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At least 289 records · Page 16Linked to original sources
PubMed1994

First morning urine pH in the diagnosis of renal tubular acidosis with nephrolithiasis.

Few reports of patients with renal stones compare fasting first morning urine pH with the lowest urine pH after a single oral dose of 0.1 g/kg ammonium chloride. We studied these values in 110 individuals, including 96 stone formers and 14 non-stone forming controls. We hypothesized that fasting first morning urine pH > or = 6.10 is abnormal. Nine of ten patients who had urine pH > or = 5.25 after NH4Cl, had pH > or = 6.10 for both a single and a second first morning urine, giving a sensitivity of 90%. In contrast, a single fasting first morning urine pH > or = 6.10 was found in 19 of 100 individuals with pH < 5.25 after ammonium chloride. However, only 4 of these 100 individuals had abnormal fasting first morning pH > or = 6.10 on two occasions, giving a specificity of 96% for the two urines. Useful prediction of urine pH > or = 5.25 after ammonium chloride occurs when two fasting first morning urines have pH > or = 6.10.

Acidosis, Renal Tubular↗
PubMed1986

Renal tubular acidosis in a case of Shwachman's syndrome.

We describe metabolic acidosis in a 15-month-old girl with clinical features of Shwachman's syndrome. Renal function tests indicated that the patient had type 1 renal tubular acidosis. Based on our findings and other reports of renal tubular dysfunction in patients with Shwachman's syndrome, we conclude that it is important to look for a possible renal tubular defect in this syndrome.

Acidosis, Renal Tubular↗
PubMed2005

Hyperammonaemia in a child with distal renal tubular acidosis.

A 5-month-old girl with distal renal tubular acidosis (RTA) and hyperammonaemia that had lasted for 12 days, despite metabolic acidosis correction, is presented in this report. The patient showed failure to thrive, poor feeding, hypotonia and vomiting crisis in absence of inborn errors of metabolism. Probably, hyperammonaemia was the result of an imbalance between the increased ammonia synthesis, in response to metabolic acidosis, and the impaired ammonia excretion, typical of distal RTA. Our case confirms that hyperammonaemia may be observed in distal RTA, mimicking an inborn error of metabolism, and it underlines that hyperammonaemia may persist several days after metabolic acidosis correction.

Acidosis, Renal Tubular↗
PubMed2000

Genetic and long-term data on a patient with permanent isolated proximal renal tubular acidosis.

UNLABELLED: A 12-year-old girl presented with permanent isolated proximal renal tubular acidosis (pRTA), glaucoma, band keratopathy, mild cataract and short stature. Severe metabolic acidosis was caused by the impairment of bicarbonate reabsorption in the proximal tubules and alkali therapy improved her acidaemia. A homozygous G to A transition at nucleotide 1,678 in the basolateral kidney type Na+/HCO3- (kNBC) cotransporter gene SLC4A4, which is critical in HCO3- resorption in renal proximal tubules, was identified. Her height and height velocity (HV) were very low (-4.0 SD and -4.4 SD, respectively) before alkali treatment, but both improved after initiating alkali therapy at the age of 2 years and 3 months. The patient's body height and HV were 131.5 cm (-2.7 SD) and 4.0 cm (-2.0 SD), respectively at the age of 12 years. CONCLUSION: This case demonstrates that early administration of alkali therapy and sustained correction of acidosis, even if inadequate to correct the metabolic acidosis, can markedly improves growth in permanent isolated proximal renal tubular acidosis.

Acidosis, Renal Tubular↗
PubMed2005

A case report and review of hypokalemic paralysis secondary to renal tubular acidosis.

A 5-year-old girl with distal renal tubular acidosis (RTA) and hypokalemic muscle paralysis is reported. RTA is a known cause of hypokalemia, but in spite of the presence of persistent hypokalemia muscular paralysis is uncommon, rarely described in children, and the onset of paralysis may initially be misinterpreted particularly if the patient is attended by a physician who is not a pediatric nephrologist. Therefore parents must be informed about this possibility. Still, as the clinical appearance of hypokalemic paralysis is quite similar to familial hypokalemic periodic paralysis, and because the emergent and prophylactic treatment of the two disorders are quite different, we discuss the diagnostic evaluation and the treatment for both of them.

Acidosis, Renal Tubular↗
PubMed2000

[Sjögren syndrome associated with renal tubular acidosis type I].

