Symptomatic Hypokalemia Research Articles

A Physiologic-Based Approach to the Treatment of a Patient With Hypokalemia

Hypokalemia is common and can be associated with serious adverse consequences, including paralysis, ileus, cardiac arrhythmias, and death. As a result, the body maintains serum potassium concentration within very narrow limits by tightly regulated feedback and feed-forward systems. Whereas the consequences of symptomatic hypokalemia and severe potassium depletion are well appreciated, chronic mild hypokalemia can accelerate the progression of chronic kidney disease, exacerbate systemic hypertension, and increase mortality. Persistent hypokalemia may reflect total-body potassium depletion or increased renal potassium clearance. In a patient with simple potassium depletion, potassium replacement therapy should correct serum potassium concentration, but may have little effect when renal potassium clearance is abnormally increased from potassium wasting. In such cases, the addition of potassium-sparing diuretics might be helpful. Serum potassium concentration is an inaccurate marker of total-body potassium deficit. Mild hypokalemia may be associated with significant total-body potassium deficits and conversely, total-body potassium stores can be normal in patients with hypokalemia due to redistribution. The speed and extent of potassium replacement should be dictated by the clinical picture and guided by frequent reassessment of serum potassium concentration(.) The goals of therapy should be to correct a potassium deficit, if present, without provoking hyperkalemia. Oral replacement is preferred except when there is no functioning bowel or in the setting of electrocardiogram changes, neurologic symptoms, cardiac ischemia, or digitalis therapy.

Hypertension and Symptomatic Hypokalemia in a Patient With Simultaneous Unilateral Stenoses of Intrarenal Arteries and Mesangioproliferative Glomerulonephritis

We present the case of a young patient with hypertension and unprovoked symptomatic hypokalemia. His workup uncovered secondary aldosteronism, moderate proteinuria, and, quite unusually, concurrent chronic hepatitis B. Detailed investigations, including renal angiography, renal vein sampling, and kidney biopsy, showed unilateral renin hypersecretion due to intrarenal arterial stenoses and mesangioproliferative glomerulonephritis, presumed to be secondary to hepatitis B infection. Targeted pharmacotherapy reversed all clinical manifestations, normalizing blood pressure and serum potassium level and achieving full remission of proteinuria and loss of hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg), and a dramatic decrease in viral load.

Lateralización de la secreción de aldosterona en la hipertensión secundaria

We present the case of a 33-year old woman with arterial hypertension and symptomatic hypokalemia who was treated with beta blockers and diuretics, with subsequent addition of telmisartan and potassium. In Nephrology, all of her medication was replaced by an alpha blocker and she was admitted for study of secondary hypertension. During her hospitalization, the existence of hypokalemia, hyperkaliuria, low basal and post-stimulation plasma renin, elevated basal and post-stimulation aldosterone, elevated aldosterone/plasma renin ratio was verified. The abdominal CT scan demonstrated the existence of a left adrenal gland mass, confirming aldosterone hypersecretion by catheterization of the adrenal veins and adrenal scintigraphy with 131Icolesterol, laparoscopically excising the mass. The diagnosis was Conn's syndrome due to left adrenal adenoma. The interest of this case is due to the diagnostic difficulty based on imaging tests and the aid of the adrenal vein catheterization.

A case of Conn's syndrome revealed after oral sodium phosphate (fleet) preparation for colonoscopy

Oral sodium phosphate solutions (Fleet Mcneil Consumer Healthcare, Guelph, Ontario, Canada) are commonly used as bowel cleansing agents in preparation for colonoscopic exams; however, serious electrolyte disorders associated with oral sodium phosphate use have been described in case reports including hyperphosphatemia, hypocalcemia, hypomagnesemia, hypernatremia, and hypokalemia. We describe a 57-year-old patient with a past history of resistant hypertension who experienced severe symptomatic hypokalemia following colonic cleansing with an oral sodium phosphate solution. Further investigations revealed a serum aldosterone of 691 pmol/L and a serum renin level of 0.02 ng/L/s with a corresponding aldosterone-to-renin ration of 34550:1. The patient was subsequently diagnosed with primary aldosteronism secondary to an adenoma of the adrenal gland. Bilateral adrenal venous sampling revealed excessive levels of aldosterone in the left adrenal vein prior to definitive surgery. This case indicates that an oral sodium phosphate bowel preparation, though safe for most patients, can be complicated by a previously not diagnosed endocrine disease like the primary aldosteronism (Conn's syndrome) reported here. This is the first report of a Conn's syndrome diagnosed after bowel cleansing with a sodium phosphate solution.

