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      Study of Erythrocyte ATPases in Infants Evaluated during the Recovery Phase of Severe Dehydration Caused by Diarrhea

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          Background/Aims: Patients severely dehydrated from diarrhea are at risk of developing hyperkalemia consequent to fluid therapy treatment. In parallel with the regulation of external potassium balance by the kidney and gastrointestinal tract, plasma potassium is rapidly regulated by redistribution of potassium between the extracellular and intracellular compartments. Erythrocytes contain ATPases that play a role in this potassium movement. In this study, erythrocyte ATPase effectiveness was evaluated in infants dehydrated from diarrhea and compared to that of healthy infants. Methods: Blood samples were collected from dehydrated and healthy infants. The activity of Na<sup>+</sup>,K<sup>+</sup>-ATPase and of an ouabain-insensitive K<sup>+</sup>-ATPase were assessed. Serum electrolytes and blood pH were also determined. Results: No hyperkalemia was found, even in dehydrated infants presenting with severe hyperchloremic metabolic acidosis. In the erythrocytes of dehydrated infants, Na<sup>+</sup>,K<sup>+</sup>-ATPase activity was increased correlating positively with the amount of sodium administered. High K<sup>+</sup>-ATPase activity in the erythrocytes correlated with low plasma potassium. The K<sup>+</sup>-ATPase activity correlated positively with the amount of potassium administered to dehydrated infants. Conclusion: These findings suggest that the erythrocytes Na<sup>+</sup>,K<sup>+</sup>-ATPase and K<sup>+</sup>-ATPase both protect against plasma potassium abnormalities in dehydrated infants. In such infants, the risk of hyperkalemia is probably low.

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          Most cited references 7

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          Aldosterone and end-organ damage.

           R. M. Brown (2005)
          This review highlights recent clinical studies demonstrating the contribution of aldosterone to cardiovascular mortality, vascular dysfunction, and renal injury in the context of advances in our understanding of the molecular biology of aldosterone. Mineralocorticoid receptor antagonism reduces mortality in patients with congestive heart failure and following myocardial infarction. Studies in animal models and in patients with congestive heart failure or hypertension indicate that aldosterone induces oxidative stress and impairs endothelial nitric oxide synthase through a mineralocorticoid receptor-dependent mechanism. Furthermore, aldosterone can cause vasoconstriction and vasodilation through rapid nongenomic mechanisms. The contribution of the nongenomic effects of aldosterone to vascular tone may depend on underlying endothelial function. In the heart and kidney, aldosterone stimulates oxidative stress and increases expression of inflammatory markers leading to fibrosis. The induction of inflammation and fibrosis appears to be both sodium and mineralocorticoid receptor dependent. The mechanisms underlying the progression from inflammation to fibrosis remain to be elucidated. Studies measuring circulating markers of collagen turnover suggest that mineralocorticoid antagonism reduces extracellular matrix turnover and cardiac remodeling in humans as well. Similarly, mineralocorticoid receptor antagonism reduces urinary albumen excretion in clinical trials in humans. Aldosterone induces oxidative stress, endothelial dysfunction, inflammation and fibrosis in the vasculature, heart and kidney. While most of these effects appear to be mediated via the mineralocorticoid receptor, better understanding of the mineralocorticoid receptor-independent effects of aldosterone, the role of nonaldosterone mineralocorticoid receptor agonists, and the mechanisms involved in the progression from inflammation to fibrosis and remodeling would enable the development of new strategies to slow the progression of cardiovascular and renal disease.
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            Extracellular fluid restoration in dehydration: a critique of rapid versus slow.

            We compared current recommendations for treatment of severe dehydration by World Health Organization physicians and by the American Academy of Pediatrics Committee on Pediatric Gastroenterology with those in general textbooks of pediatrics, written mostly by pediatric nephrologists. The former recommend rapid (1- to 2-h) and generous intravenous restoration of extracellular fluid (ECF) volume followed by oral rehydration therapy (ORT) to replace potassium, current maintenance, and diarrheal losses--the rapid rehydration regimen. Oral feedings usually are resumed in 8-24 h. General textbooks of pediatrics usually recommend giving 20 ml/kg saline "to restore circulation," followed by the deficit therapy regimen to correct serum electrolyte abnormalities and replace remaining deficits of water, sodium, chloride, and potassium over 1-2 days. Mortality for hospitalized patients with dehydration treated with rapid rehydration was <3 per 1,000; no recent results are reported for patients treated by deficit therapy. The rapid rehydration regimen improves patient well being and restores perfusion, so that oral feedings are readily tolerated and renal function corrects serum electrolyte abnormalities in 6 h. Amounts of saline given correspond to amounts given for treating various forms of shock. Deficit therapy regimens provide less ECF restoration and are slower at restoring perfusion; tolerance for oral feedings is delayed. Two hundred pediatric nephrologists were surveyed, asking how they would treat a patient with severe dehydration and a patient with 40% burns. Only 30 of 200 responded; 29 used a deficit therapy regimen, with 20-40 ml/kg ECF replacement, while a majority rapidly and generously restored ECF volume in burn shock. We recommend that fluid therapy chapters should stop teaching deficit therapy for treating severe dehydration and instead teach the rapid rehydration regimen.
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              Pediatric hydration therapy: historical review and a new approach.


                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                July 2006
                14 July 2006
                : 103
                : 4
                : p164-p169
                aInstituto da Criança, Departamento de Pediatria, and bLaboratório de Pesquisa Básica (LIM-12), Nefrologia, Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil
                92917 Nephron Physiol 2006;103:p164–p169
                © 2006 S. Karger AG, Basel

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                Figures: 4, Tables: 2, References: 20, Pages: 1
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