Cases reported "Acidosis, Renal Tubular"

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1/10. calculi complicating a renal transplant.

    Four months after a cadaver kidney transplant, kidney stones were found in the renal allograft. Three major predisposing causes of nephrolithiasis were found in the patient, including hyperparathyroidism, renal tubular acidosis, and urinary tract infection. hypercalcemia was corrected by parathyroidectomy. During the subsequent three years there was no enlargement of the renal stones and adequate kidney function was maintained. Renal tubular acidosis was not severe and seemed to be related to chronic rejection. urinary tract infection was readily corrected with antibiotics and did not recur after the immediate post-transplant period. Surgical therapy for nephrolithiasis involving a kidney allograft was defferred since urinary flow was not obstructed. This course of management is recommended for use in patients with calculi complicating renal transplantation.
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2/10. Long-term follow-up in distal renal tubular acidosis with sensorineural deafness.

    A 20-year-old man presented with failure to thrive and bilateral genu valgum. On the basis of growth failure, skeletal deformity, hyperchloremic metabolic acidosis with alkaline urine and hypokalemia, nephrocalcinosis, and hearing loss, a diagnosis of distal renal tubular acidosis (DRTA) with sensorineural deafness was made. The genu valgum was treated by corrective osteotomy. Skeletal deformity was corrected and impaired growth improved after sustained therapy of metabolic acidosis with alkali supplementation. During an 8-year follow-up period the patient's glomerular filtration rate remained stable, the nephrocalcinosis did not progress, and his height increased 10 cm. Although nephrolithiasis led to atrophy of the right kidney, at last follow-up, when the patient was 44 years old, his creatinine clearance was 50 ml/min per 1.73 m2 body surface.
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keywords = nephrolithiasis
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3/10. Atypical distal renal tubular acidosis confirmed by mutation analysis.

    In autosomal dominant distal renal tubular acidosis type I (dRTA) impaired hydrogen ion secretion is associated with metabolic acidosis, hyperchloremic hypokalemia, hypercalciuria, nephrocalcinosis, and/or nephrolithiasis. A retardation of growth is commonly observed. In this report we present a family with autosomal dominant dRTA with an atypical and discordant clinical picture. The father presented with severe nephrocalcinosis, nephrolithiasis, and isosthenuria but metabolic acidosis was absent. His 6-year-old daughter, however, suffered from metabolic acidosis, hypokalemia, and hypercalciuria. In addition, sonography revealed multiple bilateral renal cysts but no nephrocalcinosis. Mutation analysis of the AE1 gene coding for the renal Cl-/HCO3(-)-exchanger AE1 displayed a heterozygous Arg589Cys exchange in both patients but not in the healthy family members. This point mutation is frequently associated with autosomal dominant dRTA. Diagnosis of autosomal dominant dRTA is supported in this family by results of AE1 mutation analysis.
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keywords = nephrolithiasis
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4/10. Calcium nephrolithiasis and distal tubular acidosis in type 1 glycogen storage disease.

    A 36-year-old man was admitted to hospital due to right flank pain as a result of ureteral stones. He had been followed up for type 1 glycogen storage disease since the age of 11 years. He had four episodes of spontaneous stone birth during the previous 2 years, and each stone was composed mainly of calcium oxalate. Intravenous pyelography showed right hydronephrosis due to ureteral stones and bilateral multiple renal stones. We carried out transurethral ureterolithotripsy (TUL) on the right ureteral stones. The composition was a mixture of calcium oxalate and calcium phosphate. Laboratory evaluation demonstrated the association of distal renal tubular acidosis (RTA). These observations suggest that hypocitraturia and distal RTA are strongly correlated to recurrence of calcium nephrolithiasis. The patient's serum uric acid and urinary citrate excretion levels normalized after allopurinol and potassium citrate administration.
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ranking = 2.5
keywords = nephrolithiasis
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5/10. Molecular investigation and long-term clinical progress in Greek Cypriot families with recessive distal renal tubular acidosis and sensorineural deafness due to mutations in the ATP6V1B1 gene.

