Abstract
Hyperkalaemia is a common, treatable, medical emergency, often with an iatrogenic cause. This case illustrates the vulnerability of patients with pre-existing renal tubular acidosis type 4 to medications that further inhibit renin-aldosterone action. The case also illustrates the danger of keeping entirely separate case notes between different hospital disciplines.
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References
- Siamopoulos KC, Elisaf M, Katopodis K. Iatrogenic Hyperkalaemia – points to consider in diagnosis and management. Nephrology Dialysis Transplantation 1997; 13: 2402-2406
- Warren SE, O’Connor DT. Hyperkalemia resulting from captopril administration. JAMA 1980: 22; 2551-2
- Textror SC, Bravo EL, Fouad FM, et al. Hyperkalaemia in azotemic patients during ACE inhibition and aldosterone reduction with captopril. Am J Med. 1982; 73: 719-725
- Choi MJ, Fernandez PC, Patniak A et al. Trimethoprim-induced hyperkalaemia in a patient with AIDS. N Engl J Med 1993; 328: 703-706.
- Velázquez H, Perazella MA, Wright FS, et al. Renal mechanism of trimethoprim induced hyperkalaemia. Ann Intern Med 1993; 119: 296-301
- Schreiber M, Schlanger LE, Chen CB et al. Antikaliuretic action of trimethoprim is minimized by raising urinary pH. Kidney Int 1996; 50: 2063-2069
- Perazella MA, Mahnensmith RL. Trimethoprim-sulfamethoxazole: hyperkalemia is an important complication regardless of dose. Clin Nephrol 1996; 46: 187-82
- Secondary prevention in primary and secondary care for patients following a myocardial infarction. NICE CG48. May 2007.
