Disease relevance of Hypokalemia

• To assess the effect of potassium repletion in hypokalemic hypertension, we administered either potassium chloride, 60 mmol per day, or placebo tablets, each for six weeks, in a randomized, double-blind, crossover trial to 16 hypertensive patients who had diuretic-induced hypokalemia and who continued to take a constant amount of diuretic [1].
• Isoproterenol infused at 0.02 micrograms per kilogram per minute caused similar tachycardia (25 beats per minute) and elevation in plasma renin activity (6.0 to 6.5 ng per milliliter per hour), but no hypokalemia [2].
• To determine whether epinephrine-induced hypokalemia is due to beta2-adrenoceptor stimulation, and whether hypokalemia can occur at physiologic concentrations of the agonist, epinephrine was infused into six normal volunteers at a rate of 0.1 microgram per kilogram of body weight per minute [2].
• Thiazide-induced hypokalemia. Association with acute myocardial infarction and ventricular fibrillation [3].
• Both male and female survivors are fertile but exhibit hypokalemia, hypotonic polyuria, and apparent mineralocorticoid activity of corticosterone [4].

High impact information on Hypokalemia

• Hypokalemia from beta2-receptor stimulation by circulating epinephrine [2].
• With the lower-dose compound, the metabolic side effect of hypokalemia was less of a problem and there was no evidence of glucose intolerance [5].
• Response of thiazide-induced hypokalemia to amiloride [6].
• The effects of amiloride hydrochloride on thiazide-induced hypokalemia were evaluated [6].
• Deficiency of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in humans leads to the syndrome of apparent mineralocorticoid excess (SAME), in which cortisol illicitly occupies mineralocorticoid receptors, causing sodium retention, hypokalemia, and hypertension [4].

Chemical compound and disease context of Hypokalemia

• Presence of this mutation correlates with the clinical manifestations (hypertension, hypokalemia, suppressed aldosterone secretion) in this kindred [7].
• The impaired conversion of cortisol to cortisone (indicated by urinary cortisol and cortisone metabolites and failure to metabolize 11 alpha-[3H]cortisol to [3H]H2O), was associated with hypertension, hypokalemia, and suppression of the renin-angiotensin-aldosterone system [8].
• The CMA rats had significant alkalemia and hypokalemia (4-7 d: pH 7.58, HCO3 38.3 meq/liter, K+ 2.1 meq/liter; 11-14 d: pH 7.54, HCO3 38.1 meq/liter, K+ 2.5 meq/liter) [9].
• Toxic levels of theophylline were associated with hypokalemia, hypophosphatemia, hyperglycemia, metabolic acidosis, and hypotension in both the patient and the experimental series [10].
• Although clinical presentations were similar to those of patients with benign adenoma, all had significantly higher concentrations of deoxycorticosterone and aldosterone and more profound hypokalemia [11].

Biological context of Hypokalemia

• This model is characterized hemodynamically by wide variations in cardiac output and extracellular fluid volume and metabolically, by hypokalemia, suppressed plasma renin activity, and elevated plasma deoxycorticosterone values [12].
• Clinical data from our institution and others have revealed a number of characteristic features: quinidine plasma concentrations are generally low, marked QRS prolongation is absent, hypokalemia is frequent and abrupt heart rate slowing just before the initiation of a paroxysm is almost invariable [13].
• No mutations of the exons and exon-intron boundaries in the CLCN5 gene were found in one patient with LMWP, aminoaciduria, and hypokalemia [14].
• The patient's resting blood pressure was normal, and hypokalemia was not observed despite high blood corticosterone levels and reduced plasma renin activity [15].
• Administration of NaHCO3, insulin, digitalis, and calcium in patients suffering from hypothermia must be done with caution because hypokalemia may coexist with low body temperature and predispose the patients to lethal dysrhythmias [16].

Anatomical context of Hypokalemia

• The lack of the sarcolemma KATP current observed in these patients explains the symptoms of the disease, i.e., hypokalemia, depolarization of the fibers, and possibly the paralysis following insulin administration [17].
• Two control studies in which hypokalemia was allowed to ensue after hydrochlorothiazide ingestion revealed a diminution in glucose tolerance, a consequence of diminished pancreatic beta-cell response to glucose [18].
• It is concluded that the acceleration of furosemide-sensitive K+ (Rb+) transport in erythrocytes of mineralocorticoid hypertensive rats is largely caused by the hypokalemia and consecutive red cell K+ loss and shrinkage, respectively [19].
• The effect of mexiletine on normal automaticity in cardiac Purkinje fibers was studied in fibers made automatic either by hypokalemia or by isoproterenol [20].
• The hypokalemia is the result of passive and VIP-induced active secretion of potassium by colonic epithelial cells [21].

Gene context of Hypokalemia

• Recent work has shown that KCNE1-deficient mice display chronic hypokalemia and hyperaldosteronism [22].
• C-terminal HERG mutations: the role of hypokalemia and a KCNQ1-associated mutation in cardiac event occurrence [23].
• Hypokalemia causes renal tubulointerstitial injury with an elevation in renal endothelin-1 (ET-1) [24].
• It has been reported that vasoactive intestinal peptide (VIP)-producing tumors accompanied by watery diarrhea, hypokalemia, and achlorhydria (WDHA) syndrome often produce multiple hormones biochemically and immunohistochemically [25].
• In conditions with acquired nephrogenic diabetes insipidus (eg, lithium treatment, hypokalemia, postobstructive polyuria), AQP2 expression and targeting have been found to be markedly reduced, providing an explanation for the polyuria and the inability to concentrate urine associated with these conditions [26].

Analytical, diagnostic and therapeutic context of Hypokalemia

• After 60 minutes, epinephrine (10 micrograms/kg) was injected intravenously in the hypokalemia and control groups, and the arrhythmia ratio (the number of ventricular ectopic beats divided by the total heart rate) was calculated for 5 minutes [27].
• The patient had severe hypokalemia and hypertension responsive to spironolactone, and elevated supine plasma aldosterone and 18-hydroxycorticosterone values that did not increase after ambulation [28].
• Although renin-secreting tumors are rare, they must be considered in the differential diagnosis of hypertension associated with hypokalemia, which occurs commonly in the hypertensive population [29].
• Competitive effects of hypokalemia and volume depletion on plasma renin activity, aldosterone and catecholamine concentrations in hemodialysis patients [30].
• Captopril renography may be useful to differentiate Bartter's syndrome from other covert causes of hypokalemia [31].

References