PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “ACIDOSIS, RENAL TUBULAR”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 343 records · Page 19Linked to original sources
PubMed1983

Renal tubular acidosis in a patient with recurrent metabolic alkalosis.

A 7-month-old infant with failure to thrive and recurrent episodes of vomiting and metabolic alkalosis was evaluated. Urine pH, serum bicarbonate, and urine PCO2-blood PCO2 studies were consistent with the diagnosis of distal renal tubular acidosis (RTA-type I). Analysis of serum potassium and chloride levels during periods of alkalosis and acidosis revealed that potassium depletion and hypochloremic volume contraction served to maintain the alkalotic state despite the presence of an underlying chronic acidosis. This case represents an unusual presentation for renal tubular acidosis and suggests that, under certain conditions, renal tubular acidosis may predispose to the maintenance of a metabolic alkalosis.

Acidosis, Renal Tubular↗
PubMed1986

Type II renal tubular acidosis in a mare.

Persistent, severe metabolic acidosis complicated the operative and postoperative period in a 4-year-old mare with colic. On the basis of clinical and laboratory findings, a renal tubular disorder was diagnosed. Renal tubular acidosis is rare in horses. In the only report found on the subject, type I renal tubular acidosis was described in 2 horses. Bicarbonate titration studies in our case helped document type II renal tubular acidosis in this mare.

Acidosis, Renal Tubular↗
PubMed1977

Red blood cell carbonic anhydrase activity in children with distal renal tubular acidosis.

Red blood cell carbonic anhydrase activity was studied in three children with distal renal tubular acidosis, the parents of one of the patients, and in control subjects. Although each patient had distal renal tubular acidosis as defined by an inappropriately high urine pH in the face of a systemic metabolic acidosis, hyperchloremia and a low (U-B)pCO2, they differed in that two had deafness. The deafness was inherited as an autosomal recessive mode in one and by an autosomal dominant gene in the other. Red blood cell carbonic anhydrase activity was determined in hemoglobin-free hemolysate by the esterolytic action of the enzyme on the substrate p-nitrophenyl acetate. The two isoenzymes, B and C, of carbonic anhydrase were identified using polyacrylamide disc gel electrophoresis. The red blood cell carbonic anhydrase activity of nine control children aged 2-10 years was 3.8 (3.2-5.0) units/g Hb. The values obtained from the three patients were 3.0, 3.7, and 4.36 units/g Hb. These did not differ from those of the control subjects. No abnormalities were found in the ratios of the B and C peaks or in their electrophoretic mobility.

Acidosis, Renal Tubular↗
PubMed1990

Urinary constituents in an endemic area of stones and renal tubular acidosis in northeastern Thailand.

Nephrolithiasis and endemic renal distal tubular acidosis are common in northeastern Thailand. The etiology is still unknown. It is generally accepted that urine electrolytes influence the capacity of urine to inhibit or promote renal and also bladder stones. The purpose of this study was to analyse the composition of the urine in the indigenous population in the northeast area and compare their values with data obtained from a group of age matched adults, living in Bangkok. Twenty-four hour urine samples from 23 normal adult villagers from six villages within the province of Khon Kaen and 34 normal adults living in Bangkok were collected, and the daily excretion of creatinine, uric acid, calcium and inorganic phosphate, sodium, potassium, chloride, magnesium and oxalate were assayed. Daily urinary sodium, potassium, chloride and phosphate of the villagers were significantly lower than those of Bangkokians. No difference in the urinary excretion of calcium, magnesium, uric acid, oxalate and creatinine was found. The Na/Ca, and Ca/PO4 ratios of villagers were significantly lower than those of the Bangkok subjects. The villagers excreted significantly lower amounts of Na in the face of relatively higher urinary Ca. The above data, combined with our previous study showing the low values of urinary citrate in the villagers in the same areas, strongly indicate that the indigeneous population is at high risk in developing urolithiasis. The causes for these electrolyte abnormalities are still unknown. Low contents of the major electrolytes in their diets might play an important role. Low phosphate output indicates low protein diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