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PubMed1995

A study of recurrent stone formers with special reference to renal tubular acidosis.

Forty-five patients with recurrent renal stone were examined for distal renal tubular acidosis (dRTA) defects by acid challenge test (150 mg ammonium chloride/kg body weight). Their 24-h urine samples were analysed for creatinine, calcium, oxalic acid, inorganic phosphorus, uric acid, magnesium and citric acid. One-hour urine samples before acid load and hourly samples for the 7 h following acid challenge test were collected and analysed for creatinine, calcium, citric acid, inorganic phosphorus, titratable acidity, and ammonium. The incidence of distal RTA defect was 22.2% in the patients examined. The major biochemical characteristics in RTA patients compared with patients without RTA were: (a) significantly higher urinary pH, (b) significantly lower excretion of citric acid, (c) no significant difference in calcium excretion and (d) a tendency toward lower titratable acidity and ammonium excretion.

Acidosis, Renal Tubular↗
PubMed1992

Renal potassium wasting in distal renal tubular acidosis: role of aldosterone.

The pathogenesis of renal potassium wasting and hypokalemia in classic renal tubular acidosis (type 1 RTA) remains uncertain. The prevailing theory is that K(+)-Na+ exchange is stimulated due to an inability of the distal tubule to establish a normal steep lumen-peritubular H+ gradient. We encountered a 42-year-old woman with type 1 RTA associated with Sjögren's syndrome, in whom renal potassium wasting and hypokalemia persisted despite sustained correction of systemic acidosis with alkali therapy and increased intake of potassium. In addition, plasma renin activity was markedly increased and the serum aldosterone level was upper-normal despite the hypokalemia. Increased intake of sodium resulted in suppression on the serum aldosterone and correction of renal potassium wasting and hypokalemia. This case shows that secondary hyperaldosteronism, possibly due to an impairment of sodium conservation in the distal tubule, may contribute to the loss of potassium from the distal tubule even after the correction of acidosis.

Acidosis, Renal Tubular↗
PubMed1996

Renal tubular acidosis in children with vesicoureteral reflux.

PURPOSE: We evaluated renal tubular acidosis in children with primary vesicoureteral reflux. MATERIALS AND METHODS: We studied 18 children 4 to 15 years old to determine age at onset, reflux intensity, and renal scars and volume as possible associated factors of renal tubular acidosis. Patients had normal glomerular filtration rates and no urinary infections for the last 12 weeks, and they had not undergone urological surgery. Urine acidification and alkalization tests were done, and the Mann-Whitney U test was used to assess differences between the groups with and without renal tubular acidosis. RESULTS: A total of 14 patients had unilateral and 4 had bilateral reflux, which varied in severity. All children except 2 had renal scarring. Bilateral renal volume was smaller in the renal tubular acidosis group. Nine patients had distal renal tubular acidosis, including 4 with short stature. CONCLUSIONS: Several patients with vesicoureteral reflux had renal tubular acidosis and some had growth failure. Grades of reflux and renal scarring were similar in patients with and without renal tubular acidosis. A single evaluation of reflux is of slight value for predicting future functional tubular impairment, and the duration of reflux and other associated factors may be more important. Renal tubular acidosis was the main explanation for growth failure in these patients.

Acidosis, Renal Tubular↗
PubMed1983

Renal tubular acidosis. A new look at treatment of musculoskeletal and renal disease.

The clinical and laboratory manifestations, roentgenographic findings, and treatment of 48 patients with renal tubular acidosis who were examined at the Mayo Clinic during a 10-year period were reviewed. The initial clinical presentations of the 48 patients in the series included rheumatic complaints in 25 and recurrent nephrolithiasis in 23. Of the 23 patients who presented with nephrolithiasis, 8 also had musculoskeletal symptoms. Thirty-three of the 48 patients had careful follow-up of a total of 68 musculoskeletal complaints. Forty of these symptoms (59%) diminished after treatment of the renal tubular acidosis with orally administered alkali. Associated connective tissue diseases were present in 12 patients. Thirty-four patients had roentgenographic evidence of renal calculi. Of this group, 19 were followed up with sequential roentgenographic studies of the kidneys for more than 1 year during therapy. Of 15 patients treated orally with alkali, 13 had metabolically inactive renal stone disease. Three of the patients treated orally with phosphorus supplements had persistent metabolically active renal stone disease. Patients with renal tubular acidosis often present with musculoskeletal manifestations and renal lithiasis, both of which frequently subside with the treatment of the renal tubular acidosis.

