# Unraveling Acute Kidney Injury: An Intricate Case of Sepsis and Immune-Mediated Renal Damage

## TL;DR

This case study explores a complex instance of acute kidney injury involving sepsis and immune-mediated damage, highlighting the need for a broad diagnostic approach.

## Contribution

The case presents a rare combination of sepsis, antibiotic nephrotoxicity, and ANCA-negative pauci-immune glomerulonephritis in AKI.

## Key findings

- A 68-year-old patient with pneumonia and sepsis developed rapid-onset AKI linked to immune-mediated processes.
- Renal biopsy showed acute tubular injury without immune complex deposition and elevated myeloperoxidase.
- Treatment with rituximab and corticosteroids improved renal function, supporting an immune-mediated etiology.

## Abstract

Acute kidney injury (AKI) is a critical condition characterized by a sudden decline in kidney function, often posing diagnostic and therapeutic challenges due to its multifactorial nature. This case is significant, as it exemplifies the complexity of AKI in the context of coexisting sepsis, potential antibiotic nephrotoxicity, and immune-mediated processes. While AKI related to sepsis and renal toxic antibiotics is well-documented, the rapid onset and the involvement of antineutrophil cytoplasmic antibody (ANCA)-negative pauci-immune glomerulonephritis add a unique dimension to this case, contributing novel insights to the medical literature. ANCA-negative pauci-immune glomerulonephritis is characterized by a rapidly progressive glomerulonephritis that lacks the detection of antineutrophil cytoplasmic antibodies.

We report the case of a 68-year-old Hispanic male with a history of asthma and pulmonary emphysema, presenting with acute respiratory symptoms, including shortness of breath, chills, and a productive cough, accompanied by gastrointestinal symptoms. The patient was admitted to the hospital with pneumonia complicated by sepsis. Initial treatment included antibiotics known for potential renal toxicity. Within 48 hours, the patient experienced a rapid deterioration in renal function, marked by a significant increase in serum creatinine levels. A renal biopsy revealed acute tubular injury with no immune complex deposition and an elevated myeloperoxidase level, suggestive of an immune-mediated process. The patient responded positively to immunosuppressive therapy, consisting of rituximab and corticosteroids, resulting in improved renal function.

This case underscores the importance of considering a broad differential diagnosis in AKI, particularly in patients with complex clinical presentations. The involvement of ANCA-negative pauci-immune glomerulonephritis highlights the need for awareness of immune-mediated renal injuries in similar clinical scenarios. This case has implications for both nephrology and broader medical practice, as it emphasizes the necessity of integrating clinical, laboratory, and histopathological data to guide effective treatment strategies. The findings advance our understanding of the potential interplay between sepsis, drug-induced nephrotoxicity, and immune-mediated processes in AKI, offering valuable insights for future diagnostic and therapeutic approaches.