Clinicopathologic Characteristics, Etiologies, and Outcome of Secondary Oxalate Nephropathy

Abstract

Objective: To report the clinicopathologic characteristics, prognostic indicators, prognosis, and transplant outcome of secondary oxalate nephropathy (ON).

Patients and methods: We performed a retrospective analysis of 113 consecutive patients with secondary ON diagnosed at Mayo Clinic in Rochester, Minnesota, between January 1, 2001, and March 1, 2023.

Results: The incidence of secondary ON among all native biopsies from Mayo Clinic patients over the study period (n=11,617) was 0.97%. ON was attributed to enteric hyperoxaluria in 60% of the 113 patients (68; most commonly Roux-en-Y gastric bypass), excessive ingestion of foods high in oxalate or oxalate precursors in 23% (26) (most commonly vitamin C), and idiopathic in 17% (19). Most patients presented with acute kidney injury (AKI) (particularly in the ingestion group) or AKI on chronic kidney disease, and 53% (60 of 113) were diabetic. Calcium oxalate crystals were accompanied by acute tubular injury, inflammation, and interstitial fibrosis and tubular atrophy. Concurrent pathologic conditions were present in 53% of the patients (60 of 113), most commonly diabetic nephropathy. After a median follow-up of 36 months, 27% of the patients (30 of 112) had kidney recovery, 19% (21 of 112) had persistent kidney dysfunction, 54% (61 of 112) had development of kidney failure, and 29% (32 of 112) died. The mean kidney survival was worse for patients with a concurrent pathologic lesion (30 months vs 96 months for those without a concurrent pathologic lesion; P<.001). Independent predictors of kidney failure were the degree of interstitial fibrosis and tubular atrophy and nadir estimated glomerular filtration rate but not the degree of crystal deposition. After a median follow-up of 58 months in 23 patients who received kidney transplant, 4 had graft loss (due to ON in 3). The 2-, 5-, and 10-year graft survivals were 90% (18 of 20), 79% (11 of 14), and 50% (6 of 12).

Conclusion: ON is a rare cause of AKI or AKI on chronic kidney disease. Most patients have comorbid pathologic conditions, particularly diabetic nephropathy, which worsen the prognosis. Recurrence in the renal allograft and graft loss may occur if hyperoxaluria is not controlled.

FIGURE 1.

Pathologic findings in oxalate nephropathy. A, Low-power image shows numerous translucent intraluminal tubular calcium oxalate deposits with fewer intracellular and interstitial deposits, accompanied by diffuse tubular degenerative changes, interstitial edema, and patchy mononuclear cell inflammation. Glomeruli appear unremarkable (hematoxylin-eosin, original magnification ×40). B, The same field as part A is shown under polarized light. Calcium oxalate crystals are more readily identified due to their strong birefringence (hematoxylin-eosin, original magnification ×40)

FIGURE 2.

A, End-stage kidney disease (ESKD)–free survival in patients with secondary oxalate nephropathy with and without concurrent pathologic lesions. B, End-stage kidney disease–free survival in patients with secondary oxalate nephropathy stratified by cause.