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Results for “ACIDOSIS, RENAL TUBULAR”

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PubMed1989

[Primary hyperaldosteronism without arterial hypertension].

Treatment-resistant hypokalaemia (2.27 mmol/l) developed in a 43-year-old woman. Plasma renin activity was depressed (0.24 ng/ml.h), aldosterone and hydroxycorticosterone concentrations were elevated (123 ng/dl and 688 ng/dl, respectively). Mean blood pressure value (30 readings) was 133/88 mm Hg. An adrenal adenoma was diagnosed by ultrasound, computed tomography and subtraction angiography and then removed. Postoperatively the signs of hyperaldosteronism (Conn's syndrome) regressed and the average blood pressure was 112/76 mm Hg. Blood-gas analysis, which preoperatively had shown a minimal metabolic alkalosis, now revealed a mild metabolic acidosis. Preoperatively present bilateral renal calcifications in the region of the papillary tips were confirmed by computed tomography. An acid loading test revealed diminished renal acid secretion, making the diagnosis of distal renal-tubular acidosis. The latter, in combination with the primary hyperaldosteronism, may have been the cause of the low blood pressure, unusual in Conn's syndrome.

18-Hydroxycorticosterone↗

PubMed1987

Occurrence of renal tubular dysfunction in lupus nephritis.

We prospectively evaluated 30 patients who presented with active systemic lupus erythematosus (SLE) for the presence of tubular abnormalities. All patients fulfilled the American Rheumatology Association criteria for SLE. When appropriate, a renal biopsy was performed. Of the 30 patients studied, 12 had no abnormal tubular study results, whereas 18 patients had some form of defect in the handling of potassium, sodium, or hydrogen ions. Eight patients had distal renal tubular acidosis (dRTA) due to an isolated proton secretory defect. Five had dRTA of the gradient or acid back-leak type. Two had an unresponsive voltage-dependent form of dRTA; one had a responsive voltage-dependent form of dRTA. One individual had hyporeninemic hypoaldosteronism and one had dRTA plus hypoaldosteronism. Clinically, patients with the abnormal tubular study results more often presented with nephritis or nephrotic sediment, peripheral edema, or anemia. Renal biopsies failed to demonstrate any difference in glomerular histologic findings and calculated activity, chronicity, or interstitial indexes. We conclude that SLE may be associated with a variety of tubular defects.

Acidosis, Renal Tubular↗

PubMed2003

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.

Acidosis, Renal Tubular↗

PubMed1997

[Distal tubular acidosis in a patient with insulin dependent diabetes mellitus--selected pathophysiologic, diagnostic and therapeutic aspects].

This case report describes a 42 years old male patients with distal tubular renal acidosis in whom the symptomatology of this disorder was markedly changed by the presence of concomitant endocrine and exocrine insufficiency of the pancreas. Pathophysiological, diagnostic and therapeutic aspects of coexistence of these two type of pathology are stressed.

Acidosis, Renal Tubular↗

PubMed1985

Renal retinal dysplasia with diffuse glomerular cysts.

A 32-year-old male with renal retinal dysplasia is presented. He also showed hearing loss and growth retardation. Laboratory data showed mild proteinuria, renal dysfunction and type-1 renal tubular acidosis. Computed tomography showed multiple cysts at the corticomedullary junction of both kidneys. Ocular examinations disclosed retinitis pigmentosa. On light microscopy of renal biopsy specimens, diffuse cystic dilatation of Bowman's space as well as dilated tubules with interstitial fibrosis and cellular infiltration were noted. Electron microscopy revealed a peculiar chromatin condensation of epithelial cell nuclei in Bowman's capsules, glomeruli and tubules. The association of renal retinal dysplasia with diffuse glomerular cysts has not, to our knowledge, been previously reported.

Acidosis, Renal Tubular↗

PubMed1980

[Study of the renal tubular function in alcoholic hepatic cirrhosis (author's transl)].

The renal plasma flow (RPF), glomerular filtrate (GF), renal concentration strength and urinary acidification capacity in eight patients with alcoholic cirrhosis and five control subjects was studied. The maximum urinary acidification capacity was tested by means or arginine monochloride. In two patients, renal tubular acidosis (RTA) was observed. One patient manifested a slight decrease in RPF, GF, hyposthenuria, hyperchloremic metabolic acidosis and bicarbonaturia. The test for maintained acidification and the overload of bicarbonate indicated a mixed RTA. The other patient manifested incomplete distal RTA, which was briefly corrected with the administration of furosemide. These tubular defects were not associated with the loss of proteins, phosphates, glucose, aminoacids or renal lithiasis. Neither were they related to the serum levels of copper, globulins, or predisposition to hepatic encephalopathy. The association between hepatic cirrhosis and distal tubular acidosis is known, but until the present work, the fact that this hepatopathy can simultaneously affect the proximal and distal tubules had not been described.