Gitelman Syndrome

Gitelman Syndrome

Drug-Induced Hypokalaemia

Hypokalaemia (defined as a plasma potassium concentration<3.5 mEq/L) is a common electrolyte abnormality in clinical practice. Drugs are a common cause of either asymptomatic or symptomatic hypokalaemia. Drug-induced hypokalaemia is an important problem particularly in the elderly and in patients with cardiovascular, renal or hepatic disease. Hypokalaemia can complicate the use of the drug in the therapeutic concentration range, and can also be precipitated with overdose or conditions leading to drug intoxication. Because the etiologies of hypokalaemia are numerous, the diagnosis of drug-induced hypokalaemia may be overlooked. Physicians should always pay close attention to this common side effect. Evaluation and management of a hypokalaemic patient should include a careful review of medications history to determine if a drug capable of causing or aggravating this electrolyte abnormality is present.

Effect of Hydrochlorothiazide on Urinary Calcium Excretion in Dent Disease: An Uncontrolled Trial

Thiazide doses equivalent to 1 to 2 mg/kg/d of hydrochlorothiazide (HCTZ) have been proposed to correct hypercalciuria and prevent kidney failure in patients with Dent disease. However, they can cause adverse metabolic effects in the long term. In treating hypertension in children, lower thiazide doses have been shown to be as effective and well tolerated. Uncontrolled trial, with forced-titration sequential open-label study design. 7 boys with genetically confirmed Dent disease and mild phenotype (neither overt sodium wasting nor kidney failure). After a 1-month run-in period, patients sequentially received amiloride (5 mg/d) alone (1 month) and then for 3 periods of 2 months in association with increasing doses of HCTZ (<0.2, 0.2 to 0.4, and 0.4 to 0.8 mg/kg/d). Urinary calcium excretion and extracellular volume indicators. At the end of each period, 2 daily 24-hour urinary collections were performed on the days preceding admission. Blood and spot urine samples also were collected. A greater HCTZ dose increased renin, aldosterone, and plasma protein concentrations. Amiloride alone had no effect on calcium excretion. The greatest HCTZ doses decreased spot urinary calcium excretion by 42% compared with baseline (median, 0.3; minimum, maximum, 0.2, 0.8 versus median, 0.8; minimum, maximum, 0.4, 1.1, respectively; P = 0.03). However, patients developed adverse reactions, including muscle cramps (n = 2), biological (n = 7) or symptomatic hypovolemia (n = 1), hypokalemia (n = 4), and hyponatremia (n = 1), which all corrected after treatment withdrawal. Small sample size and absence of a control group. HCTZ doses greater than 0.4 mg/kg/d decreased calcium excretion, but were associated with significant adverse events. Thiazide diuretic therapy should be considered with caution in children with Dent disease.

Symptomatic hypokalemia associated with infliximab in a patient with Crohnʼs disease

Symptomatic hypokalemia associated with infliximab in a patient with Crohnʼs disease

Hypokalaemia Re-Visited: A Case Series

Hypokalaemia is a relatively common biochemical abnormality found at the emergency department. Sequential changes in the electrocardiogram occur as the serum potassium is lowered. Correction of hypokalaemia can be life-saving. It is essential for physicians to be able to recognise these changes and initiate prompt replacement when necessary. We present a case series of patients presenting to the emergency department with symptomatic hypokalaemia and discuss the electrocardiographic manifestations and recognition of hypokalaemic changes.

Hypokalemic myopathy in a patient with gluten-sensitive enteropathy and dermatitis herpetiformis Duhring: A case report

The case of a 22-year-old patient with symptomatic hypokalemia caused by rhabdomyolysis is presented as a rarely reported complication of gluten-sensitive enteropathy (GSE) and dermatitis herpetiformis Duhring. The patient's myopathy ceased on potassium supplementation and her other complaints resolved while on gluten-free diet. Recovery was otherwise uneventful with a rapid decline in serum CPK level. At the time of her last follow-up a few months later, she was free of symptoms and CPK remained stable. Patients with GSE may present with hypokalemia in association with diarrhea and emesis, and if potassium loss is rapid, rhabdomyolysis may occur.

