Nephrology

SAN DIEGO – The use of hormone therapy was associated with a lower urine albumin-to-creatinine ratio and a decreased risk of albuminuria, results from a cross-sectional study suggest.

“This may be useful information for providers taking care of menopausal women who are considering the use of hormone therapy for vasomotor symptoms and are worried about the systemic effects of these medications,” lead study author Dr. Andrea G. Kattah said in an interview after the annual meeting of the American Society of Nephrology. “Though our data only show an association and not cause and effect, hormone therapy is associated with better kidney function in this study.”

Results from many animal studies suggest that estrogen can have beneficial effects on the kidneys, noted Dr. Kattah, who conducted the research with Dr. Vesna D. Garovic and colleagues in the division of hypertension and nephrology at the Mayo Clinic, Rochester, Minn.

“In addition, in human studies of chronic kidney disease, premenopausal women tend to have slower progression of kidney disease than men,” she said. “Studies on the effects of hormone therapy on kidney function in women have had variable results. We wanted to look at the association of hormone therapy and renal function in a large, multiethnic cohort with well-defined health conditions that may confound the relationship between hormone therapy and renal disease.”

Study participants included 2,217 women enrolled in the Family Blood Pressure Program, a multinetwork effort to study the genetics of hypertension. During a study visit between 2000 and 2004, the women completed questionnaires about medical history, menopausal status, and use of hormone therapy (HT) in the past month. Clinicians also took their blood pressure, measured their body mass index, and drew blood to determine levels of serum creatinine and urine albumin-to-creatinine ratio (UACR).

Of the 2,217 women, 673 were on HT and 1,544 were not, and their mean ages were 60 years and 63 years, respectively.

In unadjusted analysis, Dr. Kattah and her associates found that UACR was significantly lower in those on HT, compared with those who were not (3.5 mg/g creatinine vs. 5.2 mg/g creatinine, respectively, P less than .001), as was the number of women with an estimated glomerular filtration rate (eGFR) of less than 60 mL/min per 1.73 m² (7% vs. 10%, P = .003).

After adjusting for renal and cardiovascular risk factors including age, race, smoking, diabetes, hypertension, and family history of hypertension, the use of HT was still significantly associated with a lower UACR and decreased risk of microalbuminuria (odds ratio, 0.61). The association between HT and eGFR of less than 60 mL/min per 1.73 m² was no longer significant after adjustment, but there was a trend toward higher eGFR and fewer women with an eGFR of less than 60 mL/min per 1.73 m² among those on HT.

“Not surprisingly, the women taking hormone therapy were different than those who were not, and they generally had fewer health problems, such as diabetes and hyperlipidemia,” Dr. Kattah said. “However, after taking these differences into account in our models, we still found a significant decrease in the risk of having microalbuminuria in those on hormone therapy.”

Dr. Kattah acknowledged certain limitations of the study, including the fact that its design is “cross-sectional and cannot answer the question of whether or not hormone therapy can improve kidney function.

In addition, “we do not have data on how long women were taking hormone therapy, which other studies have suggested is an important factor.”

The researchers reported having no financial disclosures.

[email protected]

SAN DIEGO – The use of hormone therapy was associated with a lower urine albumin-to-creatinine ratio and a decreased risk of albuminuria, results from a cross-sectional study suggest.

“This may be useful information for providers taking care of menopausal women who are considering the use of hormone therapy for vasomotor symptoms and are worried about the systemic effects of these medications,” lead study author Dr. Andrea G. Kattah said in an interview after the annual meeting of the American Society of Nephrology. “Though our data only show an association and not cause and effect, hormone therapy is associated with better kidney function in this study.”

Results from many animal studies suggest that estrogen can have beneficial effects on the kidneys, noted Dr. Kattah, who conducted the research with Dr. Vesna D. Garovic and colleagues in the division of hypertension and nephrology at the Mayo Clinic, Rochester, Minn.

“In addition, in human studies of chronic kidney disease, premenopausal women tend to have slower progression of kidney disease than men,” she said. “Studies on the effects of hormone therapy on kidney function in women have had variable results. We wanted to look at the association of hormone therapy and renal function in a large, multiethnic cohort with well-defined health conditions that may confound the relationship between hormone therapy and renal disease.”

Study participants included 2,217 women enrolled in the Family Blood Pressure Program, a multinetwork effort to study the genetics of hypertension. During a study visit between 2000 and 2004, the women completed questionnaires about medical history, menopausal status, and use of hormone therapy (HT) in the past month. Clinicians also took their blood pressure, measured their body mass index, and drew blood to determine levels of serum creatinine and urine albumin-to-creatinine ratio (UACR).

Of the 2,217 women, 673 were on HT and 1,544 were not, and their mean ages were 60 years and 63 years, respectively.

In unadjusted analysis, Dr. Kattah and her associates found that UACR was significantly lower in those on HT, compared with those who were not (3.5 mg/g creatinine vs. 5.2 mg/g creatinine, respectively, P less than .001), as was the number of women with an estimated glomerular filtration rate (eGFR) of less than 60 mL/min per 1.73 m² (7% vs. 10%, P = .003).

After adjusting for renal and cardiovascular risk factors including age, race, smoking, diabetes, hypertension, and family history of hypertension, the use of HT was still significantly associated with a lower UACR and decreased risk of microalbuminuria (odds ratio, 0.61). The association between HT and eGFR of less than 60 mL/min per 1.73 m² was no longer significant after adjustment, but there was a trend toward higher eGFR and fewer women with an eGFR of less than 60 mL/min per 1.73 m² among those on HT.

