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PubMed1996

[Primary distal renal tubular acidosis coexisting with malabsorption syndrome].

The authors present the case of 54-old man primary tubular acidosis coexisting with malabsorption syndrome. Deviation were: extension of QT interval, low level of potassium and calcium in the blood, perturbations of calcium metabolism and high level of PTH. Glucose, lactose and iron absorption curves were flat. The final diagnosis was given as a result of analysis of findings and literature. The patient underwent the vitamin D3, calcium and potassium preparations, hydrochlorotiazyd treatment. Megaloblastic anaemia was treated with vitamin B12 and folic acid. Such therapy gave considerable improvement in patient's general condition and normalisation of lab tests results. The authors try explain the etiopathogenesis of bones changes and high level of parathormone. They assume the attitude towards methods of therapy and necessary medicaments doses. Relationship between described syndromes remains inextricable. Roentgen image of ileum which suggests occlusion is still unexplainable. Described case seemed to be very interesting considering rarity of primary tubular acidosis and its coexistence with malabsorption syndrome.

Acidosis, Renal Tubular↗
PubMed1989

Familial distal renal tubular acidosis with neurosensory deafness: early nephrocalcinosis.

Nephrocalcinosis was observed in 3 children of one family with distal renal tubular acidosis (dRTA). At presentation, all 3 patients had failure to thrive, rickets, hyperchloremic metabolic acidosis, hypokalemia, hypophosphatemia and hypercalciuria. At a later age, sensorineural hearing impairment was detected. Nephrocalcinosis was diagnosed in the index case at the age of 5 years, when a plain abdominal roentgenogram was first made; in the younger brother and sister, nephrocalcinosis was detected earlier at the age of 4 months and 5 weeks, respectively. All 3 patients required large doses of alkali (7.5-9.5 mEq/kg body weight/day) during infancy and early childhood to correct the acidosis and to prevent progression of the nephrocalcinosis. Contrary to the current notion that in children with dRTA, nephrocalcinosis is observed only after the age of 3 years, it appears that in some instances nephrocalcinosis may develop in early infancy. The occurrence of nephrocalcinosis at a very young age may be a manifestation of a severe genetically transmitted variant of dRTA and emphasizes the need for early diagnosis and optimal treatment of these patients from the first days of life.

Acidosis, Renal Tubular↗
PubMed1978

Attainment and maintenance of normal stature with alkali therapy in infants and children with classic renal tubular acidosis.

Growth was evaluated in a group of 10 infants and children with familial or idiopathic classic renal tubular acidosis in whom alkali therapy was initiated at ages ranging from 8 days to 9.5 yr and administered at dosage schedules documented to sustain correction of acidosis in at least four prolonged observation periods on the Pediatric Clinical Research Ward. When alkali therapy was begun, six patients (four infants and two children) were stunted (height <2.5 SD below mean). Of the four who were not, two infants were too young (<2 wk of age) to have become stunted, and two children had been documented earlier to be nonacidotic. At the start of alkali therapy, the heights of the patients correlated inversely with the maximal possible duration of prior acidosis. WITH SUSTAINED ALKALI THERAPY: (a) each patient attained and maintained normal stature; (b) the mean height of the 10 patients increased from the 1.4+/-4 to the 37.0+/-33 percentile (of a normal age- and sex-matched population); (c) the mean height reached the 69th percentile in the eight patients whose heights could be analyzed according to parental prediction (Tanner technique); (d) the rate of growth increased two- to threefold, and normal heights were attained within 6 mo of initiating alkali therapy in the stunted infants and within 3 yr in the stunted children; (e) the height attained correlated inversely with the maximal possible duration of acidosis (before alkali therapy) only in those patients in whom alkali therapy was started after 6 mo of age, and not in those treated earlier. The amount of alkali required to sustain correction of acidosis increased substantially during the course of treatment in each patient. The maximal alkali requirement ranged from 4.8 to 14.1 meq/kg per day, and in each patient its amount was determined principally by the magnitude of renal bicarbonate wasting.

Acidosis, Renal Tubular↗
PubMed1982

Dysfunction of the proximal tubule underlies maleic acid-induced type II renal tubular acidosis.

