Nephrology

SAN DIEGO – Being catheter free and having a serum albumin level of at least 4 g/dL were among the quality indicators associated with the ability of dialysis patients to return to work, judging from the results of a large study.

"There has been limited attention to employment issues in this patient population," Nancy G. Kutner, Ph.D., said in an interview during a poster session at Kidney Week 2012. "There has been a general impression that most people aren’t going to even try to resume employment – even those who were employed immediately before starting dialysis."

Doug Brunk/IMNG Medical Media

Dr. Kutner, professor of rehabilitation medicine at Emory University, Atlanta, and her associates enrolled 509 patients who were on hemodialysis treatment for 3 months or longer during 2009-2011 for a U.S. Renal Data System study conducted in seven outpatient clinics in San Francisco and seven in Atlanta. The patients were between the ages of 18 and 64 years, and they responded to the question: "Are you now able to work for pay (full-time or part-time)?"

Using a logistic regression model adjusted for age, gender, race, educational level, diabetes, congestive heart failure, presence of symptoms of depression, length of time on dialysis, and facility clustering, the researchers investigated whether incremental achievement of certain hemodialysis quality indicator (HD QI) goals were correlated with patient-reported ability to work. The HD QI goals were standardized Kt/V of 1.2 or greater; being catheter free; and having a hemoglobin level of 10-12 g/dL, a serum albumin level of 4 g/dL or greater, and a serum phosphorus level of 3.5 mg/dL to 5.5 mg/dL.

The mean age of the patients was 50 years, and 61% were male. Of the 509 patients, 36% said that they were able to work and 13% were actually employed. The mean number of HD QI goals met was 3.31, and the patients’ likelihood of reporting being able to work increased with an increasing number of QI goals met (odds ratio 1.28; P = .02). "Achieving a quality indicator goal is likely a joint process between the provider and the patient," said Dr. Kutner, who directs the USRDS Rehabilitation/QoL Special Studies Center at Emory.

"The end result seems to be that as more of these goals are met, it furthers the potential for work and rehabilitation. This is very encouraging," she said at the meeting, which was sponsored by the American Society of Nephrology.

Compared with their counterparts who reported being unable to work, a higher proportion of those who reported being able to work met the QI goals of Kt/V of 1.2 or greater (92% vs. 90%, respectively), being catheter free (84% vs. 74%), having a hemoglobin level of 10-12 g/dL (62% vs. 60%), and having a serum albumin of 4.0 g/dL or greater (59% vs. 49%). The proportion of those reporting a serum phosphorus level of 3.5-5.5 mg/dL was similar between the two groups (48% vs. 50%).

Dr. Kutner said that she had no relevant financial conflicts to disclose.

SAN DIEGO – Being catheter free and having a serum albumin level of at least 4 g/dL were among the quality indicators associated with the ability of dialysis patients to return to work, judging from the results of a large study.

"There has been limited attention to employment issues in this patient population," Nancy G. Kutner, Ph.D., said in an interview during a poster session at Kidney Week 2012. "There has been a general impression that most people aren’t going to even try to resume employment – even those who were employed immediately before starting dialysis."

Doug Brunk/IMNG Medical Media

Dr. Kutner, professor of rehabilitation medicine at Emory University, Atlanta, and her associates enrolled 509 patients who were on hemodialysis treatment for 3 months or longer during 2009-2011 for a U.S. Renal Data System study conducted in seven outpatient clinics in San Francisco and seven in Atlanta. The patients were between the ages of 18 and 64 years, and they responded to the question: "Are you now able to work for pay (full-time or part-time)?"

Using a logistic regression model adjusted for age, gender, race, educational level, diabetes, congestive heart failure, presence of symptoms of depression, length of time on dialysis, and facility clustering, the researchers investigated whether incremental achievement of certain hemodialysis quality indicator (HD QI) goals were correlated with patient-reported ability to work. The HD QI goals were standardized Kt/V of 1.2 or greater; being catheter free; and having a hemoglobin level of 10-12 g/dL, a serum albumin level of 4 g/dL or greater, and a serum phosphorus level of 3.5 mg/dL to 5.5 mg/dL.

The mean age of the patients was 50 years, and 61% were male. Of the 509 patients, 36% said that they were able to work and 13% were actually employed. The mean number of HD QI goals met was 3.31, and the patients’ likelihood of reporting being able to work increased with an increasing number of QI goals met (odds ratio 1.28; P = .02). "Achieving a quality indicator goal is likely a joint process between the provider and the patient," said Dr. Kutner, who directs the USRDS Rehabilitation/QoL Special Studies Center at Emory.

"The end result seems to be that as more of these goals are met, it furthers the potential for work and rehabilitation. This is very encouraging," she said at the meeting, which was sponsored by the American Society of Nephrology.

Compared with their counterparts who reported being unable to work, a higher proportion of those who reported being able to work met the QI goals of Kt/V of 1.2 or greater (92% vs. 90%, respectively), being catheter free (84% vs. 74%), having a hemoglobin level of 10-12 g/dL (62% vs. 60%), and having a serum albumin of 4.0 g/dL or greater (59% vs. 49%). The proportion of those reporting a serum phosphorus level of 3.5-5.5 mg/dL was similar between the two groups (48% vs. 50%).

Dr. Kutner said that she had no relevant financial conflicts to disclose.

SAN DIEGO – Being catheter free and having a serum albumin level of at least 4 g/dL were among the quality indicators associated with the ability of dialysis patients to return to work, judging from the results of a large study.

"There has been limited attention to employment issues in this patient population," Nancy G. Kutner, Ph.D., said in an interview during a poster session at Kidney Week 2012. "There has been a general impression that most people aren’t going to even try to resume employment – even those who were employed immediately before starting dialysis."

Doug Brunk/IMNG Medical Media

Dr. Kutner, professor of rehabilitation medicine at Emory University, Atlanta, and her associates enrolled 509 patients who were on hemodialysis treatment for 3 months or longer during 2009-2011 for a U.S. Renal Data System study conducted in seven outpatient clinics in San Francisco and seven in Atlanta. The patients were between the ages of 18 and 64 years, and they responded to the question: "Are you now able to work for pay (full-time or part-time)?"

Using a logistic regression model adjusted for age, gender, race, educational level, diabetes, congestive heart failure, presence of symptoms of depression, length of time on dialysis, and facility clustering, the researchers investigated whether incremental achievement of certain hemodialysis quality indicator (HD QI) goals were correlated with patient-reported ability to work. The HD QI goals were standardized Kt/V of 1.2 or greater; being catheter free; and having a hemoglobin level of 10-12 g/dL, a serum albumin level of 4 g/dL or greater, and a serum phosphorus level of 3.5 mg/dL to 5.5 mg/dL.

The mean age of the patients was 50 years, and 61% were male. Of the 509 patients, 36% said that they were able to work and 13% were actually employed. The mean number of HD QI goals met was 3.31, and the patients’ likelihood of reporting being able to work increased with an increasing number of QI goals met (odds ratio 1.28; P = .02). "Achieving a quality indicator goal is likely a joint process between the provider and the patient," said Dr. Kutner, who directs the USRDS Rehabilitation/QoL Special Studies Center at Emory.

"The end result seems to be that as more of these goals are met, it furthers the potential for work and rehabilitation. This is very encouraging," she said at the meeting, which was sponsored by the American Society of Nephrology.

Compared with their counterparts who reported being unable to work, a higher proportion of those who reported being able to work met the QI goals of Kt/V of 1.2 or greater (92% vs. 90%, respectively), being catheter free (84% vs. 74%), having a hemoglobin level of 10-12 g/dL (62% vs. 60%), and having a serum albumin of 4.0 g/dL or greater (59% vs. 49%). The proportion of those reporting a serum phosphorus level of 3.5-5.5 mg/dL was similar between the two groups (48% vs. 50%).

Dr. Kutner said that she had no relevant financial conflicts to disclose.

SAN DIEGO – Levels of calcium, phosphorus, and parathyroid hormone are poorer in patients with heart failure at each stage of chronic kidney disease, results from a large study showed.

The finding "raises more questions than it answers," Dr. Claudine T. Jurkovitz said in an interview during a poster session at Kidney Week 2012. "The question is, are these patients less well managed for their metabolic bone disease than the patients without HF? If so, why? Is it because their HF is so severe, or is it because the nephrologists count on cardiologists or primary care physicians to treat the patients’ metabolic bone disease also? And do cardiologists identify metabolic bone disease in patients with HF?"

Doug Brunk/IMNG Medical Media

Dr. Jurkovitz, a physician scientist with Christiana Care Health System in Newark, Del., and her associates compared the management of CKD-associated metabolic bone disease between patients with and without HF who were treated at a local nephrology practice between 2000 and 2010. They evaluated the medical records of 11,883 patients with CKD stage 3 and above, and excluded dialysis and transplant patients. The researchers calculated average calcium, phosphorus, and intact parathyroid hormone (iPTH) by radioimmunoassay for each patient, and used multilinear regressions to determine the effects of CKD and HF on calcium, phosphorus, and iPTH after controlling for age, race, and gender.

The mean follow-up of the 11,883 patients was 4 years. Of these, nearly one-quarter (24%) had HF at baseline, while 76% had stage 3 CKD, 22% had stage 4 CKD, and 2% had stage 5 CKD. Patients with HF were slightly older, with a mean of 69 years, than were their counterparts without HF, who had a mean 66 years.

Dr. Jurkovitz and her associates found that the adjusted mean for calcium was significantly lower in patients with HF at each CKD stage. The interaction between CKD and HF was statistically significant. The adjusted means for phosphorus and iPTH were significantly higher in patients with HF at each CKD stage, while the interactions between CKD and HF were not significant.

"Physicians need to be concerned about the management of chronic kidney disease in their patients with HF, and the management of metabolic bone disease addressed on a case by case basis in a dialogue between the cardiologists, nephrologists, and primary care physicians," she concluded.

The meeting was sponsored by the American Society of Nephrology. Dr. Jurkovitz said that she had no relevant financial conflicts to disclose.

SAN DIEGO – Levels of calcium, phosphorus, and parathyroid hormone are poorer in patients with heart failure at each stage of chronic kidney disease, results from a large study showed.

The finding "raises more questions than it answers," Dr. Claudine T. Jurkovitz said in an interview during a poster session at Kidney Week 2012. "The question is, are these patients less well managed for their metabolic bone disease than the patients without HF? If so, why? Is it because their HF is so severe, or is it because the nephrologists count on cardiologists or primary care physicians to treat the patients’ metabolic bone disease also? And do cardiologists identify metabolic bone disease in patients with HF?"

Doug Brunk/IMNG Medical Media

Dr. Jurkovitz, a physician scientist with Christiana Care Health System in Newark, Del., and her associates compared the management of CKD-associated metabolic bone disease between patients with and without HF who were treated at a local nephrology practice between 2000 and 2010. They evaluated the medical records of 11,883 patients with CKD stage 3 and above, and excluded dialysis and transplant patients. The researchers calculated average calcium, phosphorus, and intact parathyroid hormone (iPTH) by radioimmunoassay for each patient, and used multilinear regressions to determine the effects of CKD and HF on calcium, phosphorus, and iPTH after controlling for age, race, and gender.

The mean follow-up of the 11,883 patients was 4 years. Of these, nearly one-quarter (24%) had HF at baseline, while 76% had stage 3 CKD, 22% had stage 4 CKD, and 2% had stage 5 CKD. Patients with HF were slightly older, with a mean of 69 years, than were their counterparts without HF, who had a mean 66 years.

Dr. Jurkovitz and her associates found that the adjusted mean for calcium was significantly lower in patients with HF at each CKD stage. The interaction between CKD and HF was statistically significant. The adjusted means for phosphorus and iPTH were significantly higher in patients with HF at each CKD stage, while the interactions between CKD and HF were not significant.

"Physicians need to be concerned about the management of chronic kidney disease in their patients with HF, and the management of metabolic bone disease addressed on a case by case basis in a dialogue between the cardiologists, nephrologists, and primary care physicians," she concluded.

The meeting was sponsored by the American Society of Nephrology. Dr. Jurkovitz said that she had no relevant financial conflicts to disclose.

SAN DIEGO – Levels of calcium, phosphorus, and parathyroid hormone are poorer in patients with heart failure at each stage of chronic kidney disease, results from a large study showed.

The finding "raises more questions than it answers," Dr. Claudine T. Jurkovitz said in an interview during a poster session at Kidney Week 2012. "The question is, are these patients less well managed for their metabolic bone disease than the patients without HF? If so, why? Is it because their HF is so severe, or is it because the nephrologists count on cardiologists or primary care physicians to treat the patients’ metabolic bone disease also? And do cardiologists identify metabolic bone disease in patients with HF?"

Doug Brunk/IMNG Medical Media

Dr. Jurkovitz, a physician scientist with Christiana Care Health System in Newark, Del., and her associates compared the management of CKD-associated metabolic bone disease between patients with and without HF who were treated at a local nephrology practice between 2000 and 2010. They evaluated the medical records of 11,883 patients with CKD stage 3 and above, and excluded dialysis and transplant patients. The researchers calculated average calcium, phosphorus, and intact parathyroid hormone (iPTH) by radioimmunoassay for each patient, and used multilinear regressions to determine the effects of CKD and HF on calcium, phosphorus, and iPTH after controlling for age, race, and gender.

