- Haploinsufficiency of the Mouse Atp6v1b1 Gene Leads to a Mild Acid-Base Disturbance with Implications for Kidney Stone Disease. [Journal Article]
- CPCell Physiol Biochem 2018; 47(3):1095-1107
- CONCLUSIONS: In conclusion, 1) Atp6v1b1+/- mice developed a mild incomplete dRTA. dRTA is partly compensated by respiration. 2) Compensatory mechanisms for the absence of B1 take place only in the collecting duct of Atp6v1b1-/- kidneys.
- [Primary distal renal tubular acidosis in children in the South of Tunisia: study of 15 cases]. [Journal Article]
- TMTunis Med 2013; 91(4):258-62
- CONCLUSIONS: The distal renal tubular acidosis is a rare pathology in our country but probably under diagnosed. The clinical gravity of this disease and the risk of evolution towards the terminal renal insufficiency justify an antenatal diagnosis to establish a neonatal management or propose a therapeutic interruption of the pregnancy if the distal RTA is associated with a severe pathology.
- Voluntary feed intake, acid-base balance and partitioning of urinary nitrogen in lambs fed corn silage with added sodium bicarbonate or sodium sesquicarbonate. [Journal Article]
- JAJ Anim Sci 1989; 67(8):2116-22
- An experiment with growing lambs was designed to test the hypothesis that alterations in blood acid-base status would influence intake of corn silage. Six wethers (29 kg) were fed a diet of corn sila…
An experiment with growing lambs was designed to test the hypothesis that alterations in blood acid-base status would influence intake of corn silage. Six wethers (29 kg) were fed a diet of corn silage (36% DM, 8% CP) supplemented with 1.25% urea and .2% sulfur. At feeding time, sodium bicarbonate (NaHCO3) and sodium sesquicarbonate (NaSC) were added to the silage at levels of 0, 2% or 4% of diet DM. The treatments were arranged as a 2 x 3 factorial, and the study was conducted as a 6 x 4 incomplete latin square with four 17-d periods. Voluntary intake of OM was not different (P greater than .05) between NaHCO3 (1,008 g/d) and NaSC (1,041 g/d). There was no significant interaction between type of buffer (NaHCO3 or NaSC) and level of buffer on any of the variables measured. The progressive increase in buffer load did not alter feed intake (P greater than .05), although there was a quadratic response (P less than .05) in urine pH and a linear increase (P less than .01) in blood HCO3- 2 h after feeding. There was no evidence that lambs fed corn silage experienced metabolic acid stress. Urinary excretion of ammonia and urea were indicative of changes, although not pronounced, in ammoniuria and ureapoiesis in response to bicarbonate loading. This study implies that corn silage imposes no "acid stress" on lambs and, consequently, that there is no nutritional benefit in adding buffers to corn silage for sheep.
- Renal recovery from metabolic acidosis in the rat: no role for glutamine synthetase. [Journal Article]
- RPRen Physiol 1984; 7(1):32-45
- The role of renal glutamine synthesis for the rapid decrease in renal ammoniagenesis occurring early in the recovery phase (24 h) of metabolic acidosis was studied in rats. L-Methionine-DL-sulfoximin…
The role of renal glutamine synthesis for the rapid decrease in renal ammoniagenesis occurring early in the recovery phase (24 h) of metabolic acidosis was studied in rats. L-Methionine-DL-sulfoximine (MSO), an irreversible inhibitor of glutamine synthetase, depressed the renal enzyme activity by 50% but did not impair the recovery from acidosis. Since extrarenal glutamine synthesis was decreased by this manoeuvre with lowering of blood glutamine, an intravenous load of L-glutamine sufficient to elevate blood concentration to 1 mM was superimposed on the MSO treatment. The glutamine load did not increase the ammoniuria. Infusion of glutamine alone to rats recovering from metabolic acidosis for 12-24 h did not change their ammoniuria. In contrast, glutamine administration together with HCl produced a marked ammoniuric response in rats recovering from acidosis. Conversely, the administration of bicarbonate to chronically acidotic rats acutely depressed renal ammonia production. It is concluded that glutamine synthetase activity is probably not required for recovery from metabolic acidosis, and that the post-acidosis alkaline rebound occurring in the rat may play a direct role in suppressing the ammoniagenic pathway either by drastic reduction in mitochondrial permeability for glutamine or acute inhibition of intramitochondrial deamidation of this amino acid.
- [Ammoniuria and its relation to hydroionic factors and to the precoma situation in liver cirrhosis: the kidney as an excretory organ of ammonia]. [Journal Article]
- RCRev Clin Esp 1975 Dec 31; 139(6):497-504
- [Ammoniuria in chronic hypercapnia. Study of the effects of perfusion of sodium phosphates]. [Journal Article]
- JUJ Urol Nephrol (Paris) 1968 Apr-May; 74(4):391-402
- [Alkaline reserve, ammoniuria in carnivorous animals, glycuronic acid conjugations]. [Journal Article]
- SMStrasb Med 1953; 4(4):235-40