378 Table 1 Potassium content of selected foods Foods and drinks 1 small banana (85 g) Blueberries (100 g) White mushrooms (75 g) Broccoli, cooked (75 g) Green beans, cooked (75 g) Onions, cooked (75 g) French fries (150 g) Parboiled rice (150 g) Spaghetti, without egg (150 g) Orange juice (200 ml) Milk, full fat (200 ml) Coca Cola (200 ml) Potato crisps (20 g) Milk chocolate bar (20 g) White chocolate (20 g) Wine gums (20 g) Potassium content (mmol) 8.6 1.9 8.1 5.8 3.9 1.5 17.7 2.2 2.3 7.9 7.7 0.1 5.1 2.4 1.8 1.8 mechanisms involved are not yet completely understood. The Na+/H+ antiporter is the most important system in this respect, and paracellular shunt-pathways are also present. Diffusion is driven by lumen-negative electrical potential created by the Na+/K+-ATPase in the second half of the proximal tubule, which creates high Cl- concentrations in the lumen. Approximately 15-20% of the filtered potassium is reabsorbed in the thick ascending limb of the Loop of Henle (TAL). Several co-transporters and ion channels are involved in the complex regulatory system of potassium reabsorption. The best characterized is the Na-K-2Cl cotransporter (NKCC2), which transports potassium out of the tubular fluid and is inhibited by loop diuretics (furosemide). Some of the potassium recycles back into the tubular fluid via K channel ROMK (renal outer medullary K+channel) in the apical membrane, but a fraction of it moves into the interstitial fluid. The TAL establishes the potential for countercurrent trapping of potassium in the medulla in a manner similar to that for Na+ and NHþ. Basolateral transporters include a KCl 4 cotransporter. The distal convoluted tubule (DCT) is the site of the apical sodium chloride cotransporter (NCCT), which is blocked by thiazides [3]. It modulates excretion of not only potassium but also calcium and magnesium. NCCT and ROMK channels seem to regulate potassium excretion Pediatr Nephrol (2011) 26:377–384 under the influence of serine/threonine kinases, especially lysine-deficient protein kinase-1 and 4 (WNK-1 and WNK- 4) [4]. There is evidence that the calcium-sensing receptor (CaSR) influences the renal ion transport, amongst others by inhibiting the activity of ROMK [5]. At least two circulating factors are required for the regulation of renal K+ secretion by the cortical collecting duct (CCD), the main site of renal potassium excretion, aldosterone, and a second as yet unidentified factor that increases the number of conducting K+ channels [6]. Aldosterone as key regulator of renal potassium homeo- stasis binds to the nuclear mineralocorticoid receptor (MR) within the distal tubule and the principal cells in the CCD. It activates the basolateral Na+/K+-ATPase, thereby increas- ing Na+ and water reabsorption into the blood and secretion of K+ into the urine. Aldosterone also upregulates the amiloride sensitive sodium channels (ENaCs) in the apical membrane of CCD and stimulates H+ secretion by intercalated CCD cells, thereby influencing acid/base balance [7]. K+ secretion can be partially counteracted by reabsorp- tion by the intercalated cells in the cortical and outer medullary collecting tubules [8, 9]. Vasopressin increases K+ excretion in the medullary collecting duct while promoting antidiuresis [10]. Extrarenal regulatory mechanisms of potassium metabolism Acid-base balance can affect the balance between cellular and extracellular potassium concentration. Acidosis increases the plasma K+ concentration by inducing a net shift of K+ from the cellular to the extracellular compart- ment in exchange with H+, also leading to a reduced tubular secretion of potassium. Insulin is important in preventing a large change in extracellular fluid (ECF) K+ concentration as it increases potassium uptake into liver and muscle cells by stimulating Na+/K+-ATPase. Large increases in ECF K+ concentration (>1-1.5 mmol/l) stimulate insulin secretion, which pro- motes shift of excess K+ into the intracellular compartment. Lastly, catecholamines (adrenaline, noradrenaline, dopa- mine) binding to beta-2 receptors on muscle cells stimulate the Na+/K+-ATPase and cause increased K+ shift into cells. Pathogenesis of hyperkalemia Hyperkalemia may result from an increase in total body potassium secondary to imbalance of intake vs. excretion or from maldistribution between intra- and extracellular space.