Acidosis, Renal Tubular↗

PubMed1984

Medullary sponge kidney presenting with hypokalaemic paralysis.

Medullary sponge kidney associated with a defect in urine acidification is rare and usually of no clinical significance. We report a case presenting as hypokalaemic paralysis due to associated congenital distal renal tubular acidosis.

Acidosis, Renal Tubular↗

PubMed1991

Hyperechoic renal medullary pyramids in infants and children.

Fifty-five children (34 boys, 21 girls; age range, 1 day to 18 years) with increased echogenicity of the renal medullary pyramids at ultrasound evaluation were identified. The clinical diagnoses associated with hyperechoic medullary pyramids could be separated based on the presence or absence of hypercalciuria. Patients with drug-induced hypercalciuria included 10 infants treated with furosemide, two treated with long-term steroid therapy, and one treated with excessive amounts of vitamin D. Other clinical conditions associated with hypercalciuria included renal tubular acidosis (n = 10), Bartter syndrome (n = 5), hyperparathyroidism (n = 3), Williams syndrome (n = 2) and medullary sponge kidney (n = 2). Ten children with transient renal insufficiency and three with sickle cell disease had normal urine calcium concentration. Isolated disease entities accounted for the remainder of cases. A specific diagnosis can usually be made in a patient with hyperechoic renal medullary pyramids by using a systematic clinical approach that includes evaluation of patient age, serum and urine calcium concentration, and renal function.

Acidosis, Renal Tubular↗

PubMed1987

A case report and review of band keratopathy.

A five-year-old male presented with band keratopathy as the first sign of proximal renal tubular acidosis. The band keratopathy was progressive with decreasing visual acuity. Treatment with EDTA was repeated in each eye with only minimal improvement. The pediatric renal service found the serum calcium to be no higher than 10.5 mg% and phosphorus no higher than 6.8 mg%. The calcium-phosphorus product was in the range of 60-65. Band keratopathy can be visually incapacitating and has multiple etiologies. Factors other than elevated calcium concentrations must predispose to development of this disorder. Certain of these factors and a review of band keratopathy are presented in the following article.

Acidosis, Renal Tubular↗

PubMed1996

[A patient with Sjögren syndrome with central pontine myelinolysis and hypokalemic myopathy].

We report a 42-year-old woman who presented with intermittent episodes of muscular weakness lasting approximate 7 to 10 days, about once a year, since 1985. During these episodes of weakness, hypokalemia and elevation of serum creatine kinase were noted. On admission, xerostomia, keratoconjunctivitis sicca (positive Schirmer test), abnormal sialographic findings (apple tree-like appearance), and positive serum autoantibodies against ss-A and nucleus were noted. These findings were compatible with Sjögren syndrome. She also had hyperchloremic metabolic acidosis with normal anion gap, hypokalemia and renal calcifications. Therefore, she had renal tubular acidosis (type 1) in addition to Sjögren syndrome. Brain magnetic resonance imaging (MRI) demonstrated a symmetrical circumscribed lesion in the ventral part of the central pons. We considered this lesion to be central pontine myelinolysis (CPM), because of its typical location and characteristic MRI appearance. This CPM was clinically silent. Pathogenesis and etiology of CPM are obscure, and CPM associated with hypokalemia without hyponatremia has rarely been reported in the literature. However, this is the first report of CPM associated with Sjögren syndrome and hypokalemic myopathy complicated with renal tubular acidosis.

Acidosis, Renal Tubular↗

PubMed1992

Urinary acidification in renal stone patients from northeastern Thailand.

Hypokalemia, hypokaliuria and hypocitraturia are common findings in patients with renal stone disease in Northeastern Thailand. However, hyperchloremic metabolic acidosis seldom is seen. Therefore, we studied renal acidification in 29 renal stone disease patients who were living in rural Northeast Thailand. Baseline blood and average 24-hour urine biochemical parameters were measured. Hypokalemia, hypokaliuria and hypocitraturia were found in 10%, 83% and 93% of the patients, respectively. By multiple regression, urinary citrate excretion correlated positively with serum potassium and urinary potassium excretion, and negatively with urinary ammonium (r = 0.640, p = 0.005). An abnormal response to acid loading was found in only 1 patient. Thus, hypokaliuria and hypocitraturia in our renal stone disease subjects were infrequently due to distal renal tubular acidosis. Perhaps potassium depletion might be a contributing factor in these metabolic abnormalities.

Acidosis, Renal Tubular↗

PubMed1995

Nephrocalcinosis in newborn.

