Wharton R, D'Agati V, Magun A M, Whitlock R, Kunis C L, Appel G B
Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York.
Clin Nephrol. 1990 Sep;34(3):116-21.
Enteric hyperoxaluria due to malabsorption syndromes has been well documented to cause renal calculi and chronic tubulointerstitial renal damage. Rarely, in the setting of intestinal bypass operations for morbid obesity, enteric hyperoxaluria has produced acute renal failure. We report two patients who suffered acute deterioration of renal function associated with increased intestinal absorption and renal excretion of oxalate associated with steatorrhea. One patient had a large portion of his small bowel resected many years prior to the onset of the renal failure and the second patient had chronic pancreatitis causing steatorrhea. Both patients had renal biopsy documentation of the acute nature of the tubular damage produced by oxalate deposition. The mechanisms of their deterioration of renal function may relate to sudden increases in steatorrhea in association with episodes of volume depletion. Enteric hyperoxaluria may be an easily overlooked and potentially preventable etiology of acute renal dysfunction.
因吸收不良综合征导致的肠道高草酸尿症已被充分证明可引起肾结石和慢性肾小管间质性肾损害。在病态肥胖患者接受肠道旁路手术的情况下，肠道高草酸尿症极少引发急性肾衰竭。我们报告了两名患者，他们的肾功能急性恶化，伴有肠道对草酸盐吸收增加以及肾排泄草酸盐增加，并伴有脂肪泻。一名患者在肾衰竭发作前多年就切除了大部分小肠，另一名患者患有慢性胰腺炎导致脂肪泻。两名患者的肾活检均证实了草酸盐沉积所导致的肾小管损伤的急性性质。他们肾功能恶化的机制可能与脂肪泻突然增加并伴有容量耗竭发作有关。肠道高草酸尿症可能是急性肾功能障碍一个容易被忽视且潜在可预防的病因。
