To preserve patient privacy and for didactic purposes, case descriptions and pathology reports have been anonymized and partially fictionalized. The pathology images are representative images from a mixture of similar cases.

Invited Speakers

Michael Germain
Michael GermainCase Presenter | Baystate Medical Center, Springfield, MA, USA | No conflict of interest reported
Giovanna Crisi
Giovanna CrisiNephropathology Discussant | Baystate Medical Center, Springfield, MA, USA | No conflict of interest reported
Bradley Denker
Bradley DenkerNephrology Discussant | Beth Israel Deaconess Medical Center, Boston, MA, USA | No conflict of interest reported
Helmut Rennke
Helmut RennkeNephropathology Discussant | Brigham and Women's Hospital, Boston, MA, USA | No conflict of interest reported


A young woman in her 30s presented to her primary care physician with complaints of severe lower extremity edema. One month prior to presentation, she had no complaints and on routine exam, presented without edema and a reported creatinine of 0.8 mg/dl.

As part of the work up for her edema, she was found to have AKI with a creatinine 1.7 mg/dl.

3 weeks later, she was evaluated in kidney clinic and was found to have nephrotic range proteinuria, and an active urinary sediment. Her creatinine remains mostly unchanged over the past 3 weeks.

On review of system: with exception of edema, no other complaints.

Medical History:
Bacterial bloodstream infection 1 year ago

Physical Exam:
Hypertensive with significant lower extremity edema

Laboratory and other data:
Creatinine 1.7 mg/dl.
Low C3, normal C4.
Positive cryo, pending characterization.
All SLE test negative.
Mild polyclonal IGM elevation.
Thorough infectious workup negative.

Kidney Pathology

Pathology images pending

  • Diffuse proliferative glomerulonephritis with 40% cellular crescents and full-house IF consistent with lupus-like GN

  • Acute interstitial nephritis with acute tubular injury

  • Arteries and arterioles with no significant change

The three modality findings are most suggestive of a lupus-like diffuse proliferative GN. In absence of positive serologies for lupus, the findings may be drug induced or infectious in etiology. Cryoglobulins are not identified.

Glomeruli enlarged with diffuse global endocapillary proliferative lesions obliterating capillary lumina with variable margination of neutrophils. Subendothelial deposits in most tufts in a segmental distribution.

Wire loop deposits. No subepithelial spikes or deposits.

Some focal capillary PAS+ hyaline globules. Jones with GBM double contour formation.

Mesangiolysis and focal fibrinoid deposits/necrosis associated with ruptured GBMs.

Diffuse mild interstitial expansion and scattered lymphoplasmocytic infiltrates throughout the cortex.

Acute tubular injury is present with scattered dilated tubules and cellular casts.

No vascular microthrombi.

On EM: Narrowed and occluded capillary loops by swollen endothelial cells, influx of inflammatory cells, subendothelial widening, with cell interposition and debris.

Endothelial cells are swollen and contain tubuloreticular inclusions.

Cytoplasmic dense lipid bodies are identified. Electron dense deposits are identified in subendothelial, paramesangial, and mesangial areas (no organized structures, incl no cry like structures). Overall equally dense.

IF: Diffuse segmental or global peripheral subendothelial granular and confluent with some wire loops full house staining with IgG, IgM, C1q (3+), C3, kappa/lambda and IgA, and some fibrinogen

Questions posed & summary of key discussion points

1. What are the potential differential diagnoses in this case?
2. Any further diagnostic work up to be done?
3. How would you manage this patient next?

Author(s) of case summary:

Case summary pending

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