Cases reported "Hyperkalemia"

Filter by keywords:



Filtering documents. Please wait...

1/236. adrenal insufficiency in smith-lemli-opitz syndrome.

    We describe three unrelated patients with adrenal insufficiency and RSH or smith-lemli-opitz syndrome (SLOS), a disorder due to deficient synthesis of cholesterol. These patients presented with hyponatremia, hyperkalemia, and decreased aldosterone-to-renin ratio, which is a sensitive measure of the renin-aldosterone axis. All patients had profound serum total cholesterol deficiency (14-31 mg/dl) and marked elevation of 7-dehydrocholesterol (10-45 mg/ dl). Two patients were newborn infants with 46, XY karyotypes and complete failure to masculinize; one of these patients also had cortisol deficiency. Both patients died within 10 days of birth of cardiopulmonary complications while on adrenal replacement therapy. The third patient diagnosed with SLOS at birth presented at age 7months with fever and diarrhea and was noted to have profound hyponatremia. This patient is maintaining normal serum electrolytes on mineralocorticoid replacement. We conclude that adrenal insufficiency may be a previously undetected and treatable manifestation in SLOS. We hypothesize that deficiency of cholesterol, an adrenal hormone precursor, may lead to insufficient synthesis of adrenal steroid hormones.
- - - - - - - - - -
ranking = 1
keywords = deficiency
(Clic here for more details about this article)

2/236. University of Miami Division of Clinical pharmacology therapeutic rounds: drug-induced hyperkalemia.

    Drug-induced hyperkalemia is an important but often overlooked problem encountered commonly in clinical practice. It may occur in the ambulatory as well as the impatient setting. Every evaluation of a hyperkalemic patient should include a careful review of medications to determine if a drug capable of causing or aggravating hyperkalemia is present. Medications generally produce hyperkalemia either by causing redistribution of potassium (beta2 -adrenergic blockers, succinylcholine, digitalis overdose, hypertonic mannitol) or by impairing renal potassium excretion. Drugs cause impaired renal potassium excretion by (1) interfering with the production and/or secretion of aldosterone (nonsterodial anti-inflammatory drugs, angiotensin-converting enzyme inhibitors, angiotensin-II receptor antagonists, heparin, cyclosporine, and FK 506) or (2) blocking the kaliuretic effects of aldosterone (potassium-sparing diuretics, trimethoprim, pentamidine, and nefamostat mesilate). Because severe renal insufficeiency is generally required to cause hyperkalemia, an elevated serum potassium concentration in a patient with mild-to-moderate renal failure should not be ascribed to renal failure alone. A careful search for "hidden" potassium loads and for causes of impaired tubular secretion of potassium (including drugs) is necessary. Finally, it is important to recognize that the causes of hyperkalemia may be additive. patients may have more than one cause of hyperkalemia at the same time. Therefore, all potential causes of hyperkalemia, including drugs, should be systematically evaluated in every hyperkalemic patient.
- - - - - - - - - -
ranking = 13005.09863938
keywords = potassium
(Clic here for more details about this article)

3/236. Acute hyperkalemia associated with intravenous epsilon-aminocaproic acid therapy.

    Epsilon-aminocaproic acid (Amicar) is used to treat severe hemorrhage refractory to usual medical management. This antifibrinolytic drug has been associated with a number of renal complications. However, there are no descriptions of this medication causing hyperkalemia. This report describes the development of hyperkalemia in a patient with underlying chronic renal insufficiency treated with intravenous epsilon-aminocaproic acid. The patient, who underwent coronary artery bypass grafting, had no other obvious cause for the acute increase in serum potassium concentration. Based on data in animals and humans, the cationic amino acids lysine and arginine have been shown to enter muscle cells in exchange for potassium and lead to hyperkalemia through a shift of potassium from the intracellular to the extracellular space. Epsilon-aminocaproic acid, a synthetic amino acid structurally similar to lysine and arginine, also has been noted to cause an acute increase in serum potassium in anephric dogs infused with this medication. It is probable that the mechanism underlying the increase in serum potassium with epsilon-aminocaproic acid is also based on the shift of potassium from the intracellular to the extracellular space. Hence, it appears that intravenous epsilon-aminocaproic acid can also cause hyperkalemia in humans.
- - - - - - - - - -
ranking = 11147.227405183
keywords = potassium
(Clic here for more details about this article)

4/236. Familial pseudohyperkalemia maps to the same locus as dehydrated hereditary stomatocytosis (hereditary xerocytosis).

    Familial pseudohyperkalemia is a "leaky red blood cell" condition in which the cells show a temperature-dependent loss of potassium (K) from red blood cells when stored at room temperature, manifesting as apparent hyperkalemia. The red blood cells show a reduced lifespan in vivo but there is no frank hemolysis. Studies of cation content and transport show a marginal increase in permeability at 37 degrees C and a degree of cellular dehydration, qualitatively similar to the changes seen in dehydrated hereditary stomatocytosis (hereditary xerocytosis). Physiological studies have shown that the passive leak to K has an abnormal temperature dependence, such that the leak is less sensitive to temperature than that in normal cells. We performed genetic mapping on the original family and found that the condition in this kindred maps to the same locus (16q23-ter) that we have previously identified for an Irish family with dehydrated hereditary stomatocytosis, which does not show the same temperature effects.
- - - - - - - - - -
ranking = 1857.8712341971
keywords = potassium
(Clic here for more details about this article)

5/236. A case of aldosterone-producing adenoma with severe postoperative hyperkalemia.

