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PubMed1983

Renal tubular acidosis.

In the past decade major advances in our understanding of renal tubular hydrogen ion secretion and bicarbonate reabsorption have provided new insight into the pathophysiology of renal tubular acidosis. Thus "fragment to fragment clings" and the number of disorders categorized within the syndrome grows, until we have come to know and name four types, with many subtypes. We hope this new perspective provides a basis for the physician to recognize renal tubular acidosis in its several forms so that an informed decision may be arrived at in choosing the best therapy. The physician may also be prepared to reasonably project the prognosis for each patient. We also hope that our detailed examination of renal acidification will provide a reference for delineation of new clinical expressions of acid-base disorders and kidney malfunction certain to be described in the years ahead.

Acid-Base Equilibrium↗
PubMed1996

The spectrum of endemic renal tubular acidosis in the northeast of Thailand.

We have previously reported a high prevalence of endemic renal tubular acidosis (EnRTA) in the northeast of Thailand, and our subsequent studies provided evidence that K deficiency exists in the same region. Since tubulointerstitial damage is associated with K deficiency, we postulate that this might be implicated in the pathogenesis of EnRTA and, if so, that a spectrum of tubulointerstitial abnormalities can be anticipated. In this study we evaluated renal acidification ability in 4 patients and in 11 of their relatives. We used a 3-day acid load (NH4Cl 0.1 g/kg/day) followed by 20 mg oral furosemide and monitored the maximal renal concentrating ability using water deprivation and intranasal 1-deamino-D-arginine vasopressin. The results showed that the subjects could be divided into three groups; normal relatives of the patients, those with suspected renal tubular acidosis, and patients with overt EnRTA who had chronic metabolic acidosis and a low rate of excretion of NH4+. The rate of excretion of K was very low (20 +/- 4 mmol/day) in patients with EnRTA and in their relatives with suspected EnRTA. The transtubular K concentration gradient was also very low in their relatives, especially in patients with suspected EnRTA (2.8 +/- 0.2). With a 3-day NH4Cl load, the rate of excretion of NH4+ was very low in patients with EnRTA (32 +/- 9 mmol/day), and the relatives with suspected EnRTA also had a decreased capacity to excrete NH+4 (50 +/- 14 mmol/day). In contrast, the normal relatives excreted 92 +/- 12 mmol of NH+4/day. The patients with EnRTA could lower their urine pH to less than 5.5 after the acid loading (6.2 +/- 0.3). After furosemide (20 mg), the NH4+ excretion in the patients with EnRTA was lower than in the normal relatives. Moreover, the minimum urine pH in patients with EnRTA did not fall (6.1 +/- 0.2), but there was a fall to 4.8 +/- 0.1 in the patients with suspected EnRTA after furosemide treatment. In conclusion, there was a spectrum of tubulointerstitial abnormalities ranging from suspected to overt distal RTA in a geographic area known to have a high prevalence of K deficiency. K deficiency might be the important pathogenetic factor of EnRTA in the northeast of Thailand.

Acidosis, Renal Tubular↗
PubMed1993

Sporadic distal renal tubular acidosis and periodic hypokalaemic paralysis in Kashmir.

Twenty-one cases of renal tubular acidosis presenting with periodic hypokalaemic muscular weakness, that were seen over an 8-year period, are presented. The biochemical features suggested a diagnosis of distal renal tubular acidosis and absence of family history with negative screening of eighteen families pointed towards the primary sporadic nature of the disorder in nineteen of the cases. Alkali and replacement potassium therapy resulted in immediate and sustained clinical recovery in all the cases.

Acidosis, Renal Tubular↗
PubMed1984

Effect of furosemide on urinary acidification in distal renal tubular acidosis.

