QJM Advance Access published online on December 15, 2007
QJM, doi:10.1093/qjmed/hcm110
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No elevation of blood urea level in a dehydrated patient with central diabetes insipidus
The Department of Internal Medicine
Shiga University of
Medical Science
Seta Otsu, Shiga
520-2192
Japan
email: toshiro{at}belle.shiga-med.ac.jp
Sir,
Dehydrated patients usually present with elevated blood urea nitrogen (BUN) concentrations, reflecting a low urine flow rate and increased renal reabsorption of urea. This increased renal reabsorption of urea is thought to owe at least in part to the action of antidiuretic hormone (ADH).1
A 44-year-old Japanese man with mental retardation was admitted because of the recent onset of polyposia and polyuria. As he had taken any kinds of fluids (e.g. swimming pool water) and he had not slept well due to polyuria, he was restricted fluid intake. Therefore, he showed mild hypernatrenic dehydration on admission. His blood test results were as follows: Na, 151 mEq/l; K, 3.3 mEq/l; Cl, 117 mEq/l; BUN, 12 mg/dl; creatinine, 0.82 mg/dl; uric acids, 7.0 mg/dl and blood glucose, 97 mg/dl. Although plasma osmolality was elevated to 308 mOsm/kg, his urine was markedly diluted (urinary osmolality, 183 mOsm/kg). The renal reabsorption of urea was not enhanced in spite of dehydration (fractional excretion of urea: FEUN, 40.1%; reference range, less than 35% under dehydration).2 Administering desmopressin (5 µg intranasally) markedly increased urinary osmolarity to 762 mOsm/kg. Brain magnetic resonance imaging showed the absence of the hyperintense signal of the posterior pituitary on T1-weighted images without any remarkable lesions. Therefore, he was diagnosed as having idiopathic central diabetes insipidus (CDI) and was discharged with desmopressin. In the follow-up clinic, he could not take enough fluids during fever; thus, hypernatrenic dehydration occurred again (Na, 155 mEq/l), associated with a low BUN level (7 mg/dl) due to enhanced urinary excretion (FEUN, 82.7%).
In the present case, in spite of dehydration, the level of BUN was not elevated and renal reabsorption of urea was not increased. The urea permeability in the inner medullary collecting duct rises in the presence of antidiuretic hormone,3 suggesting that urea reabsorption in the distal nephron might be decreased in CDI even when the patients are dehydrated. An observation similar to ours, low BUN levels with hypertonic dehydration, has already been reported in CDI patients;4 however, it is not mentioned in any recent textbooks of internal medicine. Our observation suggests that BUN levels can be used to distinguish dehydrated CDI patients when hypernatrenic dehydrated patients are seen.
References
1. Kokko JP. The role of the collection duct in urinary concentration. Kidney Int (1987) 31:606–10.[Web of Science][Medline]
2. Carvounis CP, Nisar S, Guro-Razuman S. Significant of the fractional excretion of urea in the differential diagnosis of acute renal failure. Kidney Int (2002) 62:2223–9.[CrossRef][Web of Science][Medline]
3. Bankir LT, Trinh-Trang Tan MM. Renal urea transporters. Direct and indirect regulation by vasopressin. Exp Physiol (2000) 85:243S–52S.[Abstract]
4. Comtois R, Bertrand S, Beauregard H, Vinay P. 2 Low serum urea level in dehydrated patients with central diabetes insipidus. CAMJ (1988) 139:965–69.
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