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At least 235 records · Page 13Linked to original sources
PubMed1993

Immune-related potassium-losing interstitial nephritis: a comparison with distal renal tubular acidosis.

Six patients with immune-related potassium-losing interstitial nephritis (IRPLIN) are described, and compared with 34 patients with immune-related distal renal tubular acidosis (IRdRTA) and 24 with familial distal renal tubular acidosis (FdRTA). Close similarities were found between IRPLIN and IRdRTA. In our experience, both syndromes are confined to postpubertal women, and are characterized by systemic features of autoimmune disease and a chronic interstitial nephritis which is probably immune-mediated and responsible for the functional tubular defects of the two syndromes. In IRPLIN, a renal potassium-losing state is the main consequence (probably mediated at least in part by renin and aldosterone hypersecretion secondary to renal sodium-losing), and urinary acidification is normal or minimally disturbed; consequently there is no systemic acidosis, and the syndrome is not complicated by nephrocalcinosis or renal bone disease. In IRdRTA, the renal tubular lesion also usually causes potassium depletion, but the most prominent tubular fault is a defect in urinary acidification, which commonly causes metabolic acidosis and often leads to nephrocalcinosis and bone disease. Familial dRTA, in contrast, is equally prevalent in the two sexes and presents at an earlier age than IRPLIN and IRdRTA. Patients with FdRTA and IRdRTA have a similar urinary acidification defect and propensity to acidosis, nephrocalcinosis and bone disease. FdRTA is frequently complicated by renal potassium-losing, but hypokalaemia is less common and less profound than in IRdRTA and IRPLIN, suggesting that immune-related interstitial nephritis has a particular tendency to cause renal potassium-losing.

Acidosis, Renal Tubular↗
PubMed2000

Renal tubular acidosis associated with zonisamide therapy.

PURPOSE: We sought to report a previously undescribed adverse effect, renal tubular acidosis associated with zonisamide (ZNS) therapy. METHODS: Ammonium chloride, bicarbonate, and furosemide loading tests were performed in an epileptic patient with metabolic acidosis and episodic hypokalemia who was treated with ZNS. RESULTS: Distal renal tubular acidosis was diagnosed. On reexamination 7 weeks after ZNS had been replaced with phenytoin, the renal tubular acidosis disappeared. CONCLUSIONS: This case indicates, for the first time, that ZNS might be a potential cause of renal tubular acidosis. Blood gases and serum electrolytes should be measured in patients undergoing ZNS therapy.

Acidosis, Renal Tubular↗
PubMed1975

Evidence for mild reversible hyperparathyroidism in distal renal tubular acidosis.

Circulating levels of immunoreactive parathyroid hormone were measured in six patients with distal renal tubular acidosis before and during two years of long-term alkali therapy. Parathyroid hormone level was elevated modestly in five patients before treatment and fell, gradually during treatment to normal or near normal levels. Urine calcium level fell, serum calcium level rose, and renal phosphorus reabsorption rose during treatment. Stopping treatment briefly caused reversion of serum parathyroid hormone and calcium levels and renal phosphorus reabsorption to pretreatment values within eight weeks. Mild hyperparathyroidism is present in renal tubular acidosis and reverses with alkali treatment.

Acidosis, Renal Tubular↗
PubMed1997

Hyperammonaemia with distal renal tubular acidosis.

The case is reported of an infant with hyperammonaemia secondary to severe distal renal tubular acidosis. A clinical association between increased concentrations of ammonia in serum and renal tubular acidosis has not previously been described. In response to acidosis the infant's kidneys presumably increased ammonia synthesis but did not excrete ammonia, resulting in hyperammonaemia. The patient showed poor feeding, frequent vomiting, and failure to thrive, but did not have an inborn error of metabolism. This case report should alert doctors to consider renal tubular acidosis in the differential diagnosis of severely ill infants with metabolic acidosis and hyperammonaemia.

Acidosis, Renal Tubular↗
PubMed1991

Evaluation of carbonic anhydrase isozymes in disorders involving osteopetrosis and/or renal tubular acidosis.

