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Obesity-Related Glomerulopathy: an Emerging Epidemic

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Obesity-Related Glomerulopathy: an Emerging Epidemic Kidney International, Vol. 59 (2001), pp. 1498±1509 Obesity-related glomerulopathy: An emerging epidemic NEERAJA KAMBHAM,GLEN S. MARKOWITZ,ANTHONY M. VALERI,JULIE LIN, and VIVETTE D. D'AGATI Departments of Pathology and Medicine, Columbia University, College of Physicians and Surgeons, New York, New York USA Obesity-related glomerulopathy: An emerging epidemic. cess fusion. The ten-fold increase in incidence over 15 years Background. We report the ®rst large renal biopsy-based suggests a newly emerging epidemic. Heightened physician clinicopathologic study on obesity-related glomerulopathy. awareness of this entity is needed to ensure accurate diagnosis Methods. Obesity was de®ned as body mass index (BMI) and appropriate therapy. Ͼ30 kg/m2. Obesity-related glomerulopathy (ORG) was de- ®ned morphologically as focal segmental glomerulosclerosis and glomerulomegaly (O-FSGS; N ϭ 57) or glomerulomegaly alone (O-GM; N ϭ 14). Cross-sectional epidemiologic studies indicate that the Results. Review of 6818 native renal biopsies received from prevalence of obesity in the United States and other 1986 to 2000 revealed a progressive increase in biopsy incidence Western countries has been steadily rising over the past of ORG from 0.2% in 1986±1990 to 2.0% in 1996±2000 (P ϭ two decades, a trend that has been linked to changing 0.0001). Mean BMI in ORG was 41.7 (range 30.9 to 62.7). dietary habits and sedentary lifestyle [1±3]. This in- Indications for renal biopsy included proteinuria (N ϭ 40) or proteinuria and renal insuf®ciency (N ϭ 31). Seventy-one creased prevalence has been reported in both children patients with ORG were compared to 50 patients with idio- and adults, and across diverse ethnic groups [1]. Ac- pathic FSGS (I-FSGS). Patients with ORG were older (mean cording to the National Health and Nutrition Examina- 42.9 vs. 32.6 years, P Ͻ 0.001) and more often Caucasian (75% ϭ tion Survey, the prevalence of obesity (de®ned as body vs. 52%; P 0.003). ORG patients had a lower incidence of Ͼ nephrotic range proteinuria (48% vs. 66%; P ϭ 0.007) and mass index, BMI 30) has increased from 14.1% to nephrotic syndrome (5.6% vs. 54%; P Ͻ 0.001), with higher 22.5% between 1971 and 1994, and 54.9% of the U.S. serum albumin (3.9 vs. 2.9 g/dL; P Ͻ 0.001), lower serum population is overweight (BMI Ͼ25) [1]. Obese patients cholesterol (229 vs. 335 mg/dL; P Ͻ 0.001), and less edema are at greater risk to develop sleep apnea, hyperlipid- ϭ (35% vs. 68%; P 0.003). On renal biopsy, patients with ORG emia, hypertension, coronary vascular disease, insulin had fewer lesions of segmental sclerosis (10 vs. 39%; P Ͻ 0.001), more glomerulomegaly (100% vs. 10%; P Ͻ 0.001), and resistance and diabetes [4±6]. less extensive foot process effacement (40 vs. 75%; P Ͻ 0.001). The renal effects of obesity in experimental animals Glomerular diameter in ORG (mean 226 ␮) was signi®cantly and humans include both structural and functional adap- larger than age- and sex-matched normal controls (mean 168 ␮; tations, such as increased glomerular ®ltration rate, in- Ͻ P 0.001). Follow-up was available in 56 ORG patients (mean creased renal blood ¯ow, and renal hypertrophy [7, 8]. 27 months) and 50 idiopathic FSGS controls (mean 38 months). A total of 75% of ORG patients received angiotensin-con- In 1974, an association between massive obesity and verting enzyme (ACE) inhibition or A2 blockade while 78% nephrotic-range proteinuria was ®rst reported [9]. Since of the I-FSGS patients received immunosuppressive therapy. that time, the development of glomerulomegaly and fo- ORG patients had less frequent doubling of serum creatinine cal segmental glomerulosclerosis (FSGS) has been linked Ͻ (14.3% vs. 50%; P 0.001) and progression to ESRD (3.6% to massive obesity [8, 10±14]. Most of these associations vs. 42%; P Ͻ 0.001). On multivariate analysis, presenting serum creatinine and severity of proteinuria were the only predictors have been limited to case reports or small autopsy series. of poor outcome in ORG. Thus, little is known about the overall prevalence of Conclusion. ORG is distinct from idiopathic FSGS, with a biopsy-documented obesity-related glomerulopathy, its lower incidence of nephrotic syndrome, more indolent course, presenting clinical features, morphologic manifestations, consistent presence of glomerulomegaly, and milder foot pro- or natural history. The current study was designed to determine the Key words: focal segmental glomerulosclerosis, nephrotic syndrome, changing biopsy incidence of obesity-related glomeru- overweight, glomerulomegaly. lopathy (ORG) over the past 15 years. To better de®ne the spectrum of clinical and pathologic features of this Received for publication June 27, 2000 and in revised form October 23, 2000 entity, a cohort of ORG was compared to controls with Accepted for publication October 26, 2000 idiopathic FSGS (I-FSGS). Our ®ndings indicate that 2001 by the International Society of Nephrology ORG is an increasingly prevalent disease that is clinically 1498 Kambham et al: Obesity-related glomerulopathy 1499 and pathologically distinct from I-FSGS. The differenti- (excluding cellular and collapsing variants) diagnosed ating clinicopathologic features of ORG have important from 1980 to 1992. implications for patient management and prognosis. Renal biopsies for the study cohort and controls were processed for light microscopy, immuno¯uorescence (IF) and electron microscopy (EM) according to stan- METHODS dard techniques. At least 11 serial sections (3 ␮m thick) All native renal biopsies accessioned in the Renal Pa- were stained with hematoxylin and eosin, periodic-acid thology Laboratory of Columbia Presbyterian Medical Schiff (PAS), Masson's trichrome and Jones methena- Center from January 1986 to April 2000 were reviewed mine-silver stains (JMS). Routine IF was performed on retrospectively for evidence of ORG. Obesity was de- ␮ Ͼ 3 m cryostat sections using polyclonal FITC-conjugated ®ned as a BMI 30, calculated as body weight in kilo- antibodies to IgG, IgM, IgA, C3, C1q, ␬, ␭, ®brinogen grams divided by the square of height in meters [1, 15]. and albumin (Dako Corporation, Carpenteria, CA, ORG was de®ned morphologically as (1) obesity-associ- USA). In 61 of 71 ORG cases, adequate glomerular ated FSGS with glomerulomegaly (O-FSGS) or (2) obe- tissue was available for EM. sity-associated glomerulomegaly alone (O-GM). Renal Juxtaglomerular apparatus (JGA) hyperplasia was de- biopsies from obese patients with other underlying con- ®ned as Ͼ8 nuclei per cross section of JGA [18]. Tubular ditions that could cause secondary FSGS (such as HIV atrophy, interstitial ®brosis and in¯ammation were infection, heroin abuse, solitary kidney, congenital heart graded semiquantitatively on a scale of 0 to 3ϩ based disease, sickle cell disease, renal dysplasia, or any other on the % cortical area affected: 0 ϭ absent; 1ϩϭ1±25%; pre-existing renal disease with loss of renal mass) were 2ϩϭ26±50% and 3ϩϾ50%. Arteriosclerosis and arte- carefully excluded. Moreover, other de®ned primary and riolosclerosis were graded as follows: 0 ϭ absent; 1ϩϭ secondary glomerular diseases including diabetic ne- ϩϭ ϩϭ phropathy and hypertensive nephrosclerosis occurring mild; 2 moderate; 3 severe. The intensity of in obese patients were eliminated. Of all 6818 native staining by immuno¯uorescence was graded on a scale ϩ Ϫ ϩ biopsies received during this period, a total of 103 cases of trace ( / )to3 . The percentage of foot process met the entry criteria. From this group, 71 cases with effacement was estimated based on examination of all adequate clinical information were studied. Because of nonsclerotic glomerular capillaries in all ®elds. the limited follow-up, newly diagnosed cases of obesity- Measurement of glomerular diameter was performed related glomerulopathy from the year 2000 were ex- using a light microscopic eyepiece with built-in micro- cluded. meter (Olympus Scienti®c, Tokyo, Japan). The conver- Patient charts were reviewed for age, sex, race, and sion factor for each objective was calibrated against a presenting clinical and laboratory features at the time standard by the manufacturer. Four levels of biopsy tis- of renal biopsy. From the height and weight at the time sue (PAS and JMS stains) were studied in each case. All of renal biopsy, BMI was calculated. Obesity was de®ned glomeruli cut at or near the hilus were measured. Two as BMI Ͼ30 kg/m2: BMI 30.0 to 34.9 kg/m2, class I obesity; perpendicular diameters extending between the farthest BMI 35.0 to 39.9 kg/m2, class II obesity; BMI Ն40 kg/m2, glomerular basement membrane points were measured ␮ class III or ªmorbidº obesity. The following de®nitions per glomerulus. The mean glomerular diameter ( m) were used: hypertension (HTN), systolic pressure Ͼ140 was calculated from a total of 5 to 30 (mean 15) glomeruli mm Hg and diastolic pressure Ͼ90 mm Hg; nephrotic examined per case. Glomerular diameter was compared range proteinuria (NRP), 24-hour urine protein excre- to that of 21 age- and sex-matched normal controls ob- tion Ն3.5 g; hematuria, presence of Ͼ5 red blood cells tained from percutaneous renal biopsies of patients with per high power ®eld on microscopic examination of the isolated asymptomatic hematuria or subnephrotic pro- urinary sediment; hypoalbuminemia, serum albumin lev- teinuria who had no evidence of glomerular disease by els Յ3.5 g/dL; hypercholesterolemia, serum cholesterol light microscopy, IF, or EM. Ͼ200 mg/dL; nephrotic syndrome, the combination of The following clinical and laboratory data at follow- NRP, hypoalbuminemia and edema; and renal insuf®- up were analyzed for the group with ORG and I-FSGS: ciency, serum creatinine Ͼ1.2 mg/dL on two separate Therapy directed to renal disease or obesity (including determinations. Creatinine clearances calculated from weight reduction, sleep apnea therapy, angiotensin-con- 24-hour urine collections were available in 58 patients.
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