Primary Sjögren's Syndrome complicated with a renal tubular acidosis type 1 and hypocalcemic paralysis, as the principal clinical manifestation, is uncommon. Although the initial manifestations of the nephropathy are not well understood, it is believed that the invasion of mononuclear cells and the high level of circulating antibodies, play an important role in the pathogenesis of the disease. We present a patient with hypocalcemic paralysis as an initial manifestation of a latent Sjögren's disease. The glandular biopsy was normal, suggesting a mayor participation of an immunological humoral factor in the renal lesion.

Acidosis, Renal Tubular↗
PubMed1993

Impaired urinary ammonium excretion in patients with isolated proximal renal tubular acidosis.

During previous studies in patients with isolated proximal renal tubular acidosis (pRTA), the rates of urinary ammonium excretion were considered inappropriately low for their state of chronic metabolic acidosis. These observations were made while the patients were on a normal diet as well as when they were undergoing a short ammonium chloride test. Because these findings suggested an impaired ability to excrete maximal amounts of ammonium, the response to the 3-day acid loading test was evaluated in eight patients with isolated pRTA and in 10 normal control subjects. Plasma creatinine, acid-base, and electrolyte values were analyzed before and after 3 days of ingesting 2 mmol/kg.24 h of ammonium chloride. Twenty-four-hour urine specimens were collected the day before and on the third day of acid loading to determine urine pH, as well as the rate of excretion of NH4+ and titratable acid in milliequivalents per 24 h per 1.73 m2. During the basal state, all patients with pRTA had hyperchloremic metabolic acidosis and they excreted urine of lower pH (5.51 +/- 0.18 versus 6.00 +/- 0.13; P < 0.05) and greater titratable acid (29.1 +/- 4.3 versus 21.8 +/- 1.4; P < 0.05); however, they had rates of NH4+ excretion similar to those of controls. On the third day of acid loading, they excreted urine of lower pH (4.66 +/- 0.03 versus 5.00 +/- 0.03; P < 0.05) and equivalent amounts of titratable acid, whereas their NH4+ excretion was significantly less than that of controls (47.7 +/- 4.4 versus 76.3 +/- 5.7; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1990

Endemic primary distal renal tubular acidosis in Thailand.

Within a period of 3 years, 103 patients with primary type I distal renal tubular acidosis were reported from two hospitals in the northeast of Thailand, with cases peaking in the summer. The patients' age ranged from 18 to 76 with a mean and mode of 39 and 47 years, respectively. The female to male ratio was 3.3:1. All patients presented with generalized muscle weakness and bone pain and nocturia were frequent manifestations. Hypokalaemia and hyperchloraemic metabolic acidosis were constant findings and were more pronounced in patients with roentgenographic evidence of nephrocalcinosis and osteomalacia. Urinary citrate was extremely low in most of the patients. Nephrocalcinosis and/or renal stones were present in 27.2% of the patients and osteomalacia was found in 23.3%. All patients were Lao-Thai. This is the first report of a large group of patients with distal renal tubular acidosis, endemic within a particular geographical region.

Acidosis, Renal Tubular↗
PubMed2003

Nitric oxide production modulates cyclosporin A-induced distal renal tubular acidosis in the rat.

Cyclosporine A (CsA) causes distal renal tubular acidosis (dRTA) in humans and rodents. Because mice deficient in nitric-oxide (NO) synthase develop acidosis, we examined how NO production modulated H+ excretion during acid loading and CsA treatment in a rat model. Rats received CsA, L-arginine (L-Arg), or N omega-nitro-L-arginine methyl ester (L-NAME), or combinations of CsA and L-NAME or L-Arg, followed by NH4Cl (acute acid load). In vehicle-treated rats, NH4Cl loading reduced serum and urine (HCO3-) and urine pH, which was associated with increases in serum [K+] and [Cl-] and urine NH3 excretion. Similar to CsA (7.5 mg/kg), L-NAME impaired H+ excretion of NH4Cl-loaded animals. The combination CsA and L-NAME reduced H+ excretion to a larger extent than either drug alone. In contrast, administration of L-Arg ameliorated the effect of CsA on H+ excretion. Urine pH after NH4Cl was 5.80 +/- 0.09, 6.11 +/- 0.13*, 6.37 +/- 0.16*, and 5.77 +/- 0.09 in the vehicle, CsA, CsA + L-NAME and CsA + L-Arg groups, respectively (*P < 0.05). The effect of CsA and alteration of NO synthesis were mediated at least in part by changes in bicarbonate absorption in perfused cortical collecting ducts. CsA or L-NAME reduced net HCO3- absorption, and, when combined, completely inhibited it. CsA + L-Arg restored HCO3- absorption to near control levels. Administration of CsA along with L-NAME reduced NO production to below levels observed with either drug alone. These results suggest that CsA causes dRTA by inhibiting H+ pumps in the distal nephron. Inhibition of NO synthesis may be one of the mechanisms underlying the CsA effect.

