Alkali therapy attenuates the progression of kidney injury via Na/H exchanger inhibition in 5/6 nephrectomized rats.
Metabolic acidosis is a cause of renal disease progression, and alkali therapy ameliorates its progression. However, there are few reports on the role of renal acid-base transporters during alkali therapy. We evaluated the effect of sodium bicarbonate therapy and the role of acid-base transporters on renal disease progression in rats with a remnant kidney. Sprague-Dawley rats consumed dietary sodium bicarbonate (NaHCO3) or sodium chloride (NaCl) with 20% casein after a 5/6 nephrectomy. After being provided with a casein diet, the NaHCO3-treated group had higher levels of serum bicarbonate than the control group. At week 4, the glomerular filtration rate in the NaHCO3 group was higher than that in the NaCl group, and the difference became prominent at week 10. The glomerulosclerosis and tubulointerstitial damage indices in the NaHCO3 group were less severe compared with controls at week 4 and 10. The expression of the Na/H exchanger (NHE) was decreased, and apical reactivity was decreased in the NaHCO3 group, compared with the NaCl group. Endothelin-1 levels in the kidney were also decreased in the NaHCO3 group. Dietary sodium bicarbonate has the effects of ameliorating renal disease progression, which may be related to the altered expression of NHE in the remaining kidney.
Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea. ; Department of Internal Medicine, Seoul National University Bundang Hospital, Seongnam, Korea.
Sejoong
0000-0002-7238-9962
S
Kim
Department of Internal Medicine, Hallym University Hangang Sacred Heart Hospital, Seoul, Korea.
Jeonghwan
0000-0003-3199-635X
J
Lee
Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea. ; Department of Internal Medicine, Healthcare System Gangnam Center, Seoul National University Hospital, Seoul, Korea.
Nam Ju
0000-0003-3721-4830
NJ
Heo
Epithelial Systems Biology Laboratory, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Jae Wook
0000-0003-0120-8164
JW
Lee
Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea.
Jin Suk
0000-0001-6892-5518
JS
Han
D000138:Acidosis / Q000188:drug therapy*; D000468:Alkalies / Q000627:therapeutic use*; D000818:Animals; D002364:Caseins / Q000008:administration & dosage; D018450:Disease Progression; D005919:Glomerular Filtration Rate / Q000187:drug effects; D005923:Glomerulosclerosis, Focal Segmental / Q000188:drug therapy; D007668:Kidney / Q000293:injuries; D008297:Male; D009392:Nephrectomy; D009395:Nephritis, Interstitial / Q000188:drug therapy; D051381:Rats; D017207:Rats, Sprague-Dawley; D051437:Renal Insufficiency / Q000188:drug therapy*; D017693:Sodium Bicarbonate / Q000627:therapeutic use*; D012965:Sodium Chloride / Q000008:administration & dosage; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors*
D000468:Alkalies; D002364:Caseins; D017923:Sodium-Hydrogen Exchangers; D012965:Sodium Chloride; D017693:Sodium Bicarbonate
Acidosis; Kidney Failure, Chronic; Sodium Bicarbonate