Pathophysiology and Management of Hyperoxaluria and Oxalate Nephropathy: A Review

Hyperoxaluria results from either inherited disorders of glyoxylate metabolism leading to hepatic oxalate overproduction (primary hyperoxaluria), or increased intestinal oxalate absorption (secondary hyperoxaluria). Hyperoxaluria may lead to urinary supersaturation of calcium oxalate and crystal formation, causing urolithiasis and deposition of calcium oxalate crystals in the kidney parenchyma, a condition termed oxalate nephropathy. Considerable progress has been made in the understanding of pathophysiological mechanisms leading to hyperoxaluria and oxalate nephropathy, whose diagnosis is frequently delayed and prognosis too often poor. Fortunately, novel promising targeted therapeutic approaches are on the horizon in patients with primary hyperoxaluria. Patients with secondary hyperoxaluria frequently have long-standing hyperoxaluria-enabling conditions, a fact suggesting the role of triggers of acute kidney injury such as dehydration. Current standard of care in these patients includes management of the underlying cause, high fluid intake, and use of calcium supplements. Overall, prompt recognition of hyperoxaluria and associated oxalate nephropathy is crucial because optimal management may improve outcomes.

Automated summary

Hyperoxaluria can result from metabolic disorders or abnormal intestinal absorption, leading to calcium oxalate supersaturation in urine and crystal formation, which causes urolithiasis and deposition of calcium oxalate crystals in the kidney. The understanding of this condition has improved, but delayed diagnosis and poor prognosis are still common. New targeted therapeutic approaches are being developed for primary hyperoxaluria, while management of secondary hyperoxaluria includes addressing underlying factors and calcium supplementation. Prompt recognition and management are crucial for improving outcomes.