ASN Kidney Week 2015

SAN DIEGO – Twice-yearly denosumab effectively increased bone mineral density in kidney transplant recipients, but was associated with more frequent episodes of urinary tract infections and hypocalcemia, results from a randomized trial showed.

“Kidney transplant recipients lose bone mass and are at increased risk for fractures, more so in females than in males,” Dr. Rudolf P. Wuthrich said at Kidney Week 2015, sponsored by the American Society of Nephrology. Results from previous studies suggest that one in five patients may develop a fracture within 5 years after kidney transplantation.

Considering that current therapeutic options to prevent bone loss are limited, Dr. Wuthrich, director of the Clinic for Nephrology at University Hospital Zurich, and his associates assessed the efficacy and safety of receptor activator of nuclear factor–kappaB ligand (RANKL) inhibition with denosumab to improve bone mineralization in the first year after kidney transplantation. They recruited 108 patients from June 2011 to May 2014. Of these, 90 were randomized within 4 weeks after kidney transplant surgery in a 1:1 ratio to receive subcutaneous injections of 60 mg denosumab at baseline and after 6 months, or no treatment. The study’s primary endpoint was the percentage change in bone mineral density measured by DXA at the lumbar spine at 12 months. The study, known as Denosumab for Prevention of Osteoporosis in Renal Transplant Recipients (POSTOP), was limited to adults who had undergone kidney transplantation within 28 days and who were on standard triple immunosuppression, including a calcineurin antagonist, mycophenolate, and steroids.

Dr. Wuthrich reported results from 46 patients in the denosumab group and 44 patients in the control group. At baseline, their mean age was 50 years, 63% were male, and 96% were white. After 12 months, the total lumbar spine BMD increased by 4.6% in the denosumab group and decreased by 0.5% in the control group, for a between-group difference of 5.1% (P less than .0001). Denosumab also significantly increased BMD at the total hip by 1.9% (P = .035) over that in the control group at 12 months.

High-resolution peripheral quantitative computed tomography in a subgroup of 24 patients showed that denosumab also significantly increased BMD and cortical thickness at the distal tibia and radius (P less than .05). Two biomarkers of bone resorption in beta C-terminal telopeptide and urine deoxypyridinoline markedly decreased in the denosumab group, as did two biomarkers of bone formation in procollagen type 1 N-terminal propeptide and bone-specific alkaline phosphatase (P less than .0001).

In terms of adverse events, there were significantly more urinary tract infections in the denosumab group, compared with the control group (15% vs. 9%, respectively), as well as more episodes of diarrhea (9% vs. 5%), and transient hypocalcemia (3% vs. 0.3%). The number of serious adverse events was similar between groups, at 17% and 19%, respectively.

“We had significantly increased bone mineral density at all measured skeletal sites in response to denosumab,” Dr. Wuthrich concluded. “We had a significant increase in bone biomarkers and we can say that denosumab was generally safe in a complex population of immunosuppressed kidney transplant recipients. But it was associated with a higher incidence of urinary tract infections. At this point we have no good explanation as to why this is. We also had a few episodes of transient and asymptomatic hypocalcemia.”

The researchers reported having no financial disclosures.

[email protected]

SAN DIEGO – Twice-yearly denosumab effectively increased bone mineral density in kidney transplant recipients, but was associated with more frequent episodes of urinary tract infections and hypocalcemia, results from a randomized trial showed.

“Kidney transplant recipients lose bone mass and are at increased risk for fractures, more so in females than in males,” Dr. Rudolf P. Wuthrich said at Kidney Week 2015, sponsored by the American Society of Nephrology. Results from previous studies suggest that one in five patients may develop a fracture within 5 years after kidney transplantation.

Considering that current therapeutic options to prevent bone loss are limited, Dr. Wuthrich, director of the Clinic for Nephrology at University Hospital Zurich, and his associates assessed the efficacy and safety of receptor activator of nuclear factor–kappaB ligand (RANKL) inhibition with denosumab to improve bone mineralization in the first year after kidney transplantation. They recruited 108 patients from June 2011 to May 2014. Of these, 90 were randomized within 4 weeks after kidney transplant surgery in a 1:1 ratio to receive subcutaneous injections of 60 mg denosumab at baseline and after 6 months, or no treatment. The study’s primary endpoint was the percentage change in bone mineral density measured by DXA at the lumbar spine at 12 months. The study, known as Denosumab for Prevention of Osteoporosis in Renal Transplant Recipients (POSTOP), was limited to adults who had undergone kidney transplantation within 28 days and who were on standard triple immunosuppression, including a calcineurin antagonist, mycophenolate, and steroids.

Dr. Wuthrich reported results from 46 patients in the denosumab group and 44 patients in the control group. At baseline, their mean age was 50 years, 63% were male, and 96% were white. After 12 months, the total lumbar spine BMD increased by 4.6% in the denosumab group and decreased by 0.5% in the control group, for a between-group difference of 5.1% (P less than .0001). Denosumab also significantly increased BMD at the total hip by 1.9% (P = .035) over that in the control group at 12 months.

