Effect of salt intake on progression of chronic kidney disease.
OBJECTIVE
The attempt of this review is to bring into focus the potential role of dietary salt intake in progression of chronic kidney disease.


RESULTS
Ongoing work has elucidated a role for dietary salt intake in modulating intrarenal production of transforming growth factor-beta1. The mechanism is independent of angiotensin II and systemic blood pressure and involves activation of vascular endothelium by dietary salt intake with release of this growth factor. In this model, transforming growth factor-beta1 serves an autacoid function by stimulating nitric oxide production by the endothelium. In turn, endothelium-derived nitric oxide modulates production of this growth factor. The model further predicts that individuals who have lost the requisite endothelial cell flexibility to adapt to this environmental stress (a high salt diet) are potentially at increased risk of developing end-organ damage from excess salt intake. Animal and human studies are presented to support this working hypothesis.


CONCLUSIONS
Overproduction of transforming growth factor-beta1 permits excess biological activity of this important fibrogenic growth factor with subsequent development or acceleration of vascular and kidney damage. In patients with diseases whose pathogenesis is related to excess production of transforming growth factor-beta1, such as chronic allograft nephropathy and diabetic nephropathy, increased salt intake may hasten loss of function, particularly if nitric oxide production does not increase. The role that endothelial cell plasticity plays in altering vascular tone and renal function, especially in response to changes in dietary salt intake, should be examined further in chronic kidney disease.
Sanders
Paul W
PW
Nephrology Research and Training Center, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, 642 Lyons-Harrison Research Building, 1530 Third Avenue South, Birmingham, AL 35294-0007, USA. psanders@uab.edu
D000818:Animals; D002908:Chronic Disease; D018450:Disease Progression; D004727:Endothelium / Q000378:metabolism*; D006801:Humans; D007674:Kidney Diseases / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012982:Sodium, Dietary / Q000009:adverse effects*; D016212:Transforming Growth Factor beta / Q000378:metabolism*; D053773:Transforming Growth Factor beta1
D012982:Sodium, Dietary; C508960:TGFB1 protein, human; C508962:Tgfb1 protein, rat; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1