ABSTRACT
After reviewing the available data on drug-induced hyperkalemia, we conclude that the situation has not improved since Lawson quantitatively documented the substantial risks of potassium chloride over a decade ago (90). As discussed, the risk of developing hyperkalemia in hospital remains at least at the range of 1 to 2% and can reach 10%, depending on the definition used (Table 2). Potassium chloride supplements and potassium-sparing diuretics remain the major culprits but they have been joined by a host of new actors, e.g., salt substitutes, beta-blockers, converting enzyme inhibitors, nonsteroidal antiinflammatory agents, and heparin, among others. Readily identifiable risk factors (other than drugs) for developing hyperkalemia are well-known but seem to be consistently ignored, even in teaching hospitals. The presence of diabetes mellitus, renal insufficiency, hypoaldosteronism, and age greater than 60 years results in a substantial increase in the risk of hyperkalemia from the use of any of the drugs we have reviewed. If prevention of hyperkalemia is the goal, as it should be, the current widespread and indiscriminate use of potassium supplements and potassium-sparing diuretics will need to end. We remain intrigued by Burchell's prescient pronouncement of over a decade ago that "more lives have been lost than saved by potassium therapy" (28).
Subject(s)
Hyperkalemia/chemically induced , Potassium/metabolism , Adrenergic Agonists/adverse effects , Adrenergic beta-Antagonists/adverse effects , Aged , Angiotensin-Converting Enzyme Inhibitors , Anti-Inflammatory Agents/adverse effects , Arginine/adverse effects , Body Fluid Compartments/metabolism , Cyclosporins/adverse effects , Digitalis Glycosides/adverse effects , Diuretics/therapeutic use , Glucose/adverse effects , Heparin/adverse effects , Heroin/adverse effects , Hormones/metabolism , Humans , Hyperkalemia/etiology , Hyperkalemia/prevention & control , Hypertonic Solutions , Kidney/metabolism , Kidney Transplantation , Lithium/adverse effects , Lithium Carbonate , Middle Aged , Potassium Chloride/adverse effects , Potassium Chloride/therapeutic use , Prostaglandins/biosynthesis , Risk , Transfusion ReactionABSTRACT
To verify the action of heparin on peritoneal transport, we selected 20 patients on acute peritoneal dialysis and performed two 2-hour cycles with 2,000 cm3 of a 1.5% solution, adding 2,000 units of heparin to the second cycle. The patients were also randomized into 2 groups: group A, adding 1.5 mg gentamycin/kg to the dialysate of cycle I (without heparin), and group B, adding the same dose of gentamycin to cycle II (with heparin). At the end of each of the two cycles blood and dialysate were drawn for urea, creatinine, glucose, proteins and gentamycin levels, using peritoneal clearances of urea and creatinine, glucose absorption and net protein loss to compare cycle I with cycle II. We found that the peritoneal transport of creatinine and urea was improved (p less than 0.02; p less than 0.05) and glucose absorption increased (p less than 0.01) with heparin, without any significant change in protein loss. Contrary to common belief, heparin in a 1,000-U/l dose improved the absorption of gentamycin from the dialysate (p less than 0.01).