The mean follow-up of the 11,883 patients was 4 years. Of these, nearly one-quarter (24%) had HF at baseline, while 76% had stage 3 CKD, 22% had stage 4 CKD, and 2% had stage 5 CKD. Patients with HF were slightly older, with a mean of 69 years, than were their counterparts without HF, who had a mean 66 years.

Dr. Jurkovitz and her associates found that the adjusted mean for calcium was significantly lower in patients with HF at each CKD stage. The interaction between CKD and HF was statistically significant. The adjusted means for phosphorus and iPTH were significantly higher in patients with HF at each CKD stage, while the interactions between CKD and HF were not significant.

"Physicians need to be concerned about the management of chronic kidney disease in their patients with HF, and the management of metabolic bone disease addressed on a case by case basis in a dialogue between the cardiologists, nephrologists, and primary care physicians," she concluded.

The meeting was sponsored by the American Society of Nephrology. Dr. Jurkovitz said that she had no relevant financial conflicts to disclose.

Medicare could save about $33 million a year on certain prostate cancer drugs if it reinstated policies that pay only the price of the least costly treatment among a group of clinically comparable drugs.

Limiting the payments for clinically comparable luteinizing hormone-releasing hormone (LHRH) agonists would bring down the cost of these prostate cancer treatments from $264.6 million to $231.3 million a year, or about 13%, according to a report from the Health and Human Services department’s Office of Inspector General (OIG). About 20% of the savings would go to patients, who would save $6.7 million in reduced coinsurance.

From 1995 until April 2010, the Centers for Medicare and Medicaid Services (CMS) imposed "least costly alternative" policies for many physician-administered drugs covered under Medicare Part B. If the patient or physician wanted to use a more expensive drug, one of them would have to pay the difference.

CMS rescinded the policies in April 2010 after a court ruled that the agency did not have the legal authority to set payments in this way.

The OIG began investigating the impact of the least costly alternative policies at the request of Rep. Ken Calvert (R-Calif.), who wanted to know if eliminating the policy had created an incentive for physicians to administer higher-priced treatments.

Based on the OIG report, that appears to have happened.

Looking at the use of triptorelin pamoate (Trelstar), goserelin acetate implant (Zoladex), and leuprolide acetate suspension (Lupron, Eligard), the OIG found that physicians favored use of the more expensive drugs while the least costly alternative policies were in place but that their use was slowly declining. At the same time, the use of the least expensive drug was slowing rising.

After the payment policies were rescinded, use of the more expensive treatments increased significantly.

In 2010, Lupron and Eligard, the most expensive drugs, were administered about twice as often as the least expensive drug, Trelstar. In the year after payment restrictions were removed, the use of Lupron and Eligard rose 31% while Trelstar use fell 74%, according to the OIG report.

Dr. Walter Stadler, professor of medicine and surgery at the University of Chicago, said that the spike in utilization of the more expensive agents is probably the result of marketing, not any clinical differences in the medications. "They are completely and totally equivalent in terms of their efficacy and how they work," he said.

Physicians may be basing their choice on which manufacturers offer them the best deal on the bulk purchase of the drugs, he said, even if that’s not the best deal for Medicare or the insurer.

The OIG report also noted another trend in the utilization of the LHRH agonists: their overall use in prostate cancer is declining. The decrease in utilization began more a year before the least costly alternative policies were rescinded and has continued, according to the OIG, making it likely that it is unrelated to the policy.

Dr. Stadler said that the overall decline is probably caused by a combination of decreasing payments to physicians for the drugs and increasing medical evidence that the LHRH agonists are not always the best treatment option.

Medicare could save about $33 million a year on certain prostate cancer drugs if it reinstated policies that pay only the price of the least costly treatment among a group of clinically comparable drugs.

Limiting the payments for clinically comparable luteinizing hormone-releasing hormone (LHRH) agonists would bring down the cost of these prostate cancer treatments from $264.6 million to $231.3 million a year, or about 13%, according to a report from the Health and Human Services department’s Office of Inspector General (OIG). About 20% of the savings would go to patients, who would save $6.7 million in reduced coinsurance.

From 1995 until April 2010, the Centers for Medicare and Medicaid Services (CMS) imposed "least costly alternative" policies for many physician-administered drugs covered under Medicare Part B. If the patient or physician wanted to use a more expensive drug, one of them would have to pay the difference.

CMS rescinded the policies in April 2010 after a court ruled that the agency did not have the legal authority to set payments in this way.

The OIG began investigating the impact of the least costly alternative policies at the request of Rep. Ken Calvert (R-Calif.), who wanted to know if eliminating the policy had created an incentive for physicians to administer higher-priced treatments.

Based on the OIG report, that appears to have happened.

Looking at the use of triptorelin pamoate (Trelstar), goserelin acetate implant (Zoladex), and leuprolide acetate suspension (Lupron, Eligard), the OIG found that physicians favored use of the more expensive drugs while the least costly alternative policies were in place but that their use was slowly declining. At the same time, the use of the least expensive drug was slowing rising.

After the payment policies were rescinded, use of the more expensive treatments increased significantly.

In 2010, Lupron and Eligard, the most expensive drugs, were administered about twice as often as the least expensive drug, Trelstar. In the year after payment restrictions were removed, the use of Lupron and Eligard rose 31% while Trelstar use fell 74%, according to the OIG report.

Dr. Walter Stadler, professor of medicine and surgery at the University of Chicago, said that the spike in utilization of the more expensive agents is probably the result of marketing, not any clinical differences in the medications. "They are completely and totally equivalent in terms of their efficacy and how they work," he said.

Physicians may be basing their choice on which manufacturers offer them the best deal on the bulk purchase of the drugs, he said, even if that’s not the best deal for Medicare or the insurer.

The OIG report also noted another trend in the utilization of the LHRH agonists: their overall use in prostate cancer is declining. The decrease in utilization began more a year before the least costly alternative policies were rescinded and has continued, according to the OIG, making it likely that it is unrelated to the policy.

Dr. Stadler said that the overall decline is probably caused by a combination of decreasing payments to physicians for the drugs and increasing medical evidence that the LHRH agonists are not always the best treatment option.

Medicare could save about $33 million a year on certain prostate cancer drugs if it reinstated policies that pay only the price of the least costly treatment among a group of clinically comparable drugs.

Limiting the payments for clinically comparable luteinizing hormone-releasing hormone (LHRH) agonists would bring down the cost of these prostate cancer treatments from $264.6 million to $231.3 million a year, or about 13%, according to a report from the Health and Human Services department’s Office of Inspector General (OIG). About 20% of the savings would go to patients, who would save $6.7 million in reduced coinsurance.

From 1995 until April 2010, the Centers for Medicare and Medicaid Services (CMS) imposed "least costly alternative" policies for many physician-administered drugs covered under Medicare Part B. If the patient or physician wanted to use a more expensive drug, one of them would have to pay the difference.

CMS rescinded the policies in April 2010 after a court ruled that the agency did not have the legal authority to set payments in this way.

The OIG began investigating the impact of the least costly alternative policies at the request of Rep. Ken Calvert (R-Calif.), who wanted to know if eliminating the policy had created an incentive for physicians to administer higher-priced treatments.

Based on the OIG report, that appears to have happened.

Looking at the use of triptorelin pamoate (Trelstar), goserelin acetate implant (Zoladex), and leuprolide acetate suspension (Lupron, Eligard), the OIG found that physicians favored use of the more expensive drugs while the least costly alternative policies were in place but that their use was slowly declining. At the same time, the use of the least expensive drug was slowing rising.

After the payment policies were rescinded, use of the more expensive treatments increased significantly.

In 2010, Lupron and Eligard, the most expensive drugs, were administered about twice as often as the least expensive drug, Trelstar. In the year after payment restrictions were removed, the use of Lupron and Eligard rose 31% while Trelstar use fell 74%, according to the OIG report.

Dr. Walter Stadler, professor of medicine and surgery at the University of Chicago, said that the spike in utilization of the more expensive agents is probably the result of marketing, not any clinical differences in the medications. "They are completely and totally equivalent in terms of their efficacy and how they work," he said.

Physicians may be basing their choice on which manufacturers offer them the best deal on the bulk purchase of the drugs, he said, even if that’s not the best deal for Medicare or the insurer.

The OIG report also noted another trend in the utilization of the LHRH agonists: their overall use in prostate cancer is declining. The decrease in utilization began more a year before the least costly alternative policies were rescinded and has continued, according to the OIG, making it likely that it is unrelated to the policy.

Dr. Stadler said that the overall decline is probably caused by a combination of decreasing payments to physicians for the drugs and increasing medical evidence that the LHRH agonists are not always the best treatment option.

SAN DIEGO – Chronic kidney disease patients with subclinical hypothyroidism who were treated with thyroid hormone had better preserved renal function than did those who did not receive the treatment, a study has shown.

In addition, thyroid hormone replacement therapy was an independent predictor of renal outcomes in this subset of patients, Dr. Shin-Wook Kang reported at Kidney Week 2012.

"Subclinical hyperthyroidism is not a rare disorder, especially in females and in the elderly, and it is frequently observed in CKD [chronic kidney disease] patients," said Dr. Kang of the department of internal medicine at Yonsei University College of Medicine, Seoul, Korea. "In contrast to overt hypothyroidism, thyroid hormone treatment is seldom necessary in patients with subclinical hypothyroidism. Even though previous studies have demonstrated that thyroid hormone improves cardiac dysfunction and reduces total and LDL cholesterol levels in patients with subclinical hypothyroidism, the impact of thyroid hormone replacement therapy on renal function has never been studied in these patients."

In an effort to investigate whether restoration of euthyroidism is beneficial in terms of preserving renal function in CKD patients with subclinical hypothyroidism, he and his associates retrospectively studied the medical records of 309 patients with stage 2-4 CKD who were diagnosed with subclinical hypothyroidism and treated at the college of medicine during 2005-2010. They assessed demographic, clinical, and biochemical data including levels of calcium/phosphorus, albumin, total cholesterol, and triglycerides and estimated glomerular filtration rate (GFR). The researchers used a linear mixed model to compare changes in estimated GFR over time between patients who received thyroid hormone replacement therapy and those who did not.

Of the 309 patients, 180 (58%) were treated with l-thyroxine at an initial dose of 25 mcg/day (treatment group) while the remaining 42% were not (nontreatment group). Among patients in the treatment group, the dose of l-thyroxine was adjusted 5-6 weeks after the start of therapy and then every 3 months based on the patient’s serum TSH levels.

At baseline, levels of serum cholesterol and triglyceride were significantly higher in the treatment vs. the nontreatment group (180.0 vs. 161.3 mg/dL and 162.7 vs. 125.6 mg/dL, respectively).

During a mean follow-up of 34.8 months, the overall rate of decline in estimated GFR was significantly greater in the nontreatment group than in the treatment group (–5.93 vs. –2.11 mL/min per year per 1.73 mm2). Dr. Kang also reported that a linear mixed model showed a significant difference in the rates of estimated GFR over time between the two groups, while Kaplan-Meier analysis also showed that renal event-free survival was significantly higher in the treatment group.

Multivariate Cox regression analysis revealed that thyroid hormone replacement therapy was an independent predictor of renal outcome (hazard ratio, 0.28; P =.01).

"Thyroid hormone therapy not only preserved renal function better but also was an independent predictor of renal outcome in CKD patients with subclinical hypothyroidism, suggesting that thyroid hormone replacement should be considered in these patients," Dr. Kang said.

Dr. Kang said he had no relevant financial conflicts to disclose.

SAN DIEGO – Chronic kidney disease patients with subclinical hypothyroidism who were treated with thyroid hormone had better preserved renal function than did those who did not receive the treatment, a study has shown.

In addition, thyroid hormone replacement therapy was an independent predictor of renal outcomes in this subset of patients, Dr. Shin-Wook Kang reported at Kidney Week 2012.

"Subclinical hyperthyroidism is not a rare disorder, especially in females and in the elderly, and it is frequently observed in CKD [chronic kidney disease] patients," said Dr. Kang of the department of internal medicine at Yonsei University College of Medicine, Seoul, Korea. "In contrast to overt hypothyroidism, thyroid hormone treatment is seldom necessary in patients with subclinical hypothyroidism. Even though previous studies have demonstrated that thyroid hormone improves cardiac dysfunction and reduces total and LDL cholesterol levels in patients with subclinical hypothyroidism, the impact of thyroid hormone replacement therapy on renal function has never been studied in these patients."

In an effort to investigate whether restoration of euthyroidism is beneficial in terms of preserving renal function in CKD patients with subclinical hypothyroidism, he and his associates retrospectively studied the medical records of 309 patients with stage 2-4 CKD who were diagnosed with subclinical hypothyroidism and treated at the college of medicine during 2005-2010. They assessed demographic, clinical, and biochemical data including levels of calcium/phosphorus, albumin, total cholesterol, and triglycerides and estimated glomerular filtration rate (GFR). The researchers used a linear mixed model to compare changes in estimated GFR over time between patients who received thyroid hormone replacement therapy and those who did not.

Of the 309 patients, 180 (58%) were treated with l-thyroxine at an initial dose of 25 mcg/day (treatment group) while the remaining 42% were not (nontreatment group). Among patients in the treatment group, the dose of l-thyroxine was adjusted 5-6 weeks after the start of therapy and then every 3 months based on the patient’s serum TSH levels.