Carbonic anhydrase II (CA II) deficiency in man is an autosomal recessive disorder manifest by osteopetrosis, renal tubular acidosis, and cerebral calcification. Other features include growth failure and mental retardation. Complications of the osteopetrosis include frequent bone fractures, cranial nerve compression symptoms, and dental malocclusion. The anemia and leukopenia seen in the recessive, lethal infantile form of osteopetrosis are not seen in CA II deficient patients. The renal tubular acidosis usually includes both proximal and distal components. Symptoms of metabolic acidosis respond to therapy, but no specific treatment is available for the osteopetrosis or cerebral calcification. We review here the role of carbonic anhydrases in bone resorption and renal acidification, and discuss clinical features and laboratory findings which distinguish CA II deficiency from other disorders producing osteopetrosis, renal tubular acidosis, or brain calcification. Methods to evaluate patients with pure proximal renal tubular acidosis for deficiency of CA IV are also discussed.

Acidosis, Renal Tubular↗
PubMed1980

A case of incomplete renal tubular acidosis (type 1) associated with medullary sponge kidney followed by nephrocalcinosis.

A case is reported of incomplete renal tubular acidosis (type 1) associated with medullary sponge kidney followed by nephrocalcinosis. Although several cases of classic renal tubular acidosis associated with medullary sponge kidney have been documented a case of incomplete renal tubular acidosis associated with medullary sponge kidney seems to be rare. We recommend examination for incomplete renal tubular acidosis in patients with medullary sponge kidney and nephrocalcinosis without systemic acidosis.

Acidosis, Renal Tubular↗
PubMed1975

Incomplete syndrome of renal tubular acidosis induced by lithium carbonate.

Renal acidification was studied in 10 control subjects and 15 lithium carbonate-treated psychiatric patients of similar age. Seven lithium-treated patients were unable to lower urine pH normally after short duration acid-loading (Li-1:5.35 to 6.25), while 8 (Li-ll:4.52 to 5.17) did not differ from control subjects (4.49 to 5.07). Li-l patients excreted significantly less titratable and net acid than the other groups. Baseline urine pH was higher in both lithium-treated groups than in control subjects, and although this was due in part to the carbonate moiety of the medication, the abnormal minimal urine pH of Li-l patients was not carbonate-dependent. Li-l patients had normal arterial pH and bicarbonate concentrations, trival bicarbonaturia, and no evidence of generalized proximal tubular dysfunction. These data demonstrate that lithium therapy can induce the syndrome of incomplete distal renal tubular acidosis at serum lithium concentrations within the accepted therapeutic range.

Acidosis, Renal Tubular↗
PubMed1979

Improvement of hypercalciuria, potassium wasting and hyperreninemia in incomplete distal renal tubular acidosis by indomethacin.

A patient with incomplete distal renal tubular acidosis (RTA) demonstrated hypercalciuria, potassium wasting and hyperreninemia. Indomethacin administration resulted in sustained improvement of these abnormalities. The results suggest that overproduction of prostaglandins contributes to hypercalciuria, potassium wasting and hyperreninemia in some patients with RTA and that indomethacin may be useful in treating patients with this disorder.

Acidosis, Renal Tubular↗
PubMed1996

Renal tubular acidosis and deafness: report of a large family.

The syndrome of distal renal tubular acidosis (dRTA) and sensorineural deafness has been reported in consanguineous families and is believed to be inherited in an autosomal recessive pattern. All affected patients also have nephrocalcinosis. We report here a family with 6 of 12 children affected with this syndrome. The parents are unaffected and are not blood related. This is the largest family described to date with distal renal tubular acidosis and sensorineural deafness.

Acidosis, Renal Tubular↗
PubMed1971

Renal potassium wasting in renal tubular acidosis (RTA): its occurrence in types 1 and 2 RTA despite sustained correction of systemic acidosis.

