Abstract: SA-PO0379
It's a Heart…It's an Infection…It's a Toxin! A Case of Multi-Hit AKI
Session Information
- AKI: Case Reports - Drug/Toxin Injury, Crystals, Obstruction, and Unusual Presentations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Paredes, William Mauricio, Cleveland Clinic, Cleveland, Ohio, United States
- Sharakova, Yuliya, Cleveland Clinic, Cleveland, Ohio, United States
Introduction
Patients admitted to cardiology service can develop AKI due to various reasons: hemodynamic ATN, CRS from heart failure, contrast-induced injury, or IRGN in setting of infective endocarditis to name a few. However, among typical triggers infrequent etiologies sometimes can be identified. Here we describe a case of AKI caused by combination of biopsy proven pigment nephropathy and IRGN with underlying CRS.
Case Description
68 yo male with rheumatic heart s/p mechanical AVR/MVR on warfarin, CHF, bladder cancer s/p TURBT and on pembrolizumab, transfusion dependent chronic anemia, and recent MSSA bacteremia s/p antimicrobial therapy, who presents with CHF exacerbation, and for potential MV surgery due to concern for prosthetic MV endocarditis (PVE) and paravalvular leak (PVL).
Diuresis was initiated, and nephrology involved for nonoliguric AKI with Cr elevation to 3.5mg/dL from a baseline 1.0-1.2. Initially kidney dysfunction was attributed to CRS iso severe volume overload with urine Na <20, however no renal improvement was noted with continued diuresis and decongestion, and kidney function remained significantly abnormal. UA showed protein 2+ (PCR 1.1 g/g), Hb 3+, along with WBCs and RBCs >20. Additional workup showed markedly elevated LD and depleted haptoglobin, and this was ascribed to MIH – mechanical intravascular hemolysis driven by mechanical MV.
Kidney biopsy was performed: IF revealed prominent mesangial deposition of C3 and polyclonal IG, likely infection related, but without aggressive proliferative lesions. Rather, the pt's AKI was explained by the presence of ATI with prominent iron-positive pigmented casts - the finding consistent with hemoglobin cast nephropathy. It was believed to be the result of MIH.
Discussion
AKI etiology in cardiac patients might seem to be clear based on underlying pathology, but unusual triggers can be present as well. It is important to remain open-minded while evaluating and consider kidney biopsy in cases when multiple risk factors are present.
Although mild subclinical MIH is seen in most cases of mechanical valve, extensive hemolysis leading to kidney injury is uncommon. PVE in this case likely caused PVL, which has described association with severe MIH. In addition, acute CHF induced shear stress on RBCs accelerating RBC destruction. This unfortunate chain of events ultimately led to significant hemoglobinuria and pt’s severe kidney dysfunction.