High-resolution peripheral quantitative computed tomography in a subgroup of 24 patients showed that denosumab also significantly increased BMD and cortical thickness at the distal tibia and radius (P less than .05). Two biomarkers of bone resorption in beta C-terminal telopeptide and urine deoxypyridinoline markedly decreased in the denosumab group, as did two biomarkers of bone formation in procollagen type 1 N-terminal propeptide and bone-specific alkaline phosphatase (P less than .0001).

In terms of adverse events, there were significantly more urinary tract infections in the denosumab group, compared with the control group (15% vs. 9%, respectively), as well as more episodes of diarrhea (9% vs. 5%), and transient hypocalcemia (3% vs. 0.3%). The number of serious adverse events was similar between groups, at 17% and 19%, respectively.

“We had significantly increased bone mineral density at all measured skeletal sites in response to denosumab,” Dr. Wuthrich concluded. “We had a significant increase in bone biomarkers and we can say that denosumab was generally safe in a complex population of immunosuppressed kidney transplant recipients. But it was associated with a higher incidence of urinary tract infections. At this point we have no good explanation as to why this is. We also had a few episodes of transient and asymptomatic hypocalcemia.”

The researchers reported having no financial disclosures.

[email protected]

SAN DIEGO – Twice-yearly denosumab effectively increased bone mineral density in kidney transplant recipients, but was associated with more frequent episodes of urinary tract infections and hypocalcemia, results from a randomized trial showed.

“Kidney transplant recipients lose bone mass and are at increased risk for fractures, more so in females than in males,” Dr. Rudolf P. Wuthrich said at Kidney Week 2015, sponsored by the American Society of Nephrology. Results from previous studies suggest that one in five patients may develop a fracture within 5 years after kidney transplantation.

Considering that current therapeutic options to prevent bone loss are limited, Dr. Wuthrich, director of the Clinic for Nephrology at University Hospital Zurich, and his associates assessed the efficacy and safety of receptor activator of nuclear factor–kappaB ligand (RANKL) inhibition with denosumab to improve bone mineralization in the first year after kidney transplantation. They recruited 108 patients from June 2011 to May 2014. Of these, 90 were randomized within 4 weeks after kidney transplant surgery in a 1:1 ratio to receive subcutaneous injections of 60 mg denosumab at baseline and after 6 months, or no treatment. The study’s primary endpoint was the percentage change in bone mineral density measured by DXA at the lumbar spine at 12 months. The study, known as Denosumab for Prevention of Osteoporosis in Renal Transplant Recipients (POSTOP), was limited to adults who had undergone kidney transplantation within 28 days and who were on standard triple immunosuppression, including a calcineurin antagonist, mycophenolate, and steroids.

Dr. Wuthrich reported results from 46 patients in the denosumab group and 44 patients in the control group. At baseline, their mean age was 50 years, 63% were male, and 96% were white. After 12 months, the total lumbar spine BMD increased by 4.6% in the denosumab group and decreased by 0.5% in the control group, for a between-group difference of 5.1% (P less than .0001). Denosumab also significantly increased BMD at the total hip by 1.9% (P = .035) over that in the control group at 12 months.

High-resolution peripheral quantitative computed tomography in a subgroup of 24 patients showed that denosumab also significantly increased BMD and cortical thickness at the distal tibia and radius (P less than .05). Two biomarkers of bone resorption in beta C-terminal telopeptide and urine deoxypyridinoline markedly decreased in the denosumab group, as did two biomarkers of bone formation in procollagen type 1 N-terminal propeptide and bone-specific alkaline phosphatase (P less than .0001).

In terms of adverse events, there were significantly more urinary tract infections in the denosumab group, compared with the control group (15% vs. 9%, respectively), as well as more episodes of diarrhea (9% vs. 5%), and transient hypocalcemia (3% vs. 0.3%). The number of serious adverse events was similar between groups, at 17% and 19%, respectively.

“We had significantly increased bone mineral density at all measured skeletal sites in response to denosumab,” Dr. Wuthrich concluded. “We had a significant increase in bone biomarkers and we can say that denosumab was generally safe in a complex population of immunosuppressed kidney transplant recipients. But it was associated with a higher incidence of urinary tract infections. At this point we have no good explanation as to why this is. We also had a few episodes of transient and asymptomatic hypocalcemia.”

The researchers reported having no financial disclosures.

[email protected]

SAN DIEGO – Among incident hemodialysis patients, high-density lipoprotein cholesterol levels remained stable over time in men but mildly decreased over time in women, regardless of age.

In addition, larger deviations in HDL cholesterol in the first 6 months of incident hemodialysis were associated with a higher risk of 5-year all-cause mortality.

Those are key findings from a large analysis of patients who received hemodialysis care over a 4-year period, which was presented at the meeting sponsored by the American Society of Nephrology.

“Elevated high-density lipoprotein cholesterol levels, although protective in the general population, can be associated with higher mortality in hemodialysis patients,” Dr. Kamyar Kalantar-Zadeh and his colleagues wrote in an abstract of the study. “Association of HDL change over time with mortality has yet to be examined.”

Dr. Kalantar-Zadeh of the division of nephrology and hypertension at the University of California, Irvine, and his associates examined changes in HDL cholesterol levels over time in 24,400 incident hemodialysis patients who received care from facilities affiliated with DaVita HealthCare Partners between 2007 and 2011.

They examined the association of delta HDL (HDL cholesterol change between the first and second 91-day interval from dialysis start) and HDL cholesterol trajectory with all-cause mortality, using mixed effect and Cox regression models and adjusted for demographics, comorbidities, and baseline HDL cholesterol. Delta HDL was treated both as a continuous variable using restricted cubic splines and in five categories ranging from less than –6 mg/dL to 6 mg/dL or greater.

The mean age of patients was 65 years, 44% were female, 31% were black, and 66% had diabetes.

Mean baseline HDL cholesterol was 40.5 mg/dL, with an HDL cholesterol change of 1.7 mg/dL. The researchers found that while male patients had no significant change in HDL cholesterol over time, females had a significant decrease in HDL cholesterol (a mean of –0.6mg/dL per year). At the same time, a 6 mg/dL or greater increase or decrease in delta HDL was associated with a 7% and 37% increase in all-cause mortality, respectively, compared with the reference group. Delta HDL mortality associations did not differ across gender.

“Patients who have a greater than 6 mg/dL change in HDL between the first and second patient [tests] have a higher risk of 5-year all-cause mortality,” the researchers concluded. “Change in HDL exhibits a reverse J-shaped association with mortality in hemodialysis patients. Further studies are needed to examine the underlying causes of these HDL changes and pathophysiology leading to higher risk of all-cause mortality.”

The study was supported by funding from the National Institute of Diabetes and Digestive and Kidney Diseases. The researchers reported having no financial disclosures.

[email protected]

SAN DIEGO – Among incident hemodialysis patients, high-density lipoprotein cholesterol levels remained stable over time in men but mildly decreased over time in women, regardless of age.

In addition, larger deviations in HDL cholesterol in the first 6 months of incident hemodialysis were associated with a higher risk of 5-year all-cause mortality.

Those are key findings from a large analysis of patients who received hemodialysis care over a 4-year period, which was presented at the meeting sponsored by the American Society of Nephrology.

“Elevated high-density lipoprotein cholesterol levels, although protective in the general population, can be associated with higher mortality in hemodialysis patients,” Dr. Kamyar Kalantar-Zadeh and his colleagues wrote in an abstract of the study. “Association of HDL change over time with mortality has yet to be examined.”

Dr. Kalantar-Zadeh of the division of nephrology and hypertension at the University of California, Irvine, and his associates examined changes in HDL cholesterol levels over time in 24,400 incident hemodialysis patients who received care from facilities affiliated with DaVita HealthCare Partners between 2007 and 2011.

They examined the association of delta HDL (HDL cholesterol change between the first and second 91-day interval from dialysis start) and HDL cholesterol trajectory with all-cause mortality, using mixed effect and Cox regression models and adjusted for demographics, comorbidities, and baseline HDL cholesterol. Delta HDL was treated both as a continuous variable using restricted cubic splines and in five categories ranging from less than –6 mg/dL to 6 mg/dL or greater.

The mean age of patients was 65 years, 44% were female, 31% were black, and 66% had diabetes.

Mean baseline HDL cholesterol was 40.5 mg/dL, with an HDL cholesterol change of 1.7 mg/dL. The researchers found that while male patients had no significant change in HDL cholesterol over time, females had a significant decrease in HDL cholesterol (a mean of –0.6mg/dL per year). At the same time, a 6 mg/dL or greater increase or decrease in delta HDL was associated with a 7% and 37% increase in all-cause mortality, respectively, compared with the reference group. Delta HDL mortality associations did not differ across gender.

“Patients who have a greater than 6 mg/dL change in HDL between the first and second patient [tests] have a higher risk of 5-year all-cause mortality,” the researchers concluded. “Change in HDL exhibits a reverse J-shaped association with mortality in hemodialysis patients. Further studies are needed to examine the underlying causes of these HDL changes and pathophysiology leading to higher risk of all-cause mortality.”

The study was supported by funding from the National Institute of Diabetes and Digestive and Kidney Diseases. The researchers reported having no financial disclosures.

[email protected]

SAN DIEGO – Among incident hemodialysis patients, high-density lipoprotein cholesterol levels remained stable over time in men but mildly decreased over time in women, regardless of age.

In addition, larger deviations in HDL cholesterol in the first 6 months of incident hemodialysis were associated with a higher risk of 5-year all-cause mortality.

Those are key findings from a large analysis of patients who received hemodialysis care over a 4-year period, which was presented at the meeting sponsored by the American Society of Nephrology.

“Elevated high-density lipoprotein cholesterol levels, although protective in the general population, can be associated with higher mortality in hemodialysis patients,” Dr. Kamyar Kalantar-Zadeh and his colleagues wrote in an abstract of the study. “Association of HDL change over time with mortality has yet to be examined.”

Dr. Kalantar-Zadeh of the division of nephrology and hypertension at the University of California, Irvine, and his associates examined changes in HDL cholesterol levels over time in 24,400 incident hemodialysis patients who received care from facilities affiliated with DaVita HealthCare Partners between 2007 and 2011.

They examined the association of delta HDL (HDL cholesterol change between the first and second 91-day interval from dialysis start) and HDL cholesterol trajectory with all-cause mortality, using mixed effect and Cox regression models and adjusted for demographics, comorbidities, and baseline HDL cholesterol. Delta HDL was treated both as a continuous variable using restricted cubic splines and in five categories ranging from less than –6 mg/dL to 6 mg/dL or greater.