“Not surprisingly, the women taking hormone therapy were different than those who were not, and they generally had fewer health problems, such as diabetes and hyperlipidemia,” Dr. Kattah said. “However, after taking these differences into account in our models, we still found a significant decrease in the risk of having microalbuminuria in those on hormone therapy.”

Dr. Kattah acknowledged certain limitations of the study, including the fact that its design is “cross-sectional and cannot answer the question of whether or not hormone therapy can improve kidney function.

In addition, “we do not have data on how long women were taking hormone therapy, which other studies have suggested is an important factor.”

The researchers reported having no financial disclosures.

[email protected]

SAN DIEGO – The use of hormone therapy was associated with a lower urine albumin-to-creatinine ratio and a decreased risk of albuminuria, results from a cross-sectional study suggest.

“This may be useful information for providers taking care of menopausal women who are considering the use of hormone therapy for vasomotor symptoms and are worried about the systemic effects of these medications,” lead study author Dr. Andrea G. Kattah said in an interview after the annual meeting of the American Society of Nephrology. “Though our data only show an association and not cause and effect, hormone therapy is associated with better kidney function in this study.”

Results from many animal studies suggest that estrogen can have beneficial effects on the kidneys, noted Dr. Kattah, who conducted the research with Dr. Vesna D. Garovic and colleagues in the division of hypertension and nephrology at the Mayo Clinic, Rochester, Minn.

“In addition, in human studies of chronic kidney disease, premenopausal women tend to have slower progression of kidney disease than men,” she said. “Studies on the effects of hormone therapy on kidney function in women have had variable results. We wanted to look at the association of hormone therapy and renal function in a large, multiethnic cohort with well-defined health conditions that may confound the relationship between hormone therapy and renal disease.”

Study participants included 2,217 women enrolled in the Family Blood Pressure Program, a multinetwork effort to study the genetics of hypertension. During a study visit between 2000 and 2004, the women completed questionnaires about medical history, menopausal status, and use of hormone therapy (HT) in the past month. Clinicians also took their blood pressure, measured their body mass index, and drew blood to determine levels of serum creatinine and urine albumin-to-creatinine ratio (UACR).

Of the 2,217 women, 673 were on HT and 1,544 were not, and their mean ages were 60 years and 63 years, respectively.

In unadjusted analysis, Dr. Kattah and her associates found that UACR was significantly lower in those on HT, compared with those who were not (3.5 mg/g creatinine vs. 5.2 mg/g creatinine, respectively, P less than .001), as was the number of women with an estimated glomerular filtration rate (eGFR) of less than 60 mL/min per 1.73 m² (7% vs. 10%, P = .003).

After adjusting for renal and cardiovascular risk factors including age, race, smoking, diabetes, hypertension, and family history of hypertension, the use of HT was still significantly associated with a lower UACR and decreased risk of microalbuminuria (odds ratio, 0.61). The association between HT and eGFR of less than 60 mL/min per 1.73 m² was no longer significant after adjustment, but there was a trend toward higher eGFR and fewer women with an eGFR of less than 60 mL/min per 1.73 m² among those on HT.

“Not surprisingly, the women taking hormone therapy were different than those who were not, and they generally had fewer health problems, such as diabetes and hyperlipidemia,” Dr. Kattah said. “However, after taking these differences into account in our models, we still found a significant decrease in the risk of having microalbuminuria in those on hormone therapy.”

Dr. Kattah acknowledged certain limitations of the study, including the fact that its design is “cross-sectional and cannot answer the question of whether or not hormone therapy can improve kidney function.

In addition, “we do not have data on how long women were taking hormone therapy, which other studies have suggested is an important factor.”

The researchers reported having no financial disclosures.

[email protected]

SAN DIEGO – Raising levels of vitamin D, deficient in many patients with chronic kidney disease, improved vascular function and reduced inflammation and vessel wall stiffness after 16 weeks, according to results of a study in a small group of early kidney disease patients in India.

“This tells us that vitamin D has the potential, at least over the short- to intermediate term, to improve vascular function,” with a promise of reducing or preventing cardiovascular outcomes in a larger study, said Dr. Vivekanand Jha, of the George Institute for Global Health in New Delhi.

©iStock/thinkstock.com

“Patients with very early kidney disease are at very high risk of developing cardiovascular complications such as heart attacks, strokes, and peripheral vascular disease – and that’s what kills them before they get to the point where they need dialysis,” Dr. Jha said. “So, many die before they need dialysis. But we don’t know the factors that cause these cardiovascular complications.”

His group hypothesized that because vitamin D has biological action on blood vessels, “if we supplemented patients with vitamin D, their vascular function would improve.”

Participants were randomized to receive directly observed oral doses of 300,000 IU of cholecalciferol at baseline and at 8 weeks, or directly observed doses of a placebo in a matched control arm.

“We measured several parameters to look at vascular function after 16 weeks and found that patients who received vitamin D showed normalized vitamin D and decreases in levels of parathyroid hormone,” Dr. Jha said at the meeting sponsored by the American Society of Nephrology.

“But most importantly, we found that vitamin D recipients showed improvement in their vascular function on two or three tests; in flow-mediated dilation, which suggests improved endothelial function; and improved augmentation index, which looks at the stiffness of blood vessels,” he explained.

The next step is a much larger study designed to show that vitamin D supplements in this population can prevent cardiovascular events. “But that’s going to be a long-term study,” Dr. Jha noted.

“I don’t want to get ahead of myself and say that this is going to cure cardiovascular problems,” Dr. Jha cautioned. “But now we know we need to do a definitive study to look at these events, and prove whether supplementation with vitamin D does or does not significantly improve those endpoints.”