Acidosis, Renal Tubular↗
PubMed2004

Mutational and functional analysis of SLC4A4 in a patient with proximal renal tubular acidosis.

Permanent isolated proximal renal tubular acidosis (pRTA) with ocular abnormalities is a systemic disease with isolated pRTA, short stature and ocular abnormalities. We identified a novel homozygous deletion of nucleotide 2,311 adenine in the kidney type Na+/HCO3- cotransporter (kNBC1) cDNA in a patient with permanent isolated pRTA. This mutation is predicted to result in a frame shift at codon 721 forming a stop codon after 29 amino acids anomalously transcribed from the SLC4A4 gene. Cosegregation of this mutation with the disease was supported by heterozygosity in the parents of the affected patient. The absence of this mutation in 156 alleles of 78 normal individuals indicates that this mutation is related to the disease and is not a common DNA sequence polymorphism. When injected into Xenopus oocytes, the mutant cRNA failed to induce electrogenic transport activity. In addition, immunofluorescence and Western blot analysis failed to detect the expression of the full-length protein in mutant-injected oocytes. Our results expand the spectrum of kNBC1 mutations in permanent isolated pRTA with ocular abnormalities and increase our understanding of the renal tubular mechanism that is essential for acid-base homeostasis.

Acidosis, Renal Tubular↗
PubMed1986

Pseudohypoaldosteronism type II: proximal renal tubular acidosis and dDAVP-sensitive renal hyperkalemia.

The mechanisms of metabolic acidosis and hyperkalemia were investigated in a patient with chronic mineralocorticoid-resistant renal hyperkalemia (5.3-6.9 mmol/l), metabolic acidosis (arterial blood pH 7.27, total CO2 17 mmol/l), arterial hypertension, undetectable plasma renin activity (less than 0.10 ng/ml/h), high plasma aldosterone level (32-100 ng/dl), and normal glomerular filtration rate (131 ml/min/1.73 m2). During the hyperkalemic period, urine was highly acidic (pH 4.6-5.0), urinary NH4 excretion (10-13 microEq/min) and urinary net acid excretion (19-24 microEq/min) were not supernormal as expected from a chronic acid load. During NaHCO3 infusion, the maximal tubular HCO3 reabsorption was markedly diminished (19.8 mmol/l glomerular filtrate), and the fractional excretion of HCO3 (FE HCO3) when plasma HCO3 was normalized was 20%. Urine minus blood PCO2 increased normally during NaHCO3 infusion (31 mm Hg), and the urinary pH remained maximally low (less than 5.3) when the buffer urinary excretion sharply increased after NH4Cl load. When serum K was returned toward normal limits, metabolic acidosis disappeared, urinary NH4 excretion rose normally after short NH4Cl loading while the urinary pH remained maximally low (4.9-5.2), the maximal tubular HCO3 reabsorption returned to normal values (24.8 mmol/l glomerular filtrate), and FE HCO3 at normal plasma HCO3 was 1%. Nasal insufflation of 1-desamino-8-D-Arginine Vasopressin (dDAVP) resulted in an acute normalization of the renal handling of K and in an increase in net urinary acid excretion. We conclude that: the effect of dDAVP on renal handling of K may be explained by the reversal of the distal chloride shunt and/or an increase in luminal membrane conductance to K; the distal acidification seems to be normal which in the event of distal chloride shunt impairing distal hydrogen secretion might be explained by the presence of systemic acidosis which is a potent stimulus of hydrogen secretion, and metabolic acidosis in the steady state was accounted for by the diminution of bicarbonate reabsorption and ammonia production in the proximal tubule secondary to chronic hyperkalemia.

Acid-Base Equilibrium↗
PubMed2005

Renal tubular acidosis: developments in our understanding of the molecular basis.