The mean age of patients was 65 years, 44% were female, 31% were black, and 66% had diabetes.

Mean baseline HDL cholesterol was 40.5 mg/dL, with an HDL cholesterol change of 1.7 mg/dL. The researchers found that while male patients had no significant change in HDL cholesterol over time, females had a significant decrease in HDL cholesterol (a mean of –0.6mg/dL per year). At the same time, a 6 mg/dL or greater increase or decrease in delta HDL was associated with a 7% and 37% increase in all-cause mortality, respectively, compared with the reference group. Delta HDL mortality associations did not differ across gender.

“Patients who have a greater than 6 mg/dL change in HDL between the first and second patient [tests] have a higher risk of 5-year all-cause mortality,” the researchers concluded. “Change in HDL exhibits a reverse J-shaped association with mortality in hemodialysis patients. Further studies are needed to examine the underlying causes of these HDL changes and pathophysiology leading to higher risk of all-cause mortality.”

The study was supported by funding from the National Institute of Diabetes and Digestive and Kidney Diseases. The researchers reported having no financial disclosures.

[email protected]

SAN DIEGO – Among patients with chronic kidney disease, LDL cholesterol level was positively associated with risk of atherosclerotic vascular events, regardless of baseline inflammation, according to a large, randomized study.

In addition, lowering LDL cholesterol with ezetimibe/simvastatin was similarly effective in the presence or absence of inflammation.

“There has been substantial interest in the relationship between LDL cholesterol and outcomes in the general population, and in particular among people with kidney disease,” study author Dr. Richard Haynes of the Nuffield Department of Population Health at the University of Oxford (England) said in an interview in advance of the meeting.

“Previous studies have found a paradoxical increased risk of death at low cholesterol levels, which may be due to another disease process – such as inflammation – both lowering cholesterol and increasing the risk of death, thereby creating a false association,” he explained.

Dr. Haynes and his associates set out to determine the relevance of LDL cholesterol and C-reactive protein (CRP) to cardiovascular risk among 9,270 patients with chronic kidney disease who were enrolled in the Study of Heart and Renal Protection (SHARP), in which they received either ezetimibe/simvastatin or placebo.

The researchers used Cox regression to analyze the hazard ratio for all atherosclerotic vascular events over a period of 4.9 years. The effect of ezetimibe/simvastatin on major atherosclerotic events was estimated in the presence and absence of inflammation, which was defined as a CRP of 3 mg/L. The mean age of SHARP participants was 62 years, and 63% were men.

Dr. Ben Storey, a colleague of Dr. Haynes at Oxford, reported the study results at the meeting sponsored by the American Society of Nephrology.

Among all patients, usual LDL was positively associated with the risk of atherosclerotic vascular events (hazard ratio, 1.34). Compared with patients who had low CRP, those with high CRP were at higher risk, but the relationship between LDL-C and atherosclerotic vascular event risk was similar in both groups (HR, 1.32 and 1.41, respectively).

Ezetimibe/simvastatin was similarly effective at reducing major atherosclerotic events in patients with low and high CRP (risk ratio, 0.84 and 0.83, respectively). Sensitivity analyses yielded similar results.

“The observational data from SHARP show that LDL cholesterol is positively associated with the risk of atherosclerotic vascular events, irrespective of baseline inflammation,” Dr. Storey concluded. “The randomized evidence showed that lowering LDL cholesterol was similarly effective in the presence or absence of inflammation, but CRP is associated with vascular risk in [chronic kidney disease].”

The findings’ clinical implications are that inflammation, “while it is relevant to patients’ outcomes, does not modify the beneficial effects of lowering LDL cholesterol,” according to Dr. Haynes, “So, clinicians should not be put off from prescribing statin-based, cholesterol-lowering therapy by the presence – or absence – of inflammation.”

Merck funded SHARP, but the University of Oxford conducted and analyzed the study independently. The Australian National Health and Medical Research Council, the British Heart Foundation, Cancer Research UK, and the UK Medical Research Council provided additional support.

[email protected]

SAN DIEGO – Among patients with chronic kidney disease, LDL cholesterol level was positively associated with risk of atherosclerotic vascular events, regardless of baseline inflammation, according to a large, randomized study.

In addition, lowering LDL cholesterol with ezetimibe/simvastatin was similarly effective in the presence or absence of inflammation.

“There has been substantial interest in the relationship between LDL cholesterol and outcomes in the general population, and in particular among people with kidney disease,” study author Dr. Richard Haynes of the Nuffield Department of Population Health at the University of Oxford (England) said in an interview in advance of the meeting.

“Previous studies have found a paradoxical increased risk of death at low cholesterol levels, which may be due to another disease process – such as inflammation – both lowering cholesterol and increasing the risk of death, thereby creating a false association,” he explained.

Dr. Haynes and his associates set out to determine the relevance of LDL cholesterol and C-reactive protein (CRP) to cardiovascular risk among 9,270 patients with chronic kidney disease who were enrolled in the Study of Heart and Renal Protection (SHARP), in which they received either ezetimibe/simvastatin or placebo.