IN TWO PATIENTS WITH CLASSIC RENAL TUBULAR ACIDOSIS (RTA) AND IN TWO PATIENTS WITH RTA ASSOCIATED WITH THE FANCONI SYNDROME, RENAL POTASSIUM WASTING PERSISTED DESPITE SUSTAINED CORRECTION OF ACIDOSIS: (a) during moderate degrees of hypokalemia, daily urinary excretion of potassium exceeded 80 mEq in each patient; (b) during more severe degrees of hypokalemia, daily urinary excretion of potassium exceeded 40 mEq in two patients and 100 mEq in another. These urinary excretion rates of potassium are more than twice those observed in potassium-depleted normal subjects with even minimal degrees of hypokalemia. The persistence of renal potassium wasting may have resulted in part from hyperaldosteronism, since urinary aldosterone was frankly increased in two patients and was probably abnormally high in the others relative to the degree of their potassium depletion. The hyperaldosteronism persisted despite sustained correction of acidosis, a normal sodium intake, and no reduction in measured plasma volume, and was not associated with hypertension; its cause was not defined. In the two patients with classic RTA, neither renal potassium wasting nor hyperaldosteronism could be explained as a consequence of a gradient restriction on renal H(+) - Na(+) exchange because the urinary pH remained greater than, or approximately equal to, the normal arterial pH or considerably greater than the minimal urinary pH attained during acidosis. The findings provide no support for the traditional view that renal potassium wasting in either classic RTA or RTA associated with the Fanconi syndrome is predictably corrected solely by sustained correction of acidosis with alkali therapy.

Acidosis, Renal Tubular↗
PubMed1976

Improvement in lacrimal and salivary secretions after alkali therapy in Sjøgren's syndrome with renal tubular acidosis.

A patient with Sjøgren's syndrome developed renal tubular acidosis which led to systemic acidosis and potassium depletion. Treatment with Shohl's solution and potassium supplements was followed by subjective improvement in tear flow, salivary flow, and by disappearance of bronchitic symptoms. Detailed objective assessments were then made during the next year, twice on treatment and twice without. These confirmed the subjective impression of improvement.

Acidosis, Renal Tubular↗
PubMed1993

Type IV renal tubular acidosis associated with Alport's syndrome.

A case of hereditary nephritis with mild reduction of renal function associated with renal tubular acidosis type IV is described. The patient was admitted with life-threatening hyperkalaemia. To our knowledge, type IV renal tubular acidosis has not been reported previously in association with Alport's syndrome in an adult patient.

Acidosis, Renal Tubular↗
PubMed1993

Urine-to-blood carbon dioxide tension gradient and maximal depression of urinary pH to distinguish rate-dependent from classic distal renal tubular acidosis in children.

We determined the prevalence and clinical features of rate-dependent distal renal tubular acidosis (dRTA) in 31 children examined for possible renal tubular acidosis by measuring the urinary-minus-blood partial pressure of carbon dioxide (U-B PCO2) gradient, minimal urinary pH, and fractional excretion of bicarbonate. Of 20 patients with low U-B PCO2 gradients, nine could not lower urinary pH < or = 5.5, indicating classic dRTA, whereas 11 could lower urinary pH < or = 5.5, as described in rate-dependent dRTA. When patients with rate-dependent dRTA and classic (type I) dRTA were compared, there was no difference in the mean U-B PCO2 gradient or in clinical findings, including age, reason for referral, presence of nephrocalcinosis, or depression of linear growth. We conclude that children with rate-dependent dRTA are susceptible to at least some of the same sequelae as children with classic dRTA. Measurement of minimal urinary pH will not detect this subtle form of dRTA. Determination of the U-B PCO2 gradient should be considered a routine part of evaluation for suspected renal tubular acidosis in a child.

Acidosis, Renal Tubular↗
PubMed1975

Proximal renal tubular acidosis in vitamin D deficiency rickets.

A proximal renal tubular acidosis (RTA) is the mechanism underlying the systemic acidosis found in vitamin D deficiency rickets. Acidotic subjects have high levels of PTH. In non-acidotic subjects proximal bicarbonate wasting can be induced by exogenous PTH injection. Carbonic anhydrase activity is not involved in this process. Calcium infusion is able to suppress both the spontaneous and the PTH-induced bicarbonate leak. The development of RTA in vitamin D deficiency is related to a particular equilibrium between two antagonizing factors at tubular level, parathyroid hormone and calcium.

Acetazolamide↗
PubMed1997

Distal renal tubular acidosis and hereditary elliptocytosis in a single family.

Distal renal tubular acidosis (RTA) and hereditary elliptocytosis (HE) are apparently distinct, genetic conditions. We report a family with 3 children having both hereditary elliptocytosis and distal renal tubular acidosis. The simultaneous occurrence of these two conditions in three siblings could be due to covariations in the same family, although a possible contiguous gene syndrome for distal RTA and HE cannot be excluded. This report emphasises the importance of excluding a renal tubular defect in any child who presents with elliptocytosis and failure to thrive.

Acidosis, Renal Tubular↗