|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Inserm Unite 652 and Universite Paris Descartes, Paris, France
2 Inserm Unite 557, INRA Unite 1125; CNAM; Paris 13 CRNH Ile de France, Paris, France
* To whom correspondence should be addressed. E-mail: bankir{at}fer-a-moulin.inserm.fr.
Men are known to be at greater risk of urolithiasis and cardiovascular and renal diseases than women. Previous studies suggest that greater urine concentration is associated with acceleration of progression of chronic kidney disease (CKD), increased urinary albumin excretion and delayed renal sodium excretion. The present review addresses possible sex-related differences in urine volume and osmolality (Uosm) which could participate in this male risk predominance. Because of the scarcity of information, we reanalyzed 24h urine data collected previously by different investigators for other purposes. In nine studies concerning healthy subjects (six studies) or patients with CKD or diabetes mellitus, Uosm (or another index of urine concentration based on the urine/plasma creatinine concentration ratio) was 21 - 39 % higher (i.e., about a 150 mosm/kg H2O difference) in men than in women. Urine volume was not statistically different. Thus, the larger osmolar load of men (related to their higher food intake) is excreted in a more concentrated urine with no difference in urine volume. This sex difference was not influenced by the level of sodium excretion and was still present in CKD patients. Sex differences in thirst threshold, AVP level, and other regulatory mediators may all contribute to the higher male Uosm. Because of the previously demonstrated adverse effects of vasopressin and/or high urine concentrating activity, the greater tendency of men to concentrate urine could participate in their greater susceptibility to urolithiasis and hypertension and to the faster progression towards end-stage renal failure.
This article has been cited by other articles:
![]() |
X. Wang, Y. Wu, C. J. Ward, P. C. Harris, and V. E. Torres Vasopressin Directly Regulates Cyst Growth in Polycystic Kidney Disease J. Am. Soc. Nephrol., January 1, 2008; 19(1): 102 - 108. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Denton and C. Baylis Physiological and molecular mechanisms governing sexual dimorphism of kidney, cardiac, and vascular function Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2007; 292(2): R697 - R699. [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |