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PubMed2005

Clinical factors associated with hyperkalemia in patients with congestive heart failure.

BACKGROUND: Patients with congestive heart failure (CHF) are at risk for hyperkalemia because of coexisting comorbidities and use of multiple medications that impair potassium (K) excretion such as angiotensin converting enzyme (ACE) inhibitors. OBJECTIVE: To identify clinical factors associated with hyperkalemia on initial presentation in patients hospitalized for CHF. DESIGN: A case-control study. SETTING: Two university-affiliated tertiary-care hospitals. SUBJECTS: Using ICD-9 code for CHF, CHF admissions with hyperkalemia on presentation (cases) were identified from a population of 938 non-dialysis-dependent CHF patients. CHF admissions with normokalemia on presentation were used as controls. Hyperkalemia was defined as serum K > or = 5.6 mmol/L, and normokalemia as serum K > or = 3.5 and < or =5.5. METHODS: Data were collected on demographic characteristics, clinical variables, comorbidity and medication use. Factors associated with hyperkalemia on initial presentation were examined. RESULTS: Mean age did not differ between cases [76 years, standard deviation (SD) = 12] and controls (75 years, SD = 12) (P = 0.824). Mean potassium levels for cases and controls were 6.2 mmol/L (range 5.6 to 8.2) and 4.3 mmol/L respectively (P < 0.001). On multivariate analysis, diabetes mellitus [odds ratio (OR) = 2.42, 95% confidence interval (CI) = 1.04-5.59], creatinine clearance <40 mL/min (OR = 8.36, CI = 2.73-25.56), use of spironolactone (OR = 4.18, CI = 1.27-13.79), and use of ACE inhibitors (OR = 2.55, CI = 1.06-6.13) were independently associated with hyperkalemia. CONCLUSIONS: In CHF patients, hyperkalemia on presentation is independently associated with diabetes, creatinine clearance <40 mL/min, use of spironolactone, and use of ACE inhibitors. Recommendations for use of spironolactone and ACE inhibitors in CHF, and the intensity of serum K monitoring need to be clarified to account for patients at higher risk for hyperkalemia.

Aged↗
PubMedDate not supplied

Trimethoprim-induced hyperkalemia: An analysis of reported cases.

BACKGROUND: Trimethoprim has been recently implicated in the development of hyperkalemia when administered at standard doses to immunocompetent patients. However, many clinicians are unaware of this potentially dangerous adverse effect. OBJECTIVE: To review reported cases of trimethoprim-induced hyperkalemia in immunocompetent patients and identify predisposing factors, treatment, and outcome. METHODS: A MEDLINE literature search was performed using the key words 'trimethoprim' and 'hyperkalemia'. All English-language case reports and bibliographies of immunocompetent patients with trimethoprim-induced hyperkalemia were reviewed. RESULTS: Nine cases were identified. The mean patient age was 77.6 years, and the mean duration of therapy was 10.2 days. Seven patients received standard oral dosages of trimethoprim-sulfamethoxazole for common infections, and 2 patients were concurrently receiving angiotensin-converting enzyme inhibitors. The mean pretreatment levels of creatinine and potassium were 1.01 mg/dl and 4.55 mmol/l, respectively. The mean peak serum potassium level was 7.0 mmol/l. No deaths attributable to hyperkalemia occurred. CONCLUSIONS: Hyperkalemia due to trimethoprim typically affects elderly patients administered standard oral dosages, even in the presence of a normal serum creatinine level. Concurrent angiotensin-converting enzyme inhibitor therapy may increase the risk of hyperkalemia. The prognosis is favorable with standard therapy for hyperkalemia and withdrawal of trimethoprim.

Aged↗
PubMed2000

Fludrocortisone for the treatment of heparin-induced hyperkalemia.

