Rapidly Progressive Glomerulonephritis due to Crescentic IgA Nephropathy in the Setting of HIV

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Introduction: In patients with HIV-related kidney diseases, the most widely recognized histological abnormality is focal segmental glomerulosclerosis (FSGS). Less commonly found is IgA nephropathy in HIV patients, which tends to have a chronic stable course. We report a case of crescentic IgA nephropathy and FSGS in a patient with rapidly progressive glomerulonephritis and newly diagnosed HIV. Case Description: A 34-year-old transgender woman with a history of alcohol use disorder presented with a petechial rash and lower extremity edema for 1 week, and was found to have a new diagnosis of HIV with an elevated creatinine. CD4 count was 143 and viral load was 103,774, and she was started on renally-dosed dolutegravir, abacavir and emtricitabine. Creatinine on admission was 1.27 mg/dL (baseline 0.7), and increased over the next several days to 5.3. Urine microscopy revealed dysmorphic RBCs and granular casts, with spot urine protein:creatinine 2.3. Renal biopsy demonstrated crescentic IgA nephropathy (Oxford classification M1 E1 S1 T1 C2) with concomitant FSGS (NOS subtype). Cellular crescents were seen in 4/7 glomeruli (figure 1), mesangial and endocapillary hypercellularity in all non-sclerotic glomeruli, and FSGS in 2/7 glomeruli. Immunofluorescence showed strong granular segmental mesangial staining for IgA (3+) and C3 (3+), and was otherwise negative. She was started on pulse-dose steroids (methylprednisolone 500mg x 3 days followed by 1 mg/kg x 2 weeks), as well as plasmapheresis every other day for 5 sessions. Her renal function had not improved by the time of discharge. Discussion: To our knowledge this is the first reported case of IgA-induced RPGN in the setting of newly diagnosed HIV. A few prior case reports describe stable IgA nephropathy in individuals with HIV, suggesting that there may be some unifying pathogenesis. This case highlights the need for investigation of this potential mechanism, which may help determine the optimal therapy for IgA nephropathy and IgA-induced RPGN in the setting of HIV.

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