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Relationship between body mass index and proteinuria in hypertensive nephrosclerosis: results from the African American Study of Kidney Disease and Hypertension (AASK) cohort.

ABSTRACT: Few studies have examined the association between obesity and markers of kidney injury in a chronic kidney disease population. We hypothesized that obesity is independently associated with proteinuria, a marker of chronic kidney disease progression.Observational cross-sectional analysis.Post hoc analysis of baseline data for 652 participants in the African American Study of Kidney Disease (AASK).Obesity, determined using body mass index (BMI).Urine total protein-creatinine ratio and albumin-creatinine ratio measured in 24-hour urine collections.AASK participants had a mean age of 60.2 ± 10.2 years and serum creatinine level of 2.3 ± 1.5 mg/dL; 61.3% were men. Mean BMI was 31.4 ± 7.0 kg/m(2). Approximately 70% of participants had a daily urine total protein excretion rate <300 mg/d. In linear regression analyses adjusted for sex, each 2-kg/m(2) increase in BMI was associated with a 6.7% (95% CI, 3.2-10.4) and 9.4% (95% CI, 4.9-14.1) increase in urine total protein-creatinine and urine albumin-creatinine ratios, respectively. In multivariable models adjusting for age, sex, systolic blood pressure, serum glucose level, uric acid level, and creatinine level, each 2-kg/m(2) increase in BMI was associated with a 3.5% (95% CI, 0.4-6.7) and 5.6% (95% CI, 1.5-9.9) increase in proteinuria and albuminuria, respectively. The interaction between older age and BMI was statistically significant, indicating that this relationship was driven by younger AASK participants.May not generalize to other populations; cross-sectional analysis precludes statements regarding causality.BMI is associated independently with urine total protein and albumin excretion in African Americans with hypertensive nephrosclerosis, particularly in younger patients.

SUBMITTER: Toto RD

PROVIDER: S-EPMC4517588 | biostudies-literature | 2010 Nov

REPOSITORIES: biostudies-literature

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Relationship between body mass index and proteinuria in hypertensive nephrosclerosis: results from the African American Study of Kidney Disease and Hypertension (AASK) cohort.

Toto Robert D RD Greene Tom T Hebert Lee A LA Hiremath Leena L Lea Janice P JP Lewis Julia B JB Pogue Velvie V Sika Mohammed M Wang Xuelei X

American journal of kidney diseases : the official journal of the National Kidney Foundation 20101101 5

<h4>Background</h4>Few studies have examined the association between obesity and markers of kidney injury in a chronic kidney disease population. We hypothesized that obesity is independently associated with proteinuria, a marker of chronic kidney disease progression.<h4>Study design</h4>Observational cross-sectional analysis.<h4>Setting & participants</h4>Post hoc analysis of baseline data for 652 participants in the African American Study of Kidney Disease (AASK).<h4>Predictors</h4>Obesity, de ...[more]

PMID: 20801567

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Project description:BackgroundAnemia is common in chronic kidney disease (CKD) and associated with poor outcomes. In cross-sectional studies, lower estimated glomerular filtration rate (eGFR) has been associated with increased risk for anemia. The aim of this study was to determine how hematocrit changes as eGFR declines and what factors impact this longitudinal association.MethodsWe followed 1094 African-Americans with hypertensive nephropathy who participated in the African-American Study of Kidney Disease and Hypertension. Mixed effects models were used to determine longitudinal change in hematocrit as a function of eGFR. Interaction terms were used to assess for differential effects of age, gender, baseline eGFR, baseline proteinuria, malnutrition and inflammation on eGFR-associated declines in hematocrit. In sensitivity analyses, models were run using iGFR (by renal clearance of I(125) iothalamate) in place of eGFR.ResultsAt baseline, mean hematocrit was 39% and 441 (40%) individuals had anemia. The longitudinal relationship between eGFR and hematocrit differed by baseline eGFR and was steeper when baseline eGFR was <45 mL/min/1.73 m(2). For example, the absolute decline in hematocrit per 10 mL/min/1.73 m(2) decline in longitudinal eGFR was -3.7, -1.3 and -0.5% for baseline eGFR values of 20, 40 and 60 mL/min/1.73 m(2), respectively (P < 0.001 comparing the longitudinal association between baseline eGFR = 40 or 60 versus baseline eGFR = 20 mL/min/1.73 m(2)). Similarly, male sex, younger age (<65 years) and higher baseline proteinuria (protein-to-creatinine ratio >0.22) were associated with greater hematocrit declines per unit decrease in longitudinal eGFR compared with female sex, older age and low baseline proteinuria, respectively (P-interaction <0.05 for each comparison). The longitudinal eGFR-hematocrit association did not differ by body mass index, serum albumin or C-reactive protein.ConclusionsMen, younger individuals and those with low baseline eGFR (<45 mL/min/1.73 m(2)) or baseline proteinuria are particularly at risk for eGFR-related declines in hematocrit.

