Hypokalemia: A Practical Approach to Diagnosis and its Genetic Basis

Abstract

Hypokalemia is a common and important finding in hospitalized patients because it may provoke cardiac arrhythmias and/or respiratory arrest. Our aim is to suggest better diagnostic tools and therapeutic principles, and summarize new molecular advances that are linked to hypokalemia. Measurements in freshly-voided urine to evaluate potassium (K+) excretion and an assessment of the acid-base status in blood can help differentiate between the various causes of hypokalemia. In patients with a low rate of K+ excretion, hypokalemia can be explained by an acute shift of K+ into cells, intestinal K+ loss, or prior renal K+ excretion. Patients with a high rate of K+ excretion usually have metabolic acid-base disorders. In patients with hyperchloremic metabolic acidosis, an assessment of the rate of excretion of ammonium (NH4+) in the urine separates those with renal tubular acidosis (RTA) (low NH4+ excretion) from those with causes other than RTA. In patients with metabolic alkalosis, a high blood pressure helps to distinguish between a state with high mineralocorticoid activity from others with extracellular fluid (ECF) volume contraction. Measurement of renin activity, aldosterone, and cortisol levels in plasma help to differentiate between the causes with mineralocorticoid excess whereas the urine chloride (Cl-) concentration may reveal the basis for renal Na+ wasting and distinguish it from non-renal Na+ loss. The treatment of hypokalemia is guided by the risk imposed by hypokalemia, magnitude of the K+ deficit, route of the K+ administration, available K+ preparations, adjuncts to therapy, and special associated conditions. Recent molecular advances in inherited hypokalemic disorders affecting transcellular K+ shift, gastrointestinal and renal K+ excretion are also discussed.

Generation and analysis of the thiazide-sensitive Na+-Cl− cotransporter (Ncc/Slc12a3) Ser707X knockin mouse as a model of Gitelman syndrome

“…It has also been noted that hypokalemia in GS is difficult to correct even with high K 1 supplementation and combined use of K 1 -sparing agents (ENaC or mineralocorticoid receptor inhibitors). ROMK channels, a lowconductance secretory channel [Wang, 2006], and Ca 21 -activated Maxi-K channels, a large-conductance channel stimulated by increased distal renal tubule flow [Pluznick and Sansom, 2006], are two important K 1 channels involved in K 1 secretion in the distal renal tubules [Lin and Halperin, 2007]. The decrease in Na 1 reabsorption via NCC would increase distal Na 1 and fluid delivery to the downstream ROMK and Maxi-K containing tubular segments and lead to K 1 wasting and hypokalemia in GS [Rodan and Huang, 2009].…”

Changes in Body Water Caused by Sleep Deprivation in Taeeum and Soyang Types in Sasang Medicine: Prospective Intervention Study

“…In addition, the effect of hormones (aldosterone, cortisol, etc.) and the interaction between cardiac output and peripheral arterial resistance may be involved in this difference in individual responses [28–30]. In future, the association between metabolic syndrome, various hormonal changes and cardiovascular diseases, and sleep deprivation and cell volume regulation should be investigated.…”

Triuret as a potential hypokalemic agent: Structure characterization of triuret and triuret–alkali metal adducts by mass spectrometric techniques

“…This observation suggests that triuret may be able to deplete potassium under certain pathophysiological conditions and should therefore be considered as a potential hypokalemic agent. Hypokalemia is an electrolyte disorder that has been associated with a plethora of pathologic conditions: cardiovascular, neuromuscular, renal, and metabolic [106–109]. A hypokalemic state results from either an increased K + shift into cells and/or excessive net loss of K + .…”