SAN DIEGO – Raising levels of vitamin D, deficient in many patients with chronic kidney disease, improved vascular function and reduced inflammation and vessel wall stiffness after 16 weeks, according to results of a study in a small group of early kidney disease patients in India.

“This tells us that vitamin D has the potential, at least over the short- to intermediate term, to improve vascular function,” with a promise of reducing or preventing cardiovascular outcomes in a larger study, said Dr. Vivekanand Jha, of the George Institute for Global Health in New Delhi.

©iStock/thinkstock.com

“Patients with very early kidney disease are at very high risk of developing cardiovascular complications such as heart attacks, strokes, and peripheral vascular disease – and that’s what kills them before they get to the point where they need dialysis,” Dr. Jha said. “So, many die before they need dialysis. But we don’t know the factors that cause these cardiovascular complications.”

His group hypothesized that because vitamin D has biological action on blood vessels, “if we supplemented patients with vitamin D, their vascular function would improve.”

Participants were randomized to receive directly observed oral doses of 300,000 IU of cholecalciferol at baseline and at 8 weeks, or directly observed doses of a placebo in a matched control arm.

“We measured several parameters to look at vascular function after 16 weeks and found that patients who received vitamin D showed normalized vitamin D and decreases in levels of parathyroid hormone,” Dr. Jha said at the meeting sponsored by the American Society of Nephrology.

“But most importantly, we found that vitamin D recipients showed improvement in their vascular function on two or three tests; in flow-mediated dilation, which suggests improved endothelial function; and improved augmentation index, which looks at the stiffness of blood vessels,” he explained.

The next step is a much larger study designed to show that vitamin D supplements in this population can prevent cardiovascular events. “But that’s going to be a long-term study,” Dr. Jha noted.

“I don’t want to get ahead of myself and say that this is going to cure cardiovascular problems,” Dr. Jha cautioned. “But now we know we need to do a definitive study to look at these events, and prove whether supplementation with vitamin D does or does not significantly improve those endpoints.”

SAN DIEGO – Raising levels of vitamin D, deficient in many patients with chronic kidney disease, improved vascular function and reduced inflammation and vessel wall stiffness after 16 weeks, according to results of a study in a small group of early kidney disease patients in India.

“This tells us that vitamin D has the potential, at least over the short- to intermediate term, to improve vascular function,” with a promise of reducing or preventing cardiovascular outcomes in a larger study, said Dr. Vivekanand Jha, of the George Institute for Global Health in New Delhi.

©iStock/thinkstock.com

“Patients with very early kidney disease are at very high risk of developing cardiovascular complications such as heart attacks, strokes, and peripheral vascular disease – and that’s what kills them before they get to the point where they need dialysis,” Dr. Jha said. “So, many die before they need dialysis. But we don’t know the factors that cause these cardiovascular complications.”

His group hypothesized that because vitamin D has biological action on blood vessels, “if we supplemented patients with vitamin D, their vascular function would improve.”

Participants were randomized to receive directly observed oral doses of 300,000 IU of cholecalciferol at baseline and at 8 weeks, or directly observed doses of a placebo in a matched control arm.

“We measured several parameters to look at vascular function after 16 weeks and found that patients who received vitamin D showed normalized vitamin D and decreases in levels of parathyroid hormone,” Dr. Jha said at the meeting sponsored by the American Society of Nephrology.

“But most importantly, we found that vitamin D recipients showed improvement in their vascular function on two or three tests; in flow-mediated dilation, which suggests improved endothelial function; and improved augmentation index, which looks at the stiffness of blood vessels,” he explained.

The next step is a much larger study designed to show that vitamin D supplements in this population can prevent cardiovascular events. “But that’s going to be a long-term study,” Dr. Jha noted.

“I don’t want to get ahead of myself and say that this is going to cure cardiovascular problems,” Dr. Jha cautioned. “But now we know we need to do a definitive study to look at these events, and prove whether supplementation with vitamin D does or does not significantly improve those endpoints.”

ORLANDO – Three simple, routinely collected measurements together provide a lot of insight into the risk faced by community-dwelling patients hospitalized for acute decompensated heart failure, according to data collected from 3,628 patients at one U.S. center.

The three measures are blood urea nitrogen (BUN), systolic blood pressure, and serum creatinine. Using dichotomous cutoffs first calculated a decade ago, these three parameters distinguish up to an eightfold range of postdischarge mortality during the 30 or 90 days following an index hospitalization, and up to a fourfold range of risk for rehospitalization for heart failure during the ensuing 30 or 90 days, Dr. Sithu Win said at the American Heart Association scientific sessions.

Applying this three-measure assessment to patients hospitalized with acute decompensated heart failure “may guide care-transition planning and promote efficient allocation of limited resources,” said Dr. Win, a cardiologist at the Mayo Clinic in Rochester, Minn. The next step is to try to figure out the best way to use this risk prognostication in routine practice, he added.

Researchers published the original analysis that identified BUN, systolic BP, and serum creatinine as key prognostic measures in 2005 using data taken from more than 65,000 U.S. heart failure patients enrolled in ADHERE (Acute Decompensated Heart Failure National Registry) (JAMA. 2005 Feb 2;293[5]:572-80). Using a classification and regression tree analysis, the 2005 study verified dichotomous cutoffs for these three parameters that identified patients at highest risk for in-hospital mortality.

The 2005 study prioritized the application of these cutoffs to define in-hospital mortality risk: first BUN, then the systolic BP criterion, and lastly the serum creatinine criterion. This resulted in five risk levels: Highest-risk patients had a BUN of at least 43 mg/dL, a systolic BP of less than 115 mm Hg, and a serum creatinine of at least 2.75 mg/dL. Lowest-risk patients had a BUN of less than 43 mg/dL and a systolic BP of more than 115 mm Hg. (In lower-risk patients, serum-creatinine level dropped out as a risk determinant.) The analysis also created three categories of patients with intermediate risk based on various combinations of the three measures.

The new study run by Dr. Win and his associates evaluated how this risk-assessment tool developed to predict in-hospital mortality performed for predicting event rates among community-based heart failure patients who had a total of 5,918 hospitalizations for acute decompensated heart failure at the Mayo Clinic during 2000-2013. They averaged 78 years old, half were women, and 48% had heart failure with preserved ejection fraction.

The risk-level distribution of the 3,628 Mayo patients closely matched the pattern seen in the original ADHERE registry: 63% were low risk, 17% were at intermediate level 3 (the lowest risk level in the intermediate range), 13% were at intermediate level 2, 5% at intermediate level 1, and 2% were categorized as high risk.

For 30-day mortality post hospitalization, patients at the highest risk level had a mortality rate eightfold higher than did the lowest-risk patients, those rated intermediate level 1 had a fivefold higher mortality rate, intermediate level 2 patients had a threefold higher rate, and those at intermediate 3 had a 50% higher rate, Dr. Win reported. During the 90 days after discharge, mortality rates relative to the lowest risk level ranged from a sixfold higher rate among the highest-risk patients to a 50% higher rate among patients with an intermediate 3 designation.

Analysis of rehospitalizations for heart failure showed that, by 30 days after hospitalization, the readmission rate ran threefold higher in the highest-risk patients, compared with those at the lowest risk and fourfold higher among those at intermediate risk level 1. Heart failure readmissions by 90 days following the index hospitalization ran threefold higher for both the highest-risk patients as well as those at intermediate level 1, compared with the patients at lowest risk.

The new analyses also showed that roughly similar risk patterns occurred regardless of whether patients had heart failure with reduced or preserved ejection fraction during their index hospitalization, although the relatively increased rate of 30-day mortality with a worse risk profile was most dramatic among patients with reduced ejection fraction. Age, sex, and comorbidity severity did not have a marked effect on the relationships between event rates and risk levels, Dr. Win said.

Dr. Win had no disclosures.

[email protected]

On Twitter @mitchelzoler

ORLANDO – Three simple, routinely collected measurements together provide a lot of insight into the risk faced by community-dwelling patients hospitalized for acute decompensated heart failure, according to data collected from 3,628 patients at one U.S. center.

The three measures are blood urea nitrogen (BUN), systolic blood pressure, and serum creatinine. Using dichotomous cutoffs first calculated a decade ago, these three parameters distinguish up to an eightfold range of postdischarge mortality during the 30 or 90 days following an index hospitalization, and up to a fourfold range of risk for rehospitalization for heart failure during the ensuing 30 or 90 days, Dr. Sithu Win said at the American Heart Association scientific sessions.

Applying this three-measure assessment to patients hospitalized with acute decompensated heart failure “may guide care-transition planning and promote efficient allocation of limited resources,” said Dr. Win, a cardiologist at the Mayo Clinic in Rochester, Minn. The next step is to try to figure out the best way to use this risk prognostication in routine practice, he added.

Researchers published the original analysis that identified BUN, systolic BP, and serum creatinine as key prognostic measures in 2005 using data taken from more than 65,000 U.S. heart failure patients enrolled in ADHERE (Acute Decompensated Heart Failure National Registry) (JAMA. 2005 Feb 2;293[5]:572-80). Using a classification and regression tree analysis, the 2005 study verified dichotomous cutoffs for these three parameters that identified patients at highest risk for in-hospital mortality.

The 2005 study prioritized the application of these cutoffs to define in-hospital mortality risk: first BUN, then the systolic BP criterion, and lastly the serum creatinine criterion. This resulted in five risk levels: Highest-risk patients had a BUN of at least 43 mg/dL, a systolic BP of less than 115 mm Hg, and a serum creatinine of at least 2.75 mg/dL. Lowest-risk patients had a BUN of less than 43 mg/dL and a systolic BP of more than 115 mm Hg. (In lower-risk patients, serum-creatinine level dropped out as a risk determinant.) The analysis also created three categories of patients with intermediate risk based on various combinations of the three measures.

The new study run by Dr. Win and his associates evaluated how this risk-assessment tool developed to predict in-hospital mortality performed for predicting event rates among community-based heart failure patients who had a total of 5,918 hospitalizations for acute decompensated heart failure at the Mayo Clinic during 2000-2013. They averaged 78 years old, half were women, and 48% had heart failure with preserved ejection fraction.

The risk-level distribution of the 3,628 Mayo patients closely matched the pattern seen in the original ADHERE registry: 63% were low risk, 17% were at intermediate level 3 (the lowest risk level in the intermediate range), 13% were at intermediate level 2, 5% at intermediate level 1, and 2% were categorized as high risk.

For 30-day mortality post hospitalization, patients at the highest risk level had a mortality rate eightfold higher than did the lowest-risk patients, those rated intermediate level 1 had a fivefold higher mortality rate, intermediate level 2 patients had a threefold higher rate, and those at intermediate 3 had a 50% higher rate, Dr. Win reported. During the 90 days after discharge, mortality rates relative to the lowest risk level ranged from a sixfold higher rate among the highest-risk patients to a 50% higher rate among patients with an intermediate 3 designation.

Analysis of rehospitalizations for heart failure showed that, by 30 days after hospitalization, the readmission rate ran threefold higher in the highest-risk patients, compared with those at the lowest risk and fourfold higher among those at intermediate risk level 1. Heart failure readmissions by 90 days following the index hospitalization ran threefold higher for both the highest-risk patients as well as those at intermediate level 1, compared with the patients at lowest risk.

