title: Renal inflammation is modulated by potassium in chronic kidney disease: possible role of Smad7.
abstract: High-potassium diets have been shown to be beneficial in cardiovascular disease partly because of a blood pressure-lowering effect. The effect of potassium on inflammation has not been studied. We investigated the influence of potassium supplementation on the degree of renal inflammation and the intracellular signaling mechanisms that could mediate inflammation in chronic kidney disease (CKD). CKD was created in male Sprague-Dawley rats by subtotal nephrectomy. Two groups of CKD rats were pair fed with diets containing 2.1% potassium (potassium-supplemented diet) or 0.4% potassium (basal diet). Body weight, blood pressure, and blood and urine electrolytes were measured biweekly. The animals were euthanized at week 8, and the remnant kidneys were analyzed by histology, immunohistochemistry, Western blotting, and real-time quantitative PCR. In the CKD pair-fed groups, blood potassium concentration did not differ significantly, but blood pressure was lower in the potassium-supplemented group. Compared with the basal diet, potassium supplementation decreased renal tubulointerstitial injury and suppressed renal inflammation as evidenced by decreased macrophage infiltration, lower expression of inflammatory cytokines, and decreased NF-kappaB activation. These renoprotective effects were associated with downregulation of renal transforming growth facto-beta, upregulation of renal Smad7, and lower blood pressure. Our results show that potassium supplementation can reduce renal inflammation and hence, could modulate the progression of kidney injury in CKD.
authors.affiliation: Dept. of Medicine-Renal Section, Baylor College of Medicine, Houston, TX 77030, USA. wanshengwang@yahoo.com
authors.forename: Wansheng
authors.initials: W
authors.lastname: Wang
authors.forename: Liliana
authors.initials: L
authors.lastname: Soltero
authors.forename: Ping
authors.initials: P
authors.lastname: Zhang
authors.forename: Xiao R
authors.initials: XR
authors.lastname: Huang
authors.forename: Hui Y
authors.initials: HY
authors.lastname: Lan
authors.forename: Horacio J
authors.initials: HJ
authors.lastname: Adrogue
mesh_terms: D000450:Aldosterone / Q000652:urine; D000804:Angiotensin II / Q000652:urine; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002908:Chronic Disease; D003404:Creatinine / Q000097:blood; D004195:Disease Models, Animal; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000378:metabolism*; D008297:Male; D016328:NF-kappa B / Q000378:metabolism; D009393:Nephritis / Q000378:metabolism*; D011188:Potassium / Q000378:metabolism*; D017419:Potassium, Dietary / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D051906:Smad7 Protein / Q000378:metabolism*; D012964:Sodium / Q000652:urine; D016212:Transforming Growth Factor beta / Q000378:metabolism
chemical_list: D016328:NF-kappa B; D017419:Potassium, Dietary; D051906:Smad7 Protein; C497808:Smad7 protein, rat; D016212:Transforming Growth Factor beta; D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D003404:Creatinine; D011188:Potassium