Effect of chronic metabolic acidosis on renal growth and renal sodium handling in uninephrectomized rats.
Paucity studies have indicated that a systemic metabolic acidosis cause a decrease in salt and water reabsorption in the kidney. The following study was undertaken on male Wistar-Hannover rats (200-250 g) to investigate the effects of a chronic, NH4Cl-induced metabolic acidosis on the renal handling of Na+ in sham-operated and uninephrectomized rats, by lithium clearance. The present study shows that chronic acidosis (blood pH, 7.16 +/- 0.13) caused a sustained increase in renal fractional Na+ excretion (267.9 +/- 36.4%), accompanied by a rise in the fractional proximal (113.3 +/- 3.6%) and post-proximal (179.7 +/- 20.2%) Na+ and fractional K+ (163.4 +/- 5.6%) excretions when compared to pair-fed rats. These differences occurred in spite of an unchanged creatinine clearance and Na+ filtered load. On the other hand, a body growth impairment was observed in the acidotic (control, 258 +/- 3.7 g versus acidotic, 232 +/- 4.6 g) and pair-fed rats (225 +/- 3.6 g), whereas there was significant enhance in the kidney weights in acidotic rats (1.73 +/- 0.05 g) compared to other experimental groups (control, 1.46 +/- 0.05 g; pair-fed, 1.4 +/- 0.05 g). The renal growth indexes after metabolic acidosis NH4Cl-induced did not shown statistical difference at 1.5, 3.0 and 12 hours after uninephrectomy when were compared with pair-fed groups. However, from the fifth to tenth day after unilateral nephrectomy the renal growth index of acidotic group was significantly greater than pair-fed groups. Unilateral nephrectomy in acidotic animals caused a striking additional but transient increase in fractional renal sodium (FENa+) and potassium (FEK+) excretion from 1.5 to 3 hours post-surgery meanly associated with an enhanced post-proximal sodium excretion when compared to pair-fed uninephrectomized rats. By the fifth postoperative day the all functional values returned to baseline levels. This altered renal Na+ handling and K+ excretion may result from a reciprocal relationship between tubular metabolic pathway stimuli and ion transport. Further studies are required to investigate the acidosis involvement on functional kidney response.
Menegon
L F
LF
Departmento de Clínica Médica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, SP, Brasil.
Figueiredo
J F
JF
Gontijo
J A
JA
D000141:Acidosis, Renal Tubular / Q000378:metabolism / Q000503:physiopathology*; D000818:Animals; D002415:Cats; D007668:Kidney / Q000254:growth & development* / Q000378:metabolism; D007684:Kidney Tubules / Q000378:metabolism*; D008297:Male; D009392:Nephrectomy; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism*
D012964:Sodium; D011188:Potassium