SummaryBackground and objectives Obesity-related glomerulopathy is a secondary form of glomerular disease that may occur in obese individuals. It is histologically characterized by marked glomerulomegaly closely related to glomerular hyperfiltration. This study examined glomerular density (nonsclerotic glomerular number per renal cortical area of biopsy specimen) in patients with obesity-related glomerulopathy to determine whether any differences in this measure is associated with disease status.Design, setting, participants, & measurements Glomerular density and glomerular volume in renal biopsy samples from patients with obesity-related glomerulopathy were compared with those of kidney transplant donors and patients with IgA nephropathy. Kidneys obtained from persons without renal diseases during autopsy were also analyzed to investigate the effects of obesity on glomerular density and glomerular volume.Results Glomerular density of kidneys from patients with obesity-related glomerulopathy (1.760.6/mm 2 ) was significantly lower than that in biopsy samples from kidney transplant donors (3.161.0/mm 2 ) and patients with IgA nephropathy (3.561.5/mm 2 ). However, an analysis of autopsy cases without renal diseases showed that the glomerular density in overweight (2.960.7/mm 2 ) or obese (3.161.1/mm 2 ) persons was similar to that in nonobese (3.160.6/mm 2 ) individuals. Biopsy specimens of patients with obesity-related glomerulopathy showed marked glomerulomegaly. However, glomerular volume was only modestly increased in the autopsy-examined kidneys from overweight or obese persons without renal diseases.Conclusions Low glomerular density associated with glomerulomegaly may be a characteristic histologic finding of patients with obesity-related glomerulopathy.

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Introduction: Obesity-related glomerulopathy (ORG) is a slowly progressive kidney disease occurring in association with obesity. It is characterized histopathologically by glomerulomegaly, likely caused by single-nephron hyperfiltration that has not been demonstrated in humans because of technical difficulty in measuring single-nephron glomerular filtration rate (SNGFR) in the clinical setting. Methods: Total glomerular number per kidney, with or without global glomerulosclerosis, was estimated by the combination of cortical volume assessment via unenhanced computed tomography and biopsybased stereology. Mean glomerular volume was calculated from the measured area of glomerular tufts. Both SNGFR and single-nephron urinary protein excretion (SNUPE) were estimated by dividing values for estimated glomerular filtration rate and urinary protein excretion by the number of nonsclerotic glomeruli. Living kidney donors were used as healthy controls. Results: A total of 48 ORG patients with average nonsclerotic glomerular numbers of 456,000 AE 235,000 per kidney were included. The values for SNGFR in ORG patients with chronic kidney disease (CKD) stages 1 and 2 were higher than for nonobese and obese controls (97 AE 43 vs. 59 AE 21 vs. 64 AE 21 nl/min, respectively, P ¼ 0.001). Nonsclerotic glomerular number decreased with advancing stages of renal functional impairment. The presence of ORG with more advanced CKD stages was associated with lower SNGFR and marked elevation in SNUPE levels, with no difference in the mean glomerular volume between the stages. Conclusions: These results provide functional evidence for single-nephron hyperfiltration in patients with ORG, and identify compensatory failure to maintain effective SNGFR as a feature of advanced-stage ORG.

A low GD together with marked glomerular enlargement characterizes renal biopsy samples of children born with a LBW at an early stage of gestation.