Nephrocalcinosis is uncommon in childhood, and almost always develops outside the newborn period. Over the last decade, nephrocalcinosis due to multifactorial pathogenesis has increased in very low birthweight infants. In this report a 23 day old full-term baby with nephrocalcinosis secondary to distal renal tubular acidosis is described.

Acidosis, Renal Tubular↗

PubMed1993

Carbonic anhydrase II deficiency.

Carbonic anhydrase (CA) isoenzyme II deficiency--formerly called the syndrome of osteopetrosis with renal tubular acidosis and cerebral calcification--is an autosomal recessive "inborn error of metabolism" that has disclosed important insight concerning osteoclast function. Nearly 50 cases have been described, predominantly from the Middle East and Mediterranean region. It is discovered late in infancy or early in childhood through developmental delay, short stature, fracture, weakness, cranial nerve compression, dental malocclusion, and/or mental subnormality. Typical radiographic features of osteopetrosis are present, and histopathologic study of the iliac crest reveals unresorbed calcified primary spongiosa. The radiographic findings are unusual, however, in that cerebral calcification appears by early childhood and the osteosclerosis and skeletal modeling defects may gradually resolve by adulthood. Patients are usually not anemic. A hyperchloremic metabolic acidosis, sometimes with hypokalemia, is caused by renal tubular acidosis that may be a proximal, distal, or combined type. Several different mutations within the CA II gene have been identified. There is no established medical therapy, and the long-term outcome remains to be characterized. Prenatal diagnosis has not been reported. Delineation of CA II deficiency establishes an important role in humans for CA II. The pathogenesis of the mental subnormality and cerebral calcification is poorly understood; however, CA II deficiency provides significant insight concerning CA II in renal regulation of acid/base homeostasis and osteoclast-mediated bone resorption.

Acidosis, Renal Tubular↗

PubMed2003

Predictive value of kidney stone composition in the detection of metabolic abnormalities.

PURPOSE: To determine if kidney stone composition can predict the underlying medical diagnosis, and vice versa. METHODS: We studied 1392 patients with kidney stones who underwent a complete ambulatory evaluation and who submitted one or more stones for analysis. We ascertained the associations between medical diagnosis and stone composition. RESULTS: The most common kidney stones were composed of calcium oxalate (n = 1041 patients [74.8%]), mixed calcium oxalate-calcium apatite (n = 485 [34.8%]), and calcium apatite alone (n = 146 [10.5%]). The most common medical diagnoses were hypocitraturia (n = 616 patients [44.3%]), absorptive hypercalciuria (n = 511 [36.7%]), and hyperuricosuria (n = 395 [28.4%]). Calcium apatite and mixed calcium oxalate-calcium apatite stones were associated with the diagnoses of renal tubular acidosis and primary hyperparathyroidism (odds ratios >/=2), but not with chronic diarrheal syndromes. As the phosphate content of the stone increased from calcium oxalate to mixed calcium oxalate-calcium apatite, and finally to calcium apatite, the percentage of patients with renal tubular acidosis increased from 5% (57/1041) to 39% (57/146), and those with primary hyperparathyroidism increased from 2% (26/1041) to 10% (14/146). Calcium oxalate stones were associated with chronic diarrheal syndromes, but not with renal tubular acidosis. Pure and mixed uric acid stones were strongly associated with a gouty diathesis, and vice versa. Chronic diarrheal syndromes and uric acid stones were associated with one another, and brushite stones were associated with renal tubular acidosis. As expected, there was a very strong association between infection stones and infection, and between cystine stones and cystinuria. CONCLUSION: Stone composition has some predictive value in diagnosing medical conditions, and vice versa, especially for noncalcareous stones.

Acidosis, Renal Tubular↗

PubMed1985

Phosphate loading attenuates renal tubular dysfunction induced by maleic acid in the dog.

The metabolic pathogenesis of the complex renal tubular dysfunction of type II renal tubular acidosis and Fanconi's syndrome (RTA II/FS) acutely induced by maleic acid could depend on the occurrence of a positive feedback loop in cells of the proximal renal tubule: impaired mitochondrial oxidation----increased glucose uptake----increased formation and concentration of phosphorylated glycolytic intermediates----limitation on availability of cellular inorganic phosphate----more severely impaired mitochondrial oxidative metabolism. To test this hypothesis we intravenously administered maleic acid both alone and after initiating intravenously administered neutral sodium phosphate, sodium sulfate, or sodium chloride to 10 unanesthetized trained female dogs undergoing water diuresis. We made the following observations: 1) Administration of maleic acid alone predictably induced dose-dependent increments in urine flow (V) and in renal clearance of HCO3-, Na+, K+, and alpha-aminonitrogen and a pronounced increase in the renal clearance and excretion of citrate. 2) Prior phosphate loading, which increased the plasma concentration of phosphate from 2.5 +/- 0.20 to 11.3 +/- 2 mg/dl: a) attenuated the increment in renal clearance of HCO3- by one-half even though the filtered load of bicarbonate was higher by 37%, owing to the higher values of both GFR and plasma bicarbonate concentration that obtained with phosphate loading; b) prevented the increment in renal clearance and excretion of alpha-aminonitrogen; c) significantly attenuated the increments in V and renal clearance of K+; but d) did not affect the increment in renal clearance and excretion of citrate.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗

PubMedDate not supplied

Acid-base transport in the collecting duct.

