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PubMed1994

[ESWL in renal tubular acidosis].

ESWL is a suitable modality for the management of lithiasis caused by RTA, especially in case of renal or ureteric stones. Smash of calculi in ducts of Bellini is worthy to be considered if the fragments can get into the renal pelvic space and the renal function improve. At present it is still a matter of discussion.

Acidosis, Renal Tubular↗
PubMed1980

Renal tubular acidosis and sensorineural deafness: an autosomal recessive syndrome.

This is the first known reported case of autosomal recessive syndrome of renal tubular acidosis and sensorineural deafness in the otorhinolaryngological literature. Ten cases in six families have been reported in the pediatric literature. Most cases manifested at birth or soon after with vomiting, dehydration, polydipsia, polyuria, hyposthenuria, and failure to thrive. Renal tubular acidosis is a clinical syndrome of disordered acidification out of proportion to the impairment of glomerular filtration, and is associated with alkaline urine. Sensorineural deafness is variable and, in most cases, present in early childhood.

Acidosis, Renal Tubular↗
PubMed1983

Pathogenetic relationships between renal tubular acidosis and sodium metabolism alterations in liver cirrhosis.

5 cirrhotic patients with latent distal renal tubular acidosis (RTA) and 5 cirrhotic patients with normal distal acidification ability were studied. All the patients were maintained on a 80 mEq/day sodium diet for at least 5 days before the study. Only 2 of the 5 patients with RTA showed a reduced daily sodium excretion while the 3 other patients with RTA had a normal natriuresis. Acidification ability was retested in all the patients after increasing sodium distal delivery by intravenous administration of ethacrynic acid. Some hours after the maximal natriuretic effect induced by ethacrynic acid, a normalization of the acidification test was seen in all patients with RTA. These findings support the concept that although sodium metabolism alterations are not the only factor in the pathogenesis of RTA in liver cirrhosis, reduced availability of sodium at the distal tubule may impair tubular acidification, probably by influencing the distal transtubular potential difference.

Acidosis, Renal Tubular↗
PubMed2005

Acute respiratory failure due to hypokalaemic muscular paralysis from renal tubular acidosis.

We report a case of hypokalaemic quadriplegia with acute respiratory failure and life-threatening cardiac arrhythmias in a 26-year-old woman who was diagnosed to have distal renal tubular acidosis. She had persistent metabolic acidosis with severe hypokalaemia and required mechanical ventilation and potassium replacement. The anaesthetic implications of renal tubular acidosis are also discussed.

Acidosis, Renal Tubular↗
PubMed1990

[Urolithiasis due to renal tubular acidosis associated with Sjögren's syndrome].

We encountered 4 patients with urolithiasis due to renal tubular acidosis (RTA) associated with Sjögren's syndrome. Laboratory results about RTA in 4 patients with Sjögrenhs syndrome were not significantly different from those in patients who suffered from urolithiasis due to RTA without Sjögren's syndrome. The incidence of urolitiasis in these cases was suspected to be higher than that in RTA patients without Sjögren's syndrome, because all 4 patients in this study had urolithiasis. When we examine patients with bilateral and multiple urolithiasis, particularly in middle-aged women, we should bear in mind that RTA and Sjögren's syndrome may exist in the background.

Acidosis, Renal Tubular↗
PubMed1986

Renal tubular acidosis in children. Diagnosis, treatment and prognosis.

To delineate the spectrum of clinical expressions of distal, type 1 renal tubular acidosis in children and to update progress in diagnosis, therapy, and prognosis, the medical records of 14 girls and 10 boys, seen over a 7 year period, who met the following criteria, were examined: persistent urinary pH more than 6, net acid excretion less than 70 microEq/min/1.73 m2, simultaneous serum total CO2 less than 17.5 mEq/1, and normal or mild impairment of the glomerular filtration rate. The mean age at diagnosis was 8 months. The presenting signs and symptoms were failure to thrive (50%), vomiting and/or diarrhea (37.5%), dehydration (12.5%), and poor feeding (8.3%). Mean values +/- SD of serum calcium (9.8 +/- 0.8 mg/dl), inorganic phosphate (5.6 +/- 0.8 mg/dl), and alkaline phosphatase (222.6 +/- 96.1 U/l) were normal. Hyperkalemia (serum potassium above 5.0 mEq/l) was present at diagnosis in 13 children. Type 4 renal tubular acidosis was ruled out by the inability to achieve a minimum urine pH. With a mean follow-up period of 28.1 +/- 25.3 months, after alkali therapy at 3.3-3.5 mEq/kg/day had been administered for at least 12 months, the growth parameters improved as follows: the percentile weight (mean +/- SD) increased from the initial 11.8 +/- 7.5 to the final 27.6 +/- 31.3 (p less than 0.003), and the length/height percentile increased from 11.5 +/- 7.3 to 29.7 +/- 24.2 (p less than 0.03). The relationship between urine calcium/creatinine ratio and serum total CO2 showed poor correlation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed1987

A study of immune responses to Tamm-Horsfall glycoprotein in the sera of patients with renal tubular acidosis.