Acidosis, Renal Tubular↗
PubMed1984

Renal tubular acidosis does not alter circulating values of calcitriol.

In 10 patients with renal tubular acidosis, seven with type I and three with Fanconi syndrome, simultaneous measurements of vitamin D metabolites and electrolytes were made. No marked abnormalities of calcidiol2, calcidiol3, 24,25(OH)2D, or calcitriol were found in these patients, whose mean serum HCO3 was 18 +/- 3 mM/L (SD). Further, no relationship between serum HCO3 and calcitriol could be found. These results suggest that either vitamin D deficiency may be required before any alterations in the production of calcitriol are seen, or that the effects of acidosis in animals may not be reflected in humans. Further, it appears less likely that the bone disease found in renal tubular acidosis is related to abnormalities in vitamin D metabolism resulting from systemic acidosis, but that bone disease is more likely related to the acidosis and hypercalcuria prevalent in this disorder.

Acidosis, Renal Tubular↗
PubMed1982

Severe hypertension, hyperkalemia, and renal tubular acidosis responding to dietary sodium restriction.

A 13-year-old girl with severe hypertension (240/140 mm Hg), short stature, marked hyperkalemia (8.6 mEq/liter), and renal tubular acidosis was studied. Renal parenchymal and renovascular diseases as well as endocrinologic causes of hypertension were ruled out by appropriate studies. The hypertension was associated with sodium retention, increased plasma volume, suppressed plasma renin activity, and decreased urinary excretion of aldosterone. Impaired renal excretion of potassium was demonstrated by sodium sulfate infusion when the patient was fed a high-sodium diet but a significant kaliuresis occurred when the test was performed on a low-sodium diet suggesting that renal sodium retention may play a role in the defect in potassium excretion. The renal tubular acidosis was associated with normal distal acidification but a low bicarbonate threshold (19 mmoles/liter) and marked suppression of urinary ammonium excretion. The hypertension, hyporeninemia, and hypoaldosteronism as well as the hyperkalemia and acid-base abnormalities were completely reversed by dietary sodium restriction or the administration of thiazides or furosemide. It is concluded that an unusual avidity for sodium chloride reabsorption by the renal tubules leading to extracellular volume expansion and renin-aldosterone suppression plays a significant pathogenic role in this syndrome and may explain the hypertension and biochemical abnormalities discussed.

Acidosis, Renal Tubular↗
PubMed1994

Sodium thiosulphate in the treatment of renal tubular acidosis I with nephrocalcinosis.

Nephrocalcinosis is a common feature in renal tubular acidosis I (RTA-I) and contributes to renal insufficiency. We describe a patient, 37 years old, with RTA-I, mild renal failure and extended nephrocalcinosis. His disease was diagnosed in age 28 and patient is under treatment with sodium bicarbonate, potassium gluconate and sodium thiosulphate for 9 years. By this treatment nephrocalcinosis and renal function have not been worsened and patient is without clinical symptoms.

Acid-Base Equilibrium↗
PubMed1975

Incomplete renal tubular acidosis: some clinical and physiological features.

17 patients with recurrent calcium-containing renal calculi were studied using the short NH4Cl test and one subject with 'incomplete renal tubular acidosis' was identified. In retrospect the only clue to this diagnosis was a fasting, morning urine pH exceeding 6.0 units. Fasting morning urine pH, which is usually less than 6.0 in subjects who acidify normally, is proposed as a simple screening test for 'incomplete RTA'. Modified high dose NH4Cl tests and Na2SO4 tests were performed in this subject and other patients with either complete or incomplete distal renal tubular acidosis. These studies suggest that the ability to lower urine pH is impaired less with the incomplete than with the complete form of the disease.

Acidosis, Renal Tubular↗
PubMedDate not supplied

Proximal renal tubular acidosis.

The proximal tubule reabsorbs approximately 80% of the filtered load of bicarbonate. Defects in the process of bicarbonate reabsorption result in loss of bicarbonate and proximal renal tubular acidosis. Global proximal tubule dysfunction is known as the Fanconi's syndrome. Both isolated proximal renal tubular acidosis and the Fanconi's syndrome can result from inherited defects or can be acquired. This review will discuss the mechanisms that cause defects in proximal tubule bicarbonate transport as well as the common causes of isolated proximal renal tubular acidosis and the Fanconi syndrome.

Acidosis, Renal Tubular↗