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Kidney Failure Risk
Q: I have many diabetic patients who do not monitor their blood sugars or watch their diet. I try to encourage them to manage their diabetes better to decrease their risk for kidney disease, blindness, or amputation. But they want to know what are their chances of ending up on dialysis. What percentage of patients develop kidney failure? What can I say to encourage my patients to take better care of themselves?
Diabetes is an epidemic in the United States and worldwide. It is the leading cause of chronic kidney disease and kidney failure.1 Diabetes is the primary diagnosis for about 44% of US patients who start dialysis, and hypertension for about 28%.2
Chronic kidney disease (CKD) can be viewed as a spectrum, ranging from mild (glomerular filtration rate [GFR] ≥ 60 mL/min/1.73 m2) to severe (GFR < 15 mL/min/1.73 m2, also referred to as end-stage renal disease [ESRD]).
A diabetic patient’s likelihood of developing diabetic nephropathy (DN) varies by race and geographic location. For patients with type 2 diabetes (T2DM), the rate is 5% to 10% for white patients and 10% to 20% for African-Americans.3 Hispanic patients develop DN at 1.5 times the rate among non-Hispanic whites.1 In the Pima Indians, who live primarily in Arizona, the incidence of DN approaches 60%. For patients with type 1 diabetes, the incidence of DN is 30% to 40%.1
While not all patients progress to ESRD, they are at increased risk for renal and cardiovascular complications, compared with nondiabetic patients.1 In general, about one in three patients with diabetes will develop significant nephropathy during the five to 10 years following diagnosis. For many years, microalbuminuria has been considered a predictor of renal disease progression.4
Previously, it was thought that patients with T2DM were more likely to die of cardiovascular complications than to progress to ESRD and require renal replacement therapy (RRT). However, researchers recently showed that patients with T2DM, DN, and proteinuria were more likely to progress to ESRD than to die of other complications.5
Given the alarming increase in the incidence of diabetes and diabetic kidney disease, a tool to predict the likelihood of an individual patient’s risk for kidney failure would be extremely helpful. As there are no widely accepted predictive instruments for CKD progression, providers must make ad hoc decisions about patients. This practice can result in treatment delays for patients whose disease does progress or unnecessary treatments for patients unlikely to experience kidney failure.6
In 2011, Tangri et al7 published a predictive model for patients with stages 3 to 5 CKD. The model relies on demographic data and clinical laboratory markers of CKD severity to accurately predict risk for future kidney failure. The study is available at http://jama.ama-assn.org/content/305/15/1553.long,7 and a smartphone app can be accessed at www.qxmd.com/Kidney-Failure-Risk-Equation.
To improve patient compliance, however, I would suggest the following steps:
• Ask yourself, “Does my patient perceive there is a problem?” Assess the patient’s readiness to modify behavior.8
• Target no more than one behavior change at each visit.
• Find at least one reason to praise the patient at each visit (eg, remembering to bring his/her glucose log, keeping the scheduled appointment, initiating an exercise program, cutting down on cigarettes).
• Use diabetes educators to reinforce teaching.
• Suggest that your patient join the ADA. The more interested and informed patients become about this chronic illness, the more likely they are to become active participants in their own long-term care.
Wanda Y. Willis, MSN, FNP-C, CNN, Renal nurse practitioner
Washington Nephrology Associates, LLC
Takoma Park, Maryland
See next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Q: I have many diabetic patients who do not monitor their blood sugars or watch their diet. I try to encourage them to manage their diabetes better to decrease their risk for kidney disease, blindness, or amputation. But they want to know what are their chances of ending up on dialysis. What percentage of patients develop kidney failure? What can I say to encourage my patients to take better care of themselves?
Diabetes is an epidemic in the United States and worldwide. It is the leading cause of chronic kidney disease and kidney failure.1 Diabetes is the primary diagnosis for about 44% of US patients who start dialysis, and hypertension for about 28%.2
Chronic kidney disease (CKD) can be viewed as a spectrum, ranging from mild (glomerular filtration rate [GFR] ≥ 60 mL/min/1.73 m2) to severe (GFR < 15 mL/min/1.73 m2, also referred to as end-stage renal disease [ESRD]).
A diabetic patient’s likelihood of developing diabetic nephropathy (DN) varies by race and geographic location. For patients with type 2 diabetes (T2DM), the rate is 5% to 10% for white patients and 10% to 20% for African-Americans.3 Hispanic patients develop DN at 1.5 times the rate among non-Hispanic whites.1 In the Pima Indians, who live primarily in Arizona, the incidence of DN approaches 60%. For patients with type 1 diabetes, the incidence of DN is 30% to 40%.1
While not all patients progress to ESRD, they are at increased risk for renal and cardiovascular complications, compared with nondiabetic patients.1 In general, about one in three patients with diabetes will develop significant nephropathy during the five to 10 years following diagnosis. For many years, microalbuminuria has been considered a predictor of renal disease progression.4
Previously, it was thought that patients with T2DM were more likely to die of cardiovascular complications than to progress to ESRD and require renal replacement therapy (RRT). However, researchers recently showed that patients with T2DM, DN, and proteinuria were more likely to progress to ESRD than to die of other complications.5
Given the alarming increase in the incidence of diabetes and diabetic kidney disease, a tool to predict the likelihood of an individual patient’s risk for kidney failure would be extremely helpful. As there are no widely accepted predictive instruments for CKD progression, providers must make ad hoc decisions about patients. This practice can result in treatment delays for patients whose disease does progress or unnecessary treatments for patients unlikely to experience kidney failure.6
In 2011, Tangri et al7 published a predictive model for patients with stages 3 to 5 CKD. The model relies on demographic data and clinical laboratory markers of CKD severity to accurately predict risk for future kidney failure. The study is available at http://jama.ama-assn.org/content/305/15/1553.long,7 and a smartphone app can be accessed at www.qxmd.com/Kidney-Failure-Risk-Equation.
To improve patient compliance, however, I would suggest the following steps:
• Ask yourself, “Does my patient perceive there is a problem?” Assess the patient’s readiness to modify behavior.8
• Target no more than one behavior change at each visit.
• Find at least one reason to praise the patient at each visit (eg, remembering to bring his/her glucose log, keeping the scheduled appointment, initiating an exercise program, cutting down on cigarettes).
• Use diabetes educators to reinforce teaching.
• Suggest that your patient join the ADA. The more interested and informed patients become about this chronic illness, the more likely they are to become active participants in their own long-term care.
Wanda Y. Willis, MSN, FNP-C, CNN, Renal nurse practitioner
Washington Nephrology Associates, LLC
Takoma Park, Maryland
See next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Q: I have many diabetic patients who do not monitor their blood sugars or watch their diet. I try to encourage them to manage their diabetes better to decrease their risk for kidney disease, blindness, or amputation. But they want to know what are their chances of ending up on dialysis. What percentage of patients develop kidney failure? What can I say to encourage my patients to take better care of themselves?
Diabetes is an epidemic in the United States and worldwide. It is the leading cause of chronic kidney disease and kidney failure.1 Diabetes is the primary diagnosis for about 44% of US patients who start dialysis, and hypertension for about 28%.2
Chronic kidney disease (CKD) can be viewed as a spectrum, ranging from mild (glomerular filtration rate [GFR] ≥ 60 mL/min/1.73 m2) to severe (GFR < 15 mL/min/1.73 m2, also referred to as end-stage renal disease [ESRD]).
A diabetic patient’s likelihood of developing diabetic nephropathy (DN) varies by race and geographic location. For patients with type 2 diabetes (T2DM), the rate is 5% to 10% for white patients and 10% to 20% for African-Americans.3 Hispanic patients develop DN at 1.5 times the rate among non-Hispanic whites.1 In the Pima Indians, who live primarily in Arizona, the incidence of DN approaches 60%. For patients with type 1 diabetes, the incidence of DN is 30% to 40%.1
While not all patients progress to ESRD, they are at increased risk for renal and cardiovascular complications, compared with nondiabetic patients.1 In general, about one in three patients with diabetes will develop significant nephropathy during the five to 10 years following diagnosis. For many years, microalbuminuria has been considered a predictor of renal disease progression.4
Previously, it was thought that patients with T2DM were more likely to die of cardiovascular complications than to progress to ESRD and require renal replacement therapy (RRT). However, researchers recently showed that patients with T2DM, DN, and proteinuria were more likely to progress to ESRD than to die of other complications.5
Given the alarming increase in the incidence of diabetes and diabetic kidney disease, a tool to predict the likelihood of an individual patient’s risk for kidney failure would be extremely helpful. As there are no widely accepted predictive instruments for CKD progression, providers must make ad hoc decisions about patients. This practice can result in treatment delays for patients whose disease does progress or unnecessary treatments for patients unlikely to experience kidney failure.6
In 2011, Tangri et al7 published a predictive model for patients with stages 3 to 5 CKD. The model relies on demographic data and clinical laboratory markers of CKD severity to accurately predict risk for future kidney failure. The study is available at http://jama.ama-assn.org/content/305/15/1553.long,7 and a smartphone app can be accessed at www.qxmd.com/Kidney-Failure-Risk-Equation.
To improve patient compliance, however, I would suggest the following steps:
• Ask yourself, “Does my patient perceive there is a problem?” Assess the patient’s readiness to modify behavior.8
• Target no more than one behavior change at each visit.
