Patient Care Endocrinology & Cardiology - December 2007 - (Page 26)

I Case & Comment Central diabetes (polyuria) regardless of the body’s vasopressin secretion and induce polyinsipidus is hydration state, leading to symptoms of uria. Patients usually remain normonaextraordinary thirst, copious water tremic despite large fluid intake, altreated with intake (up to 20 L/d), dry skin, and conthough plasma sodium and osmolality stipation.1 may be low normal or slightly reduced. desmopressin. DI can be caused by 2 different mechA clinical and laboratory diagnosis is anisms. There is either an inadequate or impaired confirmed by standard tests. The 24-hour urine secretion of vasopressin from the posterior pituitary volume must be documented and polyuria congland (neurogenic or central DI) or an impaired or firmed. Initial baseline studies include plasma elecinsufficient renal response to vasopressin (nephrotrolytes, BUN and creatinine, random plasma 1 genic DI). Vasopressin, produced in the hypothalaosmolality, and urine osmolality. If the urine osmomus, is stored in the posterior pituitary gland. Both lality is less than 200 mOsm/kg in the presence of vasopressin and its carrier protein, neurophysin, are polyuria, DI is present. synthesized in the paraventricular and supraoptic Both the desmopressin administration test and nuclei. the water deprivation test assist in making a differAbout 30% to 50% of cases are considered idioential diagnosis among the types of DI. In normal pathic. Other causes may be due to the destruction subjects and patients with psychogenic DI, the urine or degeneration of the neurons that originate in the osmolality is greater than the plasma osmolality folsupraoptic and paraventricular nuclei of the hypolowing fluid restriction, and the urine osmolality inthalamus. This may due to CNS injury from a neocreases only minimally ( 10%) after desmopressin plasm (germinoma or craniopharyngioma); Langerinjection. hans’ cell histiocytosis; sarcoidosis of the CNS; a local In comparison, patients with neurogenic DI deinflammatory, autoimmune, or vascular disease (ismonstrate urine osmolality less than plasma osmolchemia or intracranial bleeding); infection (meningiality after dehydration and increases in plasma ostis, encephalitis); trauma (cerebral edema) following molality by greater than 50% after desmopressin surgery, radiation, or an accident; psychogenic or, injection. Patients with nephrogenic DI respond with rarely, genetic defects in vasopressin biosynthesis. urine osmolality less than plasma osmolality and, These defects provide a molecular basis for central after desmopressin injection, their urine osmolality and nephrogenic DI.2 increases by less than 50%.1 In addition, measureThe maintenance of water balance is achieved by ment of urinary aquaporin-2 excretion has been used 3 interrelated determinants: thirst, vasopressin levels, in the differential diagnosis of central versus nephroand kidney function. Small changes in plasma osmogenic DI. If there is no increased aquaporin-2 excrelality regulate vasopressin release from the pituitary. tion following desmopressin administration, a diagWhen water is lost and plasma osmolality increases nosis of nephrogenic DI is likely.4 by as little as 1%, an increased secretion of vasoContributed by GEORGE D. HARRIS, MD, MS, Professor of pressin stimulates water retention by the kidneys. Medicine, Department of Community and Family Medicine, University of Missouri-Kansas City, Kansas City, Mo; Osmolality is tightly regulated around each indiand BERNADETH T. GONZALES, MD, Family Medicine— vidual’s normal value, which falls between 280 and OB Provider, Yakima Valley Farm Workers Clinic, Miramar Health Center, Pasco, Wa. 295 mOsm/kg in the general population.3 Vasopressin acts on its major target organ, the kidney, 1. Makaryus AN, McFarlane SI. Diabetes insipidus: diagnosis and treatment of a complex disease. Cleve Clin J Med. 2006;73:65-71. where it increases urine osmolality. Urine volume 2. Maghnie M. Diabetes insipidus. Horm Res. 2003;59(suppl 1):42-54. does not change markedly over wide variations of 3. Robertson GL. Posterior pituitary. In Felig P, Baxter JD, Frohman LA (eds): Endocrinology and Metabolism. 3rd ed. New York, NY: urine osmolality until the latter approaches maxiMcGraw- Hill; 1995:385-432. 4. Kanno K, Sasaki S, Hirata Y, et al. Urinary excretion of aquaporin-2 mum dilution and plasma vasopressin is completely in patients with diabetes insipidus. N Engl J Med. 1995;332:1540suppressed. Excessive fluid intake will suppress 1545. 26 PATIENT CARE ENDOCRINOLOGY & CARDIOLOGY www.patientcareonline.com http://www.patientcareonline.com

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Patient Care Endocrinology & Cardiology - December 2007 Research Digest Contents Medicine in the News Options for Managing Diabetes: Three Types of Basal Insulin Therapy Using the New AHA Guidelines for Preventing Coronary Heart Disease in Women Cardiovascular and Metabolic Implications of Polycystic Ovary Syndrome Case & Comment Classified Advertising Clinical Clips

Patient Care Endocrinology & Cardiology - December 2007

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