Furosemide stimulates urinary acidification in normal humans probably by increasing distal Na delivery and transport, thus creating a favorable electric gradient for H+ and K secretion. Therefore, furosemide should stimulate urinary acidification in patients with distal renal tubular acidosis, provided the distal nephron is capable of transporting Na and the H+ pumps can respond to the favorable electric gradient. We examined the effect of short-term furosemide administration on urinary acidification in five normal participants and 12 patients with normokalemic, hypokalemic, or hyperkalemic distal renal tubular acidosis. In controls, furosemide decreased urine pH and increased net acid and K excretion. In six of eight patients with normokalemic or hypokalemic renal tubular acidosis, furosemide decreased urine pH and increased net acid and K excretion to levels not significantly different from control values. The patients that had normal responses were interpreted as having a rate-dependent or gradient distal renal tubular acidosis, and thus increased distal Na delivery created a favorable electric gradient for H+ and K secretion. The normokalemic patients who did not have a response were considered to have a defect in the pumps (secretory defect). Of the four hyperkalemic patients, two had a voltage-dependent defect and the other two had aldosterone deficiency. The patients with selective aldosterone deficiency had low baseline urine pH values that did not change with furosemide administration, but net acid and K excretion did increase significantly. The patients with voltage-dependent defect did not lower urine pH or increase net acid and K excretion. Our data demonstrate that administration of furosemide enhances urinary acidification in certain patients with distal renal tubular acidosis. We suggest that furosemide administration may be useful in the characterization of the mechanism responsible for distal renal tubular acidosis and in the treatment of distal renal tubular acidosis in selected patients.

Acidosis, Renal Tubular↗
PubMed1976

Renal tubular acidosis: practical guides to diagnosis and treatment.

The syndrome of renal tubular acidosis in some one of its various forms should be suspected when an infant or child has failure to thrive, metabolic acidosis, constipation, diarrhea, vomiting, anorexia, polyuria, or dehydration in infancy. Confirmatory biochemical findings include an inappropriately high urinary pH, inadequate acid excretion and/or abnormal tubular reabsorption of filtered bicarbonate. Growth can be normal when there is sustained correction of the metabolic acidosis through appropriate alkaline therapy.

Acidosis, Renal Tubular↗
PubMed1998

[A young woman with metabolic acidosis and recently discovered IDDM without ketonuria. A rare autoimmune (?) combination of hypothyroidism, diabetes mellitus and distal renal tubular acidosis].

A case of a 29-year-old woman with a multiple autoimmune disorder is reported. She had a history of hypothyroidism since the age of 18. She was admitted to hospital due to hyperglycaemia. At admission she had hyperglycaemia, metabolic acidosis, but no urinary ketone bodies. Further laboratory studies revealed that the acidosis was due to distal renal tubular acidosis rather than diabetic ketoacidosis (although the patient had type 1 diabetes mellitus). Blood tests revealed antibodies to glutamic acid decarboxylase (GAD-65; associated with type 1 diabetes mellitus), thyroid and adrenal tissue, and gastric parietal cells. The patient had not developed pernicious anaemia or Addison's disease. The multiple positive antibody titres in this patient indicate that the diabetes, hypothyroidism and distal renal tubular acidosis are part of an autoimmune syndrome.

Acidosis, Renal Tubular↗
PubMed2002

Novel ATP6V1B1 and ATP6V0A4 mutations in autosomal recessive distal renal tubular acidosis with new evidence for hearing loss.

Autosomal recessive distal renal tubular acidosis (rdRTA) is characterised by severe hyperchloraemic metabolic acidosis in childhood, hypokalaemia, decreased urinary calcium solubility, and impaired bone physiology and growth. Two types of rdRTA have been differentiated by the presence or absence of sensorineural hearing loss, but appear otherwise clinically similar. Recently, we identified mutations in genes encoding two different subunits of the renal alpha-intercalated cell's apical H(+)-ATPase that cause rdRTA. Defects in the B1 subunit gene ATP6V1B1, and the a4 subunit gene ATP6V0A4, cause rdRTA with deafness and with preserved hearing, respectively. We have investigated 26 new rdRTA kindreds, of which 23 are consanguineous. Linkage analysis of seven novel SNPs and five polymorphic markers in, and tightly linked to, ATP6V1B1 and ATP6V0A4 suggested that four families do not link to either locus, providing strong evidence for additional genetic heterogeneity. In ATP6V1B1, one novel and five previously reported mutations were found in 10 kindreds. In 12 ATP6V0A4 kindreds, seven of 10 mutations were novel. A further nine novel ATP6V0A4 mutations were found in "sporadic" cases. The previously reported association between ATP6V1B1 defects and severe hearing loss in childhood was maintained. However, several patients with ATP6V0A4 mutations have developed hearing loss, usually in young adulthood. We show here that ATP6V0A4 is expressed within the human inner ear. These findings provide further evidence for genetic heterogeneity in rdRTA, extend the spectrum of disease causing mutations in ATP6V1B1 and ATP6V0A4, and show ATP6V0A4 expression within the cochlea for the first time.

