The renal concentrating mechanism and the clinical consequences of its loss

  • Emmanuel I Agaba
  • Mark Rohrscheib
  • Antonios H Tzamaloukas

Abstract

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.

Keywords: Central diabetes insipidus, hypernatremia, hypertonicity, nephrogenic diabetes insipidus, urine concentration, vasopressin

Nigerian Medical Journal | Vol. 53 | Issue 3 | July-September | 2012

Author Biographies

Emmanuel I Agaba
Departments of Medicine, Division of Nephrology, Jos University Teaching Hospital, Jos, Plateau State, Nigeria
Mark Rohrscheib
University of New Mexico School of Medicine, Albuquerque
Antonios H Tzamaloukas
Raymond G. Murphy Veterans Affairs Health Care System, Albuquerque, New Mexico, USA
Published
2014-06-29
Section
Articles

Journal Identifiers


eISSN: 2229-774X
print ISSN: 0300-1652