The new analyses also showed that roughly similar risk patterns occurred regardless of whether patients had heart failure with reduced or preserved ejection fraction during their index hospitalization, although the relatively increased rate of 30-day mortality with a worse risk profile was most dramatic among patients with reduced ejection fraction. Age, sex, and comorbidity severity did not have a marked effect on the relationships between event rates and risk levels, Dr. Win said.

Dr. Win had no disclosures.

[email protected]

On Twitter @mitchelzoler

ORLANDO – Three simple, routinely collected measurements together provide a lot of insight into the risk faced by community-dwelling patients hospitalized for acute decompensated heart failure, according to data collected from 3,628 patients at one U.S. center.

The three measures are blood urea nitrogen (BUN), systolic blood pressure, and serum creatinine. Using dichotomous cutoffs first calculated a decade ago, these three parameters distinguish up to an eightfold range of postdischarge mortality during the 30 or 90 days following an index hospitalization, and up to a fourfold range of risk for rehospitalization for heart failure during the ensuing 30 or 90 days, Dr. Sithu Win said at the American Heart Association scientific sessions.

Applying this three-measure assessment to patients hospitalized with acute decompensated heart failure “may guide care-transition planning and promote efficient allocation of limited resources,” said Dr. Win, a cardiologist at the Mayo Clinic in Rochester, Minn. The next step is to try to figure out the best way to use this risk prognostication in routine practice, he added.

Researchers published the original analysis that identified BUN, systolic BP, and serum creatinine as key prognostic measures in 2005 using data taken from more than 65,000 U.S. heart failure patients enrolled in ADHERE (Acute Decompensated Heart Failure National Registry) (JAMA. 2005 Feb 2;293[5]:572-80). Using a classification and regression tree analysis, the 2005 study verified dichotomous cutoffs for these three parameters that identified patients at highest risk for in-hospital mortality.

The 2005 study prioritized the application of these cutoffs to define in-hospital mortality risk: first BUN, then the systolic BP criterion, and lastly the serum creatinine criterion. This resulted in five risk levels: Highest-risk patients had a BUN of at least 43 mg/dL, a systolic BP of less than 115 mm Hg, and a serum creatinine of at least 2.75 mg/dL. Lowest-risk patients had a BUN of less than 43 mg/dL and a systolic BP of more than 115 mm Hg. (In lower-risk patients, serum-creatinine level dropped out as a risk determinant.) The analysis also created three categories of patients with intermediate risk based on various combinations of the three measures.

The new study run by Dr. Win and his associates evaluated how this risk-assessment tool developed to predict in-hospital mortality performed for predicting event rates among community-based heart failure patients who had a total of 5,918 hospitalizations for acute decompensated heart failure at the Mayo Clinic during 2000-2013. They averaged 78 years old, half were women, and 48% had heart failure with preserved ejection fraction.

The risk-level distribution of the 3,628 Mayo patients closely matched the pattern seen in the original ADHERE registry: 63% were low risk, 17% were at intermediate level 3 (the lowest risk level in the intermediate range), 13% were at intermediate level 2, 5% at intermediate level 1, and 2% were categorized as high risk.

For 30-day mortality post hospitalization, patients at the highest risk level had a mortality rate eightfold higher than did the lowest-risk patients, those rated intermediate level 1 had a fivefold higher mortality rate, intermediate level 2 patients had a threefold higher rate, and those at intermediate 3 had a 50% higher rate, Dr. Win reported. During the 90 days after discharge, mortality rates relative to the lowest risk level ranged from a sixfold higher rate among the highest-risk patients to a 50% higher rate among patients with an intermediate 3 designation.

Analysis of rehospitalizations for heart failure showed that, by 30 days after hospitalization, the readmission rate ran threefold higher in the highest-risk patients, compared with those at the lowest risk and fourfold higher among those at intermediate risk level 1. Heart failure readmissions by 90 days following the index hospitalization ran threefold higher for both the highest-risk patients as well as those at intermediate level 1, compared with the patients at lowest risk.

The new analyses also showed that roughly similar risk patterns occurred regardless of whether patients had heart failure with reduced or preserved ejection fraction during their index hospitalization, although the relatively increased rate of 30-day mortality with a worse risk profile was most dramatic among patients with reduced ejection fraction. Age, sex, and comorbidity severity did not have a marked effect on the relationships between event rates and risk levels, Dr. Win said.

Dr. Win had no disclosures.

[email protected]

On Twitter @mitchelzoler

THE CASE

A 94-year-old Hispanic man with hypertension, congestive heart failure (CHF), anemia of chronic disease, and end-stage renal disease (ESRD) presented to our facility with weakness and shortness of breath. We diagnosed a CHF exacerbation. Initially, he exhibited some respiratory distress that required observation in the coronary care unit and bi-level positive airway pressure therapy to maintain oxygen saturation. Our patient was then moved to a step-down unit where his primary caregiver, his granddaughter, told the medical team that he was limited at home in some of his instrumental activities of daily living. Specifically, he was unable to prepare meals or manage his finances on his own.

Nephrology was consulted for consideration of hemodialysis (HD) because our patient’s creatinine on admission was 7.2 mg/dL (normal for men is 0.7-1.3 mg/dL) and his estimated glomerular filtration rate (GFR) was 7 mL/min (normal is 90-120 mL/min). The patient’s family was conflicted over whether or not to start HD. Palliative Care was consulted to help establish goals of care.

A decision is made. In light of the patient’s limited functional status and his expressed desire to stay at home with his family and receive limited medical care there, the Nephrology and Palliative Care teams recommended delaying HD despite the patient’s worsening renal function. The patient was discharged home with home care services, and he and the family were instructed to follow up with Nephrology for supportive renal management.

