Lactitol-Induced Acute Kidney Injury with Oxalate Nephropathy: A Case Report

Oxalate nephropathy, characterized by calcium oxalate crystal deposition in renal tissue, represents an underrecognized etiology of acute and chronic kidney injury. Secondary hyperoxaluria can emerge from diverse pathogenetic mechanisms, including excessive oxalate precursor intake, augmented intestinal absorption, or iatrogenic interventions. The therapeutic potential of glucocorticoids in managing this condition remains incompletely elucidated.

A 66-year-old man with no significant prior medical history developed acute kidney injury (AKI), manifesting as a profound serum creatinine elevation from 81 µmol/L to 1,140.4 µmol/L. The patient had consumed a "corn germ powder" supplement containing lactitol for five consecutive months, concurrently experiencing persistent diarrhea. Initial laboratory investigations revealed severe renal dysfunction without notable proteinuria or hematuria. Renal ultrasonography demonstrated normal kidney morphology and dimensions. Definitive kidney biopsy revealed extensive calcium oxalate crystal deposition within renal tubular structures, conclusively diagnosing oxalate nephropathy. Therapeutic intervention comprised prednisone (60 mg daily) and comprehensive supportive management. Following a 3-month treatment protocol with gradual corticosteroid dose reduction, the patient's renal function demonstrated substantial improvement, with serum creatinine declining to 118.2 µmol/L.

This case underscores lactitol-induced secondary oxalate nephropathy as a rare yet clinically significant contributor to AKI. Prompt diagnostic recognition and targeted therapeutic intervention, potentially incorporating glucocorticoid therapy, may substantially facilitate renal functional recovery. Clinicians should maintain heightened awareness of nephrotoxic risks associated with over-the-counter laxative supplements and consider oxalate nephropathy in cryptogenic renal dysfunction scenarios.