Abstract: FR-PO048

Idiopathic Diffuse Global Hypertrophic Podocytopathy without Proteinuria with AKI in a Patient with a Solitary Kidney

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports


  • Baynes-Fields, Jaime A., Drexel University, Philadelphia, Pennsylvania, United States
  • Aggarwal, Sandeep, Drexel University College of Medicine, Philadelphia, Pennsylvania, United States
  • Vela-Ortiz, Myriam C., Drexel University, Philadelphia, Pennsylvania, United States

Podocytopathies in adults usually present as significant proteinuria but can be associated with AKI, especially in elderly patients. We present a case with AKI without proteinuria with predominant finding of diffuse podocytopathy on renal biopsy.


A 35 year old black male with history of Wilms tumor and left nephrectomy (age 2 years) presented with 2 day history of progressive anasarca, and muscle soreness. Patient denied arthralgia, upper respiratory infections, rashes, joint pain, or new prescription medications. Pertinent initial physical examination: blood pressure 140/78 mmHg, HR 106 per minute and generalized anasarca, no lymphadenopathy appreciated, and otherwise normal examination. Laboratory workup: serum creatinine (cr) 6.28mg/dl, with baseline cr 1.4 mg/dL. CPK 350 IU/L. Albumin 2.6g/dL. Paraproteinemia workup, rheumatological serologies, HIV, and Hepatitis panel were negative. Urine drug screen was positive for opiates and THC. Urinalysis specific gravity 1.019, negative for protein and blood. Urine protein/cr ratio 0.12mg/g of cr. Imaging: renal ultrasound, with enlarged right solitary kidney (17.9cm), otherwise normal. Chest xray was normal. Renal biopsy was performed with; light microscopy: diffuse global glomerulomegaly with severe glomeruli hyper cellularity without inflammatory cells, capillary lumens and glomerular space were globally obliterated without crescents. There was no glomerular sclerosis seen. No evidence of tubulitis, interstitial nephritis or vasculitis/capillaritis. Proximal tubular cells showed luminal obliteration with occasional mitotic bodies. Electron microscopy: diffuse global podocyte hypertrophy with >80% foot process effacement and microvillus changes, proximal tubular showed protein reabsorption bodies, no immune complexes were identified. Immunofluorescence: no immune deposits and negative parvovirus. Given predominant podocytopathy with otherwise preserved renal histology, patient was treated with total 3g IV methylprednisolone and transitioned to oral prednisone taper with improvement in serum creatinine.


In the emerging field of biomarkers, our case emphasizes the role of renal biopsy in diagnosing the otherwise unidentifiable causes of AKI. An atypical presentation of podocytopathy with non-proteinuric AKI was revealed by biopsy in this case.