Associations of Glomerular Number and Birth Weight With Clinicopathological Features of African Americans and Whites

Background: Hypertension and its cardiovascular complications affect African Americans more severely than whites, a disparity variously ascribed to low birth weight, low glomerular number, an exaggerated arteriolonephrosclerotic blood pressure response, and inflammation-induced oxidative stress. Study Design: Case series. Setting and Participants: Autopsy kidneys of 107 African Americans and 87 whites aged 18 to 65 years at a single medical center between 1998 and 2005. Excluded were persons with known premorbid kidney disease; pathological findings of severe arterioarteriolonephrosclerosis, nodular and diffuse diabetic glomerulosclerosis, or nonischemic cardiomyopathy. Predictors & Outcomes: Associations of: (1) race, age, sex, birth weight, obesity, and glomerular number (predictors) with hypertension and death from coronary artery (CAD) and cerebrovascular disease (CVD; outcomes); and (2) age, blood pressure, and race (predictors) with arteriolonephrosclerotic changes, including chronic tubulointerstitial inflammation (outcomes). Measurements: Hypertension ascertained from chart review and heart weight. Cause of death determined from chart review and autopsy findings. Birth weight obtained from birth records (115 persons). Total glomerular number (N) estimated by using the dissector/fractionator technique. Arteriolosclerosis, glomerulosclerosis, cortical fibrosis, and chronic inflammation by using CD68 density were measured morphometrically. Results: 59 African Americans (55%) and 32 whites (37%) were classified as hypertensive. CAD and CVD were the cause of death in 64 (33%) and 18 persons (9%), respectively. By using multiple linear regression, birth weight (P < 0.001) and sex (P < 0.01), but not race (P = 0.3) or age (P = 0.2), predicted N (P < 0.001; adjusted r = 0.176). Hypertension was associated with African American race (P = 0.04), older age (P < 0.001), and male sex (P = 0.01), but not with N (P = 0.9), body mass index (P = 0.9), or birth weight (P = 0.4). Hypertension was the only significant factor associated with CAD and CVD (P < 0.001 for both). Interactions of age and blood pressure with race showed that although African Americans had more severe hypertension (P < 0.001) and arteriolosclerosis (P = 0.01) at a younger age than whites, there were no significant racial differences in degrees of arteriolosclerosis, glomerulosclerosis, cortical fibrosis, or CD68 density for any level of increased blood pressure. Limitations: The study is observational and descriptive. Conclusions: The more severe hypertension found in African Americans could not be attributed to racial differences in N or birth weight. CAD and CVD death and increased arteriolonephrosclerosis, including CD68 density, were determined by using blood pressure without a significant interacting contribution from race