Metabolic acidosis citrate

Metabolic acidosis and hyperchioremia Potassium depletion is rarely associated with metabolic acidosis and hyperchloremia. Replace with potassium bicarbonate, citrate, acetate, or gluconate. 

Four preterm neonates with posthemorrhagic ventricular dilatation developed severe metabolic acidosis after being given acetazolamide (33). The acidosis suddenly disappeared after a transfusion of packed erythrocytes, which was attributed to the citrate contained in the blood. 

Death. Aluminum is not thought to be life-threatening to healthy humans. Studies of people receiving extremely high doses of oral aluminum in antacids have not shown any human deaths from aluminum. However, in the past, aluminum-related deaths have been reported for persons with renal disease dialyzed with aluminum -containing solutions, uremic patients exposed to dietary aluminum hydroxide to treat hyperphosphatemia and sodium citrate to correct metabolic acidosis (Kirschbaum and Schoolwerth 1989), and workers exposed by inhalation to fine powders of aluminum metal. Only very large doses (hundreds of mg/kg) of aluminum cause death in laboratory animals. 

CAIs alter renal function primarily by inhibiting carbonic anhydrase in the proximal tubule, which results in decreased bicarbonate reabsorption. The net effect of the renal actions of acetazolamide therapy is alkaliniza-tion of the urine and metabolic acidosis. Metabolic acidosis results from the initial bicarbonate loss and persists with continued acetazolamide use. Moderate metabolic acidosis develops in most patients. Reabsorption of bicarbonate independent of carbonic anhydrase prevents severe acidosis. Initially, acetazolamide produces diuresis, but urinary output decreases with the development of metabolic acidosis. In addition, decreased urinary citrate excretion follows acetazolamide therapy and has been attributed to the metabolic acidosis it produces. A high urinary pH and low urinary citrate concentration are conducive to precipitation of calcium phosphate in both the renal papillae and the urinary tract. 

Adverse effects. High doses of acetazolamide may cause drowsiness and fever, rashes and paraesthesiae may occur, and blood disorders have been reported. Renal calculi may develop, because the urine calcium is in less soluble form owing to low citrate content of the urine, a consequence of metabolic acidosis. 

Laboratory tests on a sick child reveal a low white blood cell count, metabolic acidosis, increased anion gap, and mild hyperammonemia. Measurement of plasma amino acids reveals elevated levels of glycine, and measurement of urinary organic acids reveals increased amounts of propionic acid and methyl citrate. Which of the following processes is most likely ... 

In addition to CKD as a risk factor, other contributing factors should also be considered. This includes exposure to potassium-sparing diuretics -blockers, which work predominantly via 82-antagonistic effects to interfere with the extrarenal translocation of potassium into cells and ACEls, which may cause hyperkalemia by reducing aldosterone production. Polycitra, used for the treatment of metabolic acidosis, contains potassium citrate and should not be prescribed for patients with severe CKD. If hyperkalemia develops, management options are based on the degree to which potassium is elevated (see Chap. 50). 

The main determinant of citrate excretion is probably the intracellular pH of the tubular cells (Cll, HIO, M25), as is shown by the fact that urinary citrate decreases in potassium depletion (F9), as well as after administration of maleic acid (H9) or acetazoleamide (G15, G16, HIO, OH), which produces a metabolic acidosis associated with an alkaline urine. 

Tromethamine is indicated for prevention and correction of system acidosis such as metabolic acidosis associated with cardiac bypass surgery the correction of acidity of acid citrate dextrose (ACD) blood in cardiac bypass surgery or cardiac arrest. 

The only disorder of the y-glutamyl cycle for which treatment principles have been developed is glutathione synthetase deficiency (9.2) [1]. The initial symptoms in the neonatal period may be metabolic acidosis and jaundice. Acidosis usually needs to be corrected with sodium bicarbonate, THAM or sodium citrate. Patients may benefit from oral administration of vitamin E (10 mg/kg/day) and vitamin C (100 mg/kg/day). Trials have also been made with N-acetylcysteine and glutathione esters which increased glutathione in leukocytes and plasma. Both these compounds lead to increased intracellular levels of glutathione. However, no decrease in the excretion of 5-oxoprolinuria has been reported. 

Low citrate excretion is not always adequately recognized as a risk factor in the pathogenesis of calcium-containing stones (Miller and Stapleton 1985). Low urinary citrate excretion is characteristic for the complete form of dRTA (Preminger et al. 1985). Hypocitraturia is also observed in persistent mild or latent metabolic acidosis, in hypokalemia, and in patients with malabsorption syndromes (Hoppe et al. 2005). Idiopathic hypocitraturia may be secondary to low intestinal alkali absorption (Hoppe et al. 2007). 

Some data on specific organic acids in amniotic fluid near term were given by Raiha (1963), who used enzymic and colorimetric methods to determine lactate, pyruvate, 2-oxoglutarate and citrate concentrations in an investigation of neonatal metabolic acidosis. Silicic acid chromatography was also used to demonstrate the presence of citric, lactic and pyruvic acids. Typical concentrations observed were lactate 75.69 21.29 mg (100 ml) pyruvate 0.82 0.40 mg (100 ml) citrate 5.55 1.27 mg (100 ml) and 2-oxoglutarate 0.74 0.33 mg (100 ml) (all near-term). 

The pH-buffering of extracellular fluid depends in part on the carbon dioxide/ bicarbonate equilibrium so that the intake of sodium bicarbonate is followed by a brief alkalosis and an increased excretion of sodium carbonate in the urine. Depending on its carbonate concentration, the pH of the urine may rise to 8.07. Large doses (80—100 g/day) of sodium bicarbonate were needed if the pH of stomach contents was to be maintained at 4 or over in patients with duodenal ulcers8. Oxidation of organic anions in the body to carbon dioxide and water permits the use of sodium citrate, lactate or tartrate instead of sodium bicarbonate. In an analogous manner the ingestion of ammonium chloride induces a brief acidosis as a result of the metabolic conversion of ammonia to urea and lowers the pH of the urine. 

The elimination of citric acid was shown by many workers to be decreased in diabetic patients (B24, K18, 08, 012) thus, Otto (08) found that the amount of citrate excreted in urine during diabetic coma is only 2-10 % of the normal values. It is not established whether this hypocitraturia is related to a metabolic abnormaUty, due to the disease itself, or to the acidosis, or even to a renal failure during coma (08) it appears, however, that the magnitude in the decrease of urinary citrate is not related to the severity of the acidosis (08). One must add that, if the results of Rechenberger and Benndorf (R4) concerning the decrease of blood citrate levels are confirmed, diabetic patients present a simultaneous decrease in blood and urine citrate analogous to that found by Nordmann et al. (N17) during acute renal insuflBciency. 

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