Renal tubular acidosis is a metabolic acidosis due to impaired acid excretion by the kidney. Hyperchloraemic acidosis with a normal anion gap and normal (or near normal) glomerular filtration rate, and in the absence of diarrhoea, defines this disorder. However, systemic acidosis is not always evident and renal tubular acidosis can present with hypokalaemia, medullary nephrocalcinosis and recurrent calcium phosphate stone disease, as well as growth retardation and rickets in children, or short stature and osteomalacia in adults. Renal dysfunction in renal tubular acidosis is not always confined to acid excretion and can be part of a more generalised renal tubule defect, as in the renal Fanconi syndrome. Isolated renal tubular acidosis is more usually acquired, due to drugs, autoimmune disease, post-obstructive uropathy or any cause of medullary nephrocalcinosis. Less commonly, it is inherited and may be associated with deafness, osteopetrosis or ocular abnormalities. The clinical classification of renal tubular acidosis has been correlated with our current physiological model of how the nephron excretes acid, and this has facilitated genetic studies that have identified mutations in several genes encoding acid and base ion transporters. In vitro functional studies of these mutant proteins in cell expression systems have helped to elucidate the molecular mechanisms underlying renal tubular acidosis, which ultimately may lead to new therapeutic options in what is still treatment only by giving an oral alkali.

Acidosis, Renal Tubular↗
PubMed1985

Long-term low-dose glucocorticoid therapy associated with remission of overt renal tubular acidosis in Sjögren's syndrome.

Renal tubular acidosis and focal interstitial inflammatory cell infiltrate secondary to Sjögren's syndrome remitted with low-dose glucocorticoid therapy over five and one half years in a patient with associated mild systemic lupus erythematosus. Such response has not been previously documented. This observation may have therapeutic applications for renal tubular acidosis associated with Sjögren's syndrome that deserve further investigation.

Acidosis, Renal Tubular↗
PubMed1985

Renal tubular acidosis secondary to jejunoileal bypass for morbid obesity.

Renal handling of acid and base was studied in patients with persistent metabolic acidosis 3-9 years after jejunoileal bypass for morbid obesity. Excretion of acid was studied before and after intravenous infusion of NH4Cl and excretion of bicarbonate after infusion of NaHCO3. Bypass patients showed impaired capacity for acidification of urine. The lowest urinary pH was 5.53 +/- 0.10 in 10 bypass patients and 4.76 +/- 0.06 in 6 controls. The corresponding values for standard bicarbonate in plasma were 15.0 +/- 0.3 mM and 15.8 +/- 0.3 mM. Glomerular filtration rate was identical in the two groups. Fractional loss of bicarbonate in urine was higher in controls than in bypass patients. The renal impairment is classified as distal renal tubular acidosis.

Acidosis, Renal Tubular↗
PubMed1977

Renal tubular acidosis due to the milk-alkali syndrome.

A 60-year-old man with a history of excessive ingestion of calcium carbonate presented with azotemia, hypercalcemia and hyperphosphatemia. His acid-base status was initially normal. Following the cessation of calcium carbonate treatment, the hypercalcemia and azotemia disappeared, and the patient was found to be in metabolic acidosis with blunted acid excretion and a urine pH of 6.1. Kidney biopsy showed focal tubular calcification; the tubular damage was apparently caused by hypercalcemia and had resulted in renal tubular acidosis. During the three months of observation since that time there has been a tendecy for spontaneous remission of the renal tubular acidosis. Impaired renal hydrogen ion excretion prevented the development of metabolic alkalosis despite ingestion of alkali initially, and was later responsible for the metabolic acidosis. Renal tubular acidosis occurring as a sequel to the milk-alkali syndrome may aggravate the danger of nephrocalcinosis in this syndrome.

Acidosis, Renal Tubular↗
PubMed2004

Acidosis increases magnesiuria in children with distal renal tubular acidosis.

