Nephrology Potpourri

Abstract

Acute phosphate-induced kidney injury had been known for a long time to be caused by conditions such as the acute tumor lysis syndrome (1) or rhabdomyolysis (2,3). Furthermore, after some experimental (4) and clinical (5) observations, phosphate had been discussed as one factor that aggravates acute and chronic kidney injury (6). Although on both sides of the Atlantic occasional isolated cases of acute or subacute kidney injury had been observed to be caused by oral phosphate therapy for various indications (7,8) as well as by phosphate-containing enemas (9 -11), only recently has this problem emerged as a relatively frequent complication: The use of routine colonoscopy had increased after the procedure had been recommended for early diagnosis of colon cancer. In this context, phosphatecontaining preparations had been administered more frequently (12), particularly after convenient, well-tolerated, lowvolume, hyperosmotic, low-cost oral phosphate preparations for colonoscopy had been shown to be superior to the alternative polyethylene glycol preparation (13).After several isolated reports (8 -10,14), 3 yr ago, Markowitz et al. (15) drew attention to this novel "epidemic" of what they called "acute phosphate nephropathy," caused according to a case report by intratubular deposits of hydroxyapatite with consecutive tubular damage (8). This complication had followed oral sodium phosphate bowel purgatives. The authors appropriately concluded that this type of purgative constitutes an underrecognized cause of chronic renal failure (16). Overall, the study identified during a 4-yr period 31 patients with nephrocalcinosis among 7349 native renal biopsies, 21 of whom presented with normocalcemic acute renal failure and a history of recent colonoscopy preceded by bowel cleansing with oral phosphate solution. The onset was rapid, and the median serum creatinine was 3.9 mg/dl after a median of 1 mo. The seriousness of this condition is underlined by the fact that all patients had chronic renal insufficiency, and four of the 21 patients even required permanent hemodialysis. This observation settled the issue of whether phosphate-induced acute renal failure is always a reversible condition. It was not certain, however, whether this observation represented only the peak of an iceberg. For clarification of this point, epidemiologic information was necessary.One retrospective cohort study suggested that a non-negligible proportion of patients who underwent colonoscopy using oral sodium phosphate (88 of 2325) developed incident renal dysfunction defined as estimated GFR (eGFR) Ͻ60 ml/min, although, after multivariate adjustment, no significant difference was found between oral phosphate and polyethylene glycol preparations. Importantly age Ͼ65 yr, black ethnicity, low baseline GFR, hypertension, and use of angiotensin-converting enzyme inhibitors (ACEI) and thiazides were identified as risk factors for a decrease in eGFR (17). The higher risk in older and hypertensive patients as well as in the presumably hypovolemic patients ...