Pediatr Nephrol (2011) 26:377–384 Table 3 Laboratory investigations in hyperkalemia Blood test Full blood count Blood gas analysis Serum osmolality Creatinine, urea CK ALT LDH Glucose, glycosylated hemoglobin Renin, angiotensin, aldosterone Cortisol, 11-beta hydroxylase or 21-hydroxylase or 17-OH progesterone in plasma Urine test Potassium, sodium, creatinine Albumin TTKG (S Osm * U Potassium) / (S Potassium * U Osm) Index of potassium secretory activity in the distal tubule Only valid when urine osmolality >300 and urine sodium >25 mmol/l 381 Differential diagnosis Hemolytic anemia HUS Thrombocytosis Infection & sepsis Acidosis Calculation of TTKG Acute and chronic renal insufficiency Rhabdomyolysis Hemolysis, tumor lysis Hemolysis, tumor lysis Diabetes mellitus Hyporeninemic hypoaldosteronism, pseudohypoaldosteronism Reduced enzyme activities in congenital adrenal hyperplasia Salt wasting Proteinuria TTKG expected to be high (usually >10) in hyperkalemia when renal response is intact. An inappropriately low TTKG in a hyperkalemic patient suggests hypoaldosteronism or a renal tubule defect [39] Test is most useful in distinguishing patients who have mineralocorticoid deficiency versus resistance by observing a change in TTKG values after administration of mineralocorticoid: increase in TTKG in mineralocorticoid-deficient but not aldosterone resistant states TTKG Transtubular potassium gradient, CK creatinine kinase, ALT alanine transaminase, LDH lactate dehydrogenase The following steps often have to be addressed simulta- neously. Additionally, if unknown, the cause of hyperkalemia has to be determined to prevent future episodes. Dosage and side-effects of drugs are given in Table 4. Step 1: Evaluate patient for potential toxicities and initiate ECG monitoring & & & & If patient has severe hyperkalemia or shows ECG changes, transfer to intensive care unit (ICU) immediately. Ca-Gluconate 10% can be used in patients with cardiac symptoms to stabilize membrane potential and positively influence bradycardia and ECG changes. Contraindications: digoxin-intoxication, hypercalcemic states. Step 2: Identify and immediately eliminate sources of potassium intake Review prescriptions and stop oral or parenteral potassium supplements. Stop all drugs that might cause or aggravate hyperkalemia. & Input of dieticians might be needed to identify potassium-rich foods (check for “special diets”), especially in patients with chronic renal failure. Step 3: Increase potassium shift from extra- to intracellu- lar space & & Dextrose and/or insulin infusion. An effect can often be seen immediately but response remains unpredictable. Close electrolyte and blood glucose monitoring is needed, hypoglycemia being the main side-effect. Aim to maintain blood glucose 10- 15 mmol/l. Beta-adrenergic agonists (salbutamol, reproterol) stimulate potassium to shift from extra to intracellular space via Na+/K+-ATPase as described above. Salbu- tamol can be applied via nebulizer or given intrave- nously. If given iv, the lowering effect of salbutamol is quite predictable with a mean decrease of 1.6- 1.7 mmol/l after 2 h [33]. It can cause tachycardia. Salbutamol has been shown to be safe and even superior to rectal cation-exchange resin in non- oliguric preterms with hyperkalemia [34].