Project description:Rationale & objectivePatients with a high-risk Apolipoprotein L1 (APOL1) genotype are more likely to develop chronic kidney disease and kidney failure. It is unclear whether this increased risk is entirely mediated by the development of proteinuria.Study designRetrospective observational study of the African American Study of Kidney Disease and Hypertension cohort and Chronic Renal Insufficiency Cohort.Exposures & predictorsSelf-identified race (Black/non-Black) and presence of high-risk APOL1 genotype. The primary model was adjusted for age, sex, diabetes, estimated glomerular filtration rate, and urinary protein-creatinine ratio.OutcomesTime to kidney failure defined as time to dialysis or transplantation.Analytical approachWe used Cox proportional hazard models to study how proteinuria mediates the association between APOL1 and kidney failure. We modeled proteinuria at baseline and as a time-varying covariate.ResultsA high-risk APOL1 genotype was associated with a significantly higher risk of kidney failure, even for patients with minimal proteinuria (HR, 1.87; 95% CI, 1.23-2.84). The association was not significant among patients with high proteinuria (HR, 1.22; 95% CI, 0.93-1.61). When modeling proteinuria as a time-varying covariate, a high-risk APOL1 genotype was associated with higher kidney failure risk even among patients who never developed proteinuria (HR, 2.04; 95% CI, 1.10-3.77). Compared to non-Black patients, Black patients without the high-risk genotype did not have higher risk of kidney failure (HR, 0.96; 95% CI, 0.85-1.10).LimitationsTwo datasets were combined to increase statistical power. Limited generalizability beyond the study cohorts. Residual confounding common to observational studies.ConclusionsA high-risk APOL1 genotype is significantly associated with increased kidney failure risk, especially among patients without baseline proteinuria. Although our results suggest that the risk is partially mediated through proteinuria, higher kidney failure risk was present even among patients who never developed proteinuria. Providers should consider screening for the high-risk APOL1 genotype, especially among Black patients without proteinuria in populations with chronic kidney disease.

Project description:Current research on hypertension utilizes more than fifty animal models that rely mainly on stable increases in systolic blood pressure. In experimental hypertension, grading or scoring of glomerulopathy in the majority of studies is based on a wide range of opinion-based histological changes that do not necessarily comply with lesional descriptors for glomerular injury that are well-established in clinical pathology. Here, we provide a critical appraisal of experimental hypertensive glomerulopathy with the same approach used to assess hypertensive glomerulopathy in humans. Four hypertensive models with varying pathogenesis were analyzed-chronic angiotensin II infused mice, mice expressing active human renin in the liver (TTRhRen), spontaneously hypertensive rats (SHR), and Goldblatt two-kidney one-clip rats (2K1C). Analysis of glomerulopathy utilized the same criteria applied in humans-hyalinosis, focal segmental glomerulosclerosis (FSGS), ischemic, hypertrophic and solidified glomeruli, or global glomerulosclerosis (GGS). Data from animal models were compared to human reference values. Kidneys in TTRhRen mice, SHR and the nonclipped kidneys in 2K1C rats had no sign of hyalinosis, FSGS or GGS. Glomerulopathy in these groups was limited to variations in mesangial and capillary compartment volumes, with mild increases in collagen deposition. Histopathology in angiotensin II infused mice corresponded to mesangioproliferative glomerulonephritis, but not hypertensive glomerulosclerosis. The number of nephrons was significantly reduced in TTRhRen mice and SHR, but did not correlate with severity of glomerulopathy. The most substantial human-like glomerulosclerotic lesions, including FSGS, ischemic obsolescent glomeruli and GGS, were found in the clipped kidneys of 2K1C rats. The comparison of affected kidneys to healthy control in animals produces lesion values that are numerically impressive but correspond to mild damage if compared to humans. Animal studies should be standardized by employing the criteria and classifications established in human pathology to make experimental and human data fully comparable for comprehensive analysis and model improvements.

Dataset Information

Relationship between body mass index and proteinuria in hypertensive nephrosclerosis: results from the African American Study of Kidney Disease and Hypertension (AASK) cohort.

Publications

Relationship between body mass index and proteinuria in hypertensive nephrosclerosis: results from the African American Study of Kidney Disease and Hypertension (AASK) cohort.

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