At baseline, levels of serum cholesterol and triglyceride were significantly higher in the treatment vs. the nontreatment group (180.0 vs. 161.3 mg/dL and 162.7 vs. 125.6 mg/dL, respectively).

During a mean follow-up of 34.8 months, the overall rate of decline in estimated GFR was significantly greater in the nontreatment group than in the treatment group (–5.93 vs. –2.11 mL/min per year per 1.73 mm2). Dr. Kang also reported that a linear mixed model showed a significant difference in the rates of estimated GFR over time between the two groups, while Kaplan-Meier analysis also showed that renal event-free survival was significantly higher in the treatment group.

Multivariate Cox regression analysis revealed that thyroid hormone replacement therapy was an independent predictor of renal outcome (hazard ratio, 0.28; P =.01).

"Thyroid hormone therapy not only preserved renal function better but also was an independent predictor of renal outcome in CKD patients with subclinical hypothyroidism, suggesting that thyroid hormone replacement should be considered in these patients," Dr. Kang said.

Dr. Kang said he had no relevant financial conflicts to disclose.

SAN DIEGO – Chronic kidney disease patients with subclinical hypothyroidism who were treated with thyroid hormone had better preserved renal function than did those who did not receive the treatment, a study has shown.

In addition, thyroid hormone replacement therapy was an independent predictor of renal outcomes in this subset of patients, Dr. Shin-Wook Kang reported at Kidney Week 2012.

"Subclinical hyperthyroidism is not a rare disorder, especially in females and in the elderly, and it is frequently observed in CKD [chronic kidney disease] patients," said Dr. Kang of the department of internal medicine at Yonsei University College of Medicine, Seoul, Korea. "In contrast to overt hypothyroidism, thyroid hormone treatment is seldom necessary in patients with subclinical hypothyroidism. Even though previous studies have demonstrated that thyroid hormone improves cardiac dysfunction and reduces total and LDL cholesterol levels in patients with subclinical hypothyroidism, the impact of thyroid hormone replacement therapy on renal function has never been studied in these patients."

In an effort to investigate whether restoration of euthyroidism is beneficial in terms of preserving renal function in CKD patients with subclinical hypothyroidism, he and his associates retrospectively studied the medical records of 309 patients with stage 2-4 CKD who were diagnosed with subclinical hypothyroidism and treated at the college of medicine during 2005-2010. They assessed demographic, clinical, and biochemical data including levels of calcium/phosphorus, albumin, total cholesterol, and triglycerides and estimated glomerular filtration rate (GFR). The researchers used a linear mixed model to compare changes in estimated GFR over time between patients who received thyroid hormone replacement therapy and those who did not.

Of the 309 patients, 180 (58%) were treated with l-thyroxine at an initial dose of 25 mcg/day (treatment group) while the remaining 42% were not (nontreatment group). Among patients in the treatment group, the dose of l-thyroxine was adjusted 5-6 weeks after the start of therapy and then every 3 months based on the patient’s serum TSH levels.

At baseline, levels of serum cholesterol and triglyceride were significantly higher in the treatment vs. the nontreatment group (180.0 vs. 161.3 mg/dL and 162.7 vs. 125.6 mg/dL, respectively).

During a mean follow-up of 34.8 months, the overall rate of decline in estimated GFR was significantly greater in the nontreatment group than in the treatment group (–5.93 vs. –2.11 mL/min per year per 1.73 mm2). Dr. Kang also reported that a linear mixed model showed a significant difference in the rates of estimated GFR over time between the two groups, while Kaplan-Meier analysis also showed that renal event-free survival was significantly higher in the treatment group.

Multivariate Cox regression analysis revealed that thyroid hormone replacement therapy was an independent predictor of renal outcome (hazard ratio, 0.28; P =.01).

"Thyroid hormone therapy not only preserved renal function better but also was an independent predictor of renal outcome in CKD patients with subclinical hypothyroidism, suggesting that thyroid hormone replacement should be considered in these patients," Dr. Kang said.

Dr. Kang said he had no relevant financial conflicts to disclose.

For older men with a urinary tract infection, taking antibiotics for more than 1 week does not reduce the rate of either early or late recurrence, compared with taking the drugs for 1 week, according to a report published online Dec. 3 in Archives of Internal Medicine.

Moreover, the longer course of antibiotics appeared to raise the risk of developing a Clostridium difficile infection in this retrospective observational study of 33,336 male outpatients, said Dr. Dimitri M. Drekonja of the Minneapolis Veterans Affairs Health Care System and his associates.

The study findings indicate that randomized clinical trials are needed to directly assess the benefits and harms of shorter-duration vs. longer-duration antibiotic therapy for male UTI, "to guide optimal management for this common condition," Dr. Drekonja and his colleagues noted.

The investigators used a national Veterans Affairs database to assess the effect of treatment duration on outcomes, because no study to date has evaluated the adequacy of a 7-day course of antibiotics in men as compared to a 10- or 14-day course. "The optimal treatment duration for UTI in men is unknown," they said.

For this study, the investigators searched the database for outpatient visits associated with ICD-9 codes for acute UTI and a concurrent prescription for a UTI-related antimicrobial during a single year. They identified 33,336 index cases, as well as 1,772 early recurrences (within 30 days of an index case) and 4,041 late recurrences (more than 30 days after an index case).

The mean patient age was 68 years, and comorbidities were common. The study subjects also frequently had medical conditions that predisposed them to UTI, including diabetes (35%), prostate hypertrophy (33%), and a history of prior UTI (31%).

The most commonly used agents for index cases were ciprofloxacin (63%); trimethoprim-sulfamethoxazole (27%); nitrofurantoin (6%); amoxicillin, either alone or in combination with clavulanic acid (6%); and levofloxacin (4%). Some index cases were treated with multiple antibiotics.

In a univariate analysis, rates of early recurrence were not significantly different between patients who received shorter-duration therapy (3.9%) and patients who received longer-duration therapy (4.2%).This was true in the study population as a whole and when the data were broken down by individual antibiotics.

This lack of difference in early recurrence rates persisted in a multivariate analysis, the investigators said (Arch. Intern. Med. 2012 Dec. 3 [doi: 10.1001/2013.jamainternmend.829]).

In a univariate analysis, longer duration of antibiotic therapy not only failed to cut the rate of late recurrences, but increased them slightly. Late recurrence rates were 11% in patients who received longer-duration therapy and 8.4% in those who received shorter-duration therapy. This small difference persisted in a multivariate analysis.

However, since this was an observational study, residual confounding could account for the failure to demonstrate a clinical benefit with longer duration of antibiotic therapy. "For instance, patients at increased risk for recurrence because of some unmeasured factor (e.g., catheter use) may have been overrepresented in the group that received longer-duration treatment," Dr. Drekonja and his associates said.

That is why they called for randomized clinical trials of the issue.

The researchers also examined whether longer duration of antibiotic therapy was associated with a higher rate of C. difficile infection than short-term antibiotic therapy. There was a slight increase in C. difficile infection in a univariate analysis (0.5% with long-duration vs. 0.3% with short-duration treatment), but that difference lost statistical significance in a multivariate analysis.

"Together, our findings suggest that longer-duration treatment for male UTI in the outpatient setting is not associated with a reduction in early or late recurrence and may be associated with an increase in subsequent C. difficile infection," they said.

This study was supported by the Minneapolis Veterans Affairs Health Care System. Dr. Drekonja reported no financial conflicts of interest. One of his associates reported ties to Merck, Rochester Medical, and Syntiron.

For older men with a urinary tract infection, taking antibiotics for more than 1 week does not reduce the rate of either early or late recurrence, compared with taking the drugs for 1 week, according to a report published online Dec. 3 in Archives of Internal Medicine.

Moreover, the longer course of antibiotics appeared to raise the risk of developing a Clostridium difficile infection in this retrospective observational study of 33,336 male outpatients, said Dr. Dimitri M. Drekonja of the Minneapolis Veterans Affairs Health Care System and his associates.

The study findings indicate that randomized clinical trials are needed to directly assess the benefits and harms of shorter-duration vs. longer-duration antibiotic therapy for male UTI, "to guide optimal management for this common condition," Dr. Drekonja and his colleagues noted.

The investigators used a national Veterans Affairs database to assess the effect of treatment duration on outcomes, because no study to date has evaluated the adequacy of a 7-day course of antibiotics in men as compared to a 10- or 14-day course. "The optimal treatment duration for UTI in men is unknown," they said.

For this study, the investigators searched the database for outpatient visits associated with ICD-9 codes for acute UTI and a concurrent prescription for a UTI-related antimicrobial during a single year. They identified 33,336 index cases, as well as 1,772 early recurrences (within 30 days of an index case) and 4,041 late recurrences (more than 30 days after an index case).

The mean patient age was 68 years, and comorbidities were common. The study subjects also frequently had medical conditions that predisposed them to UTI, including diabetes (35%), prostate hypertrophy (33%), and a history of prior UTI (31%).

The most commonly used agents for index cases were ciprofloxacin (63%); trimethoprim-sulfamethoxazole (27%); nitrofurantoin (6%); amoxicillin, either alone or in combination with clavulanic acid (6%); and levofloxacin (4%). Some index cases were treated with multiple antibiotics.

In a univariate analysis, rates of early recurrence were not significantly different between patients who received shorter-duration therapy (3.9%) and patients who received longer-duration therapy (4.2%).This was true in the study population as a whole and when the data were broken down by individual antibiotics.

This lack of difference in early recurrence rates persisted in a multivariate analysis, the investigators said (Arch. Intern. Med. 2012 Dec. 3 [doi: 10.1001/2013.jamainternmend.829]).

In a univariate analysis, longer duration of antibiotic therapy not only failed to cut the rate of late recurrences, but increased them slightly. Late recurrence rates were 11% in patients who received longer-duration therapy and 8.4% in those who received shorter-duration therapy. This small difference persisted in a multivariate analysis.

However, since this was an observational study, residual confounding could account for the failure to demonstrate a clinical benefit with longer duration of antibiotic therapy. "For instance, patients at increased risk for recurrence because of some unmeasured factor (e.g., catheter use) may have been overrepresented in the group that received longer-duration treatment," Dr. Drekonja and his associates said.

That is why they called for randomized clinical trials of the issue.

The researchers also examined whether longer duration of antibiotic therapy was associated with a higher rate of C. difficile infection than short-term antibiotic therapy. There was a slight increase in C. difficile infection in a univariate analysis (0.5% with long-duration vs. 0.3% with short-duration treatment), but that difference lost statistical significance in a multivariate analysis.

"Together, our findings suggest that longer-duration treatment for male UTI in the outpatient setting is not associated with a reduction in early or late recurrence and may be associated with an increase in subsequent C. difficile infection," they said.

This study was supported by the Minneapolis Veterans Affairs Health Care System. Dr. Drekonja reported no financial conflicts of interest. One of his associates reported ties to Merck, Rochester Medical, and Syntiron.

For older men with a urinary tract infection, taking antibiotics for more than 1 week does not reduce the rate of either early or late recurrence, compared with taking the drugs for 1 week, according to a report published online Dec. 3 in Archives of Internal Medicine.

Moreover, the longer course of antibiotics appeared to raise the risk of developing a Clostridium difficile infection in this retrospective observational study of 33,336 male outpatients, said Dr. Dimitri M. Drekonja of the Minneapolis Veterans Affairs Health Care System and his associates.

The study findings indicate that randomized clinical trials are needed to directly assess the benefits and harms of shorter-duration vs. longer-duration antibiotic therapy for male UTI, "to guide optimal management for this common condition," Dr. Drekonja and his colleagues noted.

The investigators used a national Veterans Affairs database to assess the effect of treatment duration on outcomes, because no study to date has evaluated the adequacy of a 7-day course of antibiotics in men as compared to a 10- or 14-day course. "The optimal treatment duration for UTI in men is unknown," they said.

For this study, the investigators searched the database for outpatient visits associated with ICD-9 codes for acute UTI and a concurrent prescription for a UTI-related antimicrobial during a single year. They identified 33,336 index cases, as well as 1,772 early recurrences (within 30 days of an index case) and 4,041 late recurrences (more than 30 days after an index case).

The mean patient age was 68 years, and comorbidities were common. The study subjects also frequently had medical conditions that predisposed them to UTI, including diabetes (35%), prostate hypertrophy (33%), and a history of prior UTI (31%).

The most commonly used agents for index cases were ciprofloxacin (63%); trimethoprim-sulfamethoxazole (27%); nitrofurantoin (6%); amoxicillin, either alone or in combination with clavulanic acid (6%); and levofloxacin (4%). Some index cases were treated with multiple antibiotics.

In a univariate analysis, rates of early recurrence were not significantly different between patients who received shorter-duration therapy (3.9%) and patients who received longer-duration therapy (4.2%).This was true in the study population as a whole and when the data were broken down by individual antibiotics.

This lack of difference in early recurrence rates persisted in a multivariate analysis, the investigators said (Arch. Intern. Med. 2012 Dec. 3 [doi: 10.1001/2013.jamainternmend.829]).

In a univariate analysis, longer duration of antibiotic therapy not only failed to cut the rate of late recurrences, but increased them slightly. Late recurrence rates were 11% in patients who received longer-duration therapy and 8.4% in those who received shorter-duration therapy. This small difference persisted in a multivariate analysis.

