Berlyne GM (ed): The Kidney Today. Selected Topics in Renal Science. Contrib Nephrol. Basel, Karger, 1992, vol 100, pp 48-57
The Metabolic Acidosis of Chronic Renal Failure: Pathophysiology and Treatment Sergio Giovannetti, Adamasco Cupisti, Giuliano Barsotti Clinica Medica J, UniversWl di Pisa, Italia
When the tubular capacity to excrete hydrogen ions becomes lower than their generation, some of them accumulate, and metabolic acidosis appears, which is indicated by low values of arterial blood pH and HCO). Several injurious effects are produced by uremic acidosis, especially if longlasting, and an adequate treatment should be instituted which, instead, is often omitted. This paper is a short review of the pathophysiology of uremic acidosis and on its conservative therapy.
The H+ that enter the body fluids under normal conditions result mostly from the oxidation of sulfur-containing amino acids and, to a minor extent, from the nonmetabolizable organic acids (uric acid, oxalic acid, etc.). Hydrogen ions may be then regarded as an end-product of proteins, like urea; indeed, the urea and H+ production are, in general, directly proportional to each other (fig. 1). Both the exogenous and endogenous proteins are equally important; hence, a catabolic condition increases the H+ production as well as a protein-rich diet. The ingested proteins are not, however, the only dietary factor modulating the H+ generation; the amount of the ingested organic anions (tartrate, acetate, citrate, etc.) which are oxidized to HCO), is equally important. HCO) plays, indeed, a key role in the physiological
Downloaded by: Université René Descartes Paris 5 193.51.85.197 - 3/15/2018 2:44:48 PM
The Origin and the Destiny of Hydrogen Ions
49
Metabolic Acidosis of Chronic Renal Failure
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The Metabolic Acidosis of Chronic Renal Failure: Pathophysiology and Treatment Sergio Giovannetti, Adamasco Cupisti, Giuliano Barsotti Clinica Medica J, UniversWl di Pisa, Italia
When the tubular capacity to excrete hydrogen ions becomes lower than their generation, some of them accumulate, and metabolic acidosis appears, which is indicated by low values of arterial blood pH and HCO). Several injurious effects are produced by uremic acidosis, especially if longlasting, and an adequate treatment should be instituted which, instead, is often omitted. This paper is a short review of the pathophysiology of uremic acidosis and on its conservative therapy.
The H+ that enter the body fluids under normal conditions result mostly from the oxidation of sulfur-containing amino acids and, to a minor extent, from the nonmetabolizable organic acids (uric acid, oxalic acid, etc.). Hydrogen ions may be then regarded as an end-product of proteins, like urea; indeed, the urea and H+ production are, in general, directly proportional to each other (fig. 1). Both the exogenous and endogenous proteins are equally important; hence, a catabolic condition increases the H+ production as well as a protein-rich diet. The ingested proteins are not, however, the only dietary factor modulating the H+ generation; the amount of the ingested organic anions (tartrate, acetate, citrate, etc.) which are oxidized to HCO), is equally important. HCO) plays, indeed, a key role in the physiological
Downloaded by: Université René Descartes Paris 5 193.51.85.197 - 3/15/2018 2:44:48 PM
The Origin and the Destiny of Hydrogen Ions
49
Metabolic Acidosis of Chronic Renal Failure
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