The researchers used Cox regression to analyze the hazard ratio for all atherosclerotic vascular events over a period of 4.9 years. The effect of ezetimibe/simvastatin on major atherosclerotic events was estimated in the presence and absence of inflammation, which was defined as a CRP of 3 mg/L. The mean age of SHARP participants was 62 years, and 63% were men.

Dr. Ben Storey, a colleague of Dr. Haynes at Oxford, reported the study results at the meeting sponsored by the American Society of Nephrology.

Among all patients, usual LDL was positively associated with the risk of atherosclerotic vascular events (hazard ratio, 1.34). Compared with patients who had low CRP, those with high CRP were at higher risk, but the relationship between LDL-C and atherosclerotic vascular event risk was similar in both groups (HR, 1.32 and 1.41, respectively).

Ezetimibe/simvastatin was similarly effective at reducing major atherosclerotic events in patients with low and high CRP (risk ratio, 0.84 and 0.83, respectively). Sensitivity analyses yielded similar results.

“The observational data from SHARP show that LDL cholesterol is positively associated with the risk of atherosclerotic vascular events, irrespective of baseline inflammation,” Dr. Storey concluded. “The randomized evidence showed that lowering LDL cholesterol was similarly effective in the presence or absence of inflammation, but CRP is associated with vascular risk in [chronic kidney disease].”

The findings’ clinical implications are that inflammation, “while it is relevant to patients’ outcomes, does not modify the beneficial effects of lowering LDL cholesterol,” according to Dr. Haynes, “So, clinicians should not be put off from prescribing statin-based, cholesterol-lowering therapy by the presence – or absence – of inflammation.”

Merck funded SHARP, but the University of Oxford conducted and analyzed the study independently. The Australian National Health and Medical Research Council, the British Heart Foundation, Cancer Research UK, and the UK Medical Research Council provided additional support.

[email protected]

SAN DIEGO – Among patients with chronic kidney disease, LDL cholesterol level was positively associated with risk of atherosclerotic vascular events, regardless of baseline inflammation, according to a large, randomized study.

In addition, lowering LDL cholesterol with ezetimibe/simvastatin was similarly effective in the presence or absence of inflammation.

“There has been substantial interest in the relationship between LDL cholesterol and outcomes in the general population, and in particular among people with kidney disease,” study author Dr. Richard Haynes of the Nuffield Department of Population Health at the University of Oxford (England) said in an interview in advance of the meeting.

“Previous studies have found a paradoxical increased risk of death at low cholesterol levels, which may be due to another disease process – such as inflammation – both lowering cholesterol and increasing the risk of death, thereby creating a false association,” he explained.

Dr. Haynes and his associates set out to determine the relevance of LDL cholesterol and C-reactive protein (CRP) to cardiovascular risk among 9,270 patients with chronic kidney disease who were enrolled in the Study of Heart and Renal Protection (SHARP), in which they received either ezetimibe/simvastatin or placebo.

The researchers used Cox regression to analyze the hazard ratio for all atherosclerotic vascular events over a period of 4.9 years. The effect of ezetimibe/simvastatin on major atherosclerotic events was estimated in the presence and absence of inflammation, which was defined as a CRP of 3 mg/L. The mean age of SHARP participants was 62 years, and 63% were men.

Dr. Ben Storey, a colleague of Dr. Haynes at Oxford, reported the study results at the meeting sponsored by the American Society of Nephrology.

Among all patients, usual LDL was positively associated with the risk of atherosclerotic vascular events (hazard ratio, 1.34). Compared with patients who had low CRP, those with high CRP were at higher risk, but the relationship between LDL-C and atherosclerotic vascular event risk was similar in both groups (HR, 1.32 and 1.41, respectively).

Ezetimibe/simvastatin was similarly effective at reducing major atherosclerotic events in patients with low and high CRP (risk ratio, 0.84 and 0.83, respectively). Sensitivity analyses yielded similar results.

“The observational data from SHARP show that LDL cholesterol is positively associated with the risk of atherosclerotic vascular events, irrespective of baseline inflammation,” Dr. Storey concluded. “The randomized evidence showed that lowering LDL cholesterol was similarly effective in the presence or absence of inflammation, but CRP is associated with vascular risk in [chronic kidney disease].”

The findings’ clinical implications are that inflammation, “while it is relevant to patients’ outcomes, does not modify the beneficial effects of lowering LDL cholesterol,” according to Dr. Haynes, “So, clinicians should not be put off from prescribing statin-based, cholesterol-lowering therapy by the presence – or absence – of inflammation.”

Merck funded SHARP, but the University of Oxford conducted and analyzed the study independently. The Australian National Health and Medical Research Council, the British Heart Foundation, Cancer Research UK, and the UK Medical Research Council provided additional support.

[email protected]

SAN DIEGO – The prevalence of kidney stone disease appears to be rising in the United States.

According to an analysis of responses from the 2007-2012 National Health and Nutrition Examination Survey (NHANES), 8.8% of people in the United States have kidney stone disease (Eur Urol. 2012 Jul;62[1]:160-5), up from a prevalence of 5.2% observed in the 1988-1994 NHANES.