However, since this was an observational study, residual confounding could account for the failure to demonstrate a clinical benefit with longer duration of antibiotic therapy. "For instance, patients at increased risk for recurrence because of some unmeasured factor (e.g., catheter use) may have been overrepresented in the group that received longer-duration treatment," Dr. Drekonja and his associates said.

That is why they called for randomized clinical trials of the issue.

The researchers also examined whether longer duration of antibiotic therapy was associated with a higher rate of C. difficile infection than short-term antibiotic therapy. There was a slight increase in C. difficile infection in a univariate analysis (0.5% with long-duration vs. 0.3% with short-duration treatment), but that difference lost statistical significance in a multivariate analysis.

"Together, our findings suggest that longer-duration treatment for male UTI in the outpatient setting is not associated with a reduction in early or late recurrence and may be associated with an increase in subsequent C. difficile infection," they said.

This study was supported by the Minneapolis Veterans Affairs Health Care System. Dr. Drekonja reported no financial conflicts of interest. One of his associates reported ties to Merck, Rochester Medical, and Syntiron.

SAN DIEGO – Since the January 2011 move to bundled Medicare payments for outpatient dialysis services, mortality and hospitalizations appear to be stable among chronic kidney disease patients – but there have been dramatic trends toward lower hemoglobin levels and less use of intravenous epoetin, along with a rise in transfusions.

The findings come from the latest review of data contained in the Dialysis Outcomes and Practice Patterns Study (DOPPS) Practice Monitor, an ongoing effort to provide up-to-date trends in clinical care for dialysis patients.

During a special session at Kidney Week 2012, Dr. Bruce M. Robinson, a nephrologist and vice president for clinical research at Arbor Research Collaborative for Health in Ann Arbor, Mich., presented findings from a stratified random sample of more than 5,000 hemodialysis patients who were treated at about 140 dialysis facilities in the United States between August 2010 and April 2012.

Over that time period, the dialysis landscape changed dramatically, Dr. Robinson said.

Not only did Medicare launch its Prospective Payment System (PPS), but the Food and Drug Administration also modified dosing recommendations for erythropoietin-stimulating agents (such as epoetin) in patients with chronic kidney disease. In addition, new anemia guidelines debuted from Kidney Disease: Improving Global Outcomes (KDIGO), a global organization managed by the National Kidney Foundation. Finally, "a lot of folks are focused on what’s going to happen with the expected introduction of oral renal medications in the bundle in January 2014," said Dr. Robinson.

Since the introduction of the PPS, there has been no clear trend in mortality or hospitalizations, based on DOPPS data corroborated by Medicare claims data. Mortality ranged between 1.5% and 2% per month, or "close to 20% per year," said Dr. Robinson. "There certainly remains substantial room for improvement."

Hospitalizations stand at around 15%, "which has been flat over the study period," he said. "This translates into about two hospitalizations per patient per year."

He went on to report four key trends related to anemia management in the DOPPS data:

• First, median hemoglobin levels declined by 0.62 g/dL over the study period. "We have about 16% of patients overall with a hemoglobin level of less than 10 g/dL, and about 4% with hemoglobin less than 9 g/dL," Dr. Robinson said.

• Second, median weekly IV epoetin doses declined by 31%. "The ceiling dose has dropped more substantially," he said. "The 90th percentile dose declined by 42%, while the 10th percentile dose declined by 21% and is now under 3,000 units per week."

• The third trend related to anemia management was observed in the rising proportion of patients who received IV iron, growing from 58% per month in August 2010 to 73% per month in April 2012.

"Clearly, there is movement toward more patients getting IV iron on a regular basis," Dr. Robinson said. "When we surveyed dialysis facility medical directors, about 75% of them told us that they’re using maintenance IV iron dosing on a weekly or biweekly basis."

• The fourth trend related to anemia management was that median serum ferritin levels have increased by 28%. In fact, 39% of hemodialysis patients have ferritin levels at or above 800 ng/mL, and 10% of patients are at or above 1,200 ng/mL.

Dr. Robinson also reported that there has been an apparent rise in the percentage of patients receiving red blood cell transfusions, presenting Medicare claims data that indicated a 0.6% increase per month between November 2010 and November 2011.

"Making some assumptions, that translates to roughly 1 in 20 to 1 in 40 patients per year, so perhaps one additional patient per dialysis shift each year," he said.

In his opinion, this unwelcome trend may be preventable. In the DOPPS data, 12% of facilities reported at least 10% of their patients had hemoglobin levels less than 9 g/dL. DOPPS survey data indicate that 15% of facilities use a lower target for hemoglobin of 9 g/dL. It’s this practice that likely raises transfusion risk.

In what Dr. Robinson characterized as a surprising finding, serum albumin levels rose during the study period, from a mean of 3.8 g/dL to a mean of 4.0 g/dL. "That’s good news," he said. "The question is, why? It may be that this is due to greater use of oral nutritional supplements; but this topic needs further investigation."

The next update of the DOPPS Practice Monitor is scheduled for December 2012.

Kidney Week 2012 was sponsored by the American Society of Nephrology. DOPPS is supported by scientific research grants from Abbott Laboratories, Amgen, Baxter Healthcare, Fresenius Medical Care, Kyowa Hakko Kirin, Sanofi Renal, and Vifor Fresenius Medical Care Renal Pharma without restrictions on publications. Dr. Robinson said that he had no other relevant financial conflicts to disclose.

SAN DIEGO – Since the January 2011 move to bundled Medicare payments for outpatient dialysis services, mortality and hospitalizations appear to be stable among chronic kidney disease patients – but there have been dramatic trends toward lower hemoglobin levels and less use of intravenous epoetin, along with a rise in transfusions.

The findings come from the latest review of data contained in the Dialysis Outcomes and Practice Patterns Study (DOPPS) Practice Monitor, an ongoing effort to provide up-to-date trends in clinical care for dialysis patients.

During a special session at Kidney Week 2012, Dr. Bruce M. Robinson, a nephrologist and vice president for clinical research at Arbor Research Collaborative for Health in Ann Arbor, Mich., presented findings from a stratified random sample of more than 5,000 hemodialysis patients who were treated at about 140 dialysis facilities in the United States between August 2010 and April 2012.

Over that time period, the dialysis landscape changed dramatically, Dr. Robinson said.

Not only did Medicare launch its Prospective Payment System (PPS), but the Food and Drug Administration also modified dosing recommendations for erythropoietin-stimulating agents (such as epoetin) in patients with chronic kidney disease. In addition, new anemia guidelines debuted from Kidney Disease: Improving Global Outcomes (KDIGO), a global organization managed by the National Kidney Foundation. Finally, "a lot of folks are focused on what’s going to happen with the expected introduction of oral renal medications in the bundle in January 2014," said Dr. Robinson.

Since the introduction of the PPS, there has been no clear trend in mortality or hospitalizations, based on DOPPS data corroborated by Medicare claims data. Mortality ranged between 1.5% and 2% per month, or "close to 20% per year," said Dr. Robinson. "There certainly remains substantial room for improvement."

Hospitalizations stand at around 15%, "which has been flat over the study period," he said. "This translates into about two hospitalizations per patient per year."

He went on to report four key trends related to anemia management in the DOPPS data:

• First, median hemoglobin levels declined by 0.62 g/dL over the study period. "We have about 16% of patients overall with a hemoglobin level of less than 10 g/dL, and about 4% with hemoglobin less than 9 g/dL," Dr. Robinson said.

• Second, median weekly IV epoetin doses declined by 31%. "The ceiling dose has dropped more substantially," he said. "The 90th percentile dose declined by 42%, while the 10th percentile dose declined by 21% and is now under 3,000 units per week."

• The third trend related to anemia management was observed in the rising proportion of patients who received IV iron, growing from 58% per month in August 2010 to 73% per month in April 2012.

"Clearly, there is movement toward more patients getting IV iron on a regular basis," Dr. Robinson said. "When we surveyed dialysis facility medical directors, about 75% of them told us that they’re using maintenance IV iron dosing on a weekly or biweekly basis."

• The fourth trend related to anemia management was that median serum ferritin levels have increased by 28%. In fact, 39% of hemodialysis patients have ferritin levels at or above 800 ng/mL, and 10% of patients are at or above 1,200 ng/mL.

Dr. Robinson also reported that there has been an apparent rise in the percentage of patients receiving red blood cell transfusions, presenting Medicare claims data that indicated a 0.6% increase per month between November 2010 and November 2011.

"Making some assumptions, that translates to roughly 1 in 20 to 1 in 40 patients per year, so perhaps one additional patient per dialysis shift each year," he said.

In his opinion, this unwelcome trend may be preventable. In the DOPPS data, 12% of facilities reported at least 10% of their patients had hemoglobin levels less than 9 g/dL. DOPPS survey data indicate that 15% of facilities use a lower target for hemoglobin of 9 g/dL. It’s this practice that likely raises transfusion risk.

In what Dr. Robinson characterized as a surprising finding, serum albumin levels rose during the study period, from a mean of 3.8 g/dL to a mean of 4.0 g/dL. "That’s good news," he said. "The question is, why? It may be that this is due to greater use of oral nutritional supplements; but this topic needs further investigation."

The next update of the DOPPS Practice Monitor is scheduled for December 2012.

Kidney Week 2012 was sponsored by the American Society of Nephrology. DOPPS is supported by scientific research grants from Abbott Laboratories, Amgen, Baxter Healthcare, Fresenius Medical Care, Kyowa Hakko Kirin, Sanofi Renal, and Vifor Fresenius Medical Care Renal Pharma without restrictions on publications. Dr. Robinson said that he had no other relevant financial conflicts to disclose.

SAN DIEGO – Since the January 2011 move to bundled Medicare payments for outpatient dialysis services, mortality and hospitalizations appear to be stable among chronic kidney disease patients – but there have been dramatic trends toward lower hemoglobin levels and less use of intravenous epoetin, along with a rise in transfusions.

The findings come from the latest review of data contained in the Dialysis Outcomes and Practice Patterns Study (DOPPS) Practice Monitor, an ongoing effort to provide up-to-date trends in clinical care for dialysis patients.

During a special session at Kidney Week 2012, Dr. Bruce M. Robinson, a nephrologist and vice president for clinical research at Arbor Research Collaborative for Health in Ann Arbor, Mich., presented findings from a stratified random sample of more than 5,000 hemodialysis patients who were treated at about 140 dialysis facilities in the United States between August 2010 and April 2012.

Over that time period, the dialysis landscape changed dramatically, Dr. Robinson said.

Not only did Medicare launch its Prospective Payment System (PPS), but the Food and Drug Administration also modified dosing recommendations for erythropoietin-stimulating agents (such as epoetin) in patients with chronic kidney disease. In addition, new anemia guidelines debuted from Kidney Disease: Improving Global Outcomes (KDIGO), a global organization managed by the National Kidney Foundation. Finally, "a lot of folks are focused on what’s going to happen with the expected introduction of oral renal medications in the bundle in January 2014," said Dr. Robinson.

Since the introduction of the PPS, there has been no clear trend in mortality or hospitalizations, based on DOPPS data corroborated by Medicare claims data. Mortality ranged between 1.5% and 2% per month, or "close to 20% per year," said Dr. Robinson. "There certainly remains substantial room for improvement."

Hospitalizations stand at around 15%, "which has been flat over the study period," he said. "This translates into about two hospitalizations per patient per year."

He went on to report four key trends related to anemia management in the DOPPS data:

• First, median hemoglobin levels declined by 0.62 g/dL over the study period. "We have about 16% of patients overall with a hemoglobin level of less than 10 g/dL, and about 4% with hemoglobin less than 9 g/dL," Dr. Robinson said.

• Second, median weekly IV epoetin doses declined by 31%. "The ceiling dose has dropped more substantially," he said. "The 90th percentile dose declined by 42%, while the 10th percentile dose declined by 21% and is now under 3,000 units per week."

• The third trend related to anemia management was observed in the rising proportion of patients who received IV iron, growing from 58% per month in August 2010 to 73% per month in April 2012.

"Clearly, there is movement toward more patients getting IV iron on a regular basis," Dr. Robinson said. "When we surveyed dialysis facility medical directors, about 75% of them told us that they’re using maintenance IV iron dosing on a weekly or biweekly basis."

• The fourth trend related to anemia management was that median serum ferritin levels have increased by 28%. In fact, 39% of hemodialysis patients have ferritin levels at or above 800 ng/mL, and 10% of patients are at or above 1,200 ng/mL.

Dr. Robinson also reported that there has been an apparent rise in the percentage of patients receiving red blood cell transfusions, presenting Medicare claims data that indicated a 0.6% increase per month between November 2010 and November 2011.

"Making some assumptions, that translates to roughly 1 in 20 to 1 in 40 patients per year, so perhaps one additional patient per dialysis shift each year," he said.

In his opinion, this unwelcome trend may be preventable. In the DOPPS data, 12% of facilities reported at least 10% of their patients had hemoglobin levels less than 9 g/dL. DOPPS survey data indicate that 15% of facilities use a lower target for hemoglobin of 9 g/dL. It’s this practice that likely raises transfusion risk.

