Pediatr Nephrol (2011) 26:377–384 DOI 10.1007/s00467-010-1699-3 EDUCATIONAL REVIEW Pathogenesis, diagnosis and management of hyperkalemia Anja Lehnhardt & Markus J. Kemper Received: 8 July 2010 / Revised: 1 October 2010 / Accepted: 4 October 2010 / Published online: 22 December 2010 # IPNA 2010 Abstract Hyperkalemia is a potentially life-threatening condition in which serum potassium exceeds 5.5 mmol/l. It can be caused by reduced renal excretion, excessive intake or leakage of potassium from the intracellular space. In addition to acute and chronic renal failure, hypoaldoster- onism, and massive tissue breakdown as in rhabdomyol- ysis, are typical conditions leading to hyperkalemia. Symptoms are non-specific and predominantly related to muscular or cardiac dysfunction. Treatment has to be initiated immediately using different therapeutic strategies to increase potassium shift into the intracellular space or to increase elimination, together with reduction of intake. Knowledge of the physiological mechanisms of potassium handling is essential in understanding the causes of hyper- kalemia as well as its treatment. This article reviews the pathomechanisms leading to hyperkalemic states, its symp- toms, and different treatment options. Keywords Hyperkalemia . Potassium . Renal failure . Salbutamol Introduction Potassium is the most abundant intracellular cation (100- 150 mmol/l) and is critical in many physiological functions. Absorption of potassium from the gastrointestinal tract is rapid and usually complete. Depending on diet, the normal daily intake can vary. Common potassium-rich foods A. Lehnhardt : M. J. Kemper (*) Department of Pediatric Nephrology, University Medical Center Hamburg-Eppendorf, Martinistr. 5, 20246, Hamburg, Germany e-mail: kemper@uke.de include fruits, potatoes, beans, and grains; in contrast, high-fat diets usually contain low amounts of potassium (Table 1). Low extracellular potassium concentrations of 3.5–5.5 mmol/l are maintained by distinct renal and extrarenal mechanisms. The major key effector is the energy-consuming enzyme Na+/K+-ATPase, located in the plasma membrane of cells, which pumps Na+ out of and K+ into the cell in a 3:2 ratio (3Na+:2K+). The Na+/K+-ATPase helps to maintain the resting potential and avail transport, and helps to regulate cellular volume as well as intracellular calcium content. Extrarenal mechanisms are able to shift K+ from extra- to intracellularly, but the excretion of potassium mainly occurs in the kidneys. Renal adaptive mechanisms allow the kidneys to maintain potassium homeostasis until the glomerular filtration rate (GFR) drops to less than 15 ml/min/1.73 m2. Approximately 10% of the daily potassium intake is cleared via the gastrointestinal tract. In the presence of renal failure, the proportion of potassium excreted through the gut can increase, but is subject to high inter-individual variability [1]. Renal mechanisms of potassium handling Handling of potassium in the nephron depends on passive and active mechanisms. Potassium is filtered in the glomerulus and almost completely reabsorbed in the proximal tubule and the loop of Henle. Excretion mainly occurs in the cortical collecting duct [2]. It should be noted, however, that reabsorption and secretion of potassium occur simultaneously, and that many modulators are important, such as diet, adrenal steroids, and acid-base balance. Approximately 60-75% of the filtered potassium is reabsorbed in the proximal tubule (PT) by diffusion and solvent drag, mainly coupled to Na+ transport. The