• Find at least one reason to praise the patient at each visit (eg, remembering to bring his/her glucose log, keeping the scheduled appointment, initiating an exercise program, cutting down on cigarettes).
• Use diabetes educators to reinforce teaching.
• Suggest that your patient join the ADA. The more interested and informed patients become about this chronic illness, the more likely they are to become active participants in their own long-term care.
Wanda Y. Willis, MSN, FNP-C, CNN, Renal nurse practitioner
Washington Nephrology Associates, LLC
Takoma Park, Maryland
See next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Statin Use
Q: I have a dialysis patient whose cholesterol numbers were getting quite high. I gave him a prescription for a lipid-lowering medication. He brought the prescription back, saying the nephrology AP told him it would make no difference since he was a dialysis patient. Is this true?
This is an excellent question that has been researched and debated over the past 10 years. Cardiovascular disease is the leading cause of death in patients with CKD and those in the dialysis population. So intuitively, it makes sense in these patients to control cholesterol—one of the main risk factors for cardiovascular disease. However, the research that has been done to date contradicts that hypothesis in dialysis patients.9
With a 2002 observational study, Iseki et al10 became the first researchers to document that cholesterol levels are inversely related to mortality in patients undergoing dialysis. However, this study team did not adjust for inflammation or infection—which, in addition to malnutrition, reduce HDL and LDL levels (and increase mortality).10
The goal of the Deutsche Diabetes and Dialysis (4D) trial,11 funded by a pharmaceutical company and involving 1,255 subjects, was to demonstrate the benefits of atorvastatin use in diabetic patients on dialysis. Although the agent was shown to improve patients’ lipid parameters, no statistically significant effect was found on the primary endpoints: all-cause mortality and cardiovascular and cerebrovascular events. In fact, the incidence of fatal stroke was significantly higher in the atorvastatin-treated patients, compared with those taking placebo.11
In the Evaluation of the Use of Rosuvastatin in Subjects on Regular Hemodialysis (AURORA) study,12 in which 2,776 patients were enrolled, the primary endpoint was time to major cardiovascular events (including fatal and nonfatal MI and stroke). No statistically significant changes were reported in mortality or primary or secondary endpoints in either treatment arm. However, the AURORA study did demonstrate an increased risk for fatal hemorrhagic stroke in the treatment arm.12
Most recently, in the seven-year-long Study of Heart and Renal Protection (SHARP),13 researchers investigated the benefits of cholesterol-lowering therapy, enrolling 9,270 patients with CKD and 3,023 patients undergoing dialysis. In the treatment arm of the CKD group (ie, those receiving simvastatin plus ezetimibe), a 17% reduction was reported in major atherosclerotic events. In the dialysis patients randomized to receive treatment, however, no significant reduction was found in mortality rates or cardiovascular events, compared with patients taking placebo.13
Thus, no cardioprotective benefit has yet been reported for statin use in patients receiving dialysis. In fact, these agents may increase patients’ risk for stroke. They surely increase the pill burden and treatment costs for dialysis patients. As for patients with CKD, a number of studies (including the SHARP study13) have demonstrated a benefit in statin use for primary prevention of cardiovascular events.
Susan Busch, MSN, CNP, Cleveland Clinic; Family NP Program
Kent State University, Ohio
For see next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Q: I have a dialysis patient whose cholesterol numbers were getting quite high. I gave him a prescription for a lipid-lowering medication. He brought the prescription back, saying the nephrology AP told him it would make no difference since he was a dialysis patient. Is this true?
This is an excellent question that has been researched and debated over the past 10 years. Cardiovascular disease is the leading cause of death in patients with CKD and those in the dialysis population. So intuitively, it makes sense in these patients to control cholesterol—one of the main risk factors for cardiovascular disease. However, the research that has been done to date contradicts that hypothesis in dialysis patients.9
With a 2002 observational study, Iseki et al10 became the first researchers to document that cholesterol levels are inversely related to mortality in patients undergoing dialysis. However, this study team did not adjust for inflammation or infection—which, in addition to malnutrition, reduce HDL and LDL levels (and increase mortality).10
The goal of the Deutsche Diabetes and Dialysis (4D) trial,11 funded by a pharmaceutical company and involving 1,255 subjects, was to demonstrate the benefits of atorvastatin use in diabetic patients on dialysis. Although the agent was shown to improve patients’ lipid parameters, no statistically significant effect was found on the primary endpoints: all-cause mortality and cardiovascular and cerebrovascular events. In fact, the incidence of fatal stroke was significantly higher in the atorvastatin-treated patients, compared with those taking placebo.11
In the Evaluation of the Use of Rosuvastatin in Subjects on Regular Hemodialysis (AURORA) study,12 in which 2,776 patients were enrolled, the primary endpoint was time to major cardiovascular events (including fatal and nonfatal MI and stroke). No statistically significant changes were reported in mortality or primary or secondary endpoints in either treatment arm. However, the AURORA study did demonstrate an increased risk for fatal hemorrhagic stroke in the treatment arm.12
Most recently, in the seven-year-long Study of Heart and Renal Protection (SHARP),13 researchers investigated the benefits of cholesterol-lowering therapy, enrolling 9,270 patients with CKD and 3,023 patients undergoing dialysis. In the treatment arm of the CKD group (ie, those receiving simvastatin plus ezetimibe), a 17% reduction was reported in major atherosclerotic events. In the dialysis patients randomized to receive treatment, however, no significant reduction was found in mortality rates or cardiovascular events, compared with patients taking placebo.13
Thus, no cardioprotective benefit has yet been reported for statin use in patients receiving dialysis. In fact, these agents may increase patients’ risk for stroke. They surely increase the pill burden and treatment costs for dialysis patients. As for patients with CKD, a number of studies (including the SHARP study13) have demonstrated a benefit in statin use for primary prevention of cardiovascular events.
Susan Busch, MSN, CNP, Cleveland Clinic; Family NP Program
Kent State University, Ohio
For see next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Q: I have a dialysis patient whose cholesterol numbers were getting quite high. I gave him a prescription for a lipid-lowering medication. He brought the prescription back, saying the nephrology AP told him it would make no difference since he was a dialysis patient. Is this true?
This is an excellent question that has been researched and debated over the past 10 years. Cardiovascular disease is the leading cause of death in patients with CKD and those in the dialysis population. So intuitively, it makes sense in these patients to control cholesterol—one of the main risk factors for cardiovascular disease. However, the research that has been done to date contradicts that hypothesis in dialysis patients.9
With a 2002 observational study, Iseki et al10 became the first researchers to document that cholesterol levels are inversely related to mortality in patients undergoing dialysis. However, this study team did not adjust for inflammation or infection—which, in addition to malnutrition, reduce HDL and LDL levels (and increase mortality).10
The goal of the Deutsche Diabetes and Dialysis (4D) trial,11 funded by a pharmaceutical company and involving 1,255 subjects, was to demonstrate the benefits of atorvastatin use in diabetic patients on dialysis. Although the agent was shown to improve patients’ lipid parameters, no statistically significant effect was found on the primary endpoints: all-cause mortality and cardiovascular and cerebrovascular events. In fact, the incidence of fatal stroke was significantly higher in the atorvastatin-treated patients, compared with those taking placebo.11
In the Evaluation of the Use of Rosuvastatin in Subjects on Regular Hemodialysis (AURORA) study,12 in which 2,776 patients were enrolled, the primary endpoint was time to major cardiovascular events (including fatal and nonfatal MI and stroke). No statistically significant changes were reported in mortality or primary or secondary endpoints in either treatment arm. However, the AURORA study did demonstrate an increased risk for fatal hemorrhagic stroke in the treatment arm.12
Most recently, in the seven-year-long Study of Heart and Renal Protection (SHARP),13 researchers investigated the benefits of cholesterol-lowering therapy, enrolling 9,270 patients with CKD and 3,023 patients undergoing dialysis. In the treatment arm of the CKD group (ie, those receiving simvastatin plus ezetimibe), a 17% reduction was reported in major atherosclerotic events. In the dialysis patients randomized to receive treatment, however, no significant reduction was found in mortality rates or cardiovascular events, compared with patients taking placebo.13
Thus, no cardioprotective benefit has yet been reported for statin use in patients receiving dialysis. In fact, these agents may increase patients’ risk for stroke. They surely increase the pill burden and treatment costs for dialysis patients. As for patients with CKD, a number of studies (including the SHARP study13) have demonstrated a benefit in statin use for primary prevention of cardiovascular events.
Susan Busch, MSN, CNP, Cleveland Clinic; Family NP Program
Kent State University, Ohio
For see next page for references...
REFERENCES
1. CDC. 2011 National Diabetes Fact Sheet. www.cdc.gov/diabetes/pubs/estimates11.htm. Accessed May 23, 2012.
2. US Renal Data System, National Institute of Diabetes and Kidney Disease, NIH. 2010 Annual Data Report, vol II: Atlas of End-Stage Renal Disease in the United States. www.usrds.org/2010/pdf/v2_00a_intros.pdf. Accessed May 23, 2012.
3. Cowie CC, Port FK, Wolfe RA, et al. Disparities in incidence of diabetic end-stage renal disease according to race and type of diabetes. N Engl J Med. 1989;312(16):1074-1079.
