Effects of Acute Acid–Base Alterations on Glutamine Metabolism and Renal Ammoniagenesis in the Dog

Fine, Adrian; Bennett, Franklyn I.; Alleyne, George A.O.

doi:10.1042/cs0540503

Cited by 8 publications

(9 citation statements)

References 12 publications

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“…This contrasts with the findings of Fine [11] who, in a short-term study, observed a decrease in serum and urinary urea excretion. The data of this group, however, are also in variance with the recent data of May et al [34], which clearly demonstrate that acidosis results in an increase in serum urea.…”

Section: Discussioncontrasting

confidence: 55%

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A Low-Protein Diet Protects Uremic Rats against the Negative Sequelae of Metabolic Acidosis

Gretz

Lasserre

Langer³

et al. 1990

Nephron

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Metabolic acidosis is a common finding in uremia. The metabolic consequences, however, are poorly understood. Thus, the aim of our study was to assess the effect of chronic metabolic acidosis in ⅚-nephrectomized male Sprague-Dawley rats given a normal (18%; n = 19) and a low-protein diet (8%; n = 23). Each of these groups was sequentially given CaCO₃ and CaCl₂ in the drinking water for a fortnight each. The animals were randomly assigned to start either with CaCO₃ or CaCl₂ (random cross-over design). The blood pH decreased significantly in both CaCl₂groups (18% protein: CaCO₃ 7.18 vs. CaCl₂ 7.11; 8% protein: CaCO₃ 7.26 vs. CaCl₂ 7.09) as did standardized base excess (18% protein: CaCO₃ -5.9 vs. CaCl₂ -9.7; 8% protein: CaCO₃ -3.6 vs. CaCl₂ -12.6). Food intake declined during acidosis in both groups, but more in the 18% protein group. The same occurred with body weight (g) in the 18% group, which decreased dramatically (8% protein: CaCO₃ 389 vs. CaCl₂ 390; 18% protein: CaCO₃ 413 vs. CaCl₂ 366). The change in body weight was reflected in the urinary urea excretion (mg/24 h/g food) (8% protein: CaCO₃ 0.9 vs. CaCl₂1.0; 18% protein: CaCO₃ 2.2 vs. CaCl₂ 30.8). There was a significant increase in proteinuria (mg/24 h) in the 8% group (CaCO₃ 10 vs. CaCl₂ 15), while in the 18% group no real change occurred (CaCO₃ 24 vs. CaCl₂ 18). Factoring the proteinuria for food intake, however, also resulted in a tendency towards an increased proteinuria in the 18% group. As expected, acidosis resulted in an increased urinary excretion of sodium, potassium and calcium, while at the same time the phosphate excretion remained fairly constant in both groups, but showed a higher excretion during CaCO₃treatment in the 8% group. In addition, osmolarity and the total amount of osmols excreted in the urine was increased during the acidotic state. Thus, we conclude that acidosis in uremic rats results in a catabolic state which may be due to anorexia and increased muscle breakdown. Furthermore, there is a tendency towards an increased proteinuria, which is probably due to changes in the permselectivity of the basal membrane. In addition, secondary hyperparathyroidism seems to be aggravated due to the high calcium losses and the reduced phosphate excretion. Thus, in order to prevent these negative sequelae of acidosis in uremics, bicarbonate therapy seems to be of considerable importance. But these data also demonstrate that most of the negative sequelae of acidosis can be overcome by a correctly followed low-protein diet.

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Section: Discussioncontrasting

confidence: 55%

“…Thus, it seems to be possible that renal function decreased during the CaCU period. Comparable phenomena concerning glomerular filtra tion rate have been described by Fine et al [11], Due to the design of our study, however, no data on GFR are avail able.…”

Section: Discussionmentioning

confidence: 72%

A Low-Protein Diet Protects Uremic Rats against the Negative Sequelae of Metabolic Acidosis

Gretz

Lasserre

Langer³

et al. 1990

Nephron

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“…Moreover, renal utilization of ammonia precursors, mainly glutamine, in these circumstances is unexplored so far. A number of investigations carried out in animals with acute metabolic acidosis provided conflicting results that also depended on species differences (14)(15)(16)(17)(18)(19)(20)(21).…”

Section: Introductionmentioning

confidence: 99%

Renal ammoniagenesis in an early stage of metabolic acidosis in man.

