Clinicopathological spectrum of Acute Kidney Injury due to Myoglobin Cast Nephropathy

Objective Myoglobin cast nephropathy is a serious yet potentially preventable cause of acute kidney injury (AKI), most commonly occurring secondary to severe rhabdomyolysis. The release of myoglobin from damaged skeletal muscle fibers leads to its filtration through the glomeruli and subsequent interaction with uromodulin within renal tubules. This results in pigment cast formation, tubular obstruction, renal vasoconstriction, and direct tubular epithelial injury, collectively contributing to acute renal dysfunction. Definitive diagnosis relies on immunohistochemical confirmation of myoglobin within tubular casts. Early recognition and timely management, including renal replacement therapy when indicated, are critical for improving patient outcomes. This retrospective observational study aims to analyze the diverse clinicopathological features of myoglobin cast nephropathy, diagnostic challenges, and various treatment approaches. Material and methods This retrospective observational study evaluated the clinicopathological spectrum of myoglobin cast nephropathy over a three-year period (July 2022–June 2025) at a tertiary care hospital in India. Twenty-five cases were identified after performing immunohistochemical staining for myoglobin on renal biopsies exhibiting pigment casts. Clinical features, biochemical parameters, histomorphological findings, and outcomes were systematically analyzed. Results The mean patient age was 34.47 years (range: 27–45 years), and all patients were male. All presented with AKI, with a mean serum creatinine level of 7.53 mg/dL (range: 3.7–10.8 mg/dL) and markedly elevated serum creatine phosphokinase levels. On light microscopy, casts appeared as granular eosinophilic pigments mimicking hemoglobin and bile casts, creating diagnostic difficulty. Immunohistochemistry confirmed myoglobin positivity in all cases. Conclusion Early clinical recognition, accurate diagnosis, and prompt therapeutic intervention in cases of myoglobin cast nephropathy are crucial to preventing fatal outcomes and long-term renal complications. Pathologists should maintain a high index of suspicion, particularly in patients with rhabdomyolysis, and routine use of immunohistochemical staining for myoglobin is recommended to establish a definitive diagnosis