OBJECTIVE: To report the use of fludrocortisone for heparin-induced hyperkalemia and to briefly review the available literature relating to heparin-induced hyperkalemia. CASE SUMMARY: A 34-year-old African-American man was admitted to the hospital for pneumococcal pneumonia and sepsis. His hospital course was complicated by the development of acute respiratory distress syndrome, severe sepsis, acute renal failure, placement of a tracheostomy, and recurrent nasopharyngeal bleeding. The patient also developed a subclavian vein thrombosis with extension to the cephalic and basilic veins secondary to placement of a pulmonary artery catheter; anticoagulation with heparin was required. On day 9 of heparin therapy, the patient developed symptomatic hyperkalemia refractory to conventional therapies. Oral fludrocortisone 0.1 mg/d was initiated with resolution of the hyperkalemia within 24 hours despite the continued administration of heparin. DATA SOURCES: A MEDLINE (1966-October 1999) search was performed to identify case reports and clinical trials discussing heparin-induced hyperkalemia or the use of fludrocortisone for hyperkalemia. DISCUSSION: Heparin has the potential to induce hyperkalemia by several mechanisms, including decreased aldosterone synthesis, reduction in number and affinity of aldosterone II receptors, and atrophy of the renal zona glomerulosa. Fludrocortisone promotes potassium excretion by its direct actions on the renal distal tubules. In this patient, fludrocortisone resulted in a significant and rapid decrease in serum potassium even with continued heparin administration and acute renal failure. CONCLUSIONS: This case suggests that fludrocortisone is a reasonable alternative therapy for patients with hyperkalemia secondary to heparin therapy when the continued administration of heparin is necessary.

Adult↗
PubMed2006

Hyperkalemia revisited.

Hyperkalemia is a common clinical condition that can induce deadly cardiac arrhythmias. Electrocardiographic manifestations of hyperkalemia vary from the classic sine-wave rhythm, which occurs in severe hyperkalemia, to nonspecific repolarization abnormalities seen with mild elevations of serum potassium. We present a case of hyperkalemia, initially diagnosed as ventricular tachycardia, to demonstrate how difficult hyperkalemia can be to diagnose. An in-depth review of hyperkalemia is presented, examining the electrophysiologic and electrocardiographic changes that occur as serum potassium levels increase. The treatment for hyperkalemia is then discussed, with an emphasis on the mechanisms by which each intervention lowers serum potassium levels. An extensive literature review has been performed to present a comprehensive review of the causes and treatment of hyperkalemia.

Aged↗
PubMedDate not supplied

Pharmacotherapy in congestive heart failure: Hyperkalemia in congestive heart failure.

Hyperkalemia is not an uncommon occurrence in the congestive heart failure patient, particularly when renal failure coexists. Hyperkalemia in CHF is typically medication-related. Its occurrence is inevitably linked to the simultaneous ingestion of angiotensin-converting enzyme inhibitors and beta-blockers, and more recently, aldosterone receptor antagonists, such as spironolactone. The most devastating consequence of hyperkalemia is its cardiotoxicity that can be fairly insidious in its rate of development. The therapy of hyperkalemia in congestive heart failure can involve both acute and semiacute management phases. Acute hyperkalemia management includes measures that block the adverse membrane effects of hyperkalemia, such as intravenous calcium administration, and efforts to shift potassium intracellularly, such as occurs with intravenous bicarbonate and/or inhaled beta-agonists. Semiacute management of hyperkalemia includes measures to increase urinary potassium excretion and administration of binding resins, such as Kayexalate®. Prevention is the cornerstone of hyperkalemia management in the heart failure patient and requires that careful attention be directed to both identifying exogenous sources of potassium and pinpointing the maximum tolerable dose of either an angiotensin-converting enzyme inhibitor or an angiotensin-receptor blocker. (c)2001 by CHF, Inc.

Journal Article↗
PubMed1992

ECG changes under hyperkalemia with nephrectomy in the rat.

Electrolyte abnormalities have become an increasingly important cause of arrhythmias. Although the electrocardiographic (ECG) changes under hyperkalemia in the rat are poorly understood, it is conceivable that excess plasma potassium may also alter the cardiac excitations in the rat. Further, effects of hyperkalemia on ECG in the rat may differ from other species that have ST-segment and longer QT intervals in ECG. The present study was designed to determine the diagnostic criteria for ECG manifestations to various levels of plasma potassium concentration. For this purpose, hyperkalemia was induced by nephrectomy with and without infusions. Because it was difficult to produce various levels of plasma potassium concentration by only nephrectomy, we used two kinds of infusions to obtain especially moderate levels of nephrectomy-induced hyperkalemia. ECGs were recorded 24, 36, and 48 hours after nephrectomy. Plasma potassium concentration and number of abnormal ECGs were increased time-dependently. Increased T wave amplitude was present with mild hyperkalemia. The typical T wave change observed with so-called sinoventricular conduction levels of potassium concentration in species with long QT intervals did not occur in the rat. PR interval and QRS duration became slightly shorter within moderate hyperkalemia. P wave disappeared in most rats at potassium levels above 8.0 mEq/l. In advanced hyperkalemia (plasma potassium concentration above 7.5 mEq/l), conduction in all parts of the heart was suppressed. Moreover, sinoventricular conduction appeared. Thus, the diagnostic criteria for ECG manifestations to various levels of plasma potassium concentration in the rat were demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Renin-angiotensin system blockade and the risk of hyperkalemia in chronic hemodialysis patients.

