The effect of a shift in sodium intake on renal hemodynamics is determined by body mass index in healthy young men

Central distribution of body fat is associated with a higher risk of renal disease, but whether it is the distribution pattern or the overall excess weight that underlies this association is not well understood. Here, we studied the association between waist-to-hip ratio (WHR), which reflects central adiposity, and renal hemodynamics in 315 healthy persons with a mean body mass index (BMI) of 24.9 kg/m 2 and a mean 125 I-iothalamate GFR of 109 ml/min per 1.73 m 2 . In multivariate analyses, WHR was associated with lower GFR, lower effective renal plasma flow, and higher filtration fraction, even after adjustment for sex, age, mean arterial pressure, and BMI. Multivariate models produced similar results regardless of whether the hemodynamic measures were indexed to body surface area. Thus, these results suggest that central body fat distribution, independent of BMI, is associated with an unfavorable pattern of renal hemodynamic measures that could underlie the increased renal risk reported in observational studies.

Section: Discussionsupporting

confidence: 78%

Central Body Fat Distribution Associates with Unfavorable Renal Hemodynamics Independent of Body Mass Index

Kwakernaak

Zelle

Bakker

et al. 2013

“…18 Thus, our data suggest that participants with high salt intake had more proteinuria at inclusion because of the association of sodium overload with urinary proteins. [8][9][10][11][24][25][26][27][28] This interpretation is consistent with evidence that, among the 172 controls on non-RAS inhibitor therapy, proteinuria was also more severe in those with high salt intake, while patient characteristics and BP control were similar among salt intake groups. The finding that BP control was independent of daily sodium intake can be explained by the fact that antihypertensive therapy was titrated to predefined BP targets.…”

Section: Discussionsupporting

confidence: 76%

“…The 500 included participants had a mean of 5.462.8 urinary sodium and creatinine measurements over a follow-up of 26.2615.6 months. Twenty-six patients (5.2%) had only one measurement.…”

Section: Baseline Characteristicsmentioning

confidence: 99%

Sodium Intake, ACE Inhibition, and Progression to ESRD

Vegter

Perna

Postma

et al. 2012

271

179

High sodium intake limits the antihypertensive and antiproteinuric effects of angiotensin-converting enzyme (ACE) inhibitors in patients with CKD; however, whether dietary sodium also associates with progression to ESRD is unknown. We conducted a post hoc analysis of the first and second Ramipril Efficacy in Nephropathy trials to evaluate the association of sodium intake with proteinuria and progression to ESRD among 500 CKD patients without diabetes who were treated with ramipril (5 mg/d) and monitored with serial 24-hour urinary sodium and creatinine measurements. Urinary sodium/creatinine excretion defined low (,100 mEq/g), medium (100 to ,200 mEq/g), and high ($200 mEq/g) sodium intake. During a follow-up of .4.25 years, 92 individuals (18.4%) developed ESRD. Among those with low, medium, and high sodium intakes, the incidence of ESRD was 6.1 (95% confidence interval [95% CI], 3.8-9.7), 7.9 (95% CI, 6.1-10.2), and 18.2 (95% CI, 11.3-29.3) per 100 patient-years, respectively (P,0.001). Patients with high dietary sodium exhibited a blunted antiproteinuric effect of ACE inhibition despite similar BP among groups. Each 100-mEq/g increase in urinary sodium/creatinine excretion associated with a 1.61-fold (95% CI, 1.15-2.24) higher risk for ESRD; adjusting for baseline proteinuria attenuated this association to 1.38-fold (95% CI, 0.95-2.00). This association was independent from BP but was lost after adjusting for changes in proteinuria. In summary, among patients with CKD but without diabetes, high dietary salt (.14 g daily) seems to blunt the antiproteinuric effect of ACE inhibitor therapy and increase the risk for ESRD, independent of BP control.

“…Although even small amounts of regular physical activity (150 min/wk) reduce all-cause and particularly, cardiovascular mortality, 75 the effects of physical activity on kidney function have not been studied in obese CKD patients. Because Krikken et al 76 showed that a high-sodium intake elicited hyperfiltration and a high filtration fraction only in subjects with a BMI$25 kg/m 2 , a low-sodium intake should be advocated in obese CKD patients. Moreover, because angiotensin II suppresses 59adenosine monophosphate-activated protein kinase activity in the kidney, which lead to enhanced salt sensitivity, 77 59adenosine monophosphate-activated protein kinase activation or angiotensin II inhibition represents a therapeutic target for obesity-related salt-sensitive hypertension.…”

Section: Treatment Of Obesity In Ckdmentioning

confidence: 99%

Obesity in CKD—What Should Nephrologists Know?

Stenvinkel

Zoccali

İkizler

2013

195

172

Obesity, the epidemic of the 21st century, carries a markedly increased risk for comorbid complications, such as type 2 diabetes, cancer, hypertension, dyslipidemia, cardiovascular disease, and sleep apnea. In addition, obesity increases the risk for CKD and its progression to ESRD. Paradoxically, even morbid obesity associates with better outcomes in studies of ESRD patients on maintenance dialysis. Because the number of obese CKD and maintenance dialysis patients is projected to increase markedly in developed as well as low-and middle-income countries, obesity is a rapidly emerging problem for the international renal community. Targeting the obesity epidemic represents an unprecedented opportunity for health officials to ameliorate the current worldwide increase in CKD prevalence. Nephrologists need more information about assessing and managing obesity in the setting of CKD. Specifically, more precise estimation of regional fat distribution and the amount of muscle mass should be introduced into regular clinical practice to complement more commonly used practical markers, such as body mass index. Studies examining the effects of obesity on kidney disease progression and other clinical outcomes along with weight management strategies are much needed in this orphan area of research. 24: 172724: -173624: , 201324: . doi: 10.1681 Obesity has emerged as the largest pandemic in near history, with important implications of not only cardiovascular disease (CVD) but also CKD. Recent data from the United States indicate that the incidence and prevalence rates of obesity in maintenance dialysis patients largely exceed the corresponding figures in the general population. 1 A large European population survey documented that a high body mass index (BMI) ranks as one of the strongest risk factors for new-onset CKD. 2 The dimension of the obesity epidemic and the impact of the same epidemic on the kidney demand efforts for understanding the epidemiology and the mechanisms of CKD associated with excess adiposity. It also sets as an absolute public health priority for the development of treatment policies integrated across specialties and general practice to halt this much concerning problem. In this scenario, it is fundamental that nephrologists are updated on current knowledge about obesity in the setting of CKD. However, little attention is still paid to this issue in major nephrology journals. The suboptimal attention to the problem by major sources of dissemination of specialty information suggests that nephrologists may have scarce knowledge of how obesity should be assessed, its epidemiology, mechanisms whereby excess fat mass is conducive to CKD, and management of obesity in the catabolic uremic milieu. 3 J Am Soc Nephrol DEFINITION AND ASSESSMENT OF OBESITYThe most common method for defining obesity is based on BMI (i.e., a person's weight as obese. It should be emphasized that population norms of BMI could be different based on ethnic and racial background (i.e., the proportion of Asian people with a high ...