Abstract: TH-PO174
IgA Nephropathy in a Patient with Alcoholic Cirrhosis
Session Information
- Fellows/Residents Case Reports: Glomerulonephritis
November 02, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Nephrology Education
- 1302 Fellows and Residents Case Reports
Authors
- Owoyemi, Itunu O., University of Virginia, Charlottesville, Virginia, United States
- Pourafshar, Negiin, None, Gainesville, Florida, United States
- Iezzoni, Julia, University of Virginia Health System, Charlottesville, Virginia, United States
- Chopra, Tushar, University of Virginia, Charlottesville, Virginia, United States
Background
Impaired removal of IgA-containing complexes in the liver is thought to predispose to IgA deposition in the kidney. Portal hypertension has been implicated in IgA nephropathy in cirrhotic patients through various mechanisms leading to decreasing hepatic processing of IgA Immune complexes. Despite the frequency of glomerular IgA deposits in advanced liver disease, most adults have no clinical signs of glomerular disease. There is a dearth of literature regarding differentiation of primary and secondary IgA nephropathy (IgAN) in cirrhotic patients.
Methods
We report a 52-year-old male with alcoholic liver cirrhosis complicated by portal hypertension who presented with a recent history of fatigue and skin rash for three weeks. The serum creatinine (SCr) had increased from baseline 2.1mg/dl to 3.2 mg/dl with proteinuria of 6.5 g/g. Measured serum IgA level was elevated at 599.2 mg/dL (68-378 mg/dL). He had a MELD score of 17. Urinalysis was significant for microscopic hematuria. His kidney biopsy revealed a mild increase in mesangial cellularity, lambda mesangial predominance, endocapillary hypercellularity with moderate tubular atrophy and moderate interstitial fibrosis consistent with a diagnosis of IgA nephropathy. Skin rash was in line with psoriasis. The patient was eventually discharged home on conservative management with losartan, and fish oil. On follow-up, his SCr was 3.1mg/dl, and proteinuria decreased to 2 g/g.
Conclusion
Our case highlights the inherent difficulty in recognition of primary and secondary IgA nephropathy in the setting of liver cirrhosis which would result in difficulty in decision making regarding proper management. We present a case of primary IgAN with diffuse staining of IgA in the glomeruli, and lambda mesangial dominance. In IgAN, lambda is usually, but not invariably, stronger than kappa. Kappa dominance and focal IgA staining not involving all the glomeruli, slightly favors secondary IgAN. Primary IgAN is rarely associated with nephrotic syndrome. Given his multiple co-morbidities, conservative management of IgA nephropathy was implemented. Cirrhotic glomerulonephritis is usually a clinically silent disease; however, the diagnosis can be suspected by finding proteinuria or abnormalities of the urine sediment. The pathogenesis may relate to defective hepatic processing and portocaval shunting of circulating immune complexes.