4. Vora JP, Ibrahim HAA. Clinical manifestations and natural history of diabetic nephropathy. In: Johnson R, Feehally J, eds. Comprehensive Clinical Nephrology. Philadelphia, PA: Mosby; 2003:425-438.
5. Packham DK, Alves TP, Dwyer JP, et al. Relative incidence of ESRD versus cardiovascular mortality in proteinuric type 2 diabetes and nephropathy: results from the DIAMETRIC (Diabetes Mellitus Treatment for Renal Insufficiency Consortium) database. Am J Kidney Dis. 2012;59(1):75-83.
6. Levey AS, Coresh J, Balk E, et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification and stratification. Ann Intern Med. 2003;139(2):137-147.
7. Tangri N, Stevens LA, Griffith J, et al. A predictive model for progression of chronic kidney disease to kidney failure. JAMA. 2011;305(15):1553-1559.
8. Prochaska JO, Velicer WF, Rossi JS, et al. Stages of change and decisional balance for 12 problem behaviors. Health Psychol. 1994;13(1):39-46.
9. Olyaei A, Lerma EV. Three strikes and statins out: a case against use of statins in dialysis patients for primary prevention. Dialysis Transplant. 2011;40(4):148-151.
10. Iseki K, Yamazato M, Tozawa M, Takishita S. Hypocholesterolemia is a significant predictor of death in a cohort of chronic hemodialysis patients. Kidney Int. 2002;61(5):1887-1893.
11. Wanner C, Krane V, März W, et al; German Diabetes and Dialysis Study Investigators. Atorvastatin in patients with type 2 diabetes mellitus undergoing hemodialysis. N Engl J Med. 2005;353(3):238-248.
12. Fellström BC, Jardine AG, Schmeider RE, et al. Rosuvastatin and cardiovascular events in patients undergoing hemodialysis. N Engl J Med. 2009; 360(14):1395-1407.
13. SHARP Collaborative Group. Study of Heart and Renal Protection (SHARP): randomized trial to assess the effects of lowering low-density lipoprotein cholesterol among 9,438 patients with chronic kidney disease. Am Heart J. 2010;160(5):785-794.
Try Abiding Instead of Hiding: An Approach to End-of-Life Care
Dialysis: How, When, and at What Dose?
Q: I work as a hospitalist PA in a large teaching hospital. In our ICU we had a patient diagnosed with acute kidney injury after a coronary artery bypass graft. We consulted nephrology and they decided to start dialysis. There was quite a discussion about whether to use hemodialysis every other day or continuous renal replacement therapy. What is the basis for this question? Is there science behind the answer, or is it determined by nephrologist preference?
The development of intermittent hemodialysis (IHD) revolutionized the care of patients with acute renal failure and allowed the medical establishment means to give these patients a chance to recover from their illness. However, IHD had (and continues to have) many downsides, and mortality in acute renal failure remains high. Thus, there is an ongoing search for the best renal replacement therapy; this search led to modern continuous therapies. Three main questions have arisen from this:
- Which Modality is Best?
- What is the optimal dose for dialysis?
- When should we initiate therapy?
Continue reading for the answers...
Which Modality is Best? IHD is a shorter treatment (2 to 4 hours), typically performed three times per week but as often as daily. Fluid and electrolyte clearance is rapid, making IHD very efficient but increasing the risk for complications, such as hemodynamic instability. Furthermore, the abrupt fluid and electrolyte shifts associated with IHD do not mimic native kidney function. Providing slower treatments delivered continuously over 24 hours has many benefits.
Continuous renal replacement therapy (CRRT) provides clearance of large amounts of fluid and electrolytes over 24 hours, with minimal hemodynamic disturbances. This allows for more gradual shifts in volume and electrolyte levels, reducing the potential for ischemic damage to the kidney and other organs. Also, CRRT more closely replicates normal renal function than IHD.
CRRT is now extremely safe and efficient, although it has been difficult to prove its superiority to IHD in regard to mortality. While there may be no actual benefit to CRRT, it is also likely that its benefit is observed only in certain subsets of patients with renal failure. For example, we do have compelling evidence of increased intracranial pressure during IHD; CRRT is much safer for patients at risk for this development.1 It is also possible that we need to further improve CRRT systems and delivery in order to see a benefit.
Because current data favor neither CRRT nor IHD, most experts recommend choosing a therapy based on patient characteristics. For instance, hemodynamically unstable patients commonly receive generous amounts of fluid daily (antibiotics, nutrition, etc), and thus are often better suited for CRRT because it is more likely to remove higher volumes of fluid successfully, and less likely to contribute to hemodynamic instability than IHD. Conversely, patients with acute electrolyte deviations may benefit more from the rapid electrolyte removal IHD provides.
Additionally, stable patients may be more suitable candidates for IHD because of location (CRRT requires intensive care monitoring) and other variables.2,3 Results from multiple studies have suggested that CRRT may also provide renal protection and consequently improve renal recovery. However, this evidence is not conclusive; the possibility needs further evaluation.1
Continue reading for the optimal dose for dialysis...
What is the optimal dose for dialysis? This question, too, is plagued by inconclusive research findings. Paganini was the first to raise it formally in patients with acute renal failure; his research team found improved survival with higher doses, but had excluded the sickest and healthiest patients (according to probability of survival) from the study.4 This was followed by two additional studies with results that also seemed to support higher doses.1,5
Then in 2008, in a a similar randomized controlled trial, Tolwani et al6 found no survival benefit with higher versus lower dosing; participants in this study were not excluded based on severity of illness. Also, Tolwani’s research team identified failure to achieve prescribed doses as one factor complicating dose comparison.6
Finally, two large randomized controlled trials were performed to evaluate dosage, one in the US7 and one in Australia and New Zealand.8 Neither research team was able to confirm survival benefits with higher-dose renal replacement therapy, and there were inconsistencies between doses used in the study and standard practice in the US. In fact, the low-dose group received dialysis exceeding what is current practice by more than 30%.
The current prevailing opinion is that we should reach a minimum dose: a Kt/V of 1.2, three times a week, for IHD; or a CRRT dose of 20 mL/kg/h. At this time, higher doses do not confer a clear survival benefit. It remains unknown whether certain patients may benefit from a higher dose. Further research is needed.
Continue reading to find out when to initiate therapy...
When should we initiate therapy? While some study results suggest that early initiation is better, this remains unconfirmed.1 In theory, renal replacement therapy should be initiated early because it improves metabolic control and corrects fluid overload, facilitating management of hemodynamics and ventilation, and reducing the potential for complications caused by uremia-induced physiologic dysfunction. However, it is still unknown which patients would benefit most from early initiation, and the appropriate triggers for when to initiate therapy remain unclear.
So, how do you choose a renal replacement therapy? This is often a matter of opinion, based on evaluation of risks and benefits specific to the patient and clinical expertise with the renal replacement therapies available.
Patient safety must be a primary consideration. IHD and CRRT have dramatically improved in safety and efficacy, but it must yet be proven beyond a doubt which is superior. Outcomes may depend on how the chosen therapy is used to treat specific patient needs—not which therapy is chosen. Further research is needed to identify the best and safest way to provide renal replacement therapy.
Catherine Wells, DNP, ACNP-BC, CNN-NP, Division of Nephrology, University of Mississippi, Jackson
Continue for references...
REFERENCES
1. Prowle JR, Bellomo R. Continuous renal replacement therapy: recent advances and future research. Nat Rev Nephrol. 2010;6(9):521-529.
2. Abi Antoun T, Palevsky PM. Selection of modality of renal replacement therapy. Semin Dial. 2009; 22(2):108-113.
3. Vanholder R, Van Biesen W, Lameire N. What is the renal replacement method of choice for intensive care patients? J Am Soc Nephrol. 2001;12 suppl 17:S40-S43.
4. Augustine JJ, Sandy D, Seifert TH, Paganini EP. A randomized controlled trial comparing intermittent with continuous dialysis in patients with ARF. Am J Kidney Dis. 2004;44(6):1000-1007.
5. Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet. 2000;356(9223):26-30.
6. Tolwani AJ, Campbell RC, Stofan BS, et al. Standard versus high-dose CVVHDF for ICU-related acute renal failure. J Am Soc Nephrol. 2008;19(6):1233-1238.
7. Palevsky PM, Zhang JH, O’Connor TZ, et al; VA/NIH Acute Renal Failure Trial Network. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med. 2008;359(1):7-20.
8. Bellomo R, Cass A, Cole L, et al; RENAL Replacement Therapy Study Investigators. Intensity of continuous renal-replacement therapy in critically ill patients. N Engl J Med. 2009;361(17):1627-1683.
Q: I work as a hospitalist PA in a large teaching hospital. In our ICU we had a patient diagnosed with acute kidney injury after a coronary artery bypass graft. We consulted nephrology and they decided to start dialysis. There was quite a discussion about whether to use hemodialysis every other day or continuous renal replacement therapy. What is the basis for this question? Is there science behind the answer, or is it determined by nephrologist preference?
The development of intermittent hemodialysis (IHD) revolutionized the care of patients with acute renal failure and allowed the medical establishment means to give these patients a chance to recover from their illness. However, IHD had (and continues to have) many downsides, and mortality in acute renal failure remains high. Thus, there is an ongoing search for the best renal replacement therapy; this search led to modern continuous therapies. Three main questions have arisen from this:
- Which Modality is Best?
- What is the optimal dose for dialysis?
- When should we initiate therapy?
