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Kidney Week

Abstract: SA-PO862

Secondary IgA Nephropathy as Red Herring in a Case of AKI

Session Information

Category: Glomerular Diseases

  • 1401 Glomerular Diseases: From Inflammation to Fibrosis

Authors

  • Aydin-Ghormoz, Emmanuel Albert, Albany Medical College, Albany, New York, United States
  • Lightle, Andrea R., Albany Medical College, Albany, New York, United States
  • Monrroy, Mauricio, Albany Medical College, Albany, New York, United States
Introduction

Liver disease, and particularly alcoholic cirrhosis, is the most common cause of secondary IgA Nephropathy (IgAN), with 50-90% of cirrhotic patients exhibiting glomerular IgA deposition. Despite this, <10% of adult patients show clinical evidence of glomerular kidney disease. We report a case of ATN with underlying diabetic kidney disease and microscopic hematuria due to cirrhotic IgAN.

Case Description

A 65-year-old man with history of type-2 diabetes mellitus and hypertension presented to our hospital after outpatient lab work showed elevated creatinine. His diabetes was managed with insulin. He had been prescribed metformin 6 months earlier but discontinued it 3 weeks before presentation due to severe diarrhea, which had partially resolved after cessation. He denied any known history of kidney disease and did not use NSAIDs. He did report heavy alcohol use for many years. Serum creatinine level was 3.7mg/dL with unknown baseline. UA was active with 3+ protein, 50-100 RBCs/HPF, and 0-5 coarse granular casts/HPF. He had ascites with nodular contour of the liver and an atrophic left kidney on imaging. Paracentesis revealed SAAG >1.1 and ascites total protein 1.6g/dL. Creatinine remained stable. ANA, dsDNA, C3, C4, cryoglobulins, ANCAs, and hepatitis panel were all negative. Serum immunofixation revealed no paraprotein. Right kidney biopsy was performed and showed ATN, significant mesangioproliferative IgA deposition, diabetic and hypertensive nephropathy with severe arteriosclerosis and arteriolar hyalinosis, and secondary FSGS. His acute rise in creatinine was attributed to ATN, hematuria and proteinuria were explained by glomerular accumulation of IgA, while FSGS was attributed to diabetic Kimmelstein-Wilson nodule formation and segmental scarring due to immune complex deposition. Kidney function slowly worsened with development of uremic symptoms, requiring initiation of hemodialysis.

Discussion

Decreased hepatic clearance of IgA complexes is the suspected etiology of secondary IgAN in patient with liver cirrhosis. Despite its infrequent presentation, this diagnosis should be suspected in cirrhotic patients presenting with AKI and active UA, with the decision to perform kidney biopsy based on the clinical presentation. Regretfully, our patient's biopsy showed advanced chronic changes due to DM, HTN, and secondary FSGS, and progression to ESRD was inevitable.