DISCUSSION

The decision to delay HD in patients with ESRD is a difficult one that requires shared decision-making between patients and medical providers. Palliative Care consultation services are often involved in this process.

Recent literature supports an “intent-to-defer” based on an evaluation of the patient’s functionality. This represents a paradigm shift from the previous “intent-to-start-early” treatment strategy. In fact, rather than starting early, the Canadian Society of Nephrology recommends delaying initiation of HD in patients with a GFR <15 mL/min.¹ Close monitoring of these patients by both a primary care physician and nephrologist is essential.

When considering initiation of HD, it’s important to look at the overall benefit of this intervention in light of the patient’s mortality risk and quality of life. Many patients who receive HD—especially the elderly—report that it takes more than 6 hours to recover following a dialysis treatment.²

Not surprisingly, depression is common in elderly HD patients. Compared to their younger cohorts, older HD patients have a 62% increased risk of developing depression.³ Also, patients who are considered frail and are receiving HD have more than 3 times the mortality risk within one year than those who are not (hazard ratio=3.42; 95% confidence interval, 2.45-4.76).⁴ (The researchers’ definition of frailty included poor self-reported physical function, exhaustion/fatigue, low physical activity, and undernutrition.⁴)

Functional status. Although a patient’s age should not be a limiting factor for HD referral, functional status should be considered. Patients with limited functionality and significant dependence have an increased risk of death during the first year of HD.⁵

Palliative approach gains acceptance. It is becoming more accepted within the nephrology community to consider a palliative approach to patients with ESRD. Organizations such as the Renal Physicians Association recommend effective prognostication, early advanced care planning, forgoing HD in patients with a poor prognosis, and involving Palliative Care early in the decision-making process.⁶ Aligning the patient’s goals of care with the appropriate treatment method—particularly in patients with comorbid conditions—is an important practice when caring for those with limited life expectancy and functionality.⁷

THE TAKEAWAY

Intent-to-defer HD may be a preferred strategy when caring for many patients with ESRD. Taking into consideration a patient’s comorbidities and functional status, while considering mortality risk and quality of life are essential. Involving palliative care and nephrology specialists can help patients and families understand HD and make an educated decision regarding when to start it.

THE CASE

A 94-year-old Hispanic man with hypertension, congestive heart failure (CHF), anemia of chronic disease, and end-stage renal disease (ESRD) presented to our facility with weakness and shortness of breath. We diagnosed a CHF exacerbation. Initially, he exhibited some respiratory distress that required observation in the coronary care unit and bi-level positive airway pressure therapy to maintain oxygen saturation. Our patient was then moved to a step-down unit where his primary caregiver, his granddaughter, told the medical team that he was limited at home in some of his instrumental activities of daily living. Specifically, he was unable to prepare meals or manage his finances on his own.

Nephrology was consulted for consideration of hemodialysis (HD) because our patient’s creatinine on admission was 7.2 mg/dL (normal for men is 0.7-1.3 mg/dL) and his estimated glomerular filtration rate (GFR) was 7 mL/min (normal is 90-120 mL/min). The patient’s family was conflicted over whether or not to start HD. Palliative Care was consulted to help establish goals of care.

A decision is made. In light of the patient’s limited functional status and his expressed desire to stay at home with his family and receive limited medical care there, the Nephrology and Palliative Care teams recommended delaying HD despite the patient’s worsening renal function. The patient was discharged home with home care services, and he and the family were instructed to follow up with Nephrology for supportive renal management.

DISCUSSION

The decision to delay HD in patients with ESRD is a difficult one that requires shared decision-making between patients and medical providers. Palliative Care consultation services are often involved in this process.

Recent literature supports an “intent-to-defer” based on an evaluation of the patient’s functionality. This represents a paradigm shift from the previous “intent-to-start-early” treatment strategy. In fact, rather than starting early, the Canadian Society of Nephrology recommends delaying initiation of HD in patients with a GFR <15 mL/min.¹ Close monitoring of these patients by both a primary care physician and nephrologist is essential.

When considering initiation of HD, it’s important to look at the overall benefit of this intervention in light of the patient’s mortality risk and quality of life. Many patients who receive HD—especially the elderly—report that it takes more than 6 hours to recover following a dialysis treatment.²

Not surprisingly, depression is common in elderly HD patients. Compared to their younger cohorts, older HD patients have a 62% increased risk of developing depression.³ Also, patients who are considered frail and are receiving HD have more than 3 times the mortality risk within one year than those who are not (hazard ratio=3.42; 95% confidence interval, 2.45-4.76).⁴ (The researchers’ definition of frailty included poor self-reported physical function, exhaustion/fatigue, low physical activity, and undernutrition.⁴)

Functional status. Although a patient’s age should not be a limiting factor for HD referral, functional status should be considered. Patients with limited functionality and significant dependence have an increased risk of death during the first year of HD.⁵

Palliative approach gains acceptance. It is becoming more accepted within the nephrology community to consider a palliative approach to patients with ESRD. Organizations such as the Renal Physicians Association recommend effective prognostication, early advanced care planning, forgoing HD in patients with a poor prognosis, and involving Palliative Care early in the decision-making process.⁶ Aligning the patient’s goals of care with the appropriate treatment method—particularly in patients with comorbid conditions—is an important practice when caring for those with limited life expectancy and functionality.⁷

THE TAKEAWAY

Intent-to-defer HD may be a preferred strategy when caring for many patients with ESRD. Taking into consideration a patient’s comorbidities and functional status, while considering mortality risk and quality of life are essential. Involving palliative care and nephrology specialists can help patients and families understand HD and make an educated decision regarding when to start it.