Continue reading for the answers...
Which Modality is Best? IHD is a shorter treatment (2 to 4 hours), typically performed three times per week but as often as daily. Fluid and electrolyte clearance is rapid, making IHD very efficient but increasing the risk for complications, such as hemodynamic instability. Furthermore, the abrupt fluid and electrolyte shifts associated with IHD do not mimic native kidney function. Providing slower treatments delivered continuously over 24 hours has many benefits.
Continuous renal replacement therapy (CRRT) provides clearance of large amounts of fluid and electrolytes over 24 hours, with minimal hemodynamic disturbances. This allows for more gradual shifts in volume and electrolyte levels, reducing the potential for ischemic damage to the kidney and other organs. Also, CRRT more closely replicates normal renal function than IHD.
CRRT is now extremely safe and efficient, although it has been difficult to prove its superiority to IHD in regard to mortality. While there may be no actual benefit to CRRT, it is also likely that its benefit is observed only in certain subsets of patients with renal failure. For example, we do have compelling evidence of increased intracranial pressure during IHD; CRRT is much safer for patients at risk for this development.1 It is also possible that we need to further improve CRRT systems and delivery in order to see a benefit.
Because current data favor neither CRRT nor IHD, most experts recommend choosing a therapy based on patient characteristics. For instance, hemodynamically unstable patients commonly receive generous amounts of fluid daily (antibiotics, nutrition, etc), and thus are often better suited for CRRT because it is more likely to remove higher volumes of fluid successfully, and less likely to contribute to hemodynamic instability than IHD. Conversely, patients with acute electrolyte deviations may benefit more from the rapid electrolyte removal IHD provides.
Additionally, stable patients may be more suitable candidates for IHD because of location (CRRT requires intensive care monitoring) and other variables.2,3 Results from multiple studies have suggested that CRRT may also provide renal protection and consequently improve renal recovery. However, this evidence is not conclusive; the possibility needs further evaluation.1
Continue reading for the optimal dose for dialysis...
What is the optimal dose for dialysis? This question, too, is plagued by inconclusive research findings. Paganini was the first to raise it formally in patients with acute renal failure; his research team found improved survival with higher doses, but had excluded the sickest and healthiest patients (according to probability of survival) from the study.4 This was followed by two additional studies with results that also seemed to support higher doses.1,5
Then in 2008, in a a similar randomized controlled trial, Tolwani et al6 found no survival benefit with higher versus lower dosing; participants in this study were not excluded based on severity of illness. Also, Tolwani’s research team identified failure to achieve prescribed doses as one factor complicating dose comparison.6
Finally, two large randomized controlled trials were performed to evaluate dosage, one in the US7 and one in Australia and New Zealand.8 Neither research team was able to confirm survival benefits with higher-dose renal replacement therapy, and there were inconsistencies between doses used in the study and standard practice in the US. In fact, the low-dose group received dialysis exceeding what is current practice by more than 30%.
The current prevailing opinion is that we should reach a minimum dose: a Kt/V of 1.2, three times a week, for IHD; or a CRRT dose of 20 mL/kg/h. At this time, higher doses do not confer a clear survival benefit. It remains unknown whether certain patients may benefit from a higher dose. Further research is needed.
Continue reading to find out when to initiate therapy...
When should we initiate therapy? While some study results suggest that early initiation is better, this remains unconfirmed.1 In theory, renal replacement therapy should be initiated early because it improves metabolic control and corrects fluid overload, facilitating management of hemodynamics and ventilation, and reducing the potential for complications caused by uremia-induced physiologic dysfunction. However, it is still unknown which patients would benefit most from early initiation, and the appropriate triggers for when to initiate therapy remain unclear.
So, how do you choose a renal replacement therapy? This is often a matter of opinion, based on evaluation of risks and benefits specific to the patient and clinical expertise with the renal replacement therapies available.
Patient safety must be a primary consideration. IHD and CRRT have dramatically improved in safety and efficacy, but it must yet be proven beyond a doubt which is superior. Outcomes may depend on how the chosen therapy is used to treat specific patient needs—not which therapy is chosen. Further research is needed to identify the best and safest way to provide renal replacement therapy.
Catherine Wells, DNP, ACNP-BC, CNN-NP, Division of Nephrology, University of Mississippi, Jackson
Continue for references...
REFERENCES
1. Prowle JR, Bellomo R. Continuous renal replacement therapy: recent advances and future research. Nat Rev Nephrol. 2010;6(9):521-529.
2. Abi Antoun T, Palevsky PM. Selection of modality of renal replacement therapy. Semin Dial. 2009; 22(2):108-113.
3. Vanholder R, Van Biesen W, Lameire N. What is the renal replacement method of choice for intensive care patients? J Am Soc Nephrol. 2001;12 suppl 17:S40-S43.
4. Augustine JJ, Sandy D, Seifert TH, Paganini EP. A randomized controlled trial comparing intermittent with continuous dialysis in patients with ARF. Am J Kidney Dis. 2004;44(6):1000-1007.
5. Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet. 2000;356(9223):26-30.
6. Tolwani AJ, Campbell RC, Stofan BS, et al. Standard versus high-dose CVVHDF for ICU-related acute renal failure. J Am Soc Nephrol. 2008;19(6):1233-1238.
7. Palevsky PM, Zhang JH, O’Connor TZ, et al; VA/NIH Acute Renal Failure Trial Network. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med. 2008;359(1):7-20.
8. Bellomo R, Cass A, Cole L, et al; RENAL Replacement Therapy Study Investigators. Intensity of continuous renal-replacement therapy in critically ill patients. N Engl J Med. 2009;361(17):1627-1683.
Q: I work as a hospitalist PA in a large teaching hospital. In our ICU we had a patient diagnosed with acute kidney injury after a coronary artery bypass graft. We consulted nephrology and they decided to start dialysis. There was quite a discussion about whether to use hemodialysis every other day or continuous renal replacement therapy. What is the basis for this question? Is there science behind the answer, or is it determined by nephrologist preference?
The development of intermittent hemodialysis (IHD) revolutionized the care of patients with acute renal failure and allowed the medical establishment means to give these patients a chance to recover from their illness. However, IHD had (and continues to have) many downsides, and mortality in acute renal failure remains high. Thus, there is an ongoing search for the best renal replacement therapy; this search led to modern continuous therapies. Three main questions have arisen from this:
- Which Modality is Best?
- What is the optimal dose for dialysis?
- When should we initiate therapy?
Continue reading for the answers...
Which Modality is Best? IHD is a shorter treatment (2 to 4 hours), typically performed three times per week but as often as daily. Fluid and electrolyte clearance is rapid, making IHD very efficient but increasing the risk for complications, such as hemodynamic instability. Furthermore, the abrupt fluid and electrolyte shifts associated with IHD do not mimic native kidney function. Providing slower treatments delivered continuously over 24 hours has many benefits.
Continuous renal replacement therapy (CRRT) provides clearance of large amounts of fluid and electrolytes over 24 hours, with minimal hemodynamic disturbances. This allows for more gradual shifts in volume and electrolyte levels, reducing the potential for ischemic damage to the kidney and other organs. Also, CRRT more closely replicates normal renal function than IHD.
CRRT is now extremely safe and efficient, although it has been difficult to prove its superiority to IHD in regard to mortality. While there may be no actual benefit to CRRT, it is also likely that its benefit is observed only in certain subsets of patients with renal failure. For example, we do have compelling evidence of increased intracranial pressure during IHD; CRRT is much safer for patients at risk for this development.1 It is also possible that we need to further improve CRRT systems and delivery in order to see a benefit.
Because current data favor neither CRRT nor IHD, most experts recommend choosing a therapy based on patient characteristics. For instance, hemodynamically unstable patients commonly receive generous amounts of fluid daily (antibiotics, nutrition, etc), and thus are often better suited for CRRT because it is more likely to remove higher volumes of fluid successfully, and less likely to contribute to hemodynamic instability than IHD. Conversely, patients with acute electrolyte deviations may benefit more from the rapid electrolyte removal IHD provides.
Additionally, stable patients may be more suitable candidates for IHD because of location (CRRT requires intensive care monitoring) and other variables.2,3 Results from multiple studies have suggested that CRRT may also provide renal protection and consequently improve renal recovery. However, this evidence is not conclusive; the possibility needs further evaluation.1
Continue reading for the optimal dose for dialysis...
What is the optimal dose for dialysis? This question, too, is plagued by inconclusive research findings. Paganini was the first to raise it formally in patients with acute renal failure; his research team found improved survival with higher doses, but had excluded the sickest and healthiest patients (according to probability of survival) from the study.4 This was followed by two additional studies with results that also seemed to support higher doses.1,5
Then in 2008, in a a similar randomized controlled trial, Tolwani et al6 found no survival benefit with higher versus lower dosing; participants in this study were not excluded based on severity of illness. Also, Tolwani’s research team identified failure to achieve prescribed doses as one factor complicating dose comparison.6
Finally, two large randomized controlled trials were performed to evaluate dosage, one in the US7 and one in Australia and New Zealand.8 Neither research team was able to confirm survival benefits with higher-dose renal replacement therapy, and there were inconsistencies between doses used in the study and standard practice in the US. In fact, the low-dose group received dialysis exceeding what is current practice by more than 30%.
