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REVIEW ARTICLE
Year : 2012  |  Volume : 53  |  Issue : 3  |  Page : 109-115

The renal concentrating mechanism and the clinical consequences of its loss


1 Department of Medicine, Division of Nephrology, Jos University Teaching Hospital, Jos, Plateau State, Nigeria
2 Department of Medicine, University of New Mexico School of Medicine, Albuquerque, USA
3 Raymond G. Murphy Veterans Affairs Health Care System, Albuquerque, New Mexico, USA

Correspondence Address:
Emmanuel I Agaba
Nephrology Division, Jos University Teaching Hospital, PMB 2076, Jos
Nigeria
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0300-1652.104376

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The integrity of the renal concentrating mechanism is maintained by the anatomical and functional arrangements of the renal transport mechanisms for solute (sodium, potassium, urea, etc) and water and by the function of the regulatory hormone for renal concentration, vasopressin. The discovery of aquaporins (water channels) in the cell membranes of the renal tubular epithelial cells has elucidated the mechanisms of renal actions of vasopressin. Loss of the concentrating mechanism results in uncontrolled polyuria with low urine osmolality and, if the patient is unable to consume (appropriately) large volumes of water, hypernatremia with dire neurological consequences. Loss of concentrating mechanism can be the consequence of defective secretion of vasopressin from the posterior pituitary gland (congenital or acquired central diabetes insipidus) or poor response of the target organ to vasopressin (congenital or nephrogenic diabetes insipidus). The differentiation between the three major states producing polyuria with low urine osmolality (central diabetes insipidus, nephrogenic diabetes insipidus and primary polydipsia) is done by a standardized water deprivation test. Proper diagnosis is essential for the management, which differs between these three conditions.


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