THE CASE

A 94-year-old Hispanic man with hypertension, congestive heart failure (CHF), anemia of chronic disease, and end-stage renal disease (ESRD) presented to our facility with weakness and shortness of breath. We diagnosed a CHF exacerbation. Initially, he exhibited some respiratory distress that required observation in the coronary care unit and bi-level positive airway pressure therapy to maintain oxygen saturation. Our patient was then moved to a step-down unit where his primary caregiver, his granddaughter, told the medical team that he was limited at home in some of his instrumental activities of daily living. Specifically, he was unable to prepare meals or manage his finances on his own.

Nephrology was consulted for consideration of hemodialysis (HD) because our patient’s creatinine on admission was 7.2 mg/dL (normal for men is 0.7-1.3 mg/dL) and his estimated glomerular filtration rate (GFR) was 7 mL/min (normal is 90-120 mL/min). The patient’s family was conflicted over whether or not to start HD. Palliative Care was consulted to help establish goals of care.

A decision is made. In light of the patient’s limited functional status and his expressed desire to stay at home with his family and receive limited medical care there, the Nephrology and Palliative Care teams recommended delaying HD despite the patient’s worsening renal function. The patient was discharged home with home care services, and he and the family were instructed to follow up with Nephrology for supportive renal management.

DISCUSSION

The decision to delay HD in patients with ESRD is a difficult one that requires shared decision-making between patients and medical providers. Palliative Care consultation services are often involved in this process.

Recent literature supports an “intent-to-defer” based on an evaluation of the patient’s functionality. This represents a paradigm shift from the previous “intent-to-start-early” treatment strategy. In fact, rather than starting early, the Canadian Society of Nephrology recommends delaying initiation of HD in patients with a GFR <15 mL/min.¹ Close monitoring of these patients by both a primary care physician and nephrologist is essential.

When considering initiation of HD, it’s important to look at the overall benefit of this intervention in light of the patient’s mortality risk and quality of life. Many patients who receive HD—especially the elderly—report that it takes more than 6 hours to recover following a dialysis treatment.²

Not surprisingly, depression is common in elderly HD patients. Compared to their younger cohorts, older HD patients have a 62% increased risk of developing depression.³ Also, patients who are considered frail and are receiving HD have more than 3 times the mortality risk within one year than those who are not (hazard ratio=3.42; 95% confidence interval, 2.45-4.76).⁴ (The researchers’ definition of frailty included poor self-reported physical function, exhaustion/fatigue, low physical activity, and undernutrition.⁴)

Functional status. Although a patient’s age should not be a limiting factor for HD referral, functional status should be considered. Patients with limited functionality and significant dependence have an increased risk of death during the first year of HD.⁵

Palliative approach gains acceptance. It is becoming more accepted within the nephrology community to consider a palliative approach to patients with ESRD. Organizations such as the Renal Physicians Association recommend effective prognostication, early advanced care planning, forgoing HD in patients with a poor prognosis, and involving Palliative Care early in the decision-making process.⁶ Aligning the patient’s goals of care with the appropriate treatment method—particularly in patients with comorbid conditions—is an important practice when caring for those with limited life expectancy and functionality.⁷

THE TAKEAWAY

Intent-to-defer HD may be a preferred strategy when caring for many patients with ESRD. Taking into consideration a patient’s comorbidities and functional status, while considering mortality risk and quality of life are essential. Involving palliative care and nephrology specialists can help patients and families understand HD and make an educated decision regarding when to start it.

A 39-year-old man presented with acute left hip pain and inability to bear weight following a minor trauma. The patient had a history of polycystic kidney disease and was on dialysis. Five years ago he had undergone bilateral nephrectomy and a renal transplantation that subsequently failed.

On examination, the active and passive range of motion of the left hip were limited due to pain. His serum laboratory values were:

• Parathyroid hormone 259.7 pmol/L (reference range 1.5–9.3)
• Calcium 2.32 mmol/L (1.15–1.32)
• Phosphate 3.26 mmol/L (0.8–1.45).

Computed tomography of the pelvis revealed an exophytic calcified lesion with multiple cystic spaces and fluid-fluid levels centered on the left pubis, extending medially into the right pubis and laterally into the left adductor muscle group. An acute pathologic fracture was documented in the left inferior pubic ramus (Figure 1). Other radiographic signs of long-standing hyperparathyroidism were present, including subperiosteal bone resorption at the radial side of the middle phalanges and the clavicle epiphysis.

The differential diagnosis of the pelvic lesion included giant cell tumor of bone with aneurysmal bone-cyst-like changes, osteitis fibrosa cystica, and, less likely, metastatic bone disease. Biopsy of the lesion showed clusters of osteoclast-type giant cells on a background of spindle cells and fibrous stroma that in this clinical context was consistent with the diagnosis of brown tumor (Figure 2).¹

BROWN TUMOR

Brown tumor has been reported in fewer than 2% of patients with primary hyperparathyroidism and in 1.5% to 1.7% of those with secondary hyperparathyroidism (ie, from chronic renal failure, malabsorption, vitamin D deficiency, or hypocalcemia).^2–4 An excess of parathyroid hormone increases the number and activity of osteoclasts, which are responsible for the lytic lesions. Brown tumor is the localized form of osteitis fibrosa cystica and is the most characteristic of the many skeletal changes that accompany secondary hyperparathyroidism.

Brown tumor is named for its color, which results from hemorrhages with accumulation of hemosiderin within the vascularized fibrous tissue. The tumor most commonly affects the pelvis, ribs, long-bone shafts, clavicle, and mandible.⁵ Clinical symptoms are nonspecific and depend on the size and location of the lesion.