Acidosis, Renal Tubular↗
PubMedDate not supplied

Secondary erythrocytosis in distal renal tubular acidosis: report of one case.

The wide spectrum of distal renal tubular acidosis (RTA) has been reported. Children with distal RTA can present with failure to thrive, gastrointestinal symptoms, nephrocalcinosis, and renal failure, etc. So far, secondary erythrocytosis in pediatric patients with distal RTA has not been reported. Here we report a case of distal RTA with failure to thrive and nephrocalcinosis accompanied by secondary erythrocytosis in a 3-year-old boy. He has been followed up for 2 years and is under treatment with NaHCO3 and potassium citrate. The treatment contributes to the improvement of metabolic acidosis and his growth. There is normal renal function and constant erythrocytosis during the follow-up period. Further studies are needed to clarify the relationship between erythrocytosis and distal RTA.

Acidosis, Renal Tubular↗
PubMedDate not supplied

[Latent renal tubular acidosis of the cirrhotic patient. Study of urinary excretion of protons and sodium].

Patients suffering from hepatic cirrhosis develop renal tubular acidosis when subjected to an acid overload. This is characterised by a fall in plasma pH and bicarbonate and by inability of the kidney to lower urine pH and to excrete a sufficient quantity of protons in the form of titratable acidy and ammonia. This disturbance is difficult to explain. It may form part of the picture of the classical functional renal insufficiency of the cirrhotic and may be a particular result of altered renal haemodynamics. Detected by the acidification test, this abnormality may be demonstrated in the absence of any other involvement of renal function. The severity of this renal tubular acidosis would appear to be related to the degree of hepatic disease.

Acidosis, Renal Tubular↗
PubMed2000

Systemic lupus erythematosus presenting initially as hydrogen ATPase pump defects of distal renal tubular acidosis.

Tubulointerstitial involvement is well recognized in systemic lupus erythematosus. The tubular dysfunction is usually latent and usually presents after diagnosis of systemic lupus erythematosus. We report a case presenting that she is well previously and initially diagnosed as periodic paralysis of hypokalemia at emergency room and final diagnosis is systemic lupus erythematosus with H+-ATPase pump defect of distal type renal tubular acidosis. Kidney biopsy showed lupus nephritis classified as mesangial proliferative glomerulonephritis WHO class II B. Her renal tubular acidosis was subsided after steroid therapy was administered.

Acidosis, Renal Tubular↗
PubMed2000

Systemic lupus erythematosus presenting initially as hydrogen ATPase pump defects of distal renal tubular acidosis.

Tubulointerstitial involvement is well recognized in systemic lupus erythematosus. The tubular dysfunction is usually latent and usually presents after diagnosis of systemic lupus erythematosus. We report a case presenting that she is well previously and initially diagnosed as periodic paralysis of hypokalemia at emergency room and final diagnosis is systemic lupus erythematosus with H+-ATPase pump defect of distal type renal tubular acidosis. Kidney biopsy showed lupus nephritis classified as mesangial proliferative glomerulonephritis WHO class II B. Her renal tubular acidosis was subsided after steroid therapy was administered.

Acidosis, Renal Tubular↗
PubMed1992

Renal tubular acidosis in children treated with trimethoprim-sulfamethoxazole during therapy for acute lymphoid leukemia.

The antibiotics trimethoprim (TMP) and sulfamethoxazole (SMZ), when used in combination, can cause metabolic acidosis, renal bicarbonate wasting, and growth failure. Retrospective review of repeated random serum chemistries from 10 children receiving TMP-SMZ and maintenance chemotherapy for acute lymphoid leukemia revealed low serum bicarbonate (P = .0002) and elevated serum chloride (P less than .0005) concentrations. These values normalized after all medications were discontinued. Prospective study of 8 children receiving TMP-SMZ and chemotherapy for acute lymphoid leukemia revealed lower serum bicarbonate concentrations and higher urine pH following a dose of TMP-SMZ than paired values obtained more than 3 days after a dose. Four children (50%) met serum bicarbonate and urinary pH criteria for the diagnosis of renal tubular acidosis soon after a dose of TMP-SMZ. The occurrence of TMP-SMZ-induced renal tubular acidosis has implications for the acid-base balance of children receiving TMP-SMZ on a long-term basis.

Acidosis, Renal Tubular↗