Antibody to Tamm-Horsfall glycoprotein in the sera of patients with distal renal tubular acidosis (dRTA) was measured by radioimmunoassay, as well as in samples of normal human serum. Normal human serum contains small amounts of IgG capable of interacting with Tamm-Horsfall glycoprotein. Appropriate assays were carried out on antiserum raised in rabbits against human Tamm-Horsfall glycoprotein serially diluted with normal human serum. Corrections were applied for the presence of interfering substances in serum. The amounts of antibody found in samples of normal and patient sera were not significantly different, although some of the patients were diagnosed as having immune as opposed to familial dRTA. Studies of cell-mediated immunity to Tamm-Horsfall glycoprotein was found not to differentiate between the normal and patient samples. dRTA does not appear to be associated with immune responses to Tamm-Horsfall glycoprotein.

Acidosis, Renal Tubular↗
PubMed1989

An in vivo study of voltage-dependent renal tubular acidosis induced by amiloride.

It has been proposed that most forms of hyperkalemic distal renal tubular acidosis (dRTA) result from a voltage-dependent acidification defect in the cortical collecting tubule (CCT) in which hydrogen and potassium secretion are decreased secondary to a reduced, transepithelial potential difference (PD) arising from impaired sodium reabsorption. The present in vivo study examines one model of hyperkalemic dRTA, induced by chronic amiloride administration, to examine the relationship between urinary excretion of hydrogen and potassium ions and CCT PD in the rat kidney. Chronic administration of amiloride produced a significant metabolic acidosis with a plasma bicarbonate of 21.3 mmol/liter compared to 25.9 mmol/liter in control rats. Plasma potassium was higher in experimental animals (4.9 mmol/liter vs. 3.3 mmol/liter in controls) and was associated with a significantly reduced fractional excretion of potassium of 11.2% versus 37.4% in controls. When animals were loaded with DOCA and infused with 4% sodium sulphate to maximize urine acidification, urine pH was significantly higher in the experimental group (6.35 vs. 5.55 in controls) while the mean PD in cortical collecting tubules was markedly lower at -21.1 mV versus -58.9 mV in controls. These results support a voltage dependent mechanism to explain the defect in hydrogen and potassium ion secretion induced by amiloride.

Acidosis, Renal Tubular↗
PubMed2003

A de novo R589C mutation of anion exchanger 1 causing distal renal tubular acidosis.

Anion exchanger 1 (AE1 or SLC4A1) mutations have been reported to cause distal renal tubular acidosis (dRTA), a disease characterized by impaired acid excretion in the distal nephron. We have recently demonstrated homozygous AE1 G701D mutation as a common molecular defect of autosomal recessive (AR) dRTA in a group of Thai pediatric patients. In the present work, we discovered a de novo heterozygous AE1 R589C mutation, previously documented in inherited autosomal dominant (AD) dRTA. Arginine at this position is conserved in all vertebrate AE proteins indicating its functional importance. Three different mutations at this position (R589C, R589H, and R589S) were all found in AD dRTA and a de novo R589H mutation has previously been recorded. Our report is the second de novo mutation but with a different substituted amino acid. A high prevalence of AE1 R589 mutations and the presence of at least two de novo mutations at this position lead us to propose that codon 589 (CGC) is a "mutational hotspot" of AE1. The mechanism of recurrent mutations probably involves methylation and deamination altering cytosine (C) to thymine (T) in the CpG dinucleotides.

Acidosis, Renal Tubular↗
PubMed1986

Renal tubular acidosis.

The clinical features and biochemical profile of 10 patients with Renal Tubular Acidosis (RTA) were described. The commonest mode of presentation was muscular weakness due to severe hypokalaemia in 5 patients while the other 5 presented with renal colic, haematuria or passage of gravel. Nine patients had nephrocalcinosis on X-rays and one had rickets. All the patients had Type I RTA, 2 of whom presenting initially with Incomplete Type I RTA which progressed to Complete Type I RTA. Two other patients had associated features of proximal tubular involvement evidenced by hypophosphatemia, hypouricemia, hyperphosphaturia, aminoaciduria and glycosuria. Six of the 10 patients had secondary RTA: 2 associated with medullary sponge kidneys, 2 with gout, 1 with idiopathic hypercalciuria and hyperuricosuria and the remaining patient with systemic lupus erythematosus.

Acidosis, Renal Tubular↗