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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied urinary acidification daily during the hospital course of 16 infants with acute gastroenteritis and metabolic acidosis. Urine pH value on admission was higher than 5.5 in 14 (87%) patients. We hypothesized that inappropriate urinary acidification was due to sodium deficiency and inadequate sodium delivery to the distal nephron. Forty-one urinary samples were collected during metabolic acidosis. The mean pH of 24 urine samples with sodium concentration less than 10 mmol/L was significantly higher than the pH of 17 samples with sodium concentration greater than 10 mmol/L (6.04 +/- 0.06 vs 5.19 +/- 0.1; p less than 0.001). The urine ratios of titratable acid to creatinine and of total acidity to creatinine were significantly higher in urine samples containing more sodium (p less than 0.02), whereas the ammonium/creatinine ratio was not. After administration of furosemide or correction of the sodium deficit, appropriate acidification was observed. We conclude that impaired urinary acidification is frequently found during metabolic acidosis in infants with acute gastroenteritis and results from a sodium deficit rather than from transient distal renal tubular acidosis.
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PMID:Transient renal acidification defect during acute infantile diarrhea: the role of urinary sodium. 188 Jun 72

In the normal human body, the extracellular fluid pH of 7.40 is closely protected. Any increase in acidity or alkalinity summons forth three lines of defense, starting immediately with the blood buffers, followed soon by the respiratory system's control of CO2, and finally purged by the renal excretion of the excess acid or base. The complex interrelated processes of the renal responses require a few days to accomplish maximum compensation. We have presented the fundamental principles governing maintenance of the acid-base equilibrium to provide a conceptual framework for understanding the clinical disorders of hydrogen ion metabolism. The somewhat elusive concepts of endogenous acid production and net acid balance have also been reviewed to help reveal the pathophysiology of metabolic acidosis caused by renal tubular acidosis, chronic renal failure, certain infant feedings, and total parenteral nutrition. The development and perpetuation of metabolic alkalosis in relationship to chloride and potassium deficiency have been examined. In the delineation of a clinical acid-base disorder, the clinician must bear in mind the continual interactions of electrolytes and hormonal systems and should be prepared to reevaluate frequently the elected therapy against the changing responses, based on a thorough understanding of physiology. The various types of renal tubular acidosis have manifold facets but the basic understanding of their pathophysiology begins with the concept of the "anion gap," a point of reference that can be used in the differential diagnosis and treatment. In this chapter a number of new causes of type IV renal tubular acidosis--currently considered to be the most common form of renal tubular acidosis--have been pointed out, along with special reference to the mineral, electrolyte, and aldosterone metabolism in the various acidoses and current means of reversing growth failure in the child, especially through bicarbonate treatment. The mechanism of metabolic acidosis in chronic renal failure including metabolic acidosis in children undergoing dialysis and in recipients of kidney transplantation, and its relationships to mineral and electrolyte metabolism have been presented. The pathophysiology of the acidosis related to certain infant formulas and the acidogenic properties of some amino acid solutions employed in total parenteral nutrition have been briefly reviewed. Finally, the metabolic alkalosis seen in a variety of chloride deficiency syndromes, such as Bartter's syndrome and dietary chloride deprivation, has been discussed and a rational approach to evaluation and treatment outlined.
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PMID:Acid-base disorders and the kidney. 642 18

Forty-five patients with recurrent renal stone were examined for distal renal tubular acidosis (dRTA) defects by acid challenge test (150 mg ammonium chloride/kg body weight). Their 24-h urine samples were analysed for creatinine, calcium, oxalic acid, inorganic phosphorus, uric acid, magnesium and citric acid. One-hour urine samples before acid load and hourly samples for the 7 h following acid challenge test were collected and analysed for creatinine, calcium, citric acid, inorganic phosphorus, titratable acidity, and ammonium. The incidence of distal RTA defect was 22.2% in the patients examined. The major biochemical characteristics in RTA patients compared with patients without RTA were: (a) significantly higher urinary pH, (b) significantly lower excretion of citric acid, (c) no significant difference in calcium excretion and (d) a tendency toward lower titratable acidity and ammonium excretion.
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PMID:A study of recurrent stone formers with special reference to renal tubular acidosis. 748 48

