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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present prospective study was undertaken to evaluate the usefulness of urinary chloride concentration in determining the cause of an abrupt decline in renal function. 99 patients from diverse clinical settings with multiple causes of acute renal failure were evaluated. Urinary chloride concentrations of less than 20 mEq/l were observed in most cases of reversible prerenal azotemia (20 of 21 cases) and were observed in more frequently than urinary sodium concentration of less than 20 mEq/l (13 of 21 cases, p less than 0.01). Only prerenal azotemia accompanying diuretic use was associated with high urinary chloride concentrations (57 +/- 7 mEq/l). When prerenal azotemia occurred in the setting of metabolic alkalosis with bicarbonaturia, urinary chloride was low (4.0 +/- 1.0 mEq/l) while urinary sodium was high (65.0 +/- 19.0 mEq/l). In patients with oliguric and nonoliguric acute tubular necrosis, and in patients with acute exacerbations of chronic renal failure, mean urinary chloride concentration ranged from 40 to 67 mEq/l and mean fractional excretions of chloride ranged from 7.2 to 8.4%. Only 11% of patients with oliguric and nonoliguric acute tubular necrosis had urinary chloride concentrations of less than 20 mEq/l. Urinary chloride concentrations exhibited greater sensitivity and equivalent specificity as urinary sodium concentrations in differentiating patients with reversible prerenal azotemia from those with oliguric and nonoliguric acute tubular necrosis.
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PMID:Urinary chloride concentration in acute renal failure. 670 May 67

There are specific clinical settings in which each of the urine electrolytes may be diagnostically useful. The urine sodium alone is not efficient in differentiating prerenal azotemia from acute tubular necrosis, but if urine sodium is coupled with some measure of the renal concentrating ability, e.g., the urine:plasma creatinine ratio. discrimination between these two conditions is much improved. Usefulness of the urine sodium in other settings (evaluation of hyponatremia, prediction of acute rejection in renal transplant recipients, index of salt balance) is controversial. Urine potassium may be useful in the evaluation of hypokalemia of obscure etiology and, occasionally, in the form of the urinary Na/K ratio, as a guide to diuretic therapy. Urine chloride is assuming importance in the differential diagnosis of metabolic alkalosis, particularly when Bartter's syndrome is a consideration.
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PMID:Measurement of urine electrolytes: clinical significance and methods. 702 36

Diagnostic kidney biopsies sometimes yield clinically unsuspected diagnoses. We present a case of a 69-year-old woman with established ANCA-associated vasculitis (AAV) of 4 years duration who was in clinical remission following cytotoxic therapy and was on maintenance immunosuppression. She presented to the hospital with acute kidney injury (AKI), symptoms suggestive of a systemic vasculitis, and in addition had hypercalcemia, metabolic alkalosis. A relapse in the AAV was suspected but a diagnostic kidney biopsy showed acute tubular necrosis, patchy interstitial inflammation, and calcium phosphate deposits. It was found that the patient recently started consuming large doses of over-the-counter calcium-containing antacids and vitamin Dcontaining multivitamin supplements. Cessation of these drugs led to improvement of renal function to baseline. This case highlights several teaching points: (1) the kidney biopsy can prove to be critically important even in cases where there appears to be a more obvious clinical diagnosis, (2) AK due to calcium-alkali syndrome has characteristic histopathological changes, and (3) that the triad of hypercalcemia, metabolic alkalosis, and AKI is exclusively associated with the ingestion of excessive quantities of calcium-containing antacids. The physician should keep this in mind, and pro-actively seek pertinent medication history from the patient. A brief review of calcium-alkali syndrome is given.
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PMID:An unexpected cause of acute kidney injury in a patient with ANCA associated vasculitis. 2693 79

Congenital chloride diarrhea of infancy is a life threatening disease. We discuss two boys with congenital chloride diarrhea over a long time period before and after kidney transplantation. In the first case, prenatal sonography revealed polyhydramnios and generalized bowel loop distention. The genetic study confirmed congenital chloride diarrhea of infancy. Multiple episodes of severe dehydration, hyponatremia and acute tubular necrosis were seen during the follow up period. He underwent a year of hemodialysis before kidney transplantation. Three periods of improvement concerning diarrhea occurred with the use of corticosteroids, taken for other reasons. These improvements were seen after prednisolone administration for mastoiditis and following prednisolone administration for kidney transplantation. The second case was a 3.5 year old boy who is the cousin of the first case. He was referred to hospital with chronic watery diarrhea, metabolic alkalosis, hypokalemia, hyponatremia and failure to thrive in the first year of life. He was also treated with prednisolone and showed significant improvement.
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PMID:Improvement Of Congenital Chloride Diarrhea With Corticosteroids: An Incidental Finding. 3182 41