BACKGROUND: Blockade of the renin-angiotensin system by angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers can cause hyperkalemia in patients with chronic renal insufficiency who are not on dialysis, but the risk of hyperkalemia in hemodialysis patients is unknown. SUBJECTS AND METHODS: We conducted a prospective study of 251 adult hemodialysis patients to determine if renin-angiotensin system blockade was associated with hyperkalemia, defined as a predialysis serum potassium concentration of 5.5 mmol/L or higher. Medication use was determined by chart review and patient interview. Predialysis serum potassium concentration was measured monthly. RESULTS: There were 367 episodes of hyperkalemia during 1877 person-months of follow-up. After adjustment for potential confounding variables and for clustering of episodes by patient, use of an ACE inhibitor or an angiotensin receptor blocker was associated with a significantly higher risk of hyperkalemia (odds ratio [OR] = 2.2; 95% confidence interval [CI]: 1.4 to 3.4). The increased risk of hyperkalemia with renin-angiotensin system blockade was seen in anuric dialysis patients (OR = 2.3; 95% CI: 1.3 to 4.2), as well as those with residual renal function (OR = 2.1; 95% CI: 1.0 to 4.1). CONCLUSION: The use of ACE inhibitors or angiotensin receptor blockers is independently associated with an increased risk of developing hyperkalemia in chronic hemodialysis patients. The serum potassium concentration should be closely monitored when these medications are prescribed for hemodialysis patients.

Aged↗
PubMed1984

Verapamil worsens rate of development and hemodynamic effects of acute hyperkalemia in halothane-anesthetized dogs: effects of calcium therapy.

The hemodynamic effects of verapamil pretreatment versus no pretreatment were evaluated in five acutely hyperkalemic dogs. Using ECG evidence for severe hyperkalemia, the halothane-anesthetized dogs were rendered acutely hyperkalemic to similar plasma levels of K+ (K+ = 8.2 +/- 0.8 mEq/l verapamil plus hyperkalemia, K+ = 9.4 +/- 0.2 mEq/l hyperkalemic controls). The verapamil-hyperkalemic group had significantly lower cardiac indexes (CI) (CI = 1.3 +/- 0.5 1 X min-1 X m-2 verapamil plus hyperkalemia vs. CI = 3.0 +/- 0.2 1 X min-1 X m-2 hyperkalemic controls) and lower mean arterial pressures (MAP = 60 +/- 13 mmHg verapamil plus hyperkalemia vs. MAP = 96 +/- 7 mmHg hyperkalemic controls). Calcium therapy for hyperkalemia that returned CI to control levels in hyperkalemic controls only partially reversed the severe hemodynamic depression and did not improve the AV block seen during hyperkalemia in the presence of the calcium entry blocker verapamil. Surprisingly, the total mEq of KCl infused at the same rate into verapamil-pretreated dogs to result in similar high serum potassium levels was only one-third that required in dogs not pretreated with verapamil (1.6 +/- 0.3 mEq/kg KCl in verapamil-hyperkalemia group vs. 5.0 +/- 0.7 mEq/kg KCl in hyperkalemic controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1998

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.

AIDS-Related Opportunistic Infections↗
PubMed2000

Regional hyperkalemia increases ventricular defibrillation energy requirements: role of electrical heterogeneity in defibrillation.