“There’s also been a marked increase in emergency room visits for kidney stones: 91% between 1994 and 2006,” Dr. Anna L. Zisman said at the meeting sponsored by the American Society of Nephrology.

“Unfortunately, it doesn’t only affect adults. There has been an increased incidence in ER visits for kids as well.” Though good national data on the incidence of kidney stone disease in children are lacking, one study conducted in South Carolina found that the incidence of ER visits in children rose from 8 per 100,000 in 1996 to more than 18 per 100,000 in 2007 (J Pediatr. 2010 Jul;157[1]:132-7).

What’s driving these increases? Dr. Zisman, a nephrologist at the University of Chicago, discussed a “recipe” for how to create a kidney stone, with heredity as the first step.

“Pick your parents well,” she said. “The familial clustering index is higher for nephrolithiasis than for diabetes and hypertension. A family history of stone disease is present in 16%-37% of stone formers, compared with 4%-12% of healthy controls. And the heritability estimates – how much of a given disease or trait can be attributable to genetic predisposition – is somewhere between 46% and 63%.”

According to Mayo Clinic researchers, heritable traits for kidney stone disease based on 24-hour urine measurements, adjusted for diet, include calcium, magnesium, pH, and citrate (Clin J Am Soc Nephrol. 2014 May;9[5]:943-50).

“Hypercalciuria is the most well-established risk factor for stone disease,” Dr. Zisman said. “Up to 50% of subjects with stones have a history of hypercalciuria, and 43% of first-degree relatives of hypercalciuric patients have hypercalciuria.”

Race and gender are two factors people can’t control in their risk for kidney stone disease. NHANES data suggest that non-Hispanic whites are at highest risk for stone formation, compared with Hispanics and non-Hispanic blacks. However, among whites and all of the racial categories, males have a higher risk than females.

Step two in the recipe for stone formation is timing: Age matters.

According to an analysis of 49,976 men who participated in the Health Professionals Follow-Up Study, the highest risk of stone formation was in male patients in their 40s (J Am Soc Nephrol. 2004 Dec;15[12]:3225-32). By the time white males reach their 70s, the prevalence is almost 19%, while the prevalence for white women in their 70s is 9.4% (Eur Urol. 2012 Jul;62[1]:160-5).

Step three in the recipe is location. According to Dr. Zisman, the prevalence of kidney stone disease across the world is quite varied. “That likely has to do with both genetic predispositions as well as environmental factors,” she noted. “For example, Iran, which has a pretty warm climate, has a prevalence of 5.7%, Greece 15.2%, whereas Argentina only 4%. In the United States, data suggest that the highest incidence of stone disease is in the south. It is suspected that this is due to more men working outside in manual labor in the heat, but that’s just a hypothesis.”

Step four in the recipe involves the role of certain nutrients. For example, a higher daily calcium intake is associated with a lower risk of kidney stone formation. “The theory is that with higher dietary calcium, your urine oxalate tends to drop,” she said. Increased intake of magnesium, protein, potassium, and fluid are also associated with decreased stone formation.

On the other hand, a higher daily vitamin C intake is associated with an increased risk of stone formation. Specifically, a daily intake of more than 1,000 mg confers a 41% increased risk, compared with a lower intake. “The theory there is that vitamin C intake, once absorbed, results in a higher urine oxalate,” Dr. Zisman said.

Current epidemiology literature draws no clear association between a high-sodium diet and the development of kidney stones. From a clinical standpoint, however, “I think everyone would recommend a low-sodium diet because of the physiologic mechanisms leading to higher urine calcium,” she said.

Higher body mass index and increased waist circumference also impact the risk of developing kidney stones, especially among women. “The higher [they are], the greater the risk,” Dr. Zisman said. “We know that as weight goes up, urinary pH drops. Another potential reason is that as body weight goes up, urinary oxalate goes up as well.”

Step five in the recipe for stone formation is occupation. A study from Israel found that lifeguards in that country faced about a 20-fold increased risk of kidney stones, compared with that of the general population (Adv Exp Med Biol. 1980;128:467-72). Meanwhile, a study of glass factory workers in Italy found that the prevalence of kidney stones was 8.5% among those exposed to blast furnace sites, compared with 2.4% among those who worked in ambient temperatures (P = .03) (J Urol 1993 Dec;150[6]:1757-60). A similar finding was observed in a more recent study of steel factory workers in Brazil (Urology 2005;65[5]:858-61).

Variations to the “recipe” for kidney stones include certain genetic diseases such as primary hyperoxaluria and Dent disease; anatomic variations such as horseshoe kidney and ileal conduits; coexisting disease such as inflammatory bowel disease and primary hyperparathyroidism; and effects from medication such as acetazolamide/topiramate and prednisone.

“Mix up genetic predisposition, environmental factors, and dietary/lifestyle factors and add the magic ingredient,” Dr. Zisman concluded. “There is something that is affecting some people and not others. We don’t know what that is, and we clearly need more research.”

Dr. Zisman reported having no financial disclosures.

[email protected]

SAN DIEGO – The prevalence of kidney stone disease appears to be rising in the United States.

According to an analysis of responses from the 2007-2012 National Health and Nutrition Examination Survey (NHANES), 8.8% of people in the United States have kidney stone disease (Eur Urol. 2012 Jul;62[1]:160-5), up from a prevalence of 5.2% observed in the 1988-1994 NHANES.