The current prevailing opinion is that we should reach a minimum dose: a Kt/V of 1.2, three times a week, for IHD; or a CRRT dose of 20 mL/kg/h. At this time, higher doses do not confer a clear survival benefit. It remains unknown whether certain patients may benefit from a higher dose. Further research is needed.
Continue reading to find out when to initiate therapy...
When should we initiate therapy? While some study results suggest that early initiation is better, this remains unconfirmed.1 In theory, renal replacement therapy should be initiated early because it improves metabolic control and corrects fluid overload, facilitating management of hemodynamics and ventilation, and reducing the potential for complications caused by uremia-induced physiologic dysfunction. However, it is still unknown which patients would benefit most from early initiation, and the appropriate triggers for when to initiate therapy remain unclear.
So, how do you choose a renal replacement therapy? This is often a matter of opinion, based on evaluation of risks and benefits specific to the patient and clinical expertise with the renal replacement therapies available.
Patient safety must be a primary consideration. IHD and CRRT have dramatically improved in safety and efficacy, but it must yet be proven beyond a doubt which is superior. Outcomes may depend on how the chosen therapy is used to treat specific patient needs—not which therapy is chosen. Further research is needed to identify the best and safest way to provide renal replacement therapy.
Catherine Wells, DNP, ACNP-BC, CNN-NP, Division of Nephrology, University of Mississippi, Jackson
Continue for references...
REFERENCES
1. Prowle JR, Bellomo R. Continuous renal replacement therapy: recent advances and future research. Nat Rev Nephrol. 2010;6(9):521-529.
2. Abi Antoun T, Palevsky PM. Selection of modality of renal replacement therapy. Semin Dial. 2009; 22(2):108-113.
3. Vanholder R, Van Biesen W, Lameire N. What is the renal replacement method of choice for intensive care patients? J Am Soc Nephrol. 2001;12 suppl 17:S40-S43.
4. Augustine JJ, Sandy D, Seifert TH, Paganini EP. A randomized controlled trial comparing intermittent with continuous dialysis in patients with ARF. Am J Kidney Dis. 2004;44(6):1000-1007.
5. Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet. 2000;356(9223):26-30.
6. Tolwani AJ, Campbell RC, Stofan BS, et al. Standard versus high-dose CVVHDF for ICU-related acute renal failure. J Am Soc Nephrol. 2008;19(6):1233-1238.
7. Palevsky PM, Zhang JH, O’Connor TZ, et al; VA/NIH Acute Renal Failure Trial Network. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med. 2008;359(1):7-20.
8. Bellomo R, Cass A, Cole L, et al; RENAL Replacement Therapy Study Investigators. Intensity of continuous renal-replacement therapy in critically ill patients. N Engl J Med. 2009;361(17):1627-1683.
Thyroid Peroxidase Antibodies
Q: I have a patient with premature ovarian failure (diagnosed when she was 32) who is now in her late 40s. She is fatigued, and a blood test revealed a thyroid peroxidase antibodies level of 587 IU/mL. Would you supplement with thyroid replacement hormone, even though she has a TSH of 1.004?
The short answer is: No. Thyroid peroxidase (TPO) antibodies are a marker for the presence of autoimmune thyroid disease. Blood test results for TPO antibodies are positive in 95% of patients with chronic lymphocytic thyroiditis, also known as Hashimoto’s disease, and in 50% to 80% of patients with Graves’ disease.
Patients with high levels of TPO antibodies are at risk for future thyroid dysfunction. Not all patients with Hashimoto’s develop hypothyroidism, and if present, it may not persist. Patients with Hashimoto’s, although rarely, can experience a change from a hypothyroid to a euthyroid or even a hyperthyroid state, because of the development of coexisting TSH-receptor antibodies (TRAb), which include thyroid-stimulating immunoglobulin (TSI) and thyrotropin-binding inhibitory immunoglobulin (TBII), as seen in Graves’ disease.
Thyroid nodules are common with Hashimoto’s and are associated with a small risk (5% to 7%) for thyroid cancer. Sudden enlargement of the thyroid gland in a patient with Hashimoto’s should raise concern about thyroid lymphoma. Some endocrinologists will give supplemental thyroid hormone to a patient with Hashimoto’s, even if the TSH is normal, in an attempt to shrink the size of the gland. However, the closer the TSH is to < 1, the less room there is to further suppress it without making the patient overtly hyperthyroid, and the less likely it is that you will achieve much shrinkage of the gland.
Therefore, in the absence of a symptomatic goiter, there is no clinical reason to initiate any therapy. Even with mildly elevated TSH levels (5 to 10 mIU/L; ie, subclinical hypothyroidism) in an asymptomatic patient, there is considerable controversy about thyroid hormone initiation when the free T4 and T3 levels are normal. Most authorities agree that treatment should be initiated in most patients when the TSH rises above 10 mIU/L, regardless of symptoms. However, there are clearer indications to start thyroid hormone in women who want to become, or who are, pregnant, to maintain a TSH of < 2.5 mIU/L. Also, individuals with depression or hyperlipidemia warrant extra consideration for the use of thyroid hormone.
Since this particular patient had premature ovarian failure, which is often autoimmune in nature, she must be considered at risk for future development of hypothyroidism. This patient should be followed annually to ensure that her TSH does not rise. Should she develop symptoms suggestive of hypothyroidism and her TSH rises above 3, some endocrinologists would initiate a brief empiric trial of thyroid replacement to see if her symptoms respond when the TSH lowers again. If they do not, the thyroid hormone might be stopped, and the patient should continue to be followed.
Note: The definition of a “normal” TSH is evolving. Levels above 3.0 (suggested normal therapeutic range: 0.5 to 3.0) are considered possibly suspicious in symptomatic young people, while levels slightly above the normal reference range (5 to 7 mIU/L) may be deemed normal for the asymptomatic geriatric population.
The other point to remember is that when a clinician initiates any thyroid therapy, some patients fixate on the thyroid as the only source of their symptoms, such as fatigue, weight gain, and obesity, to the exclusion of any other etiologies. For example, sleep deprivation is a far more common cause of fatigue in our “open 24 hours” society, and lifestyle remains the major cause of obesity. Thus, there can be unintended consequences of a diagnosis of thyroid “disease.”
SUGGESTED READING
American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. www.aace.com/publications/guidelines. Accessed March 5, 2012.
Bremner AP, Feddema P, Leedman PJ, et al. Age-related changes in thyroid function: a longitudinal study of a community-based cohort. J Clin Endocrinol Metab. 2012 Feb 16; [Epub ahead of print].
Hutfless S, Matos P, Talor MV, et al. Significance of prediagnostic thyroid antibodies in women with autoimmune thyroid disease. J Clin Endocrinol Metab. 2011;96(9):E1466-E1471.
Kauffman RP, Castracane VD. Premature ovarian failure associated with autoimmune polyglandular syndrome: pathophysiological mechanisms and future fertility. J Womens Health (Larchmt). 2003;12(5):513-520.
Q: I have a patient with premature ovarian failure (diagnosed when she was 32) who is now in her late 40s. She is fatigued, and a blood test revealed a thyroid peroxidase antibodies level of 587 IU/mL. Would you supplement with thyroid replacement hormone, even though she has a TSH of 1.004?
The short answer is: No. Thyroid peroxidase (TPO) antibodies are a marker for the presence of autoimmune thyroid disease. Blood test results for TPO antibodies are positive in 95% of patients with chronic lymphocytic thyroiditis, also known as Hashimoto’s disease, and in 50% to 80% of patients with Graves’ disease.
Patients with high levels of TPO antibodies are at risk for future thyroid dysfunction. Not all patients with Hashimoto’s develop hypothyroidism, and if present, it may not persist. Patients with Hashimoto’s, although rarely, can experience a change from a hypothyroid to a euthyroid or even a hyperthyroid state, because of the development of coexisting TSH-receptor antibodies (TRAb), which include thyroid-stimulating immunoglobulin (TSI) and thyrotropin-binding inhibitory immunoglobulin (TBII), as seen in Graves’ disease.
Thyroid nodules are common with Hashimoto’s and are associated with a small risk (5% to 7%) for thyroid cancer. Sudden enlargement of the thyroid gland in a patient with Hashimoto’s should raise concern about thyroid lymphoma. Some endocrinologists will give supplemental thyroid hormone to a patient with Hashimoto’s, even if the TSH is normal, in an attempt to shrink the size of the gland. However, the closer the TSH is to < 1, the less room there is to further suppress it without making the patient overtly hyperthyroid, and the less likely it is that you will achieve much shrinkage of the gland.
Therefore, in the absence of a symptomatic goiter, there is no clinical reason to initiate any therapy. Even with mildly elevated TSH levels (5 to 10 mIU/L; ie, subclinical hypothyroidism) in an asymptomatic patient, there is considerable controversy about thyroid hormone initiation when the free T4 and T3 levels are normal. Most authorities agree that treatment should be initiated in most patients when the TSH rises above 10 mIU/L, regardless of symptoms. However, there are clearer indications to start thyroid hormone in women who want to become, or who are, pregnant, to maintain a TSH of < 2.5 mIU/L. Also, individuals with depression or hyperlipidemia warrant extra consideration for the use of thyroid hormone.