INTRODUCTION: Increased spatial electrical heterogeneity has been associated with impaired defibrillation efficacy. The current study investigated the relationship between electrical heterogeneity and defibrillation efficacy by manipulating spatial electrical heterogeneity. METHODS AND RESULTS: We increased spatial electrical heterogeneity by infusing potassium chloride (2 to 4 mEq/hour) or placebo in the left anterior descending artery in 13 pentobarbital anesthetized swine. Electrophysiologic measurements at five myocardial sites and defibrillation energy requirement (DER) values were determined at baseline and during regional hyperkalemia (n = 7) or placebo (n = 6). Regional potassium infusion was titrated to a 20% reduction in action potential duration in the perfused region. Regional hyperkalemia increased biphasic DER values by 87% (P = 0.02), whereas infusion of placebo did not alter defibrillation efficacy. Regional hyperkalemia decreased myocardial repolarization and refractoriness in the perfused region by 21% (P < 0.001) and 18% (P = 0.01), respectively. However, regional hyperkalemia increased ventricular fibrillation cycle length (VFCL) by 39% (P = 0.008). Consequently, dispersions of repolarization, refractoriness, and VFCL were significantly increased by 169%, 92%, and 200%, respectively. Regional hyperkalemia also increased ventricular conduction time to the perfused region by 54% (P = 0.006), indicating conduction velocity dispersion, while not affecting local pacing threshold or local voltage gradient. CONCLUSION: Regional hyperkalemia increased DER values. Regional hyperkalemia likely impairs defibrillation by increasing myocardial electrical heterogeneity, which supports the theory that electrical heterogeneity promotes nonuniform propagation of early postshock activations, thereby inhibiting defibrillation.

Animals↗
PubMed1992

Hyperkalemia associated with ketorolac.

OBJECTIVE: To report and describe the apparent first case of hyperkalemia following intramuscular administration of ketorolac and to discuss the proposed mechanism of action. PATIENT: The patient was a 59-year-old man who developed hyperkalemia following a right upper lobectomy; he had received an intramuscular injection of ketorolac 30 mg for incisional pain. RESULTS: All possible causes of the hyperkalemia, including other drugs and intraoperative and postoperative events, were thoroughly evaluated and ruled out. Hyperkalemia has been reported in patients who have received other nonsteroidal antiinflammatory drugs (NSAIDs). The proposed mechanism of action for the occurrence of this hyperkalemia appears to be related to the suppression of prostaglandin synthesis. CONCLUSIONS: Considering the temporal sequence of events and drugs administered prior to the hyperkalemia in this patient and the hyperkalemic potential associated with other NSAIDs, ketorolac appears to be the precipitating agent. The possibility of hyperkalemia associated with the parenteral use of ketorolac may warrant practitioners to closely monitor the blood chemistry of patients receiving this agent.

Analgesics↗
PubMedDate not supplied

Glucose and insulin infusion versus kayexalate for the early treatment of non-oliguric hyperkalemia in very-low-birth-weight infants.

Forty very low birth weight (VLBW) infants with non-oliguric hyperkalemia in the first few days after birth were enrolled in this study. They were randomly divided into 2 groups, regular insulin (RI) infusion group and kayexalate resin enema group. Therapy was administered when serum potassium level was greater than 6 mEq/L. None of these infants received blood transfusion during this study course. In RI group (n = 20), the ratio of infusion glucose to regular insulin was 10-15 gm glucose to 1 unit RI, and the glucose infusion rate was maintained at least 6 mg/Kg/min. In Kayexalate group (n = 20), the dose of Kayexalate was 1 gm/Kg body weight given rectally every four hours. All treatment discontinued after the serum potassium level returned to normal for 6 hours. The mean gestational ages were 27.4 +/- 1.8 weeks in RI group and 28.4 +/- 2.4 weeks in Kayexalate group, respectively. Mean birth weights were 935 +/- 259 gm (RI) and 1065 +/- 214 gm (Kayexalate). The ages at onset of hyperkalemia were 24.6 +/- 8.2 (RI) and 22.2 +/- 8.1 (Kayexalate) hours after birth. The mean urine outputs during the 8-hour interval prior to development of hyperkalemia were 5.4 +/- 1.3 (RI) and 5.5 +/- 0.9 (Kayexalate) ml/kg/min. The durations of hyperkalemia were 26.4 +/- 14.9 (RI) and 38.6 +/- 13.3 (Kayexalate) hours. The peak serum potassium levels during therapy were 7.3 +/- 0.9 and 7.4 +/- 0.6 mEq/L. The incidences of grade II and above intraventricular hemorrhage (IVH) were 15% (3/20) and 50% (10/20). The incidences of cardiac dysrhythmia were 5% (1/20) and 10% (2/20). Significantly shorter duration of non-oliguric hyperkalemia and lower incidence of IVH were noted in RI group, but there were no differences in the peak potassium level or the incidence of cardiac dysrhythmia between these two groups. We conclude that to use early continuous regular insulin infusion therapy for the treatment of non-oliguric hyperkalemia in VLBW infants is more effective than kayexalate in decreasing the duration of hyperkalemia and reducing the incidence of intraventricular hemorrhage.

