Abstract: PUB466
Toxic RBC Casts as the Culprit of Irreversible AKI in IgA Nephropathy
Session Information
Category: Trainee Case Report
- 103 AKI: Mechanisms
Authors
- Syed, Bushra, Cleveland Clinic Foundation, Cleveland, Ohio, United States
- Herlitz, Leal C., Cleveland Clinic, Cleveland, Ohio, United States
- Nakhoul, Georges, Cleveland Clinic Foundation, Cleveland, Ohio, United States
Introduction
Acute tubular necrosis(ATN) driven by RBC casts occurs in 20% cases of IgA nephropathy (IgAN).Similar mechanism of AKI is observed in Henoch-Schonlein nephropathy,thin basement membrane disease and anticoagulation related nephropathy.Eventhough, glomerular hematuria in the absence of proteinuria is considered a benign entity without long term renal impact, upto 25% of patients with macrohematuria related AKI have incomplete renal recovery.Poor prognostic factors include increased age,prolonged duration of hematuria,severity of ATN and degree of interstitial fibrosis.
Case Description
A 50 year old male with cryptogenic cirrhosis presented with AKI.He had flu like symptoms 2 weeks before presentation.
Workup revealed elevated creatinine of 3.4mg/dl from a baseline of 1mg/dl.Urinalysis showed >25 RBC and protein:Cr ratio of 1.1g.On urine microscopy, dysmorphic RBCs and RBC casts were seen.Serological workup showed low C3 (77mg/dl),normal C4 and elevated ASO(476 IU/ml).
Renal biopsy showed RBC casts and tubular vacuolization.IgA and C3 deposits were seen on immunofluorescence consistent with mesangioproliferative IgAN.Crescents were absent and there was minimal interstitial fibrosis.Scant subendothelial deposits were present on electron microscopy.
Immunosuppression use was deferred in the absence of glomerular involvement and history of spontaneous bacterial peritonitis .Low dose lisinopril was initiated.After 3 months Cr had declined to 2.3.
Discussion
The ability of toxic RBC casts to independently cause AKI in the absence of glomerular involvement tends to be overlooked, but is now being increasingly recognized in cases of anticoagulant nephropathy. Intra tubular obstruction by RBCs, direct tubular toxicity by hemoglobin(Hb) byproducts and intra renal vasoconstriction play a role. Data on specific therapy is scarce and the role of renal heme oxygenase and Hb scavenging by CD163 receptors on tissue macrophages may provide a potential avenue for future therapeutic ventures.