    The spectrum of distal renal tubular acidosis (dRTA) includes a genetically heterogeneous group of inherited conditions of both autosomal-dominant and recessive mode of inheritance. The basic defect is linked to the renal part of acid-base homeostasis, which is partly achieved by the regulated luminal secretion of H at the apical surface of the alpha-intercalated cells of renal collecting ducts. This is coupled to bicarbonate reabsorption with chloride counter transport across the basolateral membranes. Here, we describe the molecular findings of the first two Greek Cypriot families with recessive dRTA and the long-term clinical findings in four of five affected members. dna linkage analysis with four polymorphic markers flanking the ATP6V1B1 gene on chromosome 2 gave evidence for positive linkage; direct dna analysis by automated dna sequencing revealed that patients in one family were homozygous for mutation 229 1G>T (IVS7 1G>T) and that patients in the second family were compound heterozygous for 229 1G>T and R157C. The mutations were found on four different haplotypes. Both the mutations were previously reported in patients of Turkish origin. Three known polymorphic variants were also identified. The five patients demonstrated the whole clinical spectrum of the disease including death in infancy, failure to thrive, rickets, nephrocalcinosis, nephrolithiasis, and episodes of hypokalemic paralysis. Some of the family members are now in their mid 30s and late 20s, and nephrolithiasis with recurrent renal colics is their main problem. Renal function has remained normal. In conclusion, early diagnosis in infancy and prompt treatment with alkali and potassium supplements is of great benefit to the patient with dRTA and ensures normal growth. The identification of responsible mutations facilitates antenatal or postnatal diagnosis in concerned families and improves the prognosis.
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ranking = 1
keywords = nephrolithiasis
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6/10. nephrocalcinosis in sjogren's syndrome: a late sequela of renal tubular acidosis.

    sjogren's syndrome (SS) is an autoimmune exocrinopathy that develops into systemic autoimmune disease in 25% of patients, leading to general complications, one of which is kidney involvement. It presents mainly as interstitial nephritis, disclosed by hyposthenuria, distal renal tubular acidosis (RTA) and diabetes insipidus. We here describe five cases of SS with type-1 RTA (hyperchloraemic metabolic acidosis with an anion gap and alkaline urine pH) who developed nephrolithiasis, nephrocalcinosis and renal insufficiency. hypercalciuria due to acidosis was the main nephrocalcinosis-prone factor in four patients; four subjects displayed diminished renal concentrating capacity, and two had hypokalaemia.
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keywords = nephrolithiasis
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7/10. Hypocitraturic and hypercalciuric renal tubular acidosis with nephrocalcinosis in a 4-year-old boy.

    A 4-year-old boy suffering from hypocitraturic and hypercalciuric renal tubular acidosis with nephrolithiasis and nephrocalcinosis is reported. Renal function tests indicated that the patient had type 1 renal tubular acidosis. potassium citrate rather than potassium bicarbonate, sodium citrate or bicarbonate is the preferred treatment for stones in RTA-I.
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ranking = 0.5
keywords = nephrolithiasis
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8/10. Hypokalemic paralysis in sjogren's syndrome secondary to renal tubular acidosis.

    A 62-year-old woman with sjogren's syndrome, distal renal tubular acidosis and hypokalemic muscle paralysis is described. The sicca syndrome was nearly subclinical and went unrecognized for several years. The main and first manifestation to be expressed was that of hypokalemic muscle paralysis secondary to renal tubular acidosis. In the last decade several reports have appeared indicating that renal tubular acidosis is associated with sjogren's syndrome. The data in this report support the view that adult onset distal renal tubular acidosis is often a disorder of an autoimmune disease, frequently that of sjogren's syndrome. The complications to renal tubular acidosis such as hypokalemic muscle paralysis or chronic muscle weakness, nephrolithiasis, and osteomalacia can be avoided if the diagnosis of renal tubular acidosis is made and corrective alkali therapy is maintained.
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ranking = 0.5
keywords = nephrolithiasis
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9/10. Complete distal renal tubular acidosis in systemic lupus: clinical and laboratory findings.

    We report two patients with systemic lupus erythematosus (SLE) who were found to have complete (acidotic) distal renal tubular acidosis (DRTA). One patient had nephrocalcinosis and renal magnesium wasting with tetany; the other patient had nephrolithiasis and nephrotic syndrome secondary to membranous glomerulopathy. Both patients had decreased urinary citrate excretion but neither had hypercalciuria. We discuss the association of DRTA with immunologic disorders and the possible role of hypocitraturia in promoting renal calcification in these patients. We suggest that patients with renal calcification be evaluated for DRTA, and that patients found to have DRTA be further evaluated for signs, symptoms, and laboratory evidence of immunologic disorders.
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ranking = 0.5
keywords = nephrolithiasis
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10/10. Hypercalciuric rickets: a rare cause of nephrolithiasis.

    An unusual case of rickets associated with hypercalciuria is described. In addition to proteinuria, the patient had phosphaturia, aminoaciduria, renal glucosuria and impaired renal concentration but no renal tubular acidosis. Studies did not support the diagnosis of primary hyperparathyroidism. The findings in the patient were very similar to those in 4 previously reported cases and are suggestive of a new combination of multiple renal tubular defects.
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ranking = 2
keywords = nephrolithiasis
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