Since this particular patient had premature ovarian failure, which is often autoimmune in nature, she must be considered at risk for future development of hypothyroidism. This patient should be followed annually to ensure that her TSH does not rise. Should she develop symptoms suggestive of hypothyroidism and her TSH rises above 3, some endocrinologists would initiate a brief empiric trial of thyroid replacement to see if her symptoms respond when the TSH lowers again. If they do not, the thyroid hormone might be stopped, and the patient should continue to be followed.
Note: The definition of a “normal” TSH is evolving. Levels above 3.0 (suggested normal therapeutic range: 0.5 to 3.0) are considered possibly suspicious in symptomatic young people, while levels slightly above the normal reference range (5 to 7 mIU/L) may be deemed normal for the asymptomatic geriatric population.
The other point to remember is that when a clinician initiates any thyroid therapy, some patients fixate on the thyroid as the only source of their symptoms, such as fatigue, weight gain, and obesity, to the exclusion of any other etiologies. For example, sleep deprivation is a far more common cause of fatigue in our “open 24 hours” society, and lifestyle remains the major cause of obesity. Thus, there can be unintended consequences of a diagnosis of thyroid “disease.”
SUGGESTED READING
American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. www.aace.com/publications/guidelines. Accessed March 5, 2012.
Bremner AP, Feddema P, Leedman PJ, et al. Age-related changes in thyroid function: a longitudinal study of a community-based cohort. J Clin Endocrinol Metab. 2012 Feb 16; [Epub ahead of print].
Hutfless S, Matos P, Talor MV, et al. Significance of prediagnostic thyroid antibodies in women with autoimmune thyroid disease. J Clin Endocrinol Metab. 2011;96(9):E1466-E1471.
Kauffman RP, Castracane VD. Premature ovarian failure associated with autoimmune polyglandular syndrome: pathophysiological mechanisms and future fertility. J Womens Health (Larchmt). 2003;12(5):513-520.
Q: I have a patient with premature ovarian failure (diagnosed when she was 32) who is now in her late 40s. She is fatigued, and a blood test revealed a thyroid peroxidase antibodies level of 587 IU/mL. Would you supplement with thyroid replacement hormone, even though she has a TSH of 1.004?
The short answer is: No. Thyroid peroxidase (TPO) antibodies are a marker for the presence of autoimmune thyroid disease. Blood test results for TPO antibodies are positive in 95% of patients with chronic lymphocytic thyroiditis, also known as Hashimoto’s disease, and in 50% to 80% of patients with Graves’ disease.
Patients with high levels of TPO antibodies are at risk for future thyroid dysfunction. Not all patients with Hashimoto’s develop hypothyroidism, and if present, it may not persist. Patients with Hashimoto’s, although rarely, can experience a change from a hypothyroid to a euthyroid or even a hyperthyroid state, because of the development of coexisting TSH-receptor antibodies (TRAb), which include thyroid-stimulating immunoglobulin (TSI) and thyrotropin-binding inhibitory immunoglobulin (TBII), as seen in Graves’ disease.
Thyroid nodules are common with Hashimoto’s and are associated with a small risk (5% to 7%) for thyroid cancer. Sudden enlargement of the thyroid gland in a patient with Hashimoto’s should raise concern about thyroid lymphoma. Some endocrinologists will give supplemental thyroid hormone to a patient with Hashimoto’s, even if the TSH is normal, in an attempt to shrink the size of the gland. However, the closer the TSH is to < 1, the less room there is to further suppress it without making the patient overtly hyperthyroid, and the less likely it is that you will achieve much shrinkage of the gland.
Therefore, in the absence of a symptomatic goiter, there is no clinical reason to initiate any therapy. Even with mildly elevated TSH levels (5 to 10 mIU/L; ie, subclinical hypothyroidism) in an asymptomatic patient, there is considerable controversy about thyroid hormone initiation when the free T4 and T3 levels are normal. Most authorities agree that treatment should be initiated in most patients when the TSH rises above 10 mIU/L, regardless of symptoms. However, there are clearer indications to start thyroid hormone in women who want to become, or who are, pregnant, to maintain a TSH of < 2.5 mIU/L. Also, individuals with depression or hyperlipidemia warrant extra consideration for the use of thyroid hormone.
Since this particular patient had premature ovarian failure, which is often autoimmune in nature, she must be considered at risk for future development of hypothyroidism. This patient should be followed annually to ensure that her TSH does not rise. Should she develop symptoms suggestive of hypothyroidism and her TSH rises above 3, some endocrinologists would initiate a brief empiric trial of thyroid replacement to see if her symptoms respond when the TSH lowers again. If they do not, the thyroid hormone might be stopped, and the patient should continue to be followed.
Note: The definition of a “normal” TSH is evolving. Levels above 3.0 (suggested normal therapeutic range: 0.5 to 3.0) are considered possibly suspicious in symptomatic young people, while levels slightly above the normal reference range (5 to 7 mIU/L) may be deemed normal for the asymptomatic geriatric population.
The other point to remember is that when a clinician initiates any thyroid therapy, some patients fixate on the thyroid as the only source of their symptoms, such as fatigue, weight gain, and obesity, to the exclusion of any other etiologies. For example, sleep deprivation is a far more common cause of fatigue in our “open 24 hours” society, and lifestyle remains the major cause of obesity. Thus, there can be unintended consequences of a diagnosis of thyroid “disease.”
SUGGESTED READING
American Association of Clinical Endocrinologists medical guidelines for clinical practice for the evaluation and treatment of hyperthyroidism and hypothyroidism. www.aace.com/publications/guidelines. Accessed March 5, 2012.
Bremner AP, Feddema P, Leedman PJ, et al. Age-related changes in thyroid function: a longitudinal study of a community-based cohort. J Clin Endocrinol Metab. 2012 Feb 16; [Epub ahead of print].
Hutfless S, Matos P, Talor MV, et al. Significance of prediagnostic thyroid antibodies in women with autoimmune thyroid disease. J Clin Endocrinol Metab. 2011;96(9):E1466-E1471.
Kauffman RP, Castracane VD. Premature ovarian failure associated with autoimmune polyglandular syndrome: pathophysiological mechanisms and future fertility. J Womens Health (Larchmt). 2003;12(5):513-520.
Seclusion and Restraint: A High-Risk Procedure With Alternative Methods
Clinicians Are Asking: Renal Diet
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: What is the renal diet? Should my patients with chronic kidney disease (CKD) restrict their protein consumption?
The CKD nondialysis diet aims to preserve remaining kidney function. A person living with kidney disease can continue to enjoy a variety of foods, including whole grains, fruits, and vegetables. These foods must be restricted only when phosphorus, parathyroid hormone, and/or potassium levels become elevated. However, many advanced practitioners recommend avoiding dark sodas because of their high phosphorus content. Sodium is limited to help maintain blood pressure control and decrease fluid buildup.
Fluid intake is not restricted unless fluid retention becomes an issue. Adequate caloric intake from carbohydrates and healthy fats is essential so as to spare protein for growth and repair. Aiming for a healthy weight through appropriate caloric intake and regular physical activity is important. A water-soluble vitamin B complex and a vitamin C supplement may be recommended as the diet becomes more restrictive. Supplemental vitamin D requirements and iron needs are based on findings from laboratory studies.
As is always the case when advising patients on food choices, the emphasis should be on optimizing nutrition and avoiding empty calories. A review of how to interpret a food label is often helpful to patients and their families.
Dietary protein recommendations continue to be controversial in CKD stages 1 through 4 (estimated glomerular filtration rate [eGFR] < 30 mL/min/1.73 m2). The renal diet emphasizes high-quality proteins but limits protein intake to approximately 0.6 to 0.8 g/kg/d so as to decrease the workload on the kidneys and reduce urea waste production. The National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for nutrition in patients with CKD1 recommend that patients who have an eGFR between 25 and 55 mL/min/1.73 m2 should eat at least 0.8 g/kg/d of protein; and that those whose eGFR is less than 25 mL/min/1.73 m2 and who are not receiving dialysis consume 0.6 g/kg/d. If a patient cannot tolerate the diet or is unable to maintain an adequate caloric intake, then protein intake can be 0.75 g/kg/d.
Once a patient is undergoing dialysis, the protein requirements may change, depending on the patient’s needs and type of dialysis. Fortunately, the renal dietician, an essential member of the interdisciplinary dialysis team, offers great assistance to the advanced practitioner in addressing the patient’s nutritional needs.
However, referral to a renal dietitian is recommended before dialysis, as diet is an important part of CKD treatment. A Medicare recipient with stage 3 or 4 CKD can see a registered dietitian through the Medical Nutrition Therapy benefit.2
Individualizing nutritional therapy is essential to optimize health in people living with the complexities of CKD. It is also very important, when assessing, monitoring, and intervening to avoid or treat malnutrition in these patients, to provide care as an interprofessional team that includes a renal dietician. (To provide the best evidence available, an experienced renal dietician was asked to contribute to this response.)
Debra Hain, PhD, APRN, GNP-BC
Assistant Professor, Christine E. Lynn College of Nursing, Florida Atlantic University, Boca Raton; Nurse Practitioner, Cleveland Clinic Florida, Weston
Susan Meese-Morris, RD, LD/N
Renal Dietitian, Pine Island, Weston, and Miramar, Florida
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: What is the renal diet? Should my patients with chronic kidney disease (CKD) restrict their protein consumption?