Tizianello¹,

Garibotto²,

Robaudo³

et al. 1982

J. Clin. Invest.

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A B S T R A C T Total renal ammonia production and ammonia precursor utilization were evaluated in patients under normal acid-base balance and in patients with 24-h NH4C1 acidosis by measuring (a) ammonia excreted with urine and that added to renal venous blood, and (b) amino acid exchange across the kidney. In 24-h acidosis not only urinary ammonia excretion is increased, but also total ammonia production is augmented (P < 0.005) in comparison with controls. By evaluating the individual role of acid-base parameters, urine pH and urine flow in influencing renal ammonia production, it was shown that the degree of acidosis and urine flow are likely major factors stimulating ammoniagenesis. Both urine pH and urine flow are determinant in the preferential shift of ammonia into urine. In 1-d acidosis, renal extraction of glutamine was not increased and the total ammonia produced/ glutamine N extracted ratio was higher than in controls (P < 0.005) and was inversely correlated with the log of arterial bicarbonate concentration (P < 0.001). In the same condition, renal glycine and ornithine uptake took place; the more severe the acidosis, the greater was the renal extraction of these amino acids (P < 0.001). These data indicate that at the early stages of metabolic acidosis, in spite of a brisk increase in ammonia production, the mechanisms responsible for the increased glutamine use, which are operative in chronic acidosis, are not activated and other ammonia precursors, besides glutamine, are probably used for ammonia production.

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“…The validity of this interpretation presupposes that renal blood flow remains constant when diets are supplemented with acid or alkali. A decrease in renal blood flow has only been reported during acute acidosis or alkalosis in the rat [14,15] and in the dog [16]. Moreover, many studies show no influence on renal blood flow of acute or chronic acidosis and/or alkalosis in the anesthetized rat [17,18] and dog [19,20], and in the awake man [4,21].…”

Section: Discussionmentioning

confidence: 98%

Arterial ammonemia changes of renal origin induced in the rat by acid and alkaline diets

et al. 1986

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The aim of this study was to investigate the influence of acid and alkali food supplementation on systemic ammonemia to explain the hyperammonemia previously observed in rats fed a high protein diet. In normal rats, arterial ammonia concentration significantly increases after 4 days of HCl-supplemented diet. Following a NaHCO3-enriched food, there is only a slight but not significant decrease in arterial ammonia level. These changes occur before any variation in arterial acid-base status and are of renal origin. Indeed, there is a positive linear correlation (r = 0.946; P less than 0.001) between arterial ammonia level and the ammonia concentration difference between the renal vein and artery (which varies proportionally to the urinary ammonium excretion). Hindquarter uptake and intestinal release of ammonia do not significantly participate in the arterial ammonia changes observed. Following HCl-enriched diets, increased renal glutamine uptake, enhanced hindquarter glutamine release, and perhaps decreased intestinal glutamine uptake occur simultaneously. In conclusion, acid and alkali food supplementation intervenes on the renal ammonia release into the circulation with concomitant arterial ammonemia changes.

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Effects of Acute Acid–Base Alterations on Glutamine Metabolism and Renal Ammoniagenesis in the Dog

Cited by 8 publications

References 12 publications

A Low-Protein Diet Protects Uremic Rats against the Negative Sequelae of Metabolic Acidosis

A Low-Protein Diet Protects Uremic Rats against the Negative Sequelae of Metabolic Acidosis

Renal ammoniagenesis in an early stage of metabolic acidosis in man.

Arterial ammonemia changes of renal origin induced in the rat by acid and alkaline diets

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