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At least 451 records · Page 25Linked to original sources
PubMed1993

Renal tubular acidosis preceding systemic lupus erythematosus.

A 10-year-old girl with distal renal tubular acidosis (RTA) for 4 years (adequately treated for 3 years) developed clinical features suggesting systemic lupus erythematosus (SLE) with supportive laboratory evidence. She had heavy proteinuria and a decreased creatinine clearance (CCr). Renal biopsy showed diffuse proliferative and sclerosing glomerulonephritis with severe tubulointerstitial changes. Following treatment with corticosteroids and cyclophosphamide, she had a clinical remission, an increase in CCr and recovery from systemic acidosis. It is likely that distal RTA in this patient was a manifestation of SLE.

Acidosis, Renal Tubular↗
PubMed1991

Distal renal tubular acidosis as the initial manifestation of systemic lupus erythematosus in an adolescent.

Distal renal tubular acidosis (dRTA) as the initial manifestation of systemic lupus erythematosus (SLE) has not been described previously. We report a 14-year-old female adolescent, first presenting with findings consistent with dRTA, whose renal biopsy demonstrated immune mesangial deposits consistent with lupus nephritis. Seven months later, she developed classic extrarenal manifestations of SLE. We recommend that adolescents with dRTA be evaluated and followed closely for the possibility of SLE.

Acidosis, Renal Tubular↗
PubMed1984

Dental features in congenital persistent renal tubular acidosis of proximal type.

The dental features in a hitherto unknown type of renal tubular acidosis (capillary blood pH 7.07-7.15) of proximal type are reported. The patient presented agenesis of three second premolars, delayed development and eruption of permanent teeth, delayed shedding of the primary dentition and severe enamel hypoplasia of the permanent teeth. Apart from exceptionally thin enamel, histologic, fluorescent and polarization microscopic and microradiographic investigation of three primary teeth did not reveal unusual findings. The changes are most probably due to a generalized, acidosis-induced defect in several highly differentiated ectodermal tissues.

Acidosis, Renal Tubular↗
PubMed1995

Hearing impairment in association with distal renal tubular acidosis among Saudi children.

A follow-up of seven patients with the autosomal recessive inherited syndrome of distal renal tubular acidosis (RTA) and sensorineural hearing loss is described. Five patients were diagnosed as having primary distal renal tubular acidosis and rickets, four were found to have severe sensorineural hearing loss of over 80 dB: two of which are brothers. Two patients were diagnosed as having secondary distal renal acidosis due to a genetic disorder called osteopetrosis; they are brothers and their audiograms showed a mild conductive hearing loss of an average 35 dB bilaterally. All patients had growth retardation with improvement due to alkaline therapy but their hearing loss was not affected by the medication. The pedigrees of two families with half sibs showed the familial incidence for consanguineous marriage. Consanguinity was found to be positive in five out of the seven patients. The tribal tradition in Saudi Arabia fosters consanguineous marriages for cultural and social reasons and pre-arranged marriages are still seen.

Acidosis, Renal Tubular↗
PubMed2003

ATP6B1 gene mutations associated with distal renal tubular acidosis and deafness in a child.

A large proportion of autosomal recessive distal renal tubular acidosis (RTA) is associated with mutations in the ATP6B1 gene encoding the B1 subunit of H+-ATPase. H+-ATPase is one of the key membrane transporters for net acid excretion in the alpha-intercalated cells of the medullary collecting duct. Sensorineural hearing loss frequently accompanies this type of distal RTA. Mutational analysis of the ATP6B1 gene in a 9-year-old Korean boy with distal RTA and sensorineural hearing loss found 2 heterozygous missense point mutations. Although a single case report, this is the second report documenting ATP6B1 mutations in recessive distal RTA with sensorineural hearing loss after the original report by Karet et al and confirms the novelty of these mutations.

Acidosis, Renal Tubular↗
PubMed1984

Renal tubular acidosis induced by dietary chloride.

Previous studies have demonstrated that dietary intake of anions with high renal reabsorbability (Cl- greater than SO4=) can result in either exacerbation of chronic metabolic acidosis or correction of chronic metabolic alkalosis. These results, however, fail to predict the renal acid-base response to Cl- administration when systemic acid-base composition is initially normal, but accompanied by an extracellular fluid (ECF) volume-mediated renal avidity for Cl- reabsorption; that is, the renal options include HCl retention, KCl retention, and phosphaturia. Accordingly, the present metabolic balance studies evaluated the response to substitution of dietary Cl- (2.5 mEq/kg/day) for Pi in five dogs previously ECF-depleted with diuretics and maintained on a dietary K+ supplement, 5.0 mEq/kg daily as neutral Pi (electrolyte-free diet) during a steady-state control period. Dietary Cl- resulted in a decrease in arterial plasma [HCO3-] from 21.2 +/- 0.7 to 17.8 +/- 0.8 mEq/liter, (P less than 0.01) and increase in [H+] from 38.5 +/- 0.7 to 43.3 +/- 0.8 nEq/liter (P less than 0.001). Urine pH increased (P less than 0.01), the cumulative change in net acid excretion decreased (-79 mEq, P less than 0.05), and Cl- retention (39 mEq, P less than 0.05) occurred. No change in Na+, K+, or Pi excretion occurred. The renal acidosis was fully corrected when SO4= was substituted for dietary Cl- and redeveloped when Cl- was resubstituted . Superimposition of a large oral buffer load (creatinine) did not ameliorate Cl- -induced renal acidosis. The results indicate that dietary reabsorbable anions can result in renal acidosis when Cl- reabsorption is stimulated and suggest that anion reabsorbability characteristics and not anion buffer properties are responsible.

Acid-Base Equilibrium↗