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Query: UMLS:C0017160 (gastroenteritis)
 11,398 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper describes an infant with gastroenteritis, who developed hypertension and oedema after administration of inaccurately prepared oral glucose salt solution. The renin aldosterone system was suppressed in this child and it was suggested that this may be a factor in the development of hypernatraemia when abnormal water losses occur in infants fed on hyperosmolar feeds. Unless salt can be given accurately in small amounts it may be safer to advise feeds of glucose only in infants with mild diarrhoea.
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PMID:Hypertension, oedema, and suppressed renin aldosterone system due to unsupervised salt administration. 119 Aug 14

Infants and young children with acute gastroenteritis have been studied with regard to stool electrolyte composition, external electrolyte balance, and aldosterone excretion. At the height of fluid depletion the stool sodium concentrations are low (median 8 m-equiv/1, range 3-58 m-equiv/1). The results indicate that in gastroenteritis the colon is responding homeostatically to a state of secondary hyperaldosteronism, thus assisting in sodium conservation.
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PMID:The homeostatic function of the colon in acute gastroenteritis. 464 94

The mean serum aldosterone concentration of 37 infants with acute gastroenteritis and dehydration was markedly elevated on admission (mean +/- SE 94.3 +/- 12.1 ng/ml) and approximated to normal values (18.2 +/- 3.7 ng/ml) following recovery from the acute disease (t=3.56 p less than 0.005). Serum aldosterone levels were significantly positively correlated with the percent weight loss (r=0.41, p less than 0.05) and with the blood urea nitrogen levels (r=0.55, p less than 0.001). There was no correlation between either serum sodium levels or blood osmolarity and aldosterone concentrations. Serum potassium levels were positively correlated with aldosterone levels (r=0.53, p less than 0.001). These findings indicate that small infants when dehydrated respond appropriately with elevated aldosterone levels. The amount of body fluid depletion and hyperkalemia are the major factors determining the amount of aldosterone response.
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PMID:Aldosterone concentrations in dehydrated infants. 670 40

Two men (61 and 81 years old) with mild impaired kidney function developed acute renal failure due to dehydration combined with the use of inhibitors of the renin-angiotensin-aldosterone system (RAAS). After rehydration, correction of hyperkalaemia and stopping RAAS-inhibition and diuretics, they recovered completely. Many patients using RAAS-inhibitors have impaired renal function. In the case of dehydration due to gastroenteritis or prolonged fever they risk developing acute renal failure. The high risk groups are elderly patients, patients with atherosclerosis or heart failure and those with co-medication of diuretics or NSAIDs. The underlying mechanism is that the normal pathways to protect kidney perfusion in case of hypovolaemia are blocked by the use of RAAS-inhibitors or NSAIDs. In the case of dehydration in patients with chronic kidney disease using RAAS-inhibitors, serum creatinine and potassium levels should be monitored. Temporary discontinuation of RAAS-inhibitors or diuretics is often necessary.
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PMID:[Acute renal failure due to RAAS-inhibitors combined with dehydration]. 2069 27

Bartter syndrome is an autosomal recessive renal tubulopathy that presents with hypokalemic, hypochloremic metabolic alkalosis associated with increased urinary loss of sodium, potassium, calcium and chloride. There is hyperreninemia and hyperaldosteronemia but normotension. A full term male neonate was referred at 20-day of age with features of sepsis and respiratory distress. He was evaluated and managed as case of septicemia with all supportive paraphernalia including mechanical ventilation. Investigations revealed electrolytes imbalance and metabolic alkalosis suggestive of Neonatal Bartter Syndrome (NBS). Raised aldosterone and renin levels confirmed the diagnosis. Electrolyte imbalance was corrected with fluids and indomethacin, treated successfully, discharged and parents counseled. He was thriving well at 9 months of age. Another 2 months old male baby presented with recurrent episodes of lethargy with dehydration and failure to gain weight. Investigations confirmed the diagnosis of NBS. He was also successfully treated with same medication. We report these 2 cases because of the rarity of NBS, presentation of which may mimic common illnesses like sepsis and gastroenteritis.
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PMID:A Rare Disorder with Common Clinical Presentation: Neonatal Bartter Syndrome. 2593 68

Kidney transplant patients (KTPs), and particularly those with advanced chronic kidney rejection, may be affected by opportunistic infections, metabolic alterations and vascular and oncologic diseases that promote clinical conditions that require a variety of treatments, the combinations of which may predispose them to hyponatremia. Salt and water imbalance can induce abnormalities in volemia and/or serum sodium depending on the nature of this alteration (increase or decrease), its absolute magnitude (mild or severe) and its relative magnitude (body sodium:water ratio). Hyponatremia appears when the body sodium:water ratio is reduced due to an increase in body water or a reduction in body sodium. Additionally, hyponatremia is classified as normotonic, hypertonic and hypotonic and while hypotonic hyponatremia is classified in hyponatremia with normal, high or low extracellular fluid. The main causes of hyponatremia in KTPs are hypotonic hyponatremia secondary to water and salt contraction with oral hydration (gastroenteritis, sepsis), free water retention (severe renal failure, syndrome of inappropriate antidiuretic hormone release, hypothyroidism), chronic hypokalemia (rapamycin, malnutrition), sodium loss (tubular dysfunction secondary to nephrocalcinosis, acute tubular necrosis, tubulitis/rejection, interstitial nephritis, adrenal insufficiency, aldosterone resistance, pancreatic drainage, kidney-pancreas transplant) and hyponatremia induced by medication (opioids, cyclophosphamide, psychoactive, potent diuretics and calcineurinic inhibitors). In conclusion, KTPs are predisposed to develop hyponatremia since they are exposed to immunologic, infectious, pharmacologic and oncologic disorders, the combinations of which alter their salt and water homeostatic capacity.
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PMID:Hyponatremia in kidney transplant patients: its pathophysiologic mechanisms. 3009 23