In experimental animals, metabolic acidosis increases renal magnesium (Mg) excretion, whereas metabolic alkalosis reduces it. The objective of this study was to examine renal magnesium handling (U(Mg)) in children with primary distal renal tubular acidosis (DRTA). We measured U(Mg) in 11 children (3 females, 8 males, aged 6.9+/-4.9 years) with primary DRTA. They were studied either during spontaneous acidosis post treatment removal (3 patients) or after ammonium chloride (100 mmol/m2) induced acidosis (8 patients), and then following oral sodium bicarbonate load (4 g/1.73 m2). During acidosis (plasma pH 7.28+/-0.09, bicarbonate 13.2+/-4.3 mEq/l), U(Mg) was elevated (U(Mg/Cr) 0.18+/-0.06 mg/mg, normal values 0.1+/-0.06, P=0.003) although plasma Mg (P(Mg)) was in the normal range (1.93+/-0.31 mg/dl, controls 1.77+/-0.19, P=NS). After acute correction of metabolic acidosis (plasma pH 7.44+/-0.05, bicarbonate 25.6+/-1.6 mEq/l, P<0.001; urine pH 7.52+/-0.28, bicarbonate 86.9+/-39.1 mEq/l), U(Mg) decreased significantly (P=0.003), returning to control values after about 2 h (U(Mg/Cr) 0.09+/-0.06 mg/mg). Bicarbonate load resulted not only in reduction in U(Mg) but also in a decrease in urinary calcium excretion (U(Ca/Cr)) from 0.46+/-0.17 mg/mg to 0.14+/-0.12 mg/mg (P<0.001). We conclude that in children with primary DRTA, urinary Mg excretion is markedly increased and that this defect, like the hypercalciuric defect, is correctable by sodium bicarbonate administration.

Acidosis, Renal Tubular↗
PubMed1986

Severe osteomalacia associated with renal tubular acidosis in Crohn's disease.

Severe renal tubular acidosis associated with massive osteomalacia is described in a patient with Crohn's disease. To our knowledge this association has not been previously recognized. The possible role of renal tubular acidosis in this patient's osteomalacia is discussed and the factors that could be involved in renal tubular acidosis in the context of Crohn's disease are analyzed.

Acidosis, Renal Tubular↗
PubMedDate not supplied

Renal tubular acidosis in horses (1980-1999).

Renal tubular acidosis (RTA) is characterized by altered renal tubular function resulting in hyperchloremic metabolic acidosis. The purpose of the study was to describe RTA in 16 horses. No breed or sex predilection was found. The mean age at onset of the disease was 7 years of age. The type of diet had no apparent effect on development of RTA. The most common clinical signs were depression, poor performance, weight loss, and anorexia. Initial blood work revealed a marked hyperchloremic metabolic acidosis in all horses and a compensatory respiratory response in most horses. Sixty-three percent (10/16) of the horses had some evidence of renal damage or disease. Initial treatment consisted of large amounts of sodium bicarbonate given intravenously and orally for the prompt correction of the acidosis. Response to treatment was largely dependent on the rate of sodium bicarbonate administration. Long-term oral supplementation with NaHCO3 was required for the maintenance of normal acid-base status in individual horses. Recurrence of RTA was noted in 56% (9/16) of the horses. Horses with evidence of renal disease had multiple relapses. RTA should be considered as a differential diagnosis in horses with vague signs of depression, weight loss, and anorexia. The pathogenesis of RTA in horses remains uncertain, but prompt recognition and early aggressive intravenous sodium bicarbonate therapy followed by long-term oral supplementation seem to be important to successful management.

Acidosis, Renal Tubular↗
PubMed1992

Might distal renal tubular acidosis be a proximal tubular cell disorder?

Incomplete renal tubular acidosis (RTA) and overt distal RTA may be different stages of the same underlying pathophysiology in certain individuals. The rationale that draws these conditions together is the relatively alkaline pH of the urine, hypocitraturia, and a possible familial association. The rate of excretion of ammonium (NH4+), on the other hand, suggests that these conditions stem from fundamentally different lesions. To explain this difference, we suggest that two possible disorders may result in the evolution from incomplete RTA to overt distal RTA. One subgroup could have gradient-limited distal RTA, while the other subgroup may have a lower pH of the intracellular fluid of the proximal convoluted tubular epithelium. Indices of proximal intracellular pH (rates of excretion of NH4+, NH3, and citrate) were culled from the literature spanning the years 1959 to 1991 on patients with incomplete RTA and overt distal RTA. Three points emerge: (1) the rate of excretion of NH4+ was lower in patients with overt distal RTA than in normals following an acute acid load (23 +/- 1 v 49 +/- 3 mumol/min); (2) the concentration of NH3 in the urine was almost 25-fold higher in incomplete RTA than in normals (69 +/- 14 v 3 +/- 0.4 nmol/min); and (3) in incomplete RTA, the pH of the urine fell to very low values (4.9 +/- 0.1) when high urine flows were induced with furosemide. The low pH of the urine would therefore suggest that many of these patients do not gradient-limited distal RTA, but more likely have proximal renal epithelial cell acidosis. We hypothesize that this high rate of excretion of NH4+ and low rate of excretion of citrate in the absence of acidosis or hypokalemia is consistent with proximal cell acidosis. To explain a transition from incomplete RTA to overt distal RTA, we speculate that toxicity of high concentrations of NH3 in the medullary interstitium as well as nephrolithiasis and nephrocalcinosis due to low urinary citrate and possibly an alkaline medullary interstitium may lead to damage of structures in this region.