The CKD nondialysis diet aims to preserve remaining kidney function. A person living with kidney disease can continue to enjoy a variety of foods, including whole grains, fruits, and vegetables. These foods must be restricted only when phosphorus, parathyroid hormone, and/or potassium levels become elevated. However, many advanced practitioners recommend avoiding dark sodas because of their high phosphorus content. Sodium is limited to help maintain blood pressure control and decrease fluid buildup.
Fluid intake is not restricted unless fluid retention becomes an issue. Adequate caloric intake from carbohydrates and healthy fats is essential so as to spare protein for growth and repair. Aiming for a healthy weight through appropriate caloric intake and regular physical activity is important. A water-soluble vitamin B complex and a vitamin C supplement may be recommended as the diet becomes more restrictive. Supplemental vitamin D requirements and iron needs are based on findings from laboratory studies.
As is always the case when advising patients on food choices, the emphasis should be on optimizing nutrition and avoiding empty calories. A review of how to interpret a food label is often helpful to patients and their families.
Dietary protein recommendations continue to be controversial in CKD stages 1 through 4 (estimated glomerular filtration rate [eGFR] < 30 mL/min/1.73 m2). The renal diet emphasizes high-quality proteins but limits protein intake to approximately 0.6 to 0.8 g/kg/d so as to decrease the workload on the kidneys and reduce urea waste production. The National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for nutrition in patients with CKD1 recommend that patients who have an eGFR between 25 and 55 mL/min/1.73 m2 should eat at least 0.8 g/kg/d of protein; and that those whose eGFR is less than 25 mL/min/1.73 m2 and who are not receiving dialysis consume 0.6 g/kg/d. If a patient cannot tolerate the diet or is unable to maintain an adequate caloric intake, then protein intake can be 0.75 g/kg/d.
Once a patient is undergoing dialysis, the protein requirements may change, depending on the patient’s needs and type of dialysis. Fortunately, the renal dietician, an essential member of the interdisciplinary dialysis team, offers great assistance to the advanced practitioner in addressing the patient’s nutritional needs.
However, referral to a renal dietitian is recommended before dialysis, as diet is an important part of CKD treatment. A Medicare recipient with stage 3 or 4 CKD can see a registered dietitian through the Medical Nutrition Therapy benefit.2
Individualizing nutritional therapy is essential to optimize health in people living with the complexities of CKD. It is also very important, when assessing, monitoring, and intervening to avoid or treat malnutrition in these patients, to provide care as an interprofessional team that includes a renal dietician. (To provide the best evidence available, an experienced renal dietician was asked to contribute to this response.)
Debra Hain, PhD, APRN, GNP-BC
Assistant Professor, Christine E. Lynn College of Nursing, Florida Atlantic University, Boca Raton; Nurse Practitioner, Cleveland Clinic Florida, Weston
Susan Meese-Morris, RD, LD/N
Renal Dietitian, Pine Island, Weston, and Miramar, Florida
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: What is the renal diet? Should my patients with chronic kidney disease (CKD) restrict their protein consumption?
The CKD nondialysis diet aims to preserve remaining kidney function. A person living with kidney disease can continue to enjoy a variety of foods, including whole grains, fruits, and vegetables. These foods must be restricted only when phosphorus, parathyroid hormone, and/or potassium levels become elevated. However, many advanced practitioners recommend avoiding dark sodas because of their high phosphorus content. Sodium is limited to help maintain blood pressure control and decrease fluid buildup.
Fluid intake is not restricted unless fluid retention becomes an issue. Adequate caloric intake from carbohydrates and healthy fats is essential so as to spare protein for growth and repair. Aiming for a healthy weight through appropriate caloric intake and regular physical activity is important. A water-soluble vitamin B complex and a vitamin C supplement may be recommended as the diet becomes more restrictive. Supplemental vitamin D requirements and iron needs are based on findings from laboratory studies.
As is always the case when advising patients on food choices, the emphasis should be on optimizing nutrition and avoiding empty calories. A review of how to interpret a food label is often helpful to patients and their families.
Dietary protein recommendations continue to be controversial in CKD stages 1 through 4 (estimated glomerular filtration rate [eGFR] < 30 mL/min/1.73 m2). The renal diet emphasizes high-quality proteins but limits protein intake to approximately 0.6 to 0.8 g/kg/d so as to decrease the workload on the kidneys and reduce urea waste production. The National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for nutrition in patients with CKD1 recommend that patients who have an eGFR between 25 and 55 mL/min/1.73 m2 should eat at least 0.8 g/kg/d of protein; and that those whose eGFR is less than 25 mL/min/1.73 m2 and who are not receiving dialysis consume 0.6 g/kg/d. If a patient cannot tolerate the diet or is unable to maintain an adequate caloric intake, then protein intake can be 0.75 g/kg/d.
Once a patient is undergoing dialysis, the protein requirements may change, depending on the patient’s needs and type of dialysis. Fortunately, the renal dietician, an essential member of the interdisciplinary dialysis team, offers great assistance to the advanced practitioner in addressing the patient’s nutritional needs.
However, referral to a renal dietitian is recommended before dialysis, as diet is an important part of CKD treatment. A Medicare recipient with stage 3 or 4 CKD can see a registered dietitian through the Medical Nutrition Therapy benefit.2
Individualizing nutritional therapy is essential to optimize health in people living with the complexities of CKD. It is also very important, when assessing, monitoring, and intervening to avoid or treat malnutrition in these patients, to provide care as an interprofessional team that includes a renal dietician. (To provide the best evidence available, an experienced renal dietician was asked to contribute to this response.)
Debra Hain, PhD, APRN, GNP-BC
Assistant Professor, Christine E. Lynn College of Nursing, Florida Atlantic University, Boca Raton; Nurse Practitioner, Cleveland Clinic Florida, Weston
Susan Meese-Morris, RD, LD/N
Renal Dietitian, Pine Island, Weston, and Miramar, Florida
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Clinicians Are Asking: Kidney Disease Education Classes
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: Our practice received a flyer for kidney disease education classes offered by the local nephrology group. Can you tell me more about these classes?
Patient education in kidney disease has been shown to delay disease progression and improve patient outcomes.4 Because of this, the Medicare Improvements for Patients and Providers Act (MIPPA) of 20085 provided for classes for patients with stage 4 CKD (GFR, 15 to 29 mL/min/1.73 m2) to receive six hours of education over their lifetime.
Classes can be taught by a physician or an advanced practitioner (a PA, an NP, or a clinical nurse specialist). Four broad areas are covered: management of comorbidities that occur with CKD; prevention of complications, including an explanation of how the kidneys work and a review of medications; renal replacement modalities, including hemodialysis, peritoneal dialysis, and transplantation; and opportunities to empower the patients as active partners in their own health care.6 Classes also include information on managing anemia, hypertension, and bone mineral disease.7
Class structure is up to the provider. Most practices offer classes to all stage 4 CKD patients, regardless of Medicare status. Classes can be taught on a one-to-one basis or in a group setting.8
Some practices design their own format, while others use programs designed for CKD education. The National Kidney Foundation developed a slide set called Your Treatment, Your Choice,8 while the Cleveland Clinic, the Mayo Clinic, and the University of Alabama at Birmingham (among others, no doubt), have developed their own in-house programs. All these programs have a prepared Power Point slide deck, and most include evaluation tools.
Tricia Howard, MHS, PA-C
South University, Savannah, Georgia
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: Our practice received a flyer for kidney disease education classes offered by the local nephrology group. Can you tell me more about these classes?
Patient education in kidney disease has been shown to delay disease progression and improve patient outcomes.4 Because of this, the Medicare Improvements for Patients and Providers Act (MIPPA) of 20085 provided for classes for patients with stage 4 CKD (GFR, 15 to 29 mL/min/1.73 m2) to receive six hours of education over their lifetime.
Classes can be taught by a physician or an advanced practitioner (a PA, an NP, or a clinical nurse specialist). Four broad areas are covered: management of comorbidities that occur with CKD; prevention of complications, including an explanation of how the kidneys work and a review of medications; renal replacement modalities, including hemodialysis, peritoneal dialysis, and transplantation; and opportunities to empower the patients as active partners in their own health care.6 Classes also include information on managing anemia, hypertension, and bone mineral disease.7
Class structure is up to the provider. Most practices offer classes to all stage 4 CKD patients, regardless of Medicare status. Classes can be taught on a one-to-one basis or in a group setting.8
Some practices design their own format, while others use programs designed for CKD education. The National Kidney Foundation developed a slide set called Your Treatment, Your Choice,8 while the Cleveland Clinic, the Mayo Clinic, and the University of Alabama at Birmingham (among others, no doubt), have developed their own in-house programs. All these programs have a prepared Power Point slide deck, and most include evaluation tools.
Tricia Howard, MHS, PA-C
South University, Savannah, Georgia
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: Our practice received a flyer for kidney disease education classes offered by the local nephrology group. Can you tell me more about these classes?
Patient education in kidney disease has been shown to delay disease progression and improve patient outcomes.4 Because of this, the Medicare Improvements for Patients and Providers Act (MIPPA) of 20085 provided for classes for patients with stage 4 CKD (GFR, 15 to 29 mL/min/1.73 m2) to receive six hours of education over their lifetime.