    It is known that some patients with primary aldosteronism show postoperative hyperkalemia, which is due to inability of the adrenal gland to secrete sufficient amounts of aldosterone. However, hyperkalemia is generally neither severe nor prolonged, in which replacement therapy with mineralocorticoid is seldom necessary. We report a case of a 46-year-old woman with an aldosterone-producing adenoma associated with severe postoperative hyperkalemia. After unilateral adrenalectomy, the patient showed episodes of severe hyperkalemia for four months, which required not only cation-exchange resin, but also mineralocorticoid replacement. plasma aldosterone concentration (PAC) was low, although PAC was increased after rapid ACTH test. Histological examination indicated the presence of adrenocortical tumor and paradoxical hyperplasia of zona glomerulosa in the adjacent adrenal. immunohistochemistry demonstrated that the enzymes involved in aldosterone synthesis, such as cholesterol side chain cleavage (P-450scc), 3beta-hydroxysteroid dehydrogenase (3beta-HSD), and 21-hydroxylase (P-450c21), or the enzyme involved in glucocorticoid synthesis, 11beta-hydroxylase (P-450c11beta), were expressed in the tumor, but they were completely absent in zona glomerulosa of the adjacent adrenal. These findings were consistent with the patterns of primary aldosteronism. serum potassium level was gradually decreased with concomitant increase in PAC. These results suggest that severe postoperative hyperkalemia of the present case was attributable to severe suppression of aldosterone synthesis in the adjacent and contralateral adrenal, which resulted in slow recovery of aldosterone secretion. It is plausible that aldosterone synthesis of adjacent and contralateral adrenal glands is severely impaired in some cases with primary aldosteronism, as glucocorticoid synthesis in cushing syndrome.
- - - - - - - - - -
ranking = 1857.8712341971
keywords = potassium
(Clic here for more details about this article)

6/236. Hyperkalaemic paralysis--a bizarre presentation of renal failure.

    paralysis due to hyperkalaemia is rare and the diagnosis may be overlooked in the first instance. However it is rapidly reversible and so long as electro-cardiography and serum potassium measurement are urgently done in all patients presenting with paralysis, it will not be missed. A case of hyperkalaemic paralysis is described and a review of the emergency management discussed.
- - - - - - - - - -
ranking = 1857.8712341971
keywords = potassium
(Clic here for more details about this article)

7/236. hyperkalemia with cardiac arrhythmia. Induction by salt substitutes, spironolactone, and azotemia.

    In two patients, severe hyperkalemia and serious cardiac arrhythmia developed after excessive use of potassium-containing salt substitutes. Both had impaired ability to handle and excrete additional potassium load due to chronic congestive heart failure, azotemia, and administration of spironolactone. Prompt recognition of the arrhythmia and immediate restoration of the cardiac rate and rhythm by pacemaker support followed by intensive regimen to lower the serum potassium prevented a potentially fatal outcome. These cases emphasize the potential danger of salt substitutes when used by patients who are predisposed to retain potassium.
- - - - - - - - - -
ranking = 7431.4849367885
keywords = potassium
(Clic here for more details about this article)

8/236. hyperkalemia probably reverses the antiarrhythmic effects of amiodarone: a case report.

    Sustained monomorphic ventricular tachycardia (VT) developed in a 58-year-old man with acute myocardial infarction and end-stage renal disease. amiodarone was effective in preventing VT recurrence. Sustained VT was not induced during an electrophysiologic study. However, VT recurred during accidental hyperkalemia, which was caused by the change of dialysis therapy from peritoneal dialysis to hemodialysis. VT subsided with correction of hyperkalemia. Thereafter, VT did not recur as long as the serum potassium concentration was kept within the normal range. Several months later, the patient died suddenly because poor dietary compliance resulted in an increase in his potassium concentration. This case suggests that hyperkalemia may reverse the potent antiarrhythmic effects of amiodarone.
- - - - - - - - - -
ranking = 3715.7424683942
keywords = potassium
(Clic here for more details about this article)

9/236. Hyperkalaemia in a Thai man.

    Blood specimens from a Thai man showed greatly increased time-dependent and temperature-dependent efflux of potassium from cells into serum. No in-vivo correlate was found, and no similar results were obtained in screening 131 other Thai men. Findings may be related to decreased Na,K-ATPase density or activity.
- - - - - - - - - -
ranking = 1857.8712341971
keywords = potassium
(Clic here for more details about this article)

10/236. Severe hyperkalaemia due to the concomitant use of salt substitutes and ACE inhibitors in hypertension: a potentially life threatening interaction.

    We report two cases of hyperkalaemia related to the use of the salt substitute 'Lo Salt' in hypertensive patients on treatment with ACE inhibitors. In each case serum potassium returned to the normal range after cessation of the salt substitute. Without vigilance the contribution of the salt substitute to hyperkalaemia would have been overlooked and an ACE inhibitor erroneously withdrawn.
- - - - - - - - - -
ranking = 1857.8712341971
keywords = potassium
(Clic here for more details about this article)
| Next ->


Leave a message about 'Hyperkalemia'


We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.