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Case report demonstrates pigment cast nephropathy in a renal transplant, highlighting complex triggers and management challenges.
Pigment cast nephropathy can cause an acute decline in renal function. The cause of pigment casts in renal allografts is poorly understood, although it has been observed in recipients of road traffic accident donors. We describe a case of pigment cast nephropathy in a renal allograft identified through several sequential biopsies performed for allograft dysfunction. A 27-year-old man underwent a deceased donor kidney transplant and developed delayed graft function with elevating creatinine levels. Early biopsies showed calcineurin inhibitor toxicity and pigment casts, and although tacrolimus was adjusted, kidney function continued to fluctuate. Over the following months, repeated biopsies consistently revealed pigment casts coexisting with pyelonephritis and antibody-mediated rejection. Despite treatment with antibiotics and intensified immunosuppression, the casts persisted. Further evaluation confirmed that the casts contained hemoglobin, and further investigations confirmed glucose-6-phosphate dehydrogenase (G6PD) deficiency as the underlying cause. After managing infections and rejection, his kidney function stabilized with creatinine at 1.55 mg/dl. Pigment cast nephropathy in the posttransplant setting can be triggered by a myriad of causes, which in the index case were deceased donor trauma–related myoglobinuria, infections, and finally G6PD deficiency–related hemoglobinuria. The trigger factors for G6PD deficiency include certain drugs and infections.
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Parvathy et al. (2026) studied this question.
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