Medical management of secondary hyperparathyroidism in dialysis patients involves some combination of phosphate binders (either calcium-containing or non-calcium-containing binders), calcitriol or synthetic vitamin D analogs, and a calcimimetic. Parathyroidectomy is required if drug therapy is ineffective. Surgical excision of brown tumor should be considered in patients who have large bone defects with spontaneous fracture risk or increasing pain. Our patient declined surgical intervention.

A 39-year-old man presented with acute left hip pain and inability to bear weight following a minor trauma. The patient had a history of polycystic kidney disease and was on dialysis. Five years ago he had undergone bilateral nephrectomy and a renal transplantation that subsequently failed.

On examination, the active and passive range of motion of the left hip were limited due to pain. His serum laboratory values were:

• Parathyroid hormone 259.7 pmol/L (reference range 1.5–9.3)
• Calcium 2.32 mmol/L (1.15–1.32)
• Phosphate 3.26 mmol/L (0.8–1.45).

Computed tomography of the pelvis revealed an exophytic calcified lesion with multiple cystic spaces and fluid-fluid levels centered on the left pubis, extending medially into the right pubis and laterally into the left adductor muscle group. An acute pathologic fracture was documented in the left inferior pubic ramus (Figure 1). Other radiographic signs of long-standing hyperparathyroidism were present, including subperiosteal bone resorption at the radial side of the middle phalanges and the clavicle epiphysis.

The differential diagnosis of the pelvic lesion included giant cell tumor of bone with aneurysmal bone-cyst-like changes, osteitis fibrosa cystica, and, less likely, metastatic bone disease. Biopsy of the lesion showed clusters of osteoclast-type giant cells on a background of spindle cells and fibrous stroma that in this clinical context was consistent with the diagnosis of brown tumor (Figure 2).¹

BROWN TUMOR

Brown tumor has been reported in fewer than 2% of patients with primary hyperparathyroidism and in 1.5% to 1.7% of those with secondary hyperparathyroidism (ie, from chronic renal failure, malabsorption, vitamin D deficiency, or hypocalcemia).^2–4 An excess of parathyroid hormone increases the number and activity of osteoclasts, which are responsible for the lytic lesions. Brown tumor is the localized form of osteitis fibrosa cystica and is the most characteristic of the many skeletal changes that accompany secondary hyperparathyroidism.

Brown tumor is named for its color, which results from hemorrhages with accumulation of hemosiderin within the vascularized fibrous tissue. The tumor most commonly affects the pelvis, ribs, long-bone shafts, clavicle, and mandible.⁵ Clinical symptoms are nonspecific and depend on the size and location of the lesion.

Medical management of secondary hyperparathyroidism in dialysis patients involves some combination of phosphate binders (either calcium-containing or non-calcium-containing binders), calcitriol or synthetic vitamin D analogs, and a calcimimetic. Parathyroidectomy is required if drug therapy is ineffective. Surgical excision of brown tumor should be considered in patients who have large bone defects with spontaneous fracture risk or increasing pain. Our patient declined surgical intervention.

A 39-year-old man presented with acute left hip pain and inability to bear weight following a minor trauma. The patient had a history of polycystic kidney disease and was on dialysis. Five years ago he had undergone bilateral nephrectomy and a renal transplantation that subsequently failed.

On examination, the active and passive range of motion of the left hip were limited due to pain. His serum laboratory values were:

• Parathyroid hormone 259.7 pmol/L (reference range 1.5–9.3)
• Calcium 2.32 mmol/L (1.15–1.32)
• Phosphate 3.26 mmol/L (0.8–1.45).

Computed tomography of the pelvis revealed an exophytic calcified lesion with multiple cystic spaces and fluid-fluid levels centered on the left pubis, extending medially into the right pubis and laterally into the left adductor muscle group. An acute pathologic fracture was documented in the left inferior pubic ramus (Figure 1). Other radiographic signs of long-standing hyperparathyroidism were present, including subperiosteal bone resorption at the radial side of the middle phalanges and the clavicle epiphysis.

The differential diagnosis of the pelvic lesion included giant cell tumor of bone with aneurysmal bone-cyst-like changes, osteitis fibrosa cystica, and, less likely, metastatic bone disease. Biopsy of the lesion showed clusters of osteoclast-type giant cells on a background of spindle cells and fibrous stroma that in this clinical context was consistent with the diagnosis of brown tumor (Figure 2).¹

BROWN TUMOR

Brown tumor has been reported in fewer than 2% of patients with primary hyperparathyroidism and in 1.5% to 1.7% of those with secondary hyperparathyroidism (ie, from chronic renal failure, malabsorption, vitamin D deficiency, or hypocalcemia).^2–4 An excess of parathyroid hormone increases the number and activity of osteoclasts, which are responsible for the lytic lesions. Brown tumor is the localized form of osteitis fibrosa cystica and is the most characteristic of the many skeletal changes that accompany secondary hyperparathyroidism.

Brown tumor is named for its color, which results from hemorrhages with accumulation of hemosiderin within the vascularized fibrous tissue. The tumor most commonly affects the pelvis, ribs, long-bone shafts, clavicle, and mandible.⁵ Clinical symptoms are nonspecific and depend on the size and location of the lesion.

Medical management of secondary hyperparathyroidism in dialysis patients involves some combination of phosphate binders (either calcium-containing or non-calcium-containing binders), calcitriol or synthetic vitamin D analogs, and a calcimimetic. Parathyroidectomy is required if drug therapy is ineffective. Surgical excision of brown tumor should be considered in patients who have large bone defects with spontaneous fracture risk or increasing pain. Our patient declined surgical intervention.