Enema↗
PubMed1991

Endocrine crises. Hyperkalemia.

Clinical disorders causing hyperkalemia require a basic understanding of normal K homeostasis, which consists of external and internal K balances. The kidney is predominant in maintaining the external balance of K, and a number of mechanisms exist to provide a renal adaptation to defend against K excess. Likewise, several factors are known to modulate internal K balance--i.e., its distribution within the body. Some of these factors may provide defense against hyperkalemia before the kidneys have time to adapt. Potassium retention by the kidney causes hyperkalemia when renal failure is advanced, or earlier in the face of impaired tubular function in a variety of disorders. Hyperkalemia out of proportion to loss of renal function also occurs in the syndrome of hyporeninemic hypoaldosteronism. Drug-induced hyperkalemia is increasingly common and usually is caused by nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors, cyclosporine, or K-sparing diuretics. Clinical disorders of internal K imbalance include diabetes mellitus, systemic acidosis, and use of beta-blockers. Hyperkalemia is usually asymptomatic, but the danger of cardiac arrest or arrhythmia in severe hyperkalemia forces prompt clinical attention. Available treatment choices include agents that antagonize the effect of K on membrane potentials, redistribute it internally into cells, and remove it altogether from the body. The diagnostic work-up can then proceed, first by distinguishing renal and extrarenal causes, then by examining the roles of specific factors outlined in the section on normal K homeostasis.

Aged↗
PubMed1989

Hyperkalemia in diabetes mellitus. Effect of a triamterene-hydrochlorothiazide combination.

Hyperkalemia is known to occur with increased frequency in the patient with diabetes mellitus and in the elderly when agents that interfere with renal potassium excretion are employed, but the precise frequency has not been established. We employed data from a post-marketing surveillance trial following the introduction of a triamterene-hydrochlorothiazide (Maxzide) combination to estimate the frequency. In patients normokalemic at baseline, hyperkalemia developed with a frequency of 0.59% in 20,809 nondiabetics and in 1.08% of 922 diabetics. Hyperkalemia was threefold to fivefold more likely in those more than 60 years of age, and all of the excess hyperkalemia in diabetics occurred in the elderly. The severity of hyperkalemia was not influenced by the diabetes mellitus. Hypokalemia occurred with a frequency of about 5% and was not influenced by either age or diabetes. In patients who were hypokalemic prior to treatment, hypokalemia was corrected in more than two thirds and hyperkalemia occurred less frequently. Although hyperkalemia indeed occurs with increased frequency in the elderly diabetic when a potassium-sparing combination is employed, the frequency is not so great that such agents should be avoided routinely when their use could be beneficial. Renal function and serum potassium concentration should be assessed prior to instituting treatment and repeated within a few days and a few weeks thereafter in the patient at risk, especially when renal function is suspected, and in the elderly.

Diabetes Complications↗
PubMed2004

Spironolactone-induced renal insufficiency and hyperkalemia in patients with heart failure.

BACKGROUND: A previous randomized controlled trial evaluating the use of spironolactone in heart failure patients reported a low risk of hyperkalemia (2%) and renal insufficiency (0%). Because treatments for heart failure have changed since the benefits of spironolactone were reported, the prevalence of these complications may differ in current clinical practice. We therefore sought to determine the prevalence and clinical associations of hyperkalemia and renal insufficiency in heart failure patients treated with spironolactone. METHODS: We performed a case control study of heart failure patients treated with spironolactone in our clinical practice. Cases were patients who developed hyperkalemia (K(+) >5.0 mEq/L) or renal insufficiency (Cr >or=2.5 mg/dL), and they were compared to 2 randomly selected controls per case. Clinical characteristics, medications, and serum chemistries at baseline and follow-up time periods were compared. RESULTS: Sixty-seven of 926 patients (7.2%) required discontinuation of spironolactone due to hyperkalemia (n = 33) or renal failure (n = 34). Patients who developed hyperkalemia were older and more likely to have diabetes, had higher baseline serum potassium levels and lower baseline potassium supplement doses, and were more likely to be treated with beta-blockers than controls (n = 134). Patients who developed renal insufficiency had lower baseline body weight and higher baseline serum creatinine, required higher doses of loop diuretics, and were more likely to be treated with thiazide diuretics than controls. CONCLUSIONS: Spironolactone-induced hyperkalemia and renal insufficiency are more common in our clinical experience than reported previously. This difference is explained by patient comorbidities and more frequent use of beta-blockers.

