riopan and Kidney-Failure--Chronic

Aluminum toxicity is becoming more and more evident as a complication of maintenance dialysis treatment. The aluminum contamination of the dialysate bath solution no longer plays an important role. The main source of aluminum overloading turns out to be the ingestion of aluminum-containing antacids as phosphate binders in the impaired renal aluminum excretion. In 19 dialysis patients an antacid poor in aluminum (Magaldrate) was compared with one rich in aluminum (compound M 70). The serum concentrations of aluminum, magnesium, phosphorus and calcium were investigated over a period of 14 days. After M 70 the aluminum and magnesium levels were markedly more elevated than after Magaldrate. Calcium remained unchanged with both compounds. Phosphorus was diminished only by M 70. The results of this short term study on dialysis patients are also important for patients with normal renal function, in particular in cases of uncontrolled long term treatment with antacids rich in aluminum.

Topics: Adolescent; Adult; Aluminum; Aluminum Hydroxide; Antacids; Clinical Trials as Topic; Female; Humans; Kidney Failure, Chronic; Magnesium; Magnesium Hydroxide; Male; Middle Aged; Random Allocation; Renal Dialysis

A significant rise in serum concentrations of aluminum was demonstrated in 23 patients prophylactically treated with the antacid magaldrate, whereas no increase in serum aluminium was observed in another 26 critically ill patients, in whom the use of antacids was avoided. In parallel, urinary excretion rates of aluminum rose to values close to maximum 72 h after antacid therapy had been started. Hyperaluminaemia was most marked in patients with acute renal failure undergoing continuous haemofiltration, but a significant increment in serum aluminium was also noted in patients with impaired renal function in the predialytic state. In the latter group and in patients with normal renal function there was a significant negative correlation between urinary excretion rates of aluminium and creatinine clearance after 48 h of treatment suggesting an enhancement of gastrointestinal absorption of aluminium in the presence of chronic renal failure. Maximum serum concentrations of aluminium did attain critical values in some patients with acute renal failure, but no overt signs of aluminium toxicity were noted. However, in light of both, possible subtle toxicity and enhanced absorption of aluminium in critically ill patients with renal failure, the prophylactic use of antacids in this setting should be re-evaluated cautiously.

Topics: Acute Kidney Injury; Adult; Aged; Aged, 80 and over; Aluminum; Aluminum Hydroxide; Antacids; Critical Care; Female; Humans; Intestinal Absorption; Kidney Diseases; Kidney Failure, Chronic; Magnesium Hydroxide; Male; Middle Aged