Contrast-induced translocational hyponatremia and hyperkalemia in advanced kidney disease

Abstract

Background: In patients with advanced kidney disease, administration of effective osmolar agents may lead to hyponatremia, hyperkalemia, metabolic acidosis, and intravascular expansion. To our knowledge, osmolar effects of contrast agents in patients with advanced kidney disease have not been previously elucidated. Methods: This retrospective case series includes 5 patients with advanced kidney disease who underwent diagnostic and/or therapeutic cardiac catheterization and developed hyponatremia. Blood chemistry tests were performed before and after the procedure. Hyponatremia is defined as a plasma sodium concentration less than 135 mEq/L (mmol/L). Results: Mean precontrast and postcontrast sodium levels were 138.6 mEq/L (mmol/L) and 122.6 mEq/L (mmol/L), respectively. Plasma potassium levels increased after contrast exposure. There was no difference in degree of hyperkalemia between patients with and without diabetes. Plasma bicarbonate levels were noted to decrease after contrast exposure in 4 of 5 patients, with the exception of a patient undergoing continuous ambulatory peritoneal dialysis. There was a strong correlation between dose of contrast administered and change in sodium level, with a correlation coefficient of 0.91. Conclusion: These data suggest that large volumes of contrast may result in hypertonic hyponatremia through a dual effect of exogenous fluid dilution and translocation. The fluid translocated from intracellular to extracellular spaces may lead to a decrease in sodium, chloride, and bicarbonate levels. All patients developed hyperkalemia, which may be caused by solvent drag and/or passive diffusion, in addition to impaired excretory capacity. Patients with advanced kidney disease exposed to large volumes of contrast should be monitored for osmolar-induced chemical changes so that timely postcontrast dialytic therapy can be instituted.