Continuously Nebulized Albuterol in Severe Exacerbations of Asthma in Adults: A Case-Controlled Study

A retrospective, case-controlled analysis comparing patients admitted to a medical intensive care unit with severe exacerbations of asthma who received continuously nebulized albuterol (CNA) versus intermittent albuterol (INA) treatments is reported. Forty matched pairs of patients with asthma are compared. CNA was administered for a mean of 11 ± 10 hr. The incidence of cardiac dysrhthmias was similar between groups. Symptomatic hypokalemia did not occur. CNA patients had higher heart rates during treatment, which may reflect severity of illness. The incidence of intubation was similar. We conclude that CNA and INA demonstrated similar profiles with regard to safety, morbidity, and mortality.

Unilateral Renal Artery Stenosis Seen Initially as Severe and Symptomatic Hypokalemia

Hypokalemia is an uncommon presentation of renovascular hypertension. Although renal artery stenosis has been associated with hypokalemia secondary to hyperreninemic hyperaldosteronism, few reports have actually evaluated the pathophysiologic changes in such a patient with renovascular hypertension. We studied a patient before and after surgical revascularization who presented with severe hypertension and marked, symptomatic hypokalemia. Before surgery, the patient had excessive urinary potassium secretion, markedly increased secretion of renin after captopril stimulation, and mild secondary hyperaldosteronism. Postoperatively, the patient's blood pressure decreased moderately and the serum and urinary potassium values normalized. After revascularization, plasma renin activity both before and after captopril stimulation and serum aldosterone levels decreased markedly. These findings demonstrate that renovascular hypertension may rarely present with symptomatic hypokalemia secondary to excessive aldosterone secretion. Improvement in the renal ischemic state is accompanied by rapid correction of the metabolic disturbances associated with hyperreninemic hyperaldosteronism.

Tetany and rhabdomyolysis due to surreptitious furosemide--importance of magnesium supplementation.

Diuretics may induce hypokalemia, hypocalcemia and hypomagnesemia. While severe hypokalemia may cause muscle weakness, severe hypomagnesemia is associated with muscle spasms and tetany which cannot be corrected by potassium and calcium supplementation alone (1,2). Surreptitious diuretic ingestion has been described, mainly in women who are concerned that they are obese or edematous. Symptomatic hypokalemia has been reported in such patients (3-7) and in one case hypocalcemia was observed (8), but the effects of magnesium depletion were not noted in these patients.

Contraception--a look forward, Part II: Mifepristone and gossypol.

Part II of this series examines two compounds that are or have been in use in countries other than the United States. Mifepristone (RU486) is the first of the clinically useful progesterone antagonists; it competes with progesterone for receptors in the uterus, ovary, and pituitary gland. When taken by women in the follicular phase, it might be capable of inhibiting folliculogenesis while still allowing endometrial proliferation for normal menstrual cycling. When the drug is taken in the late luteal phase, endometrial shedding can usually be induced even after nidation. Mifepristone could thus serve as an emergency postcoital agent. In principle, it could also be used as a monthly emmenagogue, but clinical trials have been unsuccessful due to disruption of the following cycle's length. Shorter-acting antiprogesterones now under development may overcome this difficulty. Political constraints ultimately may be more limiting than pharmacological ones. Gossypol is a Chinese cottonseed derivative, which, taken orally, inhibits spermatogenesis in men. Its efficacy is very high, but use is presently limited by two adverse effects: occasional symptomatic hypokalemia and a 10 percent chance of irreversibility of aspermia. Current research is directed at understanding and overcoming these obstacles.

Diuretic therapy and exercise performance.