In what Dr. Robinson characterized as a surprising finding, serum albumin levels rose during the study period, from a mean of 3.8 g/dL to a mean of 4.0 g/dL. "That’s good news," he said. "The question is, why? It may be that this is due to greater use of oral nutritional supplements; but this topic needs further investigation."

The next update of the DOPPS Practice Monitor is scheduled for December 2012.

Kidney Week 2012 was sponsored by the American Society of Nephrology. DOPPS is supported by scientific research grants from Abbott Laboratories, Amgen, Baxter Healthcare, Fresenius Medical Care, Kyowa Hakko Kirin, Sanofi Renal, and Vifor Fresenius Medical Care Renal Pharma without restrictions on publications. Dr. Robinson said that he had no other relevant financial conflicts to disclose.

LOS ANGELES – Patients with advanced chronic kidney disease who receive an implantable cardioverter defibrillator are not like other patients who receive these devices.

But results from a trio of studies reported at the meeting show how hard it is for researchers to get a clear handle on what makes chronic kidney disease patients different, whether they have different outcomes than defibrillator recipients without CKD, and what is the best approach for judiciously using implantable cardioverter defibrillators (ICDs) in patients with renal dysfunction.

Mitchel L. Zoler/IMNG Medical Media

It’s a particularly relevant question because CKD is linked with a substantially increased risk for sudden cardiac death (patients on dialysis have about a fivefold higher risk for sudden cardiac death, compared with patients with normal or mildly impaired renal function), but patients with CKD were excluded from the major trials that proved the efficacy of ICDs for preventing sudden cardiac death. The lack of data from randomized, prospective trials leaves questions about the efficacy, and perhaps as importantly, the cost efficiency of ICDs in CKD patients.

"Should patients with CKD get ICDs? I don’t know the answer, but I don’t think that, categorically, patients with CKD should be excluded from ICD treatment," commented Dr. Matthew Reynolds, a cardiac electrophysiologist and director of the Economics and Quality of Life Research Center at Harvard Medical School in Boston. But many patients with CKD, especially advanced disease, are not good ICD candidates.

"For a lot of patients with CKD, someone decides not to place an ICD. Those patients are not represented" in studies that focus on ICD recipients, said Dr. Reynolds, who cochaired the session where the three studies were presented.

"For every CKD patients who gets an ICD, an electrophysiologist has made a decision that this was a CKD patient who could benefit. It’s hard to extrapolate from that" to all CKD patients, agreed Dr. Paul Varosy, director of electrophysiology at the Denver Veterans Administration Medical Center. "Patients with CKD who get ICDs are fundamentally different patients."

The aim of one of the studies reported was to assess ICD efficacy in CKD patients by comparing survival between patients with ICDs divided into stage III CKD (an estimated glomerular filtration rate [GFR] of 30-59 mL/min per 1.73 m²), stage IV or V (a GFR of less than mL/min per 1.73 m²), or no CKD. The study examined 3-year follow-up data from 556 patients who received an ICD or similar device during 2006-2010 at the Minneapolis Veterans Administration Medical Center at the University of Minnesota. The series included 301 patients with no CKD, 230 with stage III CKD, and 25 patients with more severe CKD.

The analysis showed a similar incidence of appropriate and inappropriate shocks from the ICDs in all three groups, and roughly similar efficacy of the ICDs for preventing sudden cardiac death, Dr. Selcuk Adabag said at the Annual Scientific Sessions of the American Heart Association. But mortality rates rose substantially higher as renal function worsened, rising from 17% in patients without CKD to 30% in those with stage III disease, and to 56% in those with stage IV or V disease, reported Dr. Adabag, a cardiac electrophysiologist at the University of Minnesota in Minneapolis.

The mortality differences were hardly surprising, and they likely have little direct relationship to the ICDs. "In patients with CKD, the worse the disease, the worse their prognosis. CKD is a complex disease with a whole range of [mortality] risk factors; preventable sudden cardiac death is just one" of the risks these patients face, Dr. Varosy said in an interview.

Selection bias makes the ICD observations questionable, Dr. Reynolds said. "I’m very concerned about concluding that ICDs have similar effectiveness in patients with stage IV or V CKD, compared with no CKD. The study had only 25 patients with stage IV or V disease. I have to think that there was some belief that these were good candidates and that there were a lot of other patients with severe CKD where a physician decided not to implant an ICD. Those patients are not represented in the data," Dr. Reynolds said.

Another study ran a pair of meta-analyses to explore the interactions of ICDs and CKD. In both analyses, CKD was defined as patients on dialysis, those with a creatinine clearance of less than 60 mL/kg per 1.73 m², or patients with a serum creatinine of at least 1.5 mg/dL.

The first analysis looked at the impact of ICDs on all-cause death among CKD patients at high risk for sudden cardiac death. The literature search found five reports that addressed this issue, in a total of 17,460 patients, which showed that ICD placement linked with a statistically significant 35% cut in total mortality, compared with similar, propensity-score matched patients who did not get ICDs, Dr. Nader Makki said at the meeting.

The second analysis involved 15 reports with 5,333 patients, and used multivariate adjustment to find that patients who had received an ICD and also had CKD had a statistically significant, 2.9-fold higher mortality rate than did ICD recipients without CKD, highlighting the high risk for nonarrhythmic death that CKD patients face, said Dr. Makki, a researcher at the University of Iowa in Iowa City. "Despite a paucity of randomized trials in the CKD population, these data support use of ICDs for the prevention of sudden cardiac death in patients at risk," he said. "We believe that ICDs are underused in this population," patients with CKD.

But these analyses are compromised by the data they used, said Dr. Reynolds. The data were "heavily weighted with a couple of large studies that used claims data. My concern is the potential for confounding by indication. Patients who get ICDs are somehow not as sick as those who don’t."

The third study looked at the impact of CKD on the aftermath of ICD replacement among the 1,744 patients enrolled in the REPLACE (Implantable Cardiac Pulse Generator Replacement Registry) trial, which tracked the incidence of complications following replacement of ICD generators and leads. Among the enrolled patients, researchers had renal-function data for 1,662 patients. About 80% had either mild or moderate renal dysfunction, while 6% had an estimated GFR less than 30 mL/min per 1.73 m², and the remained had normal renal function.

The incidence of complications was 15% overall, and the analysis showed roughly this rate across all strata of CKD severity. Even among patients with severe CKD, the complication rate was about 20%, and not significantly different from patients with even normal renal function, Dr. Suneet Mittal reported at the meeting. The split between major and minor complications also varied little by renal function, and the incidence of infections was 1%-2% across all five levels of renal function examined.

But CKD severity played a big role in 6-month mortality. A multivariate analysis showed that CKD stage played a significant role in survival; for each stage of worsened renal function the risk of death rose by 50%. (Other significant predictors were recent heart-failure hospitalization, severe heart failure, treatment with an antiarrhythmic drug, and history of cerebrovascular disease.) In actual numbers, the 6-month mortality rate was 2% among patients with either none or mild renal dysfunction that jumped to a 9% rate in patients with an estimated GFR of 15-29 mL/min per 1.73 m², and to 16% in those on dialysis, said Dr. Mittal, a cardiac electrophysiologist at Columbia University in New York. The analyses also showed that the increased mortality risk linked to severe CKD became apparent by a month after ICD replacement, and it was not driven by procedure-related complications.

"Why do these patients [with severe CKD] do so much worse? We thought that if we looked at all their complications we’d pick up the reason, but clearly there are things that we have not yet recognized," Dr. Mittal said. "There are a lot of things that we didn’t capture in the study."

Although the analysis shed little light on what was behind the high mortality risk in severe CKD patients, it effectively highlighted how risky ICD replacements are in any patient.

"The incidence of complications, 15%-23%, was striking. It’s substantially greater than what’s been seen in any registry-based data or administrative-based data," said Dr. Varosy. He cited the unique ability of this registry to capture all the minor complications following ICD replacement.

"These are frightening numbers [because] we tell patients that there is a very small risk" from ICD replacement procedures, commented Dr. Kalyanam Shivkumar, professor and director of the University of California Los Angeles Cardiac Arrhythmia Center.

Dr. Reynolds said that he has been a consultant to Medtronic and Biosense Webster and has received research grants from Edwards Lifesciences. Dr. Varosy had no disclosures. Dr. Adabag said that he had received research grants from Medtronic and Boston Scientific. Dr. Makki had no disclosures. The REPLACE registry was sponsored by Biotronik and Dr. Mittal said that has been a consultant to Biotronik. Dr. Shivkumar had no disclosures.

LOS ANGELES – Patients with advanced chronic kidney disease who receive an implantable cardioverter defibrillator are not like other patients who receive these devices.

But results from a trio of studies reported at the meeting show how hard it is for researchers to get a clear handle on what makes chronic kidney disease patients different, whether they have different outcomes than defibrillator recipients without CKD, and what is the best approach for judiciously using implantable cardioverter defibrillators (ICDs) in patients with renal dysfunction.

Mitchel L. Zoler/IMNG Medical Media

It’s a particularly relevant question because CKD is linked with a substantially increased risk for sudden cardiac death (patients on dialysis have about a fivefold higher risk for sudden cardiac death, compared with patients with normal or mildly impaired renal function), but patients with CKD were excluded from the major trials that proved the efficacy of ICDs for preventing sudden cardiac death. The lack of data from randomized, prospective trials leaves questions about the efficacy, and perhaps as importantly, the cost efficiency of ICDs in CKD patients.

"Should patients with CKD get ICDs? I don’t know the answer, but I don’t think that, categorically, patients with CKD should be excluded from ICD treatment," commented Dr. Matthew Reynolds, a cardiac electrophysiologist and director of the Economics and Quality of Life Research Center at Harvard Medical School in Boston. But many patients with CKD, especially advanced disease, are not good ICD candidates.

"For a lot of patients with CKD, someone decides not to place an ICD. Those patients are not represented" in studies that focus on ICD recipients, said Dr. Reynolds, who cochaired the session where the three studies were presented.

"For every CKD patients who gets an ICD, an electrophysiologist has made a decision that this was a CKD patient who could benefit. It’s hard to extrapolate from that" to all CKD patients, agreed Dr. Paul Varosy, director of electrophysiology at the Denver Veterans Administration Medical Center. "Patients with CKD who get ICDs are fundamentally different patients."

The aim of one of the studies reported was to assess ICD efficacy in CKD patients by comparing survival between patients with ICDs divided into stage III CKD (an estimated glomerular filtration rate [GFR] of 30-59 mL/min per 1.73 m²), stage IV or V (a GFR of less than mL/min per 1.73 m²), or no CKD. The study examined 3-year follow-up data from 556 patients who received an ICD or similar device during 2006-2010 at the Minneapolis Veterans Administration Medical Center at the University of Minnesota. The series included 301 patients with no CKD, 230 with stage III CKD, and 25 patients with more severe CKD.

The analysis showed a similar incidence of appropriate and inappropriate shocks from the ICDs in all three groups, and roughly similar efficacy of the ICDs for preventing sudden cardiac death, Dr. Selcuk Adabag said at the Annual Scientific Sessions of the American Heart Association. But mortality rates rose substantially higher as renal function worsened, rising from 17% in patients without CKD to 30% in those with stage III disease, and to 56% in those with stage IV or V disease, reported Dr. Adabag, a cardiac electrophysiologist at the University of Minnesota in Minneapolis.

The mortality differences were hardly surprising, and they likely have little direct relationship to the ICDs. "In patients with CKD, the worse the disease, the worse their prognosis. CKD is a complex disease with a whole range of [mortality] risk factors; preventable sudden cardiac death is just one" of the risks these patients face, Dr. Varosy said in an interview.

Selection bias makes the ICD observations questionable, Dr. Reynolds said. "I’m very concerned about concluding that ICDs have similar effectiveness in patients with stage IV or V CKD, compared with no CKD. The study had only 25 patients with stage IV or V disease. I have to think that there was some belief that these were good candidates and that there were a lot of other patients with severe CKD where a physician decided not to implant an ICD. Those patients are not represented in the data," Dr. Reynolds said.

Another study ran a pair of meta-analyses to explore the interactions of ICDs and CKD. In both analyses, CKD was defined as patients on dialysis, those with a creatinine clearance of less than 60 mL/kg per 1.73 m², or patients with a serum creatinine of at least 1.5 mg/dL.

The first analysis looked at the impact of ICDs on all-cause death among CKD patients at high risk for sudden cardiac death. The literature search found five reports that addressed this issue, in a total of 17,460 patients, which showed that ICD placement linked with a statistically significant 35% cut in total mortality, compared with similar, propensity-score matched patients who did not get ICDs, Dr. Nader Makki said at the meeting.

The second analysis involved 15 reports with 5,333 patients, and used multivariate adjustment to find that patients who had received an ICD and also had CKD had a statistically significant, 2.9-fold higher mortality rate than did ICD recipients without CKD, highlighting the high risk for nonarrhythmic death that CKD patients face, said Dr. Makki, a researcher at the University of Iowa in Iowa City. "Despite a paucity of randomized trials in the CKD population, these data support use of ICDs for the prevention of sudden cardiac death in patients at risk," he said. "We believe that ICDs are underused in this population," patients with CKD.

But these analyses are compromised by the data they used, said Dr. Reynolds. The data were "heavily weighted with a couple of large studies that used claims data. My concern is the potential for confounding by indication. Patients who get ICDs are somehow not as sick as those who don’t."

