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At least 379 records · Page 21Linked to original sources
PubMed1978

Urinary sulfate excretion in children with classic renal tubular acidosis.

These studies quantitat the significantly elevated sulfate excretion in the urine of children with classic renal tubular acidosis as compared to six weight-matched controls (1.4 +/-0.5 vs. 0.7 +/- 0.2 mEq/kg/day;p less than 0.05). This sulfate loss may result in a subclinical sulfate deficiency which may contribute to a chondroitin sulfate metabolic disorder.,and thus contribute to the growth failure in children with real tubular acidosis. Futhermore, elevated urinary sulfate excretion may be an early diagnostic finding in infancy prior to the manifestation of renal acidification defects. It is not known whether the sulfate loss is related to a primary renal tubular defect or secondary to metabolic acidosis, although the increased sulfate excretion persisting after correction of metabolic acidosis would tend to suggest a primary defect. However, the normal plasma sulfate concentration and the relatively short period of study permit no definitive answer at this time.

Acidosis, Renal Tubular↗
PubMed1983

Renal hypoprostaglandism, hypertension, and type IV renal tubular acidosis reversed by furosemide.

A 13-year-old white girl with severe hypertension and type IV renal tubular acidosis had decreased renal chloride clearance and exaggerated sodium chloride reabsorption by the ascending limb of Henle during hypotonic saline diuresis. Urinary prostaglandin E2 excretion was markedly diminished and often undetectable (0 to 37 ng/24 h). Treatment with oral furosemide completely reversed the hypertension and hyperkalemic acidosis, and effected a 20-fold rise in urinary prostaglandin E2. Sodium chloride reabsorption by the thick ascending limb of Henle decreased from 93.5% to 79.3%. Renal hypoprostaglandism may have a pathogenic role in this syndrome by enhancing chloride reabsorption in the ascending limb of Henle leading to extracellular fluid volume expansion, hypertension, and suppression of the renin-angiotensin-aldosterone axis. The therapeutic effects of furosemide may be partially mediated by enhancing the biosynthesis of renal prostaglandins or inhibiting their breakdown.

Absorption↗
PubMed2001

Renal tubular acidosis: a new look at an old problem.

Although the definition of renal tubular acidosis (RTA) is simple, understanding the physiologic basis underlying the various types of this clinical entity is much more difficult. The pathophysiology of this disorder is reviewed using the normal acid-base functions of the involved segments of the nephron as a guide to understanding. Clinical and laboratory features of the subtypes of RTA are addressed, and diagnosis and treatment discussed. New developments in the knowledge and understanding of the associated growth disturbances, mineral metabolism, and molecular biology of RTA are also reviewed to provide the most current view of this relatively common pediatric entity.

Acidosis, Renal Tubular↗
PubMed2002

Distal renal tubular acidosis associated with isolated large vestibular aqueduct and sensorineural hearing loss.

Distal renal tubular acidosis (dRTA) is characterized by a defect in urinary acidification with various degrees of metabolic acidosis; it can be inherited either as an autosomal dominant trait or as a recessive trait. The recessive form is associated in about one third of cases with progressive sensorineural hearing loss (SNHL). We performed a neuroradiological study in 3 consecutive unrelated pediatric patients affected with sporadic dRTA and progressive SNHL that disclosed an enlarged vestibular aqueduct (VA) and endolymphatic sac (ES) in each. The presence of an enlarged VA in our patients with dRTA and SNHL could contribute to the development, or at least the progression, of the hearing impairment. We suppose that the same molecular defect present in both the kidney and the inner ear could be the cause of dRTA and of the development of the enlarged VA and ES.

Acidosis, Renal Tubular↗
PubMed1997

Renal tubular acidosis and osteopetrosis with carbonic anhydrase II deficiency: pathogenesis of impaired acidification.

Renal tubular acidosis with osteopetrosis is an autosomal recessive disorder due to deficiency of carbonic anhydrase II (CAII). A 3.5-year-old Egyptian boy with osteopetrosis and cerebral calcification has a persistent normal anion gap type of metabolic acidosis (plasma pH 7.26) and a mild degree of hypokalemia. A baseline urine pH was 7.0; ammonium (NH4+) excretion was low at 11 mumol/min per 1.73 m2; fractional excretion of bicarbonate HCO3 (FEHCO3) was high at 9% when plasma HCO3 was 20 mmol/l; citrate excretion rate was high for the degree of acidosis at 0.35 mmol/mmol creatinine. Intravenous administration of sodium bicarbonate led to a urine pH of 7.6, a FEHCO3 of 14%, a urine-blood PCO2 difference of 7 mmHg, NH4+ excretion fell to close to nil, and citrate excretion remained at 0.38 mmol/mmol creatinine. Intravenous administration of arginine hydrochloride caused the urine pH to fall to 5.8, the FEHCO3 to fall to 0, the NH4+ excretion rate to rise to 43 mumol/min per 1.73 m2, and citrate excretion to fall to < 0.01 mmol/mmol creatinine. These results show that our patient had a low rate of NH4+ excretion, a low urine minus blood PCO2 difference in alkaline urine, and a low urinary citrate excretion, but only when he was severely acidotic. He failed to achieve a maximally low urine pH. These findings indicate that his renal acidification mechanisms were impaired in both the proximal and distal tubule, the result of his CAII deficiency.

Acidosis, Renal Tubular↗
PubMed1992

Hypokalemic paralysis associated with distal renal tubular acidosis.

A 68-year-old man had hydronephrosis due to ureteral stones for two months earlier and then increasing muscle weakness developed. A 30-year-old woman had rapidly progressive quadriparesis. In both cases, severe hypokalemia with metabolic acidosis was observed and the diagnosis of distal renal tubular acidosis was made. The former was considered to be an idiopathic incomplete form and the latter was a secondary complete form associated with Sjögren syndrome. Hypokalemic paralysis may occur as a complication of distal renal tubular acidosis.

Acidosis, Renal Tubular↗