Drugs that induce an increased urine flow are used both legitimately (treatment of hypertension and oedema) and otherwise (rapid weight loss) in sports and exercise. There are 5 major categories of diuretic drugs based on their mechanisms and loci of action. Common to all classes is hypohydration, which has been shown to have an array of adverse effects on performance, including impaired strength, power and endurance. Postural hypotension can be particularly troublesome in the elderly. Also common to all diuretics, except those interfering with the aldosterone mechanism in the distal nephron, is hypokalaemia. Severe symptomatic hypokalaemia (serum K+ concentration less than 3.0 mmol/L) is rare except in clinical situations in which additional hypokalaemic factors are present. Moderate levels of hypokalaemia (serum K+ concentration 3.0 to 3.5 mmol/L) can increase the risk of adverse reactions as has been shown in a variety of prospective clinical studies. Hypokalaemia has effects on cardiac rhythm, muscle function and integrity, local blood flow, carbohydrate metabolism, and the blood lipid profile. Performance studies generally show diminished exercise tolerance in direct proportion to the degree of hypohydration induced. This is not the case, however, in a clinical setting of compromised cardiopulmonary function, in which diuresis has direct and indirect inotropic effects which augment exercise tolerance and decrease symptoms. The ability of the carbonic anhydrase inhibitor, acetazolamide, to induce a hyperventilatory response to the obligatory metabolic acidosis is taken advantage of in mountaineering to prevent or ameliorate the symptoms of acute mountain sickness, thereby improving exercise performance at high altitude. It is suggested that in clinical situations in which the use of a diuretic is considered appropriate, every effort be made to maintain or restore the serum concentration and the total body store of potassium to normal. To some degree this can be accomplished through diet, although potassium chloride supplements or potassium-sparing diuretics or diuretic combinations may be necessary.

Profound Hypokalemia in Continuous Ambulatory Peritoneal Dialysis

Symptomatic hypokalemia is not known to complicate continuous ambulatory peritoneal dialysis (CAPD), although this treatment is associated with continuous peritoneal potassium losses. Severe hypokalemia and muscular abnormalities associated with potassium loss developed in a patient undergoing CAPD, illustrating that oral supplementation and/or intraperitoneal potassium administration may be needed to treat patients with chronically poor nutritional intake or increased gastrointestinal potassium losses. Intraperitoneal potassium administration may be indicated in patients who cannot tolerate oral potassium supplements.

The role of vertebral angiography in the investigation of third nerve palsy.

The association between intracranial aneurysm and third nerve palsy in a series of fifty patients presenting to this unit over a six year period has been studied. All aneurysms causing a third nerve palsy were found to be in the anterior circulation and all were adequately demonstrated by carotid angiography alone. None of the thirty cases of posterior circulation aneurysm was associated with a third nerve palsy. Vertebral angiography carries a higher risk of serious complications than carotid angiography. We feel that the added risk of vertebral angiography is not justified for the investigation of an isolated third nerve palsy.

Symptomatic Hypokalemia Resulting From Surreptitious Diuretic Ingestion

We report five cases of symptomatic hypokalemia caused by surreptitious diuretic ingestion. A positive diagnosis was made in four patients by a colorimetric detection of the diuretic in urine by simple chemical means. Patients who surreptitiously ingest diuretics appear to be mainly women, among whom there appears to be high prevalence of diagnoses involving the reproductive system. Many of these patients have health-related occupations. They seem to be very concerned with appearing obese or edematous. A high urine potassium level in the presence of a low serum potassium level can suggest this diagnosis.

Hyperglycemia and inhibition of insulin secretion during administration of diazoxide and trichlormethiazide in man.

Reversible “diabetes” was produced in eight normal male subjects by administering between 400 mg. and 645 mg. of diazoxide and 8 mg. of trichlormethiazide per day for four to seven days. Insulin secretory responses to oral and intravenous glucose loads were determined on the last treatment day and the following morning, respectively. Four to six weeks later both tests were repeated to obtain control data. The speed of breakdown in glucose tolerance was proportional to daily diazoxide dosage, which in turn was limited by the severity of side effects. Carbohydrate turnover tended to worsen each day, even after correction of severe symptomatic hypokalemia in two subjects. The induced “diabetic” state was associated with sluggish insulin release as blood glucose rose, and with greatly decreased hormonal output per unit of glycemic stimulus—the same two secretory defects which characterize the clinical onset of hereditary diabetes mellitus. The dala suggest that the potent diabetogenicity of diazoxide given with trichlormethiazide may be almost entirely due io blockade of insulin release, either by direct action or by stimulating alpha adrenergic receptor sites in the beta cell. The synergistic effect of natriuretic analogues like trichlormethiazide probably reflects superimposed potassium deficiency, evidence of which consistently underlies the weaker hyperglycemic property of diuretic benzothiadiazines but is not caused by diazoxide itself. Thus, “diazoxide diabetes” appears to be functionally distinct from ordinary “thiazide diabetes” and, in fact, closely resembles spontaneous diabetes mellitus clinically. Since the condition can be predictably induced and is entirely reversible, it may provide a useful experimental model for further study of the inherited disease in man.