The collecting duct is responsible for the final secretion or reabsorption of protons and bicarbonate, respectively. Approximately 2% of the total filtered bicarbonate is reabsorbed in this segment. At least two different types of cells are involved in the transport of protons and bicarbonate, namely, type A and B intercalated cells. Their relative abundance differs in zonal distribution in the collecting duct. A variety of transport proteins and enzymes take part in the transcellular movement of protons and bicarbonate, some of them identified on a molecular level. These proteins are tightly regulated by hormones such as angiotensin II, aldosterone or endothelin or by the metabolic status of the organism. Alterations in acid-base intake or electrolyte status have profound effects on the collecting duct. Moreover, drugs interacting with renal electrolyte or bicarbonate handling (i.e. diuretics, glucocorticoids) also often affect acid-base transport in the collecting duct. For some of the identified proteins mutations have been found in various genetic diseases and syndromes of distal renal tubular acidosis leading to metabolic acidosis and an increased risk of nephrocalcinosis or -lithiasis.

Acidosis↗

PubMed1991

[The effect of metabolic acidosis on amino acid and keto acid metabolism in chronic renal failure].

The effect of metabolic acidosis (MA) on amino acid and keto acid metabolism was studied in fourteen patients with chronic renal failure (CRF) under the low protein diet (0.6-0.8 g/kgBW). The comparative study of five patients with renal tubular acidosis was carried out. Each patient was investigated before [MA(+)period] and after correction with sodium bicarbonate administration lasting 10 days [MA(-)period]. The correction of MA improved nitrogen balance and elevated plasma branched-chain amino acids (BCAA), keto acids (BCKA), glutamine and alanine concentrations. No effect was however, observed in change of plasma insulin and glucagon. Oral administration of the keto-analogues of BCKA [0.1 g/kgBW of alpha-ketoisovalerates (KIV) and alpha-keto-isocaproic acid (KIC)] is made for the purpose of investigating the change in the metabolic conversion rate to amino acids. As a result, MA (+) suppressed an increase in plasma KIV and KIC concentrations. Moreover, an increase in plasma valine and leucine concentrations were suppressed by MA (+). These results suggested that MA stimulates BCKA oxidation and suppresses the protein sparing effect of leucine and KIC, and accelerates the catabolism in CRF under the low protein diet. The correction of MA is ineffective in severe renal failure (serum creatinine above 10.0 mg/dl), because the other uremic factors appear to be affecting protein and amino acid metabolism. Therefore, it might be concluded that MA should be corrected at an earlier stage of CRF.

Acidosis, Renal Tubular↗

PubMed1986

Coordinately increased lysozymuria and lysosomal enzymuria induced by maleic acid.

During the acute renal tubular dysfunction of Fanconi syndrome and type 2 renal tubular acidosis (FS/RTA2) induced by maleic acid in the unanesthetized dog, we observed: 30 minutes after the onset of FS/RTA2, the urinary excretion of lysosomal enzymes, N-acetyl-beta-glucosaminidase (NAG), beta-glucuronidase (beta-gluc) and beta-galactosidase (beta-galac), increased simultaneously with the anticipated increase in renal clearance of lysozyme; the severities of all these hyperenzymurias increased rapidly, progressively, and in parallel, all reaching a peak some 60 to 80 minutes after their onset; thereafter, while the FS/RTA2 continued undiminished in severity, the severity of the hyperenzymurias decreased rapidly, greatly, progressively, and in parallel; and sodium phosphate loading strikingly attenuated the FS/RTA2 and the hyperenzymurias. Thus, the maleic acid-induced FS/RTA2 is attended by an acute reversible-complex derangement in the renal tubular processing of proteins that: affects not only lysozyme which is normally filtered, but also NAG and other lysosomal enzymes, which are not; and is to some extent functionally separable from that of FS/RTA2. The findings suggest that the derangements in renal processing of lysozyme and lysosomal enzymes are linked, and that a phosphate-dependent metabolic abnormality in the proximal tubule can participate in the pathogenesis of both these derangements and the FS/RTA2.

Acetylglucosaminidase↗