Late-onset primary hyperoxaluria diagnosed after renal transplantation presented with early recurrence of disease.

Intratubular crystal deposition in transplanted patients is very rare and can be a cause of renal graft failure. Oxalate is a major component of the most common type of kidney stones, calcium oxalate stones. Hyperoxaluria is either inborn or acquired. Primary hyperoxaluria (PH) is a rare autosomal recessive disease resulting from deficiency of hepatic alanine:glyoxylate aminotransferase (AGT) (type I, PH-I) or glyoxylate reductase/D-glycerate dehydrogenase (type II, PH-II). Urinary excretion of both oxalate and glycolate is increased in PH-I, and that of both oxalate and L-glyceric acid is elevated in PH-II. PH results in urolithiasis and systemic oxalosis, often progressing to end-stage renal disease (ESRD) in young people. Late manifestations of PH-I are reported in a few middle-aged patients with recurrent renal stones or systemic oxalosis [1–3]. Recurrence of PH in renal transplants is common [4]. In a few patients, very rapid recurrence of disease has also been described [2]. Here, we report a case of late-onset PH-I, with the diagnosis being made only after transplantation presented with rapid intratubular calcium oxalate crystal deposition in a renal graft.