Alkali reserve

Renal calculi occurred in 2 children being treated with a low-galactose diet (B7, C5). In one case it was shown that the serum alkali reserve was low (B7). It is impossible to decide whether this was due to galactose damaging the kidney and causing continued dysfunction after exposure to galactose had stopped, or to some characteristic of the low-galactose diet. 

Metabolic ac/dos/s Triamterene may cause decreasing alkali reserve with a possibility of metabolic acidosis. 

Including consideration of acid/alkali reserve capacity, if appropriate. 

Firstly, the influence of main dietary representants, the carbohydrates, the fats, and the proteins on the acid—base balance should be mentioned. In addition, the function of the biosynthesized uric acid on the alkali reserve will be discussed in some detail. Subsequently, some quantitative aspects of uric acid synthesis, turnover, and renal and extrarenal excretion in healthy persons and gouty patients will be dealt with, followed by the detailed description of a special mechanism, preserving the serum bicarbonate by mobilization of bone phosphates. Finally, some clinical observations, supporting our concep- tion of the interrelation between hyperproduced uric acid and acid-base balance, will be discussed briefly. 

The reported pKi values range from 3.9 to 5.7 (21,48). For our considerations it is essential that the pK value of uric acid is lower than that of bicarbonate, the latter being 6.1. All acids with a pK value of less than 6.1 are able to release carbon dioxide from bicarbonate. Our gasometric measurements showed a slow but clear release of carbon dioxide after addition of uric acid to sodium bicarbonate. A prolonged overproduction of acids (even weak acids such as uric acid inevitably impairs the alkali reserve if this is not compensated for. 

Organic acids like lactic, pyruvic, di- and tricarboxylic acids of the Krebs cycle, and uric acid, which con tribe essentially to the titratable acidity of urine, can at low urinary pH combine with excreted hydrogen ions and prevent depletion of the alkali reserve in this way. 

A dietary deficiency of chlorine may lead to an abnormal increase of the alkali reserve of the blood (alkalosis) caused by an excess of bicarbonate, since inadequate levels of chlorine in the body are partly compensated for by increases in bicarbonate. Experiments with rats on chlorine-deficient diets have shown that growth was retarded, but no other symptoms developed. 

A variation on the gasometric type of analysis is the alkali reserve or the CO2 combining power . This is the plasma CO2 content after equilibration of the plasma at a PCO2 of 5.3 kPa (40mmHg). It is an attempt to replace the CO2 which has been lost during the collection of the specimen with the alveolar air of a normal person. 

This term designates the substances in the blood and body fluid which will neutralize acids. The main alkali in the blood is the bicarbonate ion. The alkali reserve protects the body against the damaging effects of the acids which arise from metabolism. The most significant of these acids are the ketone bodies, phosphoric acid, sulfuric acid, hydrochloric acid, and lactic acid. 

Name used by lay people to designate antacids that contain baking soda or sodium bicarbonate. The chemical definition of bicarbonate is a salt produced by the reaction of carbonic acid with an alkali. Sometimes, the term bicarbonate is used to designate the major alkali present in the blood. However, the correct term for the so-called alkali reserve is bicarbonate ion. 

Also see ACID-BALANCE ALKALI RESERVE BAKING POWDER AND BAKING SODA and BICARBONATE ION.)... 

Alkali Reserve and Acidosis. Since HCOs"" can neutralize the H ions of a strong acid (entering the blood stream, for example) according to the equation H+ - - HCO " = H CO, the quantity of HCOs" is often, but somewhat incorrectly, called alkali reserve. The normal value of the alkali reserve in blood is 25 meq/liter. A situation in which the alkali reserve is diminished greatly is called compensated acidosis, as long as the pH remains normal if the pH drops, it is called uncompensated acidosis. Alkalosis refers to the reverse situation and is characterized by a strongly elevated HCOs concentration. 

A partial failure of kidney function consequently is reflected by the ionic composition, by the alkali reserve, and possibly by the pH of blood. The regulation by the lungs also may lose its effectiveness and permit corresponding shifts of the alkali reserve (= respiratory acidosis or alkalosis). Finally, a metabolic defect may cause overproduction of organic acids, as has been known longest in the case of diabetes mellitus. The last situation is termed metabolic acidosis. There are other pathological shifts of acid-base equilibria and of the electrolyte balance that are not discussed here. 

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