Fludrocortisone for the Treatment of Heparin-Induced Hyperkalemia

2000 ◽  
Vol 34 (5) ◽  
pp. 606-610 ◽  
Author(s):  
Deb S Sherman ◽  
Carrie L Kass ◽  
Douglas N Fish

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.

2006 ◽  
Vol 116 (3) ◽  
pp. 165-172 ◽  
Author(s):  
Dirk Henrich ◽  
Martin Hoffmann ◽  
Michael Uppenkamp ◽  
Raoul Bergner

2020 ◽  
Vol 2020 ◽  
pp. 1-6
Author(s):  
Gisela Marcelino ◽  
Ould Maouloud Hemett ◽  
Eric Descombes

Direct oral anticoagulants (DOACs) are among the most commonly prescribed medications, and DOAC-associated kidney dysfunction may be a problem that is underrecognized by clinicians. We report on the case of an 82-year-old patient who, two weeks after the prescription of rivaroxaban for atrial fibrillation, was hospitalized for a drug-induced hypersensitivity syndrome whose main clinical manifestations were low-grade fever with a petechial rash in the legs and acute renal failure (ARF). Within one week after rivaroxaban withdrawal, the patient’s clinical condition improved and the renal function normalized. In a review of the literature, we only found five case reports of rivaroxaban-related ARF: two patients had tubulo-interstitial nephritis (TIN), two had anticoagulant-related nephropathy (ARN), and the last one had IgA nephropathy. As some recent publications suggest that kidney injury due to anticoagulation drugs may be largely underdiagnosed, we also analyzed the data from the VigiAccess database, the World Health Organization pharmacovigilance program that collects drug-related adverse events from 134 national registries worldwide. Among all the rivaroxaban-associated adverse events reported in VigiAccess since 2006, 4,323 (3.5%) were renal side effects, of which 2,351 (54.3%) were due to unspecified ARF, 363 (8.4%) were due to renal hemorrhage (characteristically associated with ARN), and 24 (0.6%) were due to TIN. We also compared these results with those reported in VigiAccess for other DOACs and vitamin K antagonists. This analysis suggests that the frequency of renal adverse events associated with rivaroxaban and other DOACs may be appreciably higher than what one might currently consider based only on the small number of fully published cases.


2019 ◽  
Vol 2019 ◽  
pp. 1-5
Author(s):  
D. Kelsey ◽  
A. J. Berry ◽  
R. A. Swain ◽  
S. Lorenz

Energy drinks are nonalcoholic beverages that are widely consumed in the general population, and worldwide usage is increasing. The main stimulant component of energy drinks is typically caffeine. Few case reports exist that link energy drink consumption to psychosis, and similarly few reports exist that associate energy drink consumption with acute renal failure. We present a patient who simultaneously developed psychosis and acute renal failure associated with excessive energy drink consumption. The patient required haemodialysis, and his psychosis resolved on cessation of energy drinks and a brief course of antipsychotic medication. We perform a review of similar cases where excessive caffeinated energy drink consumption has been linked to psychosis or acute renal failure. To our knowledge, this is the first case report describing both renal failure and psychosis occurring simultaneously in a patient. Recognising the spectrum of disorders associated with excessive energy drink consumption is vital for both physicians and psychiatrists, as this has important implications for both prognosis and treatment.


2003 ◽  
Vol 37 (7-8) ◽  
pp. 1014-1017 ◽  
Author(s):  
A Scott Mathis ◽  
Vicky Chan ◽  
Margaret Gryszkiewicz ◽  
Robert T Adamson ◽  
Gary S Friedman

OBJECTIVE: To describe a case of levofloxacin-induced partial Achilles tendon rupture; this occurred in the presence of known risk factors and acute renal failure. CASE SUMMARY: A 79-year-old white man received levofloxacin for presumed pneumonia, developed acute renal failure in the setting of dehydration, and began having ankle pain on the 12th day of admission. Levofloxacin was discontinued, and magnetic resonance imaging revealed a 6-cm partial tear and degenerative changes. DISCUSSION: The Naranjo probability scale indicates a possible association between levofloxacin and tendon rupture because the event occurred in the setting of known risk factors such as steroid use, renal failure, older age, and male gender. CONCLUSIONS: Levofloxacin, like other fluoroquinolones, may cause Achilles tendon rupture, and this may be particularly likely with known risk factors.


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