Classes can be taught by a physician or an advanced practitioner (a PA, an NP, or a clinical nurse specialist). Four broad areas are covered: management of comorbidities that occur with CKD; prevention of complications, including an explanation of how the kidneys work and a review of medications; renal replacement modalities, including hemodialysis, peritoneal dialysis, and transplantation; and opportunities to empower the patients as active partners in their own health care.6 Classes also include information on managing anemia, hypertension, and bone mineral disease.7
Class structure is up to the provider. Most practices offer classes to all stage 4 CKD patients, regardless of Medicare status. Classes can be taught on a one-to-one basis or in a group setting.8
Some practices design their own format, while others use programs designed for CKD education. The National Kidney Foundation developed a slide set called Your Treatment, Your Choice,8 while the Cleveland Clinic, the Mayo Clinic, and the University of Alabama at Birmingham (among others, no doubt), have developed their own in-house programs. All these programs have a prepared Power Point slide deck, and most include evaluation tools.
Tricia Howard, MHS, PA-C
South University, Savannah, Georgia
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Clinicians Are Asking: Dialysis Patients Requiring Surgery
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: We scheduled a total knee replacement for a patient on dialysis, and anesthesia balked because the patient had a potassium level of 5.5 mEq/L. The nephrology practice, apparently not concerned, agreed to dialyze the patient, but only because anesthesia insisted. If the practice uses our facility, where 5.3 mEq/L is the upper limit of serum potassium, how can a potassium level of 5.5 mEq/L not be of concern in a hemodialysis patient?
This is a question that occurs frequently regarding patients receiving dialysis. Hyperkalemia is a problem faced by many dialysis patients as a result of the kidneys’ inability to remove potassium with the loss of renal function. Patients’ potassium levels are monitored routinely, and low-potassium diets are a staple of any nephrology clinic or dialysis unit.
For patients in our dialysis unit, the normal potassium range is 3.5 to 6.0 mEq/L, which is 0.9 mEq/L higher than for a patient without end-stage renal disease (ESRD). Dialysis patients with ESRD often have an increased tolerance for hyperkalemia.
When potassium levels are elevated, a 12-lead ECG is used to detect any physiological cardiac changes. These are generally not seen until the serum potassium exceeds 6.0 to 6.5 mEq/L. ECG changes seen in hyperkalemia include peaked T waves, a prolonged PR interval, and absent P waves with a widened QRS complex. These changes, which can lead to ventricular tachycardia or ventricular fibrillation, are not based on numbers or values of serum potassium, but are thought to reflect the transcellular potassium gradient.3
When questioning a potassium level in a dialysis patient and considering whether presurgical dialysis is needed, it is important to consider the surgery planned. In surgeries during which potassium might be released secondary to tissue trauma, potassium levels can rise higher during surgery.3
It is important to assess hypokalemia as well. Arrhythmias such as premature atrial and ventricular beats, sinus bradycardia, paroxysmal atrial or junctional tachycardia, atrioventricular block, and ventricular tachycardia or fibrillation can occur with hypokalemia. ECG changes include depression of the ST segment, a decrease in the amplitude of the T wave, and an increase in the amplitude of U waves, which occur at the end of the T wave. U waves are often seen in the lateral precordial leads V4 to V6.3
Laura MacGregor, RN, MS, NP-C
Grand Street Medical Associates, Kingston, New York
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: We scheduled a total knee replacement for a patient on dialysis, and anesthesia balked because the patient had a potassium level of 5.5 mEq/L. The nephrology practice, apparently not concerned, agreed to dialyze the patient, but only because anesthesia insisted. If the practice uses our facility, where 5.3 mEq/L is the upper limit of serum potassium, how can a potassium level of 5.5 mEq/L not be of concern in a hemodialysis patient?
This is a question that occurs frequently regarding patients receiving dialysis. Hyperkalemia is a problem faced by many dialysis patients as a result of the kidneys’ inability to remove potassium with the loss of renal function. Patients’ potassium levels are monitored routinely, and low-potassium diets are a staple of any nephrology clinic or dialysis unit.
For patients in our dialysis unit, the normal potassium range is 3.5 to 6.0 mEq/L, which is 0.9 mEq/L higher than for a patient without end-stage renal disease (ESRD). Dialysis patients with ESRD often have an increased tolerance for hyperkalemia.
When potassium levels are elevated, a 12-lead ECG is used to detect any physiological cardiac changes. These are generally not seen until the serum potassium exceeds 6.0 to 6.5 mEq/L. ECG changes seen in hyperkalemia include peaked T waves, a prolonged PR interval, and absent P waves with a widened QRS complex. These changes, which can lead to ventricular tachycardia or ventricular fibrillation, are not based on numbers or values of serum potassium, but are thought to reflect the transcellular potassium gradient.3
When questioning a potassium level in a dialysis patient and considering whether presurgical dialysis is needed, it is important to consider the surgery planned. In surgeries during which potassium might be released secondary to tissue trauma, potassium levels can rise higher during surgery.3
It is important to assess hypokalemia as well. Arrhythmias such as premature atrial and ventricular beats, sinus bradycardia, paroxysmal atrial or junctional tachycardia, atrioventricular block, and ventricular tachycardia or fibrillation can occur with hypokalemia. ECG changes include depression of the ST segment, a decrease in the amplitude of the T wave, and an increase in the amplitude of U waves, which occur at the end of the T wave. U waves are often seen in the lateral precordial leads V4 to V6.3
Laura MacGregor, RN, MS, NP-C
Grand Street Medical Associates, Kingston, New York
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.
Your renal practitioners/department editors have chosen three typical situations you might encounter in practice.
• Nutrition and diet help control kidney disease, but also heart disease, diabetes, and other comorbid states.
• Renal patients, like many others, often require surgeries; what specific concerns exist for surgical patients requiring dialysis?
• The Medicare education benefit has been a particular bonus for advanced practitioners, as we teach many of the classes.
We welcome your questions and comments.
Q: We scheduled a total knee replacement for a patient on dialysis, and anesthesia balked because the patient had a potassium level of 5.5 mEq/L. The nephrology practice, apparently not concerned, agreed to dialyze the patient, but only because anesthesia insisted. If the practice uses our facility, where 5.3 mEq/L is the upper limit of serum potassium, how can a potassium level of 5.5 mEq/L not be of concern in a hemodialysis patient?
This is a question that occurs frequently regarding patients receiving dialysis. Hyperkalemia is a problem faced by many dialysis patients as a result of the kidneys’ inability to remove potassium with the loss of renal function. Patients’ potassium levels are monitored routinely, and low-potassium diets are a staple of any nephrology clinic or dialysis unit.
For patients in our dialysis unit, the normal potassium range is 3.5 to 6.0 mEq/L, which is 0.9 mEq/L higher than for a patient without end-stage renal disease (ESRD). Dialysis patients with ESRD often have an increased tolerance for hyperkalemia.
When potassium levels are elevated, a 12-lead ECG is used to detect any physiological cardiac changes. These are generally not seen until the serum potassium exceeds 6.0 to 6.5 mEq/L. ECG changes seen in hyperkalemia include peaked T waves, a prolonged PR interval, and absent P waves with a widened QRS complex. These changes, which can lead to ventricular tachycardia or ventricular fibrillation, are not based on numbers or values of serum potassium, but are thought to reflect the transcellular potassium gradient.3
When questioning a potassium level in a dialysis patient and considering whether presurgical dialysis is needed, it is important to consider the surgery planned. In surgeries during which potassium might be released secondary to tissue trauma, potassium levels can rise higher during surgery.3
It is important to assess hypokalemia as well. Arrhythmias such as premature atrial and ventricular beats, sinus bradycardia, paroxysmal atrial or junctional tachycardia, atrioventricular block, and ventricular tachycardia or fibrillation can occur with hypokalemia. ECG changes include depression of the ST segment, a decrease in the amplitude of the T wave, and an increase in the amplitude of U waves, which occur at the end of the T wave. U waves are often seen in the lateral precordial leads V4 to V6.3
Laura MacGregor, RN, MS, NP-C
Grand Street Medical Associates, Kingston, New York
REFERENCES
1. National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF-K/DOQI) Clinical Practice Guidelines for Nutrition in Chronic Renal Failure (2000). www.kidney.org/professionals/kdoqi/guidelines_updates/doqi_nut.html. Accessed February 16, 2012.
2. Medicare.gov. Medical nutrition therapy. www.medicare.gov/navigation/manage-your-health/preventive-services/medical-nutrition-therapy.aspx?AspxAutoDetectCookieSupport=1. Accessed February 16, 2012.
3. Soundararajan R, Golper T. Medical management of the dialysis patient undergoing surgery. www.uptodate.com/contents/medical-management-of-the-dialysis-patient-undergoing-surgery. Accessed February 16, 2012.
4. Young HN, Chan MR, Yevzlin AS, Becker BN. The rationale, implementation and effects of the Medicare CKD education benefit. Am J Kidney Dis. 2011;57(3):381-386.
5. H. R. 6331: Medicare Improvements for Patients and Providers Act of 2008. www.govtrack.us/congress/bill.xpd?bill=h110-6331. Accessed February 16, 2012.
6. §410.48. Kidney disease education services. Federal Register. 2009;74(226):62003.
7. Lazarus JM. National health care policy and its effect on renal care. Presented at: NKFI Multi-Disciplinary Conference; September 24, 2009; Chicago, IL.
8. National Kidney Foundation. MIPPA Kidney Disease Education Benefit. Your Treatment, Your Choice (2010). www.kidney.org/professionals/KLS/YTYC.cfm. Accessed February 16, 2012.