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PubMed1992

[A case of Hashimoto's thyroiditis associated with renal tubular acidosis, Sjögren syndrome and empty sella syndrome].

This report describes a 48-year old female patient with Hashimoto's thyroiditis, distal-type renal tubular acidosis (d-RTA), Sjögren syndrome (SjS), and empty sella syndrome (ESS). She has been receiving replacement of thyroxine for Hashimoto's thyroiditis since 1967. She felt muscle weakness and numbness in the extremities and was found to have low serum potassium (2.9 mEq/l) in 1987. Since then she has been administrated potassium chloride orally. She was admitted to our hospital because of recurrence of muscle weakness and numbness of the extremities in November 1990. Laboratory examination revealed that her serum levels of antimicrosomal antibody and anti-thyroglobulin antibody were highly positive (MCHA: x 2(10) x 100, and TGHA: x 100). Furthermore, she was revealed to have 1) d-RTA by oral tolerance tests with the administration of NH4Cl and NaHCO3, 2) SjS by Schirmer test and sialography, and 3) ESS by computed tomography and magnetic resonance imaging examinations of the pituitary. Association of Hashimoto's thyroiditis, d-RTA, SjS and ESS in this case may possibly be caused by common autoimmune mechanism.

Acidosis, Renal Tubular↗

PubMed1989

[Hypokalemic quadriplegia and coma in renal tubular acidosis].

A case is reported of an acute episode of severe hypokalaemia (K+ = 1.1 mmol.l-1) associated with hyperchloraemic acidosis and simultaneous high urine pH (pH = 7) in a 24 year old woman with type I distal tubular acidosis and nephrocalcinosis. The flaccid paralysis involved the trunk, neck, facial and pharyngeal muscles. She was in areflexic quadriplegia, coma and respiratory failure requiring endotracheal intubation and positive pressure ventilation. There were no cardiac disturbances, presumably because of the chronic potassium depletion, the patient's youth and healthy myocardium. Despite the usually recommended maximal potassium infusion rate (0.25 mmol.kg-1.h-1), there was a transient worsening of her neuromuscular status. Only 12 h later, the first movements were noticed. In order to prevent such a deterioration, a more rapid potassium infusion could have been used. However, in our case, the occurrence of hypokalaemic extrasystoles was reduced and the patient was still intubated and ventilated. It was therefore decided not to run the risk of myocardial inexcitability carried out with supramaximal infusion rates and to keep the usual protocol. Besides, several pitfalls have to be avoided during the treatment of the numerous metabolic disorders coexisting with severe hypokalaemia, such as metabolic acidosis and hyperglycaemia.

Acidosis, Renal Tubular↗

PubMed2000

Prevalence and characterization of renal tubular acidosis in patients with osteopenia and osteoporosis and in non-porotic controls.

BACKGROUND: Chronic metabolic acidosis may increase alkali mobilization from the bone and thus promote the development of osteoporosis. The objective of the current study was to compare urinary acidification in patients with reduced bone mineral content with that in control subjects with normal bone density. METHODS: Forty-six subjects (41 females, 5 males) with osteopenia or osteoporosis were studied. In none of the subjects were overt metabolic acidosis, derangement of potassium homeostasis, or renal insufficiency present. Distal tubular acidification was studied by means of oral ammonium chloride loading test (0.1 g/kg body weight) and the oral frusemide test (40 mg). In addition the frusemide test was performed in 20 healthy age- and sex-matched controls (17 females, 3 males). RESULTS: In all control subjects a urinary pH <5. 5 was observed following the ingestion of 40 mg frusemide. In contrast, in patients with reduced bone mineral density incomplete renal tubular acidosis type I (RTA I) was diagnosed in 10 of 46 subjects (22%) by oral ammonium chloride loading test. Disorders possibly related to RTA I were detected in eight of these 10 patients. Thirty-six patients had a normal urinary pH response following oral ammonium chloride loading. Oral frusemide, 40 mg, failed to lower urinary pH <5.5 in sixteen patients (35%), these included 10 subjects with incomplete RTA I, and six subjects with a normal oral ammonium chloride loading test. An abnormal frusemide test was found in 35% of patients with reduced bone mass and in none of the normal controls (chi(2)=7.39; P<0.01). With the ammonium chloride test as the gold standard for diagnosis of distal RTA, the frusemide test showed a sensitivity of 1.0 (95% CI, 0.69-1.0) and a specificity of 0.89 (95% CI, 0.78-0.96) for the diagnosis of distal RTA. Patients with incomplete RTA I were younger than those without incomplete RTA I (42+/-16 vs 54+/-14 years; P=0.025; mean+/-SD). Basal serum bicarbonate concentrations and capillary pH did not differ between the groups. CONCLUSION: Incomplete RTA I may be prevalent in a significant proportion of patients suffering from osteopenia or osteoporosis. The outcome of the frusemide test suggests either a defect of the H(+)ATPase in the cortical collecting tubule (CCT) or a defective Na(+) reabsorption in the CCT. Prospective studies are needed to further elucidate the impact of incomplete RTA I on the development of reduced bone mineral content.

Acidosis, Renal Tubular↗

PubMed1986

The Spitzer-Weinstein syndrome: one form of type IV renal tubular acidosis and its response to hydrochlorothiazide