© FD-Communications Inc. Obesity Surgery, 15, 2005 137 Obesity Surgery, 15, 137-140 There is experimental evidence but very few human studies that suggest a role for obesity in the forma- tion and progression of some glomerular lesions. We report the case of a morbidly obese male with hema- turia and proteinuria that was subsequently diag- nosed with renal failure which required dialysis. Histological findings of the renal biopsy performed during a laparoscopic gastric bypass are presented. His renal failure resolved with the weight loss. Key words: Morbid obesity, renal failure, dialysis, laparo- scopic gastric bypass, IgA nephropathy Introduction The prevalence of obesity is increasing worldwide and the impact of obesity on metabolic and cardio- vascular diseases has been well documented. However, less attention has been paid to the impact of obesity on the kidney. Obesity is a risk factor for progressive loss of renal function in patients with known kidney disease, and there is increasing evi- dence that obesity may also damage the kidney in otherwise healthy individuals. 1 Increased renal blood flow and glomerular filtration rate as well as microalbuminuria have been described in obesity. 2 It has previously been shown that an increased body mass index (BMI) is associated with microalbumin- uria, especially in hypertensive individuals. 2 The incidence of obesity-related glomerulopathy, defined as focal segmental glomerulosclerosis (FSGS) on biopsy, has increased ten-fold over the last 15 years. 3 In 1974, an association between massive obesity and nephrotic range proteinuria was first reported. 4 Since that time, the development of FSGS has been linked to massive obesity. 5 This obesity-related glomerulopathy (ORG) is an increasingly prevalent disease that is clinically and pathologically distinct from idiopathic FSGS (I-FSGS). 3 Previous experi- mental and clinical evidence suggests that excess body weight and/or obesity are associated with hyperfiltration and glomerulomegaly, with intra- glomerular hypertension as the genesis of a sclerotic lesion. 2,3,6 IgA nephropathy remains an uncommon finding in obesity-associated glomerulonephritis, and the role of excess body weight in both the clinical and patho- logical progression of IgA nephropathy has not been precisely investigated. 7,8 Bonnet et al 8 in their study of IgA nephropathy found a correlation between the disease and the presence of an elevated BMI. 6 Case Report Renal Failure, Glomerulonephritis and Morbid Obesity: Improvement after Rapid Weight Loss following Laparoscopic Gastric Bypass Flavia C. Soto, MD; Guillermo Higa-Sansone, MD; John B. Copley, MD, FACD 1 ; Mariana Berho, MD 2 ; Colleen Kennedy, MD; Emanuelle LoMenzo, MD; David Podkameni, MD; Samuel Szomstein, MD, FACS; Raul J. Rosenthal, MD, FACS The Bariatric Institute and Departments of 1 Nephrology and 2 Pathology, Cleveland Clinic Florida, Weston, FL, USA Reprint requests to: Dr. R. Rosenthal, The Bariatric Institute, Cleveland Clinic Florida, 2950 Cleveland Clinic Blvd., Weston, FL 33331, USA. Fax: 954-659-5256; e-mail: rosentr@ccf.org