scholarly journals Urinary acid profiles in asymptomatic and symptomatic siblings with propionyl CoA carboxylase deficiency.

1989 ◽  
Vol 7 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Tomiko KUHARA ◽  
Masahiro MATSUMOTO ◽  
Yoshito INOUE ◽  
Takashi OHKURA ◽  
Tsuneo AOYAMA ◽  
...  
Keyword(s):  
Urinary Acid ◽  
Propionyl Coa Carboxylase Deficiency

Urinary acid profiles of asymptomatic propionyl CoA carboxylase deficiency

1988 ◽  
Vol 113 (4) ◽  
pp. 787 ◽  
Author(s):  
Tomiko Kuhara ◽  
Yoshito Inoue ◽  
Isamu Matsumoto
Keyword(s):  
Urinary Acid ◽  
Propionyl Coa Carboxylase Deficiency

scholarly journals 48 Urinary Acid Excretion in the Intact Lamb Fetus

1967 ◽  
Vol 1 (3) ◽  
pp. 212-212
Author(s):  
Fred G Smith ◽  
Richard Bashore
Keyword(s):  
Acid Excretion ◽  
Urinary Acid

The response of the kidney of the freshwater rainbow trout to true metabolic acidosis

1980 ◽  
Vol 84 (1) ◽  
pp. 227-244 ◽  
Author(s):  
K. A. Kobayashi ◽  
C. M. Wood
Keyword(s):  
Lactic Acid ◽  
Metabolic Acidosis ◽  
Blood Lactate ◽  
Renal Excretion ◽  
Total Acid ◽  
Time Courses ◽  
Lactate Levels ◽  
Urinary Acid ◽  
Proton Load ◽  
Lactate Excretion

Infusion of lactic acid into the bloodstream of trout produced a short-lived depression of blood pH and a long-lasting elevation of blood lactate. The lactate injected was distributed in a volume of 198 ml/kg. Renal excretion of lactate anion and total acid increased by approximately equal amounts during the period of high blood lactate levels, but total renal loss over 72 h accounted for only 2% of the lactate load and 6% of the proton load. Comparable differences in the time courses of blood lactate and pH changes occurred when lactacidosis was induced endogenously by normocapnic hypoxia. The immediate response of the kidney was similar to that with lactic acid infusion, but there was a long-lasting (12–72 + h) elevation of urinary acid efflux that was not associated with lactate excretion. Following hypoxia, renal excretion over 72 h accounted for 1% of the estimated lactate load and 12–25% of the proton load. A renal lactate threshold of 4–10 muequiv/ml prevents significant urinary lactate excretion. The response of the trout kidney to true metabolic acidosis is similar to that of the mammalian kidney.

A mathematical model of rat collecting duct II. Effect of buffer delivery on urinary acidification

2002 ◽  
Vol 283 (6) ◽  
pp. F1252-F1266 ◽  
Author(s):  
Alan M. Weinstein
Keyword(s):  
Mathematical Model ◽  
Carbonic Anhydrase ◽  
Collecting Duct ◽  
Phosphate Concentration ◽  
Rate Coefficients ◽  
Urinary Flow ◽  
Urinary Acidification ◽  
Model Predictions ◽  
Disequilibrium Ph ◽  
Urinary Acid

A mathematical model of the rat collecting duct (CD) is used to examine the effect of delivered load of bicarbonate and nonbicarbonate buffer on urinary acidification. Increasing the delivered load of HCO[Formula: see text] produces bicarbonaturia, and, with luminal carbonic anhydrase absent, induces a disequilibrium luminal pH and a postequilibration increase in urinary Pco 2. At baseline flows, this disequilibrium disappears when luminal carbonic anhydrase rate coefficients reach 1% of full catalysis. The magnitude of the equilibration Pco 2 depends on the product of urinary acid phosphate concentration and the disequilibrium pH. Thus, although increasing phosphate delivery to the CD decreases the disequilibrium pH, the increase in urinary phosphate concentration yields an overall increase in postequilibration Pco 2. In simulations of experimental HCO[Formula: see text] loading in the rat, model predictions of urinary Pco 2 exceed the measured Pco 2 of bladder urine. In part, the higher model predictions for urinary Pco 2 may reflect higher urinary flow rates and lower urinary phosphate concentrations in the experimental preparations. However, when simulation of CD function during HCO[Formula: see text] loading acknowledges the high ambient renal medullary Pco 2 (5), the predicted urinary Pco 2 of the model CD is yet that much greater. This discrepancy cannot be resolved within the model but requires additional experimental data, namely, concomitant determination of urinary buffer concentrations within the tubule fluid sampled for Pco 2 and pH. This model should provide a means for simulating formal testing of urinary acidification and thus for examining hypotheses regarding transport defects underlying distal renal tubular acidosis.

A4982 Effects of obesity on urinary acid excretion and kidney injury in chronic kidney disease

2018 ◽  
Vol 36 ◽  
pp. e40
Author(s):  
Yuichiro Izumi ◽  
Koji Eguchi ◽  
Yushi Nakayama ◽  
Naomi Matsuo ◽  
Akiko Hara ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Kidney Injury ◽  
Acid Excretion ◽  
Urinary Acid

scholarly journals Propionyl-CoA carboxylase deficiency (propionicacidemia): A cause of non-ketotic hyperglycinemia

1971 ◽  
Vol 5 (8) ◽  
pp. 395-395 ◽  
Author(s):  
Maurice J Mahonev ◽  
Y Edward Hsia ◽  
Leon E Rosenberg
Keyword(s):  
Propionyl Coa Carboxylase Deficiency
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