Catabolism in Uremia: Metabolic Acidosis and Activation of Specific Pathways1

Greiber, S.

doi:10.1159/000421597

Cited by 20 publications

(23 citation statements)

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“…Na + /H + exchange may be involved in these effects. In contrast to our findings and those of Corry et al [20], Greiber and Mitch found that the antiport was decreased in thymocytes of uraemic rats [30]. Additional studies will be necessary to elucidate these issues.…”

Section: Discussioncontrasting

confidence: 99%

Light-chain-induced renal tubular acidosis: effect of sodium bicarbonate on sodium-proton exchange

Reusch

Mann²,

Mihatch

et al. 1995

Nephrology Dialysis Transplantation

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Abstract. We measured sodium-proton (Na + /H + ) exchange in lymphocytes and platelets of a 46-yearold woman with the adult Fanconi syndrome before, during, and after treatment with NaHCO 3 . Kappa light chains in her urine and unique but rarely observed crystalline structures confirmed the presence of lightchain nephropathy. Her glomerular nitration rate was only moderately impaired at 72 ml/min. NaHCO 3 at 1, 3, and 5 mmol/kg/day for 5 days increased her serum HCO 3 and pH from 17 to 21 mmol/1 and 7.28 to 7.39 respectively. Plasma renin and aldosterone values were decreased by NaHCO 3 . Na + /H + exchange (ciHi/min) was measured with the fluorescent marker BCECF after acidification of lymphocytes and platelets with sodium propionate at five (10-50mM) doses. Na + /H + exchange was accelerated in this patient compared to normal controls. NaHCO 3 treatment significantly decreased Na + /H + exchange in lymphocytes, but not in platelets. These findings suggest that Na + /H + exchange can be influenced by NaHCO 3 ingestion at doses that only modestly affect systemic pH. Since Na + /H + exchange is involved in stimulus response coupling, cell growth regulation, cell differentiation, and perhaps the progression of nephrosclerosis, these observations may have clinical relevance.

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Section: Discussioncontrasting

confidence: 99%

Light-chain-induced renal tubular acidosis: effect of sodium bicarbonate on sodium-proton exchange

Reusch

Mann²,

Mihatch

et al. 1995

Nephrology Dialysis Transplantation

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“…The acidosis-induced alterations in protein metabolism involve various endocrine systems, including a decrease in insulin-like growth factor 1 levels (due to a loss of peripheral growth hormone sensitivity), moderate hyperthyroidism and hyperglucorticoidism (Greiber & Mitch, 1992;Wiederkehr & Krapf, 2001). In addition, various metabolic disturbances liable to be accompanied by acidosis (diabetes, sepsis) result in a decrease in insulin action on protein synthesis or degradation but, in contrast, the antiproteolytic action of insulin could be improved during hyperthyroidism (Grizard et al 1999).…”

Section: Acid-base Status and Protein Metabolismmentioning

confidence: 99%

Organic anions and potassium salts in nutrition and metabolism

et al. 2004

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The present review examines the importance of dietary organic anions in preventive nutrition. Organic anions are chiefly supplied by plant foods, as partially neutralised K salts such as potassium citrate, potassium malate and, to a lesser extent, oxalate or tartrate salts. Animal products may also supply K anions, essentially as phosphate, but also as lactate as a result of fermentative or maturation processes, but these K salts have little alkalinising significance. Citrate and malate anions are absorbed in the upper digestive tract, while a substantial proportion is probably metabolised in the splanchnic area. Whatever their site of metabolism, these anions finally yield KHCO 3 which is used by the kidneys to neutralise fixed acidity. This acidity essentially reflects the oxidation of excess S amino acids to sulfate ions, which is mainly related to the dietary protein level. Failure to neutralise acidity leads to low-grade metabolic acidosis, with possible long-term deleterious effects on bone Ca status and on protein status. Furthermore, low-grade acidosis is liable to affect other metabolic processes, such as peroxidation of biological structures. These metabolic disturbances could be connected with the relatively high incidence of osteoporosis and muscle-protein wasting problems observed in ageing individuals in Europe and Northern America. Providing a sufficient supply of K organic anions through fruit and vegetable intake should be recommended, fostering the actual motivational campaigns ('five (or ten) per d') already launched to promote the intake of plant foods rich in complex carbohydrates and various micronutrients.

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“…Glutamine metabolism by kidneys is a major process to counteract acidosis through bicarbonate and ammonium production (hence H + trapping) and urine measurements have actually shown that ammonium excretion was higher with the 26% protein diet. In fact, the effect of protein intake on acid-base status is equivocal since, besides sulfur amino acid catabolism (defi nitely acidogenic), the catabolism of some other amino acids is potentially alkalinizing (dicarboxylic amino acid oxidation, branched chain amino acid metabolism and glutamine generation) and this catabolism is induced by high-protein diets [3,14,15] .…”

Section: Discussionmentioning

confidence: 99%

“…This process can lead to a base defi cit, hence a situation of low-grade metabolic acidosis [1,2] . Such an alteration in acid base status is liable, in turn, to trigger various metabolic disturbances affecting bones, kidneys or muscles [3,4] and pathological consequences of major importance have been identifi ed, such as osteoporosis, kidney stone formation or osteopenia [5] . Metabolic acidity is normally controlled by specifi c processes such as glutamine breakdown in kidneys (generating both ammonia and HCO 3 -) or HCO 3 -generation resulting from the metabolism of dietary K organic anions salts, K citrate or K malate for example.…”

Section: Introductionmentioning

confidence: 99%

Excess Casein in the Diet Is Not the Unique Cause of Low-Grade Metabolic Acidosis: Role of a Deficit in Potassium Citrate in a Rat Model

Sabboh¹,

Besson²,

Tressol³

et al. 2006

Ann Nutr Metab

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This study examined the effects of a dietary model of protein excess and K anion salt deficit on the occurrence of metabolic acidosis in rat. Rats were adapted to diets containing either 13 or 26% casein, together with mineral imbalance, through lowering K/increasing sodium/omitting alkalinizing anions. For each protein level, a group of rats was supplemented with K citrate. Dietary K citrate resulted in neutral urinary pH, whatever the protein level. Urea excretion was higher in rats adapted to 26% casein than 13% casein diets, but K citrate enhanced this excretion and suppressed ammonium elimination. No citraturia could be observed in acidotic rats, whereas K citrate greatly stimulated citraturia and 2-ketoglutarate excretion. In conclusion, low-grade metabolic acidosis can occur with a moderate protein level in the diet. K citrate was apparently less effective in rats adapted to the 26% casein level than in those adapted to the 13% casein level with regard to magnesium, citrate and 2-ketoglutarate concentrations in urine.

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Catabolism in Uremia: Metabolic Acidosis and Activation of Specific Pathways1

Cited by 20 publications

References 0 publications

Light-chain-induced renal tubular acidosis: effect of sodium bicarbonate on sodium-proton exchange

Light-chain-induced renal tubular acidosis: effect of sodium bicarbonate on sodium-proton exchange

Organic anions and potassium salts in nutrition and metabolism

Excess Casein in the Diet Is Not the Unique Cause of Low-Grade Metabolic Acidosis: Role of a Deficit in Potassium Citrate in a Rat Model

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