“There’s also been a marked increase in emergency room visits for kidney stones: 91% between 1994 and 2006,” Dr. Anna L. Zisman said at the meeting sponsored by the American Society of Nephrology.

“Unfortunately, it doesn’t only affect adults. There has been an increased incidence in ER visits for kids as well.” Though good national data on the incidence of kidney stone disease in children are lacking, one study conducted in South Carolina found that the incidence of ER visits in children rose from 8 per 100,000 in 1996 to more than 18 per 100,000 in 2007 (J Pediatr. 2010 Jul;157[1]:132-7).

What’s driving these increases? Dr. Zisman, a nephrologist at the University of Chicago, discussed a “recipe” for how to create a kidney stone, with heredity as the first step.

“Pick your parents well,” she said. “The familial clustering index is higher for nephrolithiasis than for diabetes and hypertension. A family history of stone disease is present in 16%-37% of stone formers, compared with 4%-12% of healthy controls. And the heritability estimates – how much of a given disease or trait can be attributable to genetic predisposition – is somewhere between 46% and 63%.”

According to Mayo Clinic researchers, heritable traits for kidney stone disease based on 24-hour urine measurements, adjusted for diet, include calcium, magnesium, pH, and citrate (Clin J Am Soc Nephrol. 2014 May;9[5]:943-50).

“Hypercalciuria is the most well-established risk factor for stone disease,” Dr. Zisman said. “Up to 50% of subjects with stones have a history of hypercalciuria, and 43% of first-degree relatives of hypercalciuric patients have hypercalciuria.”

Race and gender are two factors people can’t control in their risk for kidney stone disease. NHANES data suggest that non-Hispanic whites are at highest risk for stone formation, compared with Hispanics and non-Hispanic blacks. However, among whites and all of the racial categories, males have a higher risk than females.

Step two in the recipe for stone formation is timing: Age matters.

According to an analysis of 49,976 men who participated in the Health Professionals Follow-Up Study, the highest risk of stone formation was in male patients in their 40s (J Am Soc Nephrol. 2004 Dec;15[12]:3225-32). By the time white males reach their 70s, the prevalence is almost 19%, while the prevalence for white women in their 70s is 9.4% (Eur Urol. 2012 Jul;62[1]:160-5).

Step three in the recipe is location. According to Dr. Zisman, the prevalence of kidney stone disease across the world is quite varied. “That likely has to do with both genetic predispositions as well as environmental factors,” she noted. “For example, Iran, which has a pretty warm climate, has a prevalence of 5.7%, Greece 15.2%, whereas Argentina only 4%. In the United States, data suggest that the highest incidence of stone disease is in the south. It is suspected that this is due to more men working outside in manual labor in the heat, but that’s just a hypothesis.”

Step four in the recipe involves the role of certain nutrients. For example, a higher daily calcium intake is associated with a lower risk of kidney stone formation. “The theory is that with higher dietary calcium, your urine oxalate tends to drop,” she said. Increased intake of magnesium, protein, potassium, and fluid are also associated with decreased stone formation.

On the other hand, a higher daily vitamin C intake is associated with an increased risk of stone formation. Specifically, a daily intake of more than 1,000 mg confers a 41% increased risk, compared with a lower intake. “The theory there is that vitamin C intake, once absorbed, results in a higher urine oxalate,” Dr. Zisman said.

Current epidemiology literature draws no clear association between a high-sodium diet and the development of kidney stones. From a clinical standpoint, however, “I think everyone would recommend a low-sodium diet because of the physiologic mechanisms leading to higher urine calcium,” she said.

Higher body mass index and increased waist circumference also impact the risk of developing kidney stones, especially among women. “The higher [they are], the greater the risk,” Dr. Zisman said. “We know that as weight goes up, urinary pH drops. Another potential reason is that as body weight goes up, urinary oxalate goes up as well.”

Step five in the recipe for stone formation is occupation. A study from Israel found that lifeguards in that country faced about a 20-fold increased risk of kidney stones, compared with that of the general population (Adv Exp Med Biol. 1980;128:467-72). Meanwhile, a study of glass factory workers in Italy found that the prevalence of kidney stones was 8.5% among those exposed to blast furnace sites, compared with 2.4% among those who worked in ambient temperatures (P = .03) (J Urol 1993 Dec;150[6]:1757-60). A similar finding was observed in a more recent study of steel factory workers in Brazil (Urology 2005;65[5]:858-61).

Variations to the “recipe” for kidney stones include certain genetic diseases such as primary hyperoxaluria and Dent disease; anatomic variations such as horseshoe kidney and ileal conduits; coexisting disease such as inflammatory bowel disease and primary hyperparathyroidism; and effects from medication such as acetazolamide/topiramate and prednisone.

“Mix up genetic predisposition, environmental factors, and dietary/lifestyle factors and add the magic ingredient,” Dr. Zisman concluded. “There is something that is affecting some people and not others. We don’t know what that is, and we clearly need more research.”

Dr. Zisman reported having no financial disclosures.

[email protected]

SAN DIEGO – The prevalence of kidney stone disease appears to be rising in the United States.

