Kidney transplantation (KT) is the preferred treatment for end-stage renal disease, yet post-transplant complications and graft dysfunction remain significant challenges. Oxalate nephropathy, resulting from calcium oxalate crystal deposition due to hyperoxaluria, represents an under-recognised contributor to graft injury. We describe a woman in her 60s with obesity, chronic pancreatitis and type 2 diabetes who underwent KT after dialysis. Post-transplant, she developed recurrent pyelonephritis and impaired graft function. The biopsy revealed oxalate crystal deposits, tubular injury and interstitial nephritis and fibrosis consistent with oxalate nephropathy. Contributing factors included chronic pancreatitis-related malabsorption and high dietary vitamin C intake. Supportive measures, including a low-oxalate diet and hydration, were introduced. This case illustrates the multifactorial nature of allograft dysfunction and highlights the importance of considering oxalate nephropathy in at-risk patients. Early recognition and preventive strategies may help preserve graft function and improve long-term outcomes.
Rodrigues et al. (Sun,) studied this question.