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.

高草酸尿症是由于遗传性乙醛酸代谢紊乱导致肝脏草酸过量产生（原发性高草酸尿症），或肠道草酸吸收增加（继发性高草酸尿症）。高草酸尿症可能导致尿液中草酸钙过饱和和结晶形成，导致尿路结石和草酸钙结晶沉积在肾实质中，这种情况称为草酸盐肾病。在了解导致高草酸尿症和草酸盐肾病的病理生理机制方面取得了相当大的进展，其诊断经常被延迟并且预后往往很差。幸运的是，针对原发性高草酸尿症患者的新的有前途的靶向治疗方法即将出现。继发性高草酸尿症患者经常有长期的高草酸尿症，这一事实表明急性肾损伤的触发因素（如脱水）的作用。这些患者目前的护理标准包括根本原因的管理、大量液体摄入和钙补充剂的使用。总的来说，及时识别高草酸尿症和相关的草酸盐肾病是至关重要的，因为最佳管理可能会改善结果。