According to an analysis of responses from the 2007-2012 National Health and Nutrition Examination Survey (NHANES), 8.8% of people in the United States have kidney stone disease (Eur Urol. 2012 Jul;62[1]:160-5), up from a prevalence of 5.2% observed in the 1988-1994 NHANES.

“There’s also been a marked increase in emergency room visits for kidney stones: 91% between 1994 and 2006,” Dr. Anna L. Zisman said at the meeting sponsored by the American Society of Nephrology.

“Unfortunately, it doesn’t only affect adults. There has been an increased incidence in ER visits for kids as well.” Though good national data on the incidence of kidney stone disease in children are lacking, one study conducted in South Carolina found that the incidence of ER visits in children rose from 8 per 100,000 in 1996 to more than 18 per 100,000 in 2007 (J Pediatr. 2010 Jul;157[1]:132-7).

What’s driving these increases? Dr. Zisman, a nephrologist at the University of Chicago, discussed a “recipe” for how to create a kidney stone, with heredity as the first step.

“Pick your parents well,” she said. “The familial clustering index is higher for nephrolithiasis than for diabetes and hypertension. A family history of stone disease is present in 16%-37% of stone formers, compared with 4%-12% of healthy controls. And the heritability estimates – how much of a given disease or trait can be attributable to genetic predisposition – is somewhere between 46% and 63%.”

According to Mayo Clinic researchers, heritable traits for kidney stone disease based on 24-hour urine measurements, adjusted for diet, include calcium, magnesium, pH, and citrate (Clin J Am Soc Nephrol. 2014 May;9[5]:943-50).

“Hypercalciuria is the most well-established risk factor for stone disease,” Dr. Zisman said. “Up to 50% of subjects with stones have a history of hypercalciuria, and 43% of first-degree relatives of hypercalciuric patients have hypercalciuria.”

Race and gender are two factors people can’t control in their risk for kidney stone disease. NHANES data suggest that non-Hispanic whites are at highest risk for stone formation, compared with Hispanics and non-Hispanic blacks. However, among whites and all of the racial categories, males have a higher risk than females.

Step two in the recipe for stone formation is timing: Age matters.

According to an analysis of 49,976 men who participated in the Health Professionals Follow-Up Study, the highest risk of stone formation was in male patients in their 40s (J Am Soc Nephrol. 2004 Dec;15[12]:3225-32). By the time white males reach their 70s, the prevalence is almost 19%, while the prevalence for white women in their 70s is 9.4% (Eur Urol. 2012 Jul;62[1]:160-5).

Step three in the recipe is location. According to Dr. Zisman, the prevalence of kidney stone disease across the world is quite varied. “That likely has to do with both genetic predispositions as well as environmental factors,” she noted. “For example, Iran, which has a pretty warm climate, has a prevalence of 5.7%, Greece 15.2%, whereas Argentina only 4%. In the United States, data suggest that the highest incidence of stone disease is in the south. It is suspected that this is due to more men working outside in manual labor in the heat, but that’s just a hypothesis.”

Step four in the recipe involves the role of certain nutrients. For example, a higher daily calcium intake is associated with a lower risk of kidney stone formation. “The theory is that with higher dietary calcium, your urine oxalate tends to drop,” she said. Increased intake of magnesium, protein, potassium, and fluid are also associated with decreased stone formation.

On the other hand, a higher daily vitamin C intake is associated with an increased risk of stone formation. Specifically, a daily intake of more than 1,000 mg confers a 41% increased risk, compared with a lower intake. “The theory there is that vitamin C intake, once absorbed, results in a higher urine oxalate,” Dr. Zisman said.

Current epidemiology literature draws no clear association between a high-sodium diet and the development of kidney stones. From a clinical standpoint, however, “I think everyone would recommend a low-sodium diet because of the physiologic mechanisms leading to higher urine calcium,” she said.

Higher body mass index and increased waist circumference also impact the risk of developing kidney stones, especially among women. “The higher [they are], the greater the risk,” Dr. Zisman said. “We know that as weight goes up, urinary pH drops. Another potential reason is that as body weight goes up, urinary oxalate goes up as well.”

Step five in the recipe for stone formation is occupation. A study from Israel found that lifeguards in that country faced about a 20-fold increased risk of kidney stones, compared with that of the general population (Adv Exp Med Biol. 1980;128:467-72). Meanwhile, a study of glass factory workers in Italy found that the prevalence of kidney stones was 8.5% among those exposed to blast furnace sites, compared with 2.4% among those who worked in ambient temperatures (P = .03) (J Urol 1993 Dec;150[6]:1757-60). A similar finding was observed in a more recent study of steel factory workers in Brazil (Urology 2005;65[5]:858-61).

Variations to the “recipe” for kidney stones include certain genetic diseases such as primary hyperoxaluria and Dent disease; anatomic variations such as horseshoe kidney and ileal conduits; coexisting disease such as inflammatory bowel disease and primary hyperparathyroidism; and effects from medication such as acetazolamide/topiramate and prednisone.

“Mix up genetic predisposition, environmental factors, and dietary/lifestyle factors and add the magic ingredient,” Dr. Zisman concluded. “There is something that is affecting some people and not others. We don’t know what that is, and we clearly need more research.”

Dr. Zisman 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 – 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.”