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.
Departmento de Clínica Médica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, SP, Brasil.
L F
LF
Menegon
J F
JF
Figueiredo
J A
JA
Gontijo
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