The third study looked at the impact of CKD on the aftermath of ICD replacement among the 1,744 patients enrolled in the REPLACE (Implantable Cardiac Pulse Generator Replacement Registry) trial, which tracked the incidence of complications following replacement of ICD generators and leads. Among the enrolled patients, researchers had renal-function data for 1,662 patients. About 80% had either mild or moderate renal dysfunction, while 6% had an estimated GFR less than 30 mL/min per 1.73 m², and the remained had normal renal function.

The incidence of complications was 15% overall, and the analysis showed roughly this rate across all strata of CKD severity. Even among patients with severe CKD, the complication rate was about 20%, and not significantly different from patients with even normal renal function, Dr. Suneet Mittal reported at the meeting. The split between major and minor complications also varied little by renal function, and the incidence of infections was 1%-2% across all five levels of renal function examined.

But CKD severity played a big role in 6-month mortality. A multivariate analysis showed that CKD stage played a significant role in survival; for each stage of worsened renal function the risk of death rose by 50%. (Other significant predictors were recent heart-failure hospitalization, severe heart failure, treatment with an antiarrhythmic drug, and history of cerebrovascular disease.) In actual numbers, the 6-month mortality rate was 2% among patients with either none or mild renal dysfunction that jumped to a 9% rate in patients with an estimated GFR of 15-29 mL/min per 1.73 m², and to 16% in those on dialysis, said Dr. Mittal, a cardiac electrophysiologist at Columbia University in New York. The analyses also showed that the increased mortality risk linked to severe CKD became apparent by a month after ICD replacement, and it was not driven by procedure-related complications.

"Why do these patients [with severe CKD] do so much worse? We thought that if we looked at all their complications we’d pick up the reason, but clearly there are things that we have not yet recognized," Dr. Mittal said. "There are a lot of things that we didn’t capture in the study."

Although the analysis shed little light on what was behind the high mortality risk in severe CKD patients, it effectively highlighted how risky ICD replacements are in any patient.

"The incidence of complications, 15%-23%, was striking. It’s substantially greater than what’s been seen in any registry-based data or administrative-based data," said Dr. Varosy. He cited the unique ability of this registry to capture all the minor complications following ICD replacement.

"These are frightening numbers [because] we tell patients that there is a very small risk" from ICD replacement procedures, commented Dr. Kalyanam Shivkumar, professor and director of the University of California Los Angeles Cardiac Arrhythmia Center.

Dr. Reynolds said that he has been a consultant to Medtronic and Biosense Webster and has received research grants from Edwards Lifesciences. Dr. Varosy had no disclosures. Dr. Adabag said that he had received research grants from Medtronic and Boston Scientific. Dr. Makki had no disclosures. The REPLACE registry was sponsored by Biotronik and Dr. Mittal said that has been a consultant to Biotronik. Dr. Shivkumar had no disclosures.

LOS ANGELES – Patients with advanced chronic kidney disease who receive an implantable cardioverter defibrillator are not like other patients who receive these devices.

But results from a trio of studies reported at the meeting show how hard it is for researchers to get a clear handle on what makes chronic kidney disease patients different, whether they have different outcomes than defibrillator recipients without CKD, and what is the best approach for judiciously using implantable cardioverter defibrillators (ICDs) in patients with renal dysfunction.

Mitchel L. Zoler/IMNG Medical Media

It’s a particularly relevant question because CKD is linked with a substantially increased risk for sudden cardiac death (patients on dialysis have about a fivefold higher risk for sudden cardiac death, compared with patients with normal or mildly impaired renal function), but patients with CKD were excluded from the major trials that proved the efficacy of ICDs for preventing sudden cardiac death. The lack of data from randomized, prospective trials leaves questions about the efficacy, and perhaps as importantly, the cost efficiency of ICDs in CKD patients.

"Should patients with CKD get ICDs? I don’t know the answer, but I don’t think that, categorically, patients with CKD should be excluded from ICD treatment," commented Dr. Matthew Reynolds, a cardiac electrophysiologist and director of the Economics and Quality of Life Research Center at Harvard Medical School in Boston. But many patients with CKD, especially advanced disease, are not good ICD candidates.

"For a lot of patients with CKD, someone decides not to place an ICD. Those patients are not represented" in studies that focus on ICD recipients, said Dr. Reynolds, who cochaired the session where the three studies were presented.

"For every CKD patients who gets an ICD, an electrophysiologist has made a decision that this was a CKD patient who could benefit. It’s hard to extrapolate from that" to all CKD patients, agreed Dr. Paul Varosy, director of electrophysiology at the Denver Veterans Administration Medical Center. "Patients with CKD who get ICDs are fundamentally different patients."

The aim of one of the studies reported was to assess ICD efficacy in CKD patients by comparing survival between patients with ICDs divided into stage III CKD (an estimated glomerular filtration rate [GFR] of 30-59 mL/min per 1.73 m²), stage IV or V (a GFR of less than mL/min per 1.73 m²), or no CKD. The study examined 3-year follow-up data from 556 patients who received an ICD or similar device during 2006-2010 at the Minneapolis Veterans Administration Medical Center at the University of Minnesota. The series included 301 patients with no CKD, 230 with stage III CKD, and 25 patients with more severe CKD.

The analysis showed a similar incidence of appropriate and inappropriate shocks from the ICDs in all three groups, and roughly similar efficacy of the ICDs for preventing sudden cardiac death, Dr. Selcuk Adabag said at the Annual Scientific Sessions of the American Heart Association. But mortality rates rose substantially higher as renal function worsened, rising from 17% in patients without CKD to 30% in those with stage III disease, and to 56% in those with stage IV or V disease, reported Dr. Adabag, a cardiac electrophysiologist at the University of Minnesota in Minneapolis.

The mortality differences were hardly surprising, and they likely have little direct relationship to the ICDs. "In patients with CKD, the worse the disease, the worse their prognosis. CKD is a complex disease with a whole range of [mortality] risk factors; preventable sudden cardiac death is just one" of the risks these patients face, Dr. Varosy said in an interview.

Selection bias makes the ICD observations questionable, Dr. Reynolds said. "I’m very concerned about concluding that ICDs have similar effectiveness in patients with stage IV or V CKD, compared with no CKD. The study had only 25 patients with stage IV or V disease. I have to think that there was some belief that these were good candidates and that there were a lot of other patients with severe CKD where a physician decided not to implant an ICD. Those patients are not represented in the data," Dr. Reynolds said.

Another study ran a pair of meta-analyses to explore the interactions of ICDs and CKD. In both analyses, CKD was defined as patients on dialysis, those with a creatinine clearance of less than 60 mL/kg per 1.73 m², or patients with a serum creatinine of at least 1.5 mg/dL.

The first analysis looked at the impact of ICDs on all-cause death among CKD patients at high risk for sudden cardiac death. The literature search found five reports that addressed this issue, in a total of 17,460 patients, which showed that ICD placement linked with a statistically significant 35% cut in total mortality, compared with similar, propensity-score matched patients who did not get ICDs, Dr. Nader Makki said at the meeting.

The second analysis involved 15 reports with 5,333 patients, and used multivariate adjustment to find that patients who had received an ICD and also had CKD had a statistically significant, 2.9-fold higher mortality rate than did ICD recipients without CKD, highlighting the high risk for nonarrhythmic death that CKD patients face, said Dr. Makki, a researcher at the University of Iowa in Iowa City. "Despite a paucity of randomized trials in the CKD population, these data support use of ICDs for the prevention of sudden cardiac death in patients at risk," he said. "We believe that ICDs are underused in this population," patients with CKD.

But these analyses are compromised by the data they used, said Dr. Reynolds. The data were "heavily weighted with a couple of large studies that used claims data. My concern is the potential for confounding by indication. Patients who get ICDs are somehow not as sick as those who don’t."

The third study looked at the impact of CKD on the aftermath of ICD replacement among the 1,744 patients enrolled in the REPLACE (Implantable Cardiac Pulse Generator Replacement Registry) trial, which tracked the incidence of complications following replacement of ICD generators and leads. Among the enrolled patients, researchers had renal-function data for 1,662 patients. About 80% had either mild or moderate renal dysfunction, while 6% had an estimated GFR less than 30 mL/min per 1.73 m², and the remained had normal renal function.

The incidence of complications was 15% overall, and the analysis showed roughly this rate across all strata of CKD severity. Even among patients with severe CKD, the complication rate was about 20%, and not significantly different from patients with even normal renal function, Dr. Suneet Mittal reported at the meeting. The split between major and minor complications also varied little by renal function, and the incidence of infections was 1%-2% across all five levels of renal function examined.

But CKD severity played a big role in 6-month mortality. A multivariate analysis showed that CKD stage played a significant role in survival; for each stage of worsened renal function the risk of death rose by 50%. (Other significant predictors were recent heart-failure hospitalization, severe heart failure, treatment with an antiarrhythmic drug, and history of cerebrovascular disease.) In actual numbers, the 6-month mortality rate was 2% among patients with either none or mild renal dysfunction that jumped to a 9% rate in patients with an estimated GFR of 15-29 mL/min per 1.73 m², and to 16% in those on dialysis, said Dr. Mittal, a cardiac electrophysiologist at Columbia University in New York. The analyses also showed that the increased mortality risk linked to severe CKD became apparent by a month after ICD replacement, and it was not driven by procedure-related complications.

"Why do these patients [with severe CKD] do so much worse? We thought that if we looked at all their complications we’d pick up the reason, but clearly there are things that we have not yet recognized," Dr. Mittal said. "There are a lot of things that we didn’t capture in the study."

Although the analysis shed little light on what was behind the high mortality risk in severe CKD patients, it effectively highlighted how risky ICD replacements are in any patient.

"The incidence of complications, 15%-23%, was striking. It’s substantially greater than what’s been seen in any registry-based data or administrative-based data," said Dr. Varosy. He cited the unique ability of this registry to capture all the minor complications following ICD replacement.

"These are frightening numbers [because] we tell patients that there is a very small risk" from ICD replacement procedures, commented Dr. Kalyanam Shivkumar, professor and director of the University of California Los Angeles Cardiac Arrhythmia Center.

Dr. Reynolds said that he has been a consultant to Medtronic and Biosense Webster and has received research grants from Edwards Lifesciences. Dr. Varosy had no disclosures. Dr. Adabag said that he had received research grants from Medtronic and Boston Scientific. Dr. Makki had no disclosures. The REPLACE registry was sponsored by Biotronik and Dr. Mittal said that has been a consultant to Biotronik. Dr. Shivkumar had no disclosures.

Q:  How much of a bump in serum creatinine (SCr) can I expect after I start a patient on an ACE inhibitor or an angiotensin II receptor blocker (ARB)? How often should I check the patient’s SCr?

ACE inhibitors and ARBs inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the glomerular microcirculation. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by these medications reduces both intraglomerular filtration pressure and proteinuria, delaying the progression of kidney disease.⁶ In response to RAAS inhibition, the GFR is slightly decreased and SCr is increased, reflecting the beneficial effects of the ACE inhibitor or the ARB on renal hemodynamics.^7,8 SCr may rise 10% to 30% from baseline within the first two weeks and generally stabilizes within two to four weeks.⁸

Patients with normal renal function initiated on an ACE inhibitor or an ARB experience a rise in SCr of about 0.2 mg/dL over a two- to three-week period, returning to baseline during week 4. Patients with abnormal renal function will have an increase in SCr of approximately 0.5 mg/dL over a four-week period.⁹ A progressive increase in SCr as great as 2.0 mg/dL may be seen in patients with bilateral renal artery stenosis, extensive atherosclerotic cardiovascular disease, or dehydration. In these instances, treatment with the ACE inhibitor or the ARB should be discontinued.⁹ 

Close monitoring is recommended in patients with chronic kidney disease Stage 3 through Stage 5 who are started on an ACE inhibitor or an ARB. SCr and K should be evaluated before and four weeks after initiating or titrating therapy.⁹ If SCr has increased by less than 0.5 mg/dL from a baseline measurement of 2.5 mg/dL or less; or if the rise in SCr is 1.0 mg/dL or less when the baseline SCr exceeds 2.5 mg/dL and K is 5.5 mEq/L or less, continue to titrate the agents, rechecking blood pressure (BP) and levels of SCr and K every four weeks until BP is at goal.⁸ Once SCr, K, and BP are stable, they should be rechecked annually.⁹

The adverse effects of ACE inhibitor/ARB use include angioedema and hyperkalemia, while only ACE inhibitors cause patients to cough. 

Afix Kehinde, PharmD, College of Pharmacy, University of Illinois at Chicago; Cheryl L. Gilmartin, PharmD, Clinical Assistant Professor, Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago; Clinical Pharmacist, Ambulatory Pharmacy Services, University of Illinois Hospital & Health Sciences System, Chicago

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q:  How much of a bump in serum creatinine (SCr) can I expect after I start a patient on an ACE inhibitor or an angiotensin II receptor blocker (ARB)? How often should I check the patient’s SCr?

