Exp Clin Endocrinol Diabetes 2004; 112 - P26
DOI: 10.1055/s-2004-832904

Central diabetes insipidus as a complication of Malaria tropica

CA Koch 1, H Achenbach 1, L Engelmann 2, G Borte 3, M Stumvoll 1, S Schubert 4
  • 1Department of Medicine/Endocrinology and Nephrology, University of Leipzig, Germany
  • 2Department of Critical Care, University of Leipzig, Germany
  • 3Department of Radiology, University of Leipzig, Germany
  • 4Department of Tropical Diseases, University of Leipzig, Germany

Malaria tropica is caused by Plasmodium falciparum and associated with renal failure. Nephrogenic diabetes insipidus with a mean 24h urine output of 3018ml has been described in approximately 21% of patients (Grimwade et al. 2004). Central diabetes insipidus in malaria tropica, however, has not yet been reported. A 39-yo man spent vacation in Kenia without taking chemophrophylaxis for malaria. 5 days after he had returned to Germany, the patient developed chills. Malaria was suspected and he was admitted to the intensive care unit of the University of Leipzig. His plasmodium index was 30%. Treatment was initiated with quinine and doxycycline. He developed acute renal failure, paralytic ileus, and dyspnea requiring intubation and ventilation. His serum creatinine was 404 nmol (normal, <82). A renal ultrasound showed enlarged kidneys. His 24h urine output was 7 l in combination with an increased sodium excretion, low urine osmolality, a serum Na of 124 mmol/l, and serum K of 6,2 mmol/l. His plasma was hyperosmolar. Diabetes insipidus was suspected in combination with adrenal insufficiency. Intravenous hydrocortisone was started. Serum Na increased but the patient remained polyuric. Serum cortisol showed a normal stimulation to CRH. Hydrocortisone was discontinued and fludrocortisone 150 mcg/die given. In addition, intranasal desmopressin 0,5 2 times per day and 6g NaCl tablets were administered. The 24h urine output decreased to 1,5 l per day. Serum Na and creatinine remained normal. An insulin-hypoglycemia test showed a normal serum cortisol response. Therefore, adrenal insufficiency seemed unlikely and fludrocortisone was discontinued. An MRT of the pituitary showed a 3×2mm hypoenhancing area in the posterior pituitary. Hormones of the anterior pituitary and IGF-1 matched for age and gender were normal. We suspect that in this patient malaria tropica caused an infarction of the neurohypophysis. Repeat MRT of the pituitary and a trial of dismissing desmopressin are planned in 5 months. To our knowledge, this is the first case of a patient with malaria tropica complicated by central diabetes insipidus.