Adrenergic beta-Antagonists↗
PubMed2006

Management of severe hyperkalemia without hemodialysis: case report and literature review.

PURPOSE: To report a case of severe hyperkalemia successfully managed without the use of hemodialysis and to provide a review of the literature regarding the management of severe hyperkalemia. METHODS: A clinical case report from the medical-surgical intensive care unit of a teaching hospital and a literature review are presented. The case involves a 59-year old man with diabetes mellitus, essential hypertension, and gout, who presented to hospital with severe hyperkalemia (K(+) = 10.4 mEq/L) and normal renal function. He was treated with intravenous fluids, sodium bicarbonate, calcium chloride, insulin, calcium resonium, and furosemide. RESULTS: The hyperkalemia resolved with conservative treatment within 8 hours, and dialytic therapy was not required. The literature review supported an initial conservative management approach in stable patients with intact renal function. CONCLUSIONS: Hemodialysis is not necessary for all cases of severe hyperkalemia and should be reserved for patients with acute or chronic renal failure or those with life-threatening hyperkalemia unresponsive to more conservative measures.

Bradycardia↗
PubMed2003

Hyperkalemia with concomitant watery diarrhea: an unusual association.

Four patients presented to the emergency room with life-threatening hyperkalemia and concomitant watery diarrhea. Hypovolemia, acidosis, and renal insufficiency were present in all 4 cases. In 2 patients, hyperkalemia followed initiation of angiotensin-converting enzyme (ACE) inhibitor therapy, whereas 1 patient experienced hyperkalemia after a dose increase of an ACE inhibitor, and the fourth patient was on continuous ACE-inhibitor therapy at the time of the hyperkalemia episode. Two of the 3 patients with functioning kidneys required hemodialysis to correct the hyperkalemia, whereas the other patient was on long-term hemodialysis therapy. In the 2 patients in whom transtubular potassium (K+) gradients were available, their values ranged far below normal, indicating tubular failure to secrete K+. This abnormality was attributed to decreased distal delivery of sodium and water and to renin/angiotensin II/aldosterone blockade. It has been proposed that aldosterone blockade impairs the capacity of the colonic epithelial cells to secrete K+. In all 4 patients the watery diarrhea ceased in parallel with the correction of serum K+ to normal values. It is suggested that hyperkalemia, most likely by stimulating intestinal motility, induced the watery diarrhea in all 4 patients. The watery diarrhea, however, failed to compensate for the renal tubular failure to secrete K+.

Aged↗
PubMed1999

Hyperkalemia in patients infected with the human immunodeficiency virus: involvement of a systemic mechanism.

BACKGROUND: The appearance of hyperkalemia has been described in human immunodeficiency virus (HIV)-positive patients treated with drugs with amiloride-like properties. Recent in vitro data suggest that individuals infected with HIV have alterations in transcellular K+ transport. METHODS: With the objective of examining the presence of alterations in transmembrane K+ equilibrium in HIV-positive patients, we designed a prospective, interventional study involving 10 HIV-positive individuals and 10 healthy controls, all with normal renal function. An infusion of L-arginine (6%, intravenously, in four 30-min periods at 50, 100, 200, and 300 ml/hr) was administered, and plasma and urine electrolytes, creatinine, pH and osmolality, total and fractional sodium and potassium excretion, transtubular potassium gradient, plasma insulin, renin, aldosterone, and cortisol were measured. RESULTS: A primary disturbance consisting of a significant rise in plasma [K+] induced by L-arginine was detected in only the HIV patients but not in the controls (P < 0.001 between groups). A K+ redistribution origin of the hyperkalemia was supported by its rapid development (within 60 min) and the lack of significant differences between HIV-positive individuals and controls in the amount of K+ excreted in the urine. The fact that the HIV-positive individuals had an inhibited aldosterone response to the increase in plasma K+ suggested a putative mechanism for the deranged K+ response. CONCLUSIONS: These results reveal that HIV-infected individuals have a significant abnormality in systemic K+ equilibrium. This abnormality, which leads to the development of hyperkalemia after the L-arginine challenge, may be related, in part, to a failure in the aldosterone response to hyperkalemia. These results provide a new basis for understanding the pathogenesis of hyperkalemia in HIV individuals, and demonstrate that the risk of HIV-associated hyperkalemia exists even in the absence of amiloride-mimicking drugs or overt hyporeninemic hypoaldosteronism.

Adult↗