ACE inhibitors and ARBs inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the glomerular microcirculation. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by these medications reduces both intraglomerular filtration pressure and proteinuria, delaying the progression of kidney disease.⁶ In response to RAAS inhibition, the GFR is slightly decreased and SCr is increased, reflecting the beneficial effects of the ACE inhibitor or the ARB on renal hemodynamics.^7,8 SCr may rise 10% to 30% from baseline within the first two weeks and generally stabilizes within two to four weeks.⁸

Patients with normal renal function initiated on an ACE inhibitor or an ARB experience a rise in SCr of about 0.2 mg/dL over a two- to three-week period, returning to baseline during week 4. Patients with abnormal renal function will have an increase in SCr of approximately 0.5 mg/dL over a four-week period.⁹ A progressive increase in SCr as great as 2.0 mg/dL may be seen in patients with bilateral renal artery stenosis, extensive atherosclerotic cardiovascular disease, or dehydration. In these instances, treatment with the ACE inhibitor or the ARB should be discontinued.⁹ 

Close monitoring is recommended in patients with chronic kidney disease Stage 3 through Stage 5 who are started on an ACE inhibitor or an ARB. SCr and K should be evaluated before and four weeks after initiating or titrating therapy.⁹ If SCr has increased by less than 0.5 mg/dL from a baseline measurement of 2.5 mg/dL or less; or if the rise in SCr is 1.0 mg/dL or less when the baseline SCr exceeds 2.5 mg/dL and K is 5.5 mEq/L or less, continue to titrate the agents, rechecking blood pressure (BP) and levels of SCr and K every four weeks until BP is at goal.⁸ Once SCr, K, and BP are stable, they should be rechecked annually.⁹

The adverse effects of ACE inhibitor/ARB use include angioedema and hyperkalemia, while only ACE inhibitors cause patients to cough. 

Afix Kehinde, PharmD, College of Pharmacy, University of Illinois at Chicago; Cheryl L. Gilmartin, PharmD, Clinical Assistant Professor, Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago; Clinical Pharmacist, Ambulatory Pharmacy Services, University of Illinois Hospital & Health Sciences System, Chicago

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q:  How much of a bump in serum creatinine (SCr) can I expect after I start a patient on an ACE inhibitor or an angiotensin II receptor blocker (ARB)? How often should I check the patient’s SCr?

ACE inhibitors and ARBs inhibit the angiotensin-induced vasoconstriction of the efferent arterioles of the glomerular microcirculation. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by these medications reduces both intraglomerular filtration pressure and proteinuria, delaying the progression of kidney disease.⁶ In response to RAAS inhibition, the GFR is slightly decreased and SCr is increased, reflecting the beneficial effects of the ACE inhibitor or the ARB on renal hemodynamics.^7,8 SCr may rise 10% to 30% from baseline within the first two weeks and generally stabilizes within two to four weeks.⁸

Patients with normal renal function initiated on an ACE inhibitor or an ARB experience a rise in SCr of about 0.2 mg/dL over a two- to three-week period, returning to baseline during week 4. Patients with abnormal renal function will have an increase in SCr of approximately 0.5 mg/dL over a four-week period.⁹ A progressive increase in SCr as great as 2.0 mg/dL may be seen in patients with bilateral renal artery stenosis, extensive atherosclerotic cardiovascular disease, or dehydration. In these instances, treatment with the ACE inhibitor or the ARB should be discontinued.⁹ 

Close monitoring is recommended in patients with chronic kidney disease Stage 3 through Stage 5 who are started on an ACE inhibitor or an ARB. SCr and K should be evaluated before and four weeks after initiating or titrating therapy.⁹ If SCr has increased by less than 0.5 mg/dL from a baseline measurement of 2.5 mg/dL or less; or if the rise in SCr is 1.0 mg/dL or less when the baseline SCr exceeds 2.5 mg/dL and K is 5.5 mEq/L or less, continue to titrate the agents, rechecking blood pressure (BP) and levels of SCr and K every four weeks until BP is at goal.⁸ Once SCr, K, and BP are stable, they should be rechecked annually.⁹

The adverse effects of ACE inhibitor/ARB use include angioedema and hyperkalemia, while only ACE inhibitors cause patients to cough. 

Afix Kehinde, PharmD, College of Pharmacy, University of Illinois at Chicago; Cheryl L. Gilmartin, PharmD, Clinical Assistant Professor, Department of Pharmacy Practice, College of Pharmacy, University of Illinois at Chicago; Clinical Pharmacist, Ambulatory Pharmacy Services, University of Illinois Hospital & Health Sciences System, Chicago

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: Is there any science behind the use of acetylcysteine/fluid prep for cardiac catheterizations, or is that just “voodoo” medicine?

Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute kidney injury. In recent years, the use of iodinated radiocontrast medium has increased significantly, due to increased use of both percutaneous coronary interventions and CT scanning. The radiocontrast medium causes vasoconstriction, which leads to a reduction in renal blood flow, with a resulting decrease in GFR. Preexisting impaired kidney function results in increased risk due to slower clearance of the contrast materials, and the resulting prolonged exposure increases the risk for further renal injury.¹⁰

A GFR below 60 mL/min/1.73m², volume depletion, and diabetes all increase the risk for CIN. Among patients who experience an acute kidney injury due to contrast medium, the risk for adverse outcomes increases, including early or late cardiovascular events, prolonged hospitalizations, and death. As no FDA-approved treatment yet exists for CIN, the best medicine is to try to prevent it.¹¹

Several interventions can reduce the patient’s risk for CIN. These include IV hydration, acetylcysteine/fluid prep, selection of the safest possible type and volume of radiocontrast medium, and avoidance of nephrotoxic medications immediately before the patient’s exposure to contrast medium.

In multiple randomized clinical trials, the efficacy of IV hydration in reducing the risk for CIN has been examined. Most notably, the REMEDIAL trial¹² demonstrated that IV hydration with sodium bicarbonate was superior to 0.9% hydration with normal saline. However, the largest trial to date did not show any benefit in using sodium bicarbonate, compared with normal saline.¹³ There is no consensus regarding the optimal hydration solution or timing, rate, or total volume of fluid administered, although the current literature does show that IV hydration in some form appears to decrease the risk for CIN.¹¹

The recently released Kidney Disease Improving Global Outcomes (K/DIGO) Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend IV volume expansion with normal saline or sodium bicarbonate solution. No particular regimen is recommended.

Acetylcysteine is an antioxidant with vasodilatory properties. A number of clinical trials and meta-analyses have been conducted to examine its efficacy. For instance, Kelly et al¹⁵ have suggested the benefit of acetylcysteine in the prevention of CIN, but several studies included in their meta-analysis were criticized for being of low quality. While the findings among these studies vary, none of the research teams reported any negative outcomes from the use of acetylcysteine. Although there is no definitive proof of its benefit, acetylcysteine is well tolerated, economical, and easily accessible; the general consensus is to use it.¹¹ The K/DIGO Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend using acetylcysteine in conjunction with isotonic solution in patients at increased risk for acute kidney injury.¹⁵

Other interventions include careful consideration of the type of radiocontrast agent to be used. Use of a low-osmolality agent such as iohexol (Omnipaque™ 350) or an iso-osmolar agent such as iodixanol (Visipaque™ 320) incurs much lower risk than do older, higher-osmolarity agents.¹⁶ In addition, although there are no scientific data to support this, withholding all potentially nephrotoxic medications (eg, ACE inhibitors, ARBs, NSAIDs, aminoglycosides, high-dose loop diuretics) prior to exposure to contrast medium is a prudent measure to reduce a patient’s risk profile.¹⁰

In summary, there are considerable conflicting data from multiple clinical studies regarding the use of acetylcysteine or IV hydration to minimize the risk for CIN. In fact, new guidelines are due to be published soon that may take a more definitive stand. Nevertheless, categorization as “voodoo” medicine seems inappropriate when an intervention appears to offer positive impact on patient care.
Kimberley Brinkman, MS, CNN, GNP-BC, Nephrology, Hypertension, and

Internal Medicine, Lawrence, MA

REFERENCES

1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: Is there any science behind the use of acetylcysteine/fluid prep for cardiac catheterizations, or is that just “voodoo” medicine?

Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute kidney injury. In recent years, the use of iodinated radiocontrast medium has increased significantly, due to increased use of both percutaneous coronary interventions and CT scanning. The radiocontrast medium causes vasoconstriction, which leads to a reduction in renal blood flow, with a resulting decrease in GFR. Preexisting impaired kidney function results in increased risk due to slower clearance of the contrast materials, and the resulting prolonged exposure increases the risk for further renal injury.¹⁰

A GFR below 60 mL/min/1.73m², volume depletion, and diabetes all increase the risk for CIN. Among patients who experience an acute kidney injury due to contrast medium, the risk for adverse outcomes increases, including early or late cardiovascular events, prolonged hospitalizations, and death. As no FDA-approved treatment yet exists for CIN, the best medicine is to try to prevent it.¹¹

Several interventions can reduce the patient’s risk for CIN. These include IV hydration, acetylcysteine/fluid prep, selection of the safest possible type and volume of radiocontrast medium, and avoidance of nephrotoxic medications immediately before the patient’s exposure to contrast medium.

In multiple randomized clinical trials, the efficacy of IV hydration in reducing the risk for CIN has been examined. Most notably, the REMEDIAL trial¹² demonstrated that IV hydration with sodium bicarbonate was superior to 0.9% hydration with normal saline. However, the largest trial to date did not show any benefit in using sodium bicarbonate, compared with normal saline.¹³ There is no consensus regarding the optimal hydration solution or timing, rate, or total volume of fluid administered, although the current literature does show that IV hydration in some form appears to decrease the risk for CIN.¹¹

The recently released Kidney Disease Improving Global Outcomes (K/DIGO) Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend IV volume expansion with normal saline or sodium bicarbonate solution. No particular regimen is recommended.

Acetylcysteine is an antioxidant with vasodilatory properties. A number of clinical trials and meta-analyses have been conducted to examine its efficacy. For instance, Kelly et al¹⁵ have suggested the benefit of acetylcysteine in the prevention of CIN, but several studies included in their meta-analysis were criticized for being of low quality. While the findings among these studies vary, none of the research teams reported any negative outcomes from the use of acetylcysteine. Although there is no definitive proof of its benefit, acetylcysteine is well tolerated, economical, and easily accessible; the general consensus is to use it.¹¹ The K/DIGO Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend using acetylcysteine in conjunction with isotonic solution in patients at increased risk for acute kidney injury.¹⁵

Other interventions include careful consideration of the type of radiocontrast agent to be used. Use of a low-osmolality agent such as iohexol (Omnipaque™ 350) or an iso-osmolar agent such as iodixanol (Visipaque™ 320) incurs much lower risk than do older, higher-osmolarity agents.¹⁶ In addition, although there are no scientific data to support this, withholding all potentially nephrotoxic medications (eg, ACE inhibitors, ARBs, NSAIDs, aminoglycosides, high-dose loop diuretics) prior to exposure to contrast medium is a prudent measure to reduce a patient’s risk profile.¹⁰

In summary, there are considerable conflicting data from multiple clinical studies regarding the use of acetylcysteine or IV hydration to minimize the risk for CIN. In fact, new guidelines are due to be published soon that may take a more definitive stand. Nevertheless, categorization as “voodoo” medicine seems inappropriate when an intervention appears to offer positive impact on patient care.
Kimberley Brinkman, MS, CNN, GNP-BC, Nephrology, Hypertension, and

Internal Medicine, Lawrence, MA

REFERENCES

1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: Is there any science behind the use of acetylcysteine/fluid prep for cardiac catheterizations, or is that just “voodoo” medicine?

Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute kidney injury. In recent years, the use of iodinated radiocontrast medium has increased significantly, due to increased use of both percutaneous coronary interventions and CT scanning. The radiocontrast medium causes vasoconstriction, which leads to a reduction in renal blood flow, with a resulting decrease in GFR. Preexisting impaired kidney function results in increased risk due to slower clearance of the contrast materials, and the resulting prolonged exposure increases the risk for further renal injury.¹⁰

A GFR below 60 mL/min/1.73m², volume depletion, and diabetes all increase the risk for CIN. Among patients who experience an acute kidney injury due to contrast medium, the risk for adverse outcomes increases, including early or late cardiovascular events, prolonged hospitalizations, and death. As no FDA-approved treatment yet exists for CIN, the best medicine is to try to prevent it.¹¹

Several interventions can reduce the patient’s risk for CIN. These include IV hydration, acetylcysteine/fluid prep, selection of the safest possible type and volume of radiocontrast medium, and avoidance of nephrotoxic medications immediately before the patient’s exposure to contrast medium.

In multiple randomized clinical trials, the efficacy of IV hydration in reducing the risk for CIN has been examined. Most notably, the REMEDIAL trial¹² demonstrated that IV hydration with sodium bicarbonate was superior to 0.9% hydration with normal saline. However, the largest trial to date did not show any benefit in using sodium bicarbonate, compared with normal saline.¹³ There is no consensus regarding the optimal hydration solution or timing, rate, or total volume of fluid administered, although the current literature does show that IV hydration in some form appears to decrease the risk for CIN.¹¹

The recently released Kidney Disease Improving Global Outcomes (K/DIGO) Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend IV volume expansion with normal saline or sodium bicarbonate solution. No particular regimen is recommended.

Acetylcysteine is an antioxidant with vasodilatory properties. A number of clinical trials and meta-analyses have been conducted to examine its efficacy. For instance, Kelly et al¹⁵ have suggested the benefit of acetylcysteine in the prevention of CIN, but several studies included in their meta-analysis were criticized for being of low quality. While the findings among these studies vary, none of the research teams reported any negative outcomes from the use of acetylcysteine. Although there is no definitive proof of its benefit, acetylcysteine is well tolerated, economical, and easily accessible; the general consensus is to use it.¹¹ The K/DIGO Clinical Practice Guidelines for Acute Kidney Injury¹⁴ recommend using acetylcysteine in conjunction with isotonic solution in patients at increased risk for acute kidney injury.¹⁵

Other interventions include careful consideration of the type of radiocontrast agent to be used. Use of a low-osmolality agent such as iohexol (Omnipaque™ 350) or an iso-osmolar agent such as iodixanol (Visipaque™ 320) incurs much lower risk than do older, higher-osmolarity agents.¹⁶ In addition, although there are no scientific data to support this, withholding all potentially nephrotoxic medications (eg, ACE inhibitors, ARBs, NSAIDs, aminoglycosides, high-dose loop diuretics) prior to exposure to contrast medium is a prudent measure to reduce a patient’s risk profile.¹⁰

In summary, there are considerable conflicting data from multiple clinical studies regarding the use of acetylcysteine or IV hydration to minimize the risk for CIN. In fact, new guidelines are due to be published soon that may take a more definitive stand. Nevertheless, categorization as “voodoo” medicine seems inappropriate when an intervention appears to offer positive impact on patient care.
Kimberley Brinkman, MS, CNN, GNP-BC, Nephrology, Hypertension, and

Internal Medicine, Lawrence, MA

REFERENCES

1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: I know that I have to tell my patients to be careful with dietary potassium when they are taking spironolactone and ACE inhibitors or angiotensin II receptor blockers (ARBs). However, what foods are bad? What is an acceptable K+ level for patients with chronic kidney disease (CKD)? 

Potassium (K) is a mineral that aids in the regulation of osmotic pressure and acid–base balance. It is essential for normal excitability of muscle tissue, in particular the cardiac muscle, and it plays a role in the conduction of nerve impulses. A safe serum potassium level for a patient with CKD is 4.0 to 5.0 mmol/L. A serum level between 5.0 and 5.5 mmol/L is considered a caution zone, requiring potassium restriction and laboratory monitoring¹ (note: values and ranges vary according to lab). Prescription and OTC medications, herbs, herbals, and dietary intake affect serum potassium. 

Medications such as ACE inhibitors and ARBs can cause hyperkalemia by blocking aldosterone production. The Kidney Disease Outcomes Quality Initiative (K/DOQI)² defines hyperkalemia resulting from ACE inhibitor/ARB use as an increase of serum potassium exceeding 5.0 mmol/L. Therapeutic options to reduce serum potassium include:

•Lowering the dose of the ACE inhibitor or ARB by 50%

•Stopping or reducing other medications that can cause hyperkalemia

•Starting or increasing the dosage of a loop diuretic; or

•Reinforcing dietary restriction.²

Alkali replacement or the use of Kayexalate® (sodium polystyrene sulfonate) may also be used to treat persistent or significant increases in serum potassium.

Diets high in potassium may lead to hyperkalemia in patients with CKD, particularly in patients with a glomerular filtration rate (GFR) below 60 mL/min/1.73 m². K/DOQI² recommends 4 g/d of potassium for patients with CKD Stage 1 or Stage 2 and 2 to 4 g/d for patients with CKD Stage 3 or Stage 4. In the latter group, daily recommendations for potassium intake should be based on the individual patient’s serum potassium level.³

Foods containing more than 200 mg of potassium per serving are considered high-potassium foods. Fruits in this designation include avocado, bananas, cantaloupe, honeydew, kiwi, orange, mango, nectarines, bananas, and prunes. High-potassium vegetables include artichokes, dried beans (including baked beans, refried beans, and black beans), broccoli, carrots, canned mushrooms, potatoes (white or sweet), pumpkin, spinach, and tomatoes. Other foods that are high in potassium include bran products, chocolate, milk, molasses, nuts, seeds, peanut butter, salt substitutes, and yogurt.¹

Leaching is a helpful way to “pull out” some of the potassium in high-potassium vegetables.^4,5 For potatoes, sweet potatoes, or carrots, cut the peeled vegetable into 1/8-inch-thick slices, rinse in warm water, and soak in water 10 times the volume of the vegetables’ volume for a minimum of two hours. Rinse under warm water again, then cook the vegetable in water five times the volume of the vegetables’.
Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: I know that I have to tell my patients to be careful with dietary potassium when they are taking spironolactone and ACE inhibitors or angiotensin II receptor blockers (ARBs). However, what foods are bad? What is an acceptable K+ level for patients with chronic kidney disease (CKD)? 

Potassium (K) is a mineral that aids in the regulation of osmotic pressure and acid–base balance. It is essential for normal excitability of muscle tissue, in particular the cardiac muscle, and it plays a role in the conduction of nerve impulses. A safe serum potassium level for a patient with CKD is 4.0 to 5.0 mmol/L. A serum level between 5.0 and 5.5 mmol/L is considered a caution zone, requiring potassium restriction and laboratory monitoring¹ (note: values and ranges vary according to lab). Prescription and OTC medications, herbs, herbals, and dietary intake affect serum potassium. 

Medications such as ACE inhibitors and ARBs can cause hyperkalemia by blocking aldosterone production. The Kidney Disease Outcomes Quality Initiative (K/DOQI)² defines hyperkalemia resulting from ACE inhibitor/ARB use as an increase of serum potassium exceeding 5.0 mmol/L. Therapeutic options to reduce serum potassium include:

•Lowering the dose of the ACE inhibitor or ARB by 50%

•Stopping or reducing other medications that can cause hyperkalemia

•Starting or increasing the dosage of a loop diuretic; or

•Reinforcing dietary restriction.²

Alkali replacement or the use of Kayexalate® (sodium polystyrene sulfonate) may also be used to treat persistent or significant increases in serum potassium.

Diets high in potassium may lead to hyperkalemia in patients with CKD, particularly in patients with a glomerular filtration rate (GFR) below 60 mL/min/1.73 m². K/DOQI² recommends 4 g/d of potassium for patients with CKD Stage 1 or Stage 2 and 2 to 4 g/d for patients with CKD Stage 3 or Stage 4. In the latter group, daily recommendations for potassium intake should be based on the individual patient’s serum potassium level.³

Foods containing more than 200 mg of potassium per serving are considered high-potassium foods. Fruits in this designation include avocado, bananas, cantaloupe, honeydew, kiwi, orange, mango, nectarines, bananas, and prunes. High-potassium vegetables include artichokes, dried beans (including baked beans, refried beans, and black beans), broccoli, carrots, canned mushrooms, potatoes (white or sweet), pumpkin, spinach, and tomatoes. Other foods that are high in potassium include bran products, chocolate, milk, molasses, nuts, seeds, peanut butter, salt substitutes, and yogurt.¹

Leaching is a helpful way to “pull out” some of the potassium in high-potassium vegetables.^4,5 For potatoes, sweet potatoes, or carrots, cut the peeled vegetable into 1/8-inch-thick slices, rinse in warm water, and soak in water 10 times the volume of the vegetables’ volume for a minimum of two hours. Rinse under warm water again, then cook the vegetable in water five times the volume of the vegetables’.
Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.

Q: I know that I have to tell my patients to be careful with dietary potassium when they are taking spironolactone and ACE inhibitors or angiotensin II receptor blockers (ARBs). However, what foods are bad? What is an acceptable K+ level for patients with chronic kidney disease (CKD)? 

Potassium (K) is a mineral that aids in the regulation of osmotic pressure and acid–base balance. It is essential for normal excitability of muscle tissue, in particular the cardiac muscle, and it plays a role in the conduction of nerve impulses. A safe serum potassium level for a patient with CKD is 4.0 to 5.0 mmol/L. A serum level between 5.0 and 5.5 mmol/L is considered a caution zone, requiring potassium restriction and laboratory monitoring¹ (note: values and ranges vary according to lab). Prescription and OTC medications, herbs, herbals, and dietary intake affect serum potassium. 

Medications such as ACE inhibitors and ARBs can cause hyperkalemia by blocking aldosterone production. The Kidney Disease Outcomes Quality Initiative (K/DOQI)² defines hyperkalemia resulting from ACE inhibitor/ARB use as an increase of serum potassium exceeding 5.0 mmol/L. Therapeutic options to reduce serum potassium include:

•Lowering the dose of the ACE inhibitor or ARB by 50%

•Stopping or reducing other medications that can cause hyperkalemia

•Starting or increasing the dosage of a loop diuretic; or

•Reinforcing dietary restriction.²

Alkali replacement or the use of Kayexalate® (sodium polystyrene sulfonate) may also be used to treat persistent or significant increases in serum potassium.

Diets high in potassium may lead to hyperkalemia in patients with CKD, particularly in patients with a glomerular filtration rate (GFR) below 60 mL/min/1.73 m². K/DOQI² recommends 4 g/d of potassium for patients with CKD Stage 1 or Stage 2 and 2 to 4 g/d for patients with CKD Stage 3 or Stage 4. In the latter group, daily recommendations for potassium intake should be based on the individual patient’s serum potassium level.³

Foods containing more than 200 mg of potassium per serving are considered high-potassium foods. Fruits in this designation include avocado, bananas, cantaloupe, honeydew, kiwi, orange, mango, nectarines, bananas, and prunes. High-potassium vegetables include artichokes, dried beans (including baked beans, refried beans, and black beans), broccoli, carrots, canned mushrooms, potatoes (white or sweet), pumpkin, spinach, and tomatoes. Other foods that are high in potassium include bran products, chocolate, milk, molasses, nuts, seeds, peanut butter, salt substitutes, and yogurt.¹

Leaching is a helpful way to “pull out” some of the potassium in high-potassium vegetables.^4,5 For potatoes, sweet potatoes, or carrots, cut the peeled vegetable into 1/8-inch-thick slices, rinse in warm water, and soak in water 10 times the volume of the vegetables’ volume for a minimum of two hours. Rinse under warm water again, then cook the vegetable in water five times the volume of the vegetables’.
Kristy Washinger, MSN, CRNP, Nephrology Associates of Central Pennsylvania, Camp Hill, PA

REFERENCES
1. Greene JH. Restricting dietary sodium and potassium intake: a dietitian’s perspective. In: Daugirdas JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins; 2011:81-96.

2. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 6: Dietary and other therapeutic lifestyle changes in adults. www.kidney .org/professionals/kdoqi/guidelines_bp/guide_6.htm. Accessed November 21, 2012.

3. National Kidney Foundation. K/DOQI Clinical Practice Guidelines on Hypertension and Antihypertensive Agents in Chronic Kidney Disease. Guideline 11: Use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in CKD. www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11 .htm. Accessed November 21, 2012.

4. Nutrition 411. Renal diet preparation in-service for kitchen staff: leaching potassium from vegetables. www.rd411.com/renalcenter/ article1.php?ID=8pro. Accessed November 21, 2012.

5. Burrowes JD, Ramer NJ. Removal of potassium from tuberous root vegetables by leaching. J Ren Nutr. 2006;16(4):304-311.

6. Bargman JM, Skorecki K. Chapter 280. Chronic kidney disease. In: Longo D, Fauci A, Kasper E, et al, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York, NY: McGraw-Hill; 2012. www.accesspharmacy

.com/content.aspx?aid=9130075. Accessed November 21, 2012.

7. Ryan MJ, Tuttle KR. Elevations in serum creatinine with RAAS blockade: why isn’t it a sign of kidney injury? Curr Opin Nephrol Hypertens. 2008;17(5):443–449.

8. Schoolwerth AC, Sica DA, Ballermann BJ, Wilcox CS. Renal considerations in angiotensin converting enzyme inhibitor therapy: a statement for healthcare professionals from the Council on the Kidney in Cardiovascular Disease and the Council for High Blood Pressure Research of the American Heart Association. Circulation. 2001;104(16):1985-1991.

9. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: Is this a cause for concern? Arch Intern Med. 2000;160(5):685-693.

10. Coca SG, Perazella MA. Use of iodinated and gadolinium-containing contrast media. In: Gaudiras JT. Handbook of Chronic Kidney Disease Management. Philadelphia, PA: Lippincott Williams & Wilkins: 2011:363-375.

11. Rudnick MR, Tumlin JA. Prevention of contrast-induced nephropathy (2012). www .uptodate.com/contents/prevention-of-

contrast-induced-nephropathy. Accessed November 21, 2012.

12. Briguori C, Airoldi F, D’Andrea D, et al. Renal Insufficiency Following Contrast Media Administration Trial (REMEDIAL): a randomized comparison of 3 preventive strategies. Circulation. 2007;115(10):1211-1217.

13. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium–induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300(9):1038-1046.

14. National Kidney Foundation. K/DIGO Clinical Practice Guideline for Acute Kidney Injury. www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO%20AKI%20Guideline

.pdf. Accessed November 21, 2012.

15. Kelly AM, Dwamena B, Cronin P, et al. Meta-analysis: effectiveness of drugs for preventing radiocontrast-induced nephropathy. Ann Intern Med. 2008;148(4):284-294.

16. Rudnick M, Feldman H. Contrast-induced nephropathy: what are the true clinical consequences? Clin J Am Soc Nephrol. 2008; 3(1):263-272.