To investigate whether dysfunction of the proximal tubule underlies maleic acid-(MA) induced type II ("proximal") renal tubular acidosis (RTA II), we intravenously administered either MA or acetazolamide to eight conscious trained dogs undergoing water diuresis and examined the relationship between fractional solute-free water clearance (Ch2o/GFR), a measure of NaCl reabsorption in the post-proximal nephron, and either fractional urine flow (V/GFR), a measure of total solute rejected by the proximal tubule, or the sum of fractional excretion of Cl- and Ch2o/GFR [(Ccl + Ch2o)/GFR], a measure of proximally rejected solute that is potentially reabsorbable by the thick ascending limb. When MA or acetazolamide induced brisk bicarbonaturia at normal plasma bicarbonate concentrations: 1) V/GFR, (Ccl + Ch20)GFR, and Ch2o/GFR increased strikingly; 2) at any increment of Ch2o/GFR ws not; 3) the increments of V/GFR correlated positively with those of fractional excretion of bicarbonate (P less than 0.001); 4) during hyperchloremic acidosis, MA-induced bicarbonaturia was greatly attenuated; the increment in V/GFR was halved and approximated that in Ch20/GFR, which was unchanged; 5) when plasma bicarbonate was abruptly increased, bicarbonaturia increased strikingly and V/GFR increased further but Ch20/GFR and aminoaciduria did not. We conclude that MA induces a reduction in the net rate at which the proximal tubule reabsorbs HCO-3, Na+, and Cl-. This dysfunction underlies RTA II and evokes greatly increased reabsorption of Cl- and Na+ in the post-proximal tubule.

Acetazolamide↗
PubMed1998

Correction of renal tubular acidosis in carbonic anhydrase II-deficient mice with gene therapy.

Carbonic anhydrase II (CAII) deficiency in humans is associated with a syndrome of renal tubular acidosis, osteopetrosis, and cerebral calcification. A strain of mice of CAII deficiency due to a point mutation also manifests renal tubular acidosis. We report here that retrograde injection of cationic liposome complexed with a CAII chimeric gene, using a cytomegalovirus (CMV) promoter/enhancer as an expression cassette to drive human CAII cDNA, into the renal pelvis of CAII-deficient mice results in expression of CAII in the kidney. The levels of both the CAII gene and its corresponding mRNA were highest by day 3 after treatment, diminishing thereafter, but remaining detectable by 1 mo. After gene therapy, CAII-deficient mice restored the ability to acidify urine after oral administration of ammonium chloride. The ability to acidify urine was maintained at 3 wk after gene therapy, and was eventually lost by 6 wk. Immunohistochemistry studies using anti-CAII antibodies showed that CAII was expressed in tubular cells of the outer medulla and corticomedullary junction. The gene therapy was not associated with nephrotoxicity as assessed by blood urea nitrogen levels and renal histology. To our knowledge, this is the first successful gene therapy of a genetic renal disease. Our results demonstrate the potential of gene therapy as a novel treatment for hereditary renal tubular defects.

Acidosis, Renal Tubular↗
PubMed1982

Distal renal tubular acidosis with intact capacity to lower urinary pH.

The sine qua non for the diagnosis of distal renal tubular acidosis requires that the urinary pH cannot decrease maximally during systemic acidosis. A defect in distal acidification however, could also result from a decrease in the capacity (or rate) of distal hydrogen ion secretion. In this type of defect, the ability to lower the urinary pH during acidemia could be preserved as long as a certain capacity for hydrogen ion secretion remained. In this report, we describe four patients with deranged distal urinary acidification, in whom urinary pH was able to decrease (4.99 +/- 0.11) during acidemia. One of the patients had hyperchloremic metabolic acidosis whereas the remaining three were not spontaneously acidotic. In these patients, the defect for distal urinary acidification was disclosed by the inability of the urine-blood pCO2 gradient to increase normally (i.e., above 30 mm Hg) during bicarbonate loading. In contrast, a normal increase in the urine-blood pCO2 gradient was observed in each patient in response to neutral sodium phosphate infusion. The reabsorptive capacity of bicarbonate was not depressed in these patients, which indicated that the acidification process in the proximal nephron was intact. We propose that our four patients had a defect in distal urinary acidification caused by a reduction in the rate of distal hydrogen ion secretion rather than an inability to generate a steep pH gradient across the distal nephron. Our data also suggest that the inability to raise urinary pCO2 normally during sodium bicarbonate loading may be the most sensitive index of decreased distal urinary acidification available.

Acidosis, Renal Tubular↗