Foscarnet is used as therapy of cytomegalovirus (CMV) infection in immunosuppressed subjects. We present a patient with human immunodeficiency virus infection under treatment with foscarnet for CMV retinitis who complained of thirst and polyuria. Laboratory data showed hypernatremia with increased plasma osmolality and metabolic hyperchloremic acidosis. A water deprivation test demonstrated a nephrogenic diabetes insipidus. Other laboratory studies, including urine pH, anion gap, titratable acidity, and bicarbonate, showed a distal tubular acidification defect. All abnormalities were transient, with recovery a few days after foscarnet withdrawal. No cases of renal acidosis, and only one case of nephrogenic diabetes insipidus, has been previously reported as a complication of foscarnet treatment. Our patient developed both nephrogenic diabetes insipidus and renal tubular acidosis with a temporal pattern that demonstrated a link between foscarnet therapy and these abnormalities.
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PMID:Nephrogenic diabetes insipidus and renal tubular acidosis secondary to foscarnet therapy. 860 15

Renal stone disease may ensue from either derangements of urine biochemistries or anatomic abnormalities of kidneys and urinary tract. Genetic, environmental and dietary factors may also cooperate in the pathophysiology of nephrolithiasis. An adequate metabolic evaluation should focus on the urinary excretion of promoters and inhibitors of stone formation as well as on the occurrence of systemic diseases potentially related to secondary nephrolithiasis (i.e., endocrine disturbances, malabsorption, bone diseases). Moreover, metabolic investigations should provide reliable information on patient's dietary habits, guide towards the best therapeutic approach and enable the physician to verify patient's compliance to prescribed therapies.AN EXTENSIVE METABOLIC EVALUATION IS RECOMMENDED IN PATIENTS WITH ACTIVE STONE DISEASE (NAMELY, AT LEAST ONE NEW STONE WITHIN THE LAST TWO YEARS), OR IN THOSE HAVING HAD A SINGLE STONE EPISODE OCCURRED IN PECULIAR CONDITIONS: familial history of disease, childhood, menopause, pregnancy, systemic diseases. Simplified protocols may be adequate in non-active nephrolithiasis or in patients with single stone and no relevant risk factors.In our Stone Centre, a so-called "first level screening" is performed by routine, in order to assess urinary supersaturation with stone forming salts and evaluate the excretion of dietary-related metabolites in urine. Relative blood and urine determinations are reported below.IN VENOUS BLOOD: urea, creatinine, uric acid, Na, K, total and ionised Ca, Mg, P, Cl, alkaline phosphatase, gas analysis. In 24-hr urine samples: urea, creatinine, uric acid, Na, K, Ca, Mg, P, Cl, oxalate, inorganic sulphate, citrate, pH, ammonia and titratable acidity. IN FASTING URINE SAMPLES: Ca, citrate, creatinine, hydroxyproline, Brand's test for cistinuria, urine sediment, urine culture. If the first-level evaluation suggested an abnormal bone turnover, then further determinations are warranted, namely, calciotropic hormones (blood Vitamin D and PTH), markers of bone resorption (urine pyridinium crosslinks, serum crosslaps) and formation (serum osteocalcin) bone mineral density.EVENTUALLY, MORE SOPHISTICATED INVESTIGATIONS ARE REQUIRED TO IMPROVE THE DIAGNOSIS OF PECULIAR DISEASES: serum oxalate and glycolate, urine glycolate and L-glycerate, hepatic AGT activity (primary hyperoxalurias); genetic tests (hereditary nephrolithiasis); acidification tests (renal tubular acidosis).
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PMID:Biochemical evaluation in renal stone disease. 2246 Sep 94