Acid-Base Equilibrium↗
PubMedDate not supplied

Nephrology rounds, University of Iowa Hospitals: renal tubular acidosis.

We have discussed two patients who had renal tubular acidosis complicated by hypokalemia. The first patient had a distal acidifying defect. Circumstantial evidence has been presented suggesting that exposure to toluene-diisocyanate or toluene-diamine played a role in the pathogenesis. The acidosis and the hypokalemia of this patient were easily corrected by the administration of small amounts of sodium bicarbonate without potassium supplementation. The second patient had an interstitial nephritis of unknown etiology and presented with moderate renal insufficiency, renal tubular acidosis, and proximal as well as distal acidifying defects. The proximal tubular dysfunction was associated with general aminoaciduria and glucosuria. This patient required large quantities of both alkali and potassium to correct the electrolyte abnormalities. The mechanisms of potassium wasting in proximal and distal renal tubular acidosis are reviewed. A classification is presented of cellular defects that may underlie the different renal acidifying defects. Attempts to distinguish between pump and permeability defects from urinary pCO2 levels must take into account the simultaneous HCO-3 concentration, since large pCO2 elevations require the presence of ample HCO-3 in the urine. Permeability defects may impair urinary acidification by either abnormal back flux of H+ out of the lumen or increased influx of HCO-3 into the lumen. In studies of acidification in vitro, amphotericin B causes increased H+ permeability and has little effect on HCO-3 permeability. Toluene-diamine causes a marked permeability defect which is reversible, but remains to be defined in terms of the ion species, HCO-3 or H+, affected. At times, hyperchloremic acidosis is caused by distal defects in net acid excretion that occur without impairment of the H+ gradient. In certain patients with hypoaldosteronism, for example, distal H+ secretion may be reduced without change in the force of the H+ pump.

Acidosis, Renal Tubular↗
PubMed1984

Amelioration of hyperchloremic acidosis with furosemide therapy in patients with chronic renal insufficiency and type 4 renal tubular acidosis.

In hypoaldosteronemic patients with chronic renal insufficiency, administration of a mineralocorticoid steroid such as fludrocortisone can ameliorate hyperkalemia and metabolic acidosis, but this therapy is not always safe owing to the deleterious consequences of extracellular fluid volume expansion resulting from mineralocorticoid-induced sodium chloride retention. In the present study of 8 patients with renal hyperchloremic acidosis, mild hyperkalemia and chronic glomerular insufficiency, we evaluated the therapeutic effect of chronic administration of a natriuretic/chloruretic agent, furosemide, a renoactive drug that is known to increase renal acid excretion in experimental animals without increasing body content of sodium chloride. 4 patients had hyporeninemic hypoaldosteronism. During 8 days of treatment in 6 patients who received furosemide alone, metabolic acidosis was significantly ameliorated. Urinary net acid excretion increased, except in the 2 patients who had the most severe hypoaldosteronism. For the group as a whole, the cumulative change in net acid excretion correlated positively with the rate of aldosterone excretion (r = 0.94, p less than 0.01). Thus, the aciduric response to furosemide is attenuated by aldosterone deficiency. When furosemide was administered in combination with fludrocortisone (4 subjects), an amelioration of metabolic acidosis occurred that was greater than that observed in the group treated with furosemide alone. Combined therapy ameliorated acidosis in the patient with the most severe degree of hypoaldosteronism, the same patient in whom administration of furosemide without fludrocortisone was ineffective even after 6 months of treatment. The findings in this study indicate that chronic furosemide therapy, alone or in combination with fludrocortisone, is a safe and effective means of ameliorating metabolic acidosis in patients with chronic renal insufficiency, including those with hypoaldosteronism.

Acidosis↗