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Obesity Related Glomerulopathy

Updated: Jun 7


By Jonathan E. Zuckerman, M.D. Ph.D. HS Assistant Clinical Professor Service Chief, Renal Pathology Director, Surgical Pathology Fellowship UCLA Department of Pathology and Laboratory Medicine

A representative clinical presentation:

The patient is a 45 year old man with worsening proteinuria that is now ~2g. His past medical history is significant for long-standing hypertension, pre-diabetes, obstructive sleep apnea, and obesity (BMI 36). Serologic workup including ANA, ANCA, SPEP/UPEP, RF, cryocrit, HIV, and hepatitis serologies are negative. His complement levels are normal. His serum creatinine is mildly elevated. A renal biopsy was performed and was significant for the following findings.


Obesity-related glomerulopathy

Key points:

  • Defined as glomerulomegaly (glomerular hypertrophy) with or without secondary adaptive segmental glomerulosclerosis arising in obese patients with body mass index >30 kg/m2

  • Obesity-associated glomerular hyperfiltration results in prolonged podocyte shear stress with loss of adhesions and detachment ultimately with segmental sclerosis formation

  • Similar findings reported in “moderate obesity” (BMI 25-30) suggest some degree of an undetermined genetic component

  • Generally presents as slowly progressive proteinuria that may eventually reach nephrotic range but not a true nephrotic syndrome

  • Histologic features

  • Enlarged glomeruli (>1/2 of a 40x high powered field)

  • Thickened GBM

  • May see increased mesangial matrix

  • Segmental sclerosis, most often a perihilar variant

  • Tubular cross-sections enlarged

  • Often less interstitial fibrosis/tubular atrophy than other cause of maladaptive glomerular injury

  • IF studies are negative (non-specific IgM, C3, and C1q staining of segments of sclerosis may be present)

  • EM with patchy partial podocyte foot process effacement (usually ranges from 25-40%)

  • Differential diagnoses

  • Diabetic nephropathy may show overlapping features and may be indistinguishable. May show hyalinization of both afferent and efferent arterioles

  • Primary FSGS will show more extensive podocyte foot process effacement (>75%) and present as true nephrotic syndrome

  • Other causes of maladaptive glomerular injury (e.g, renal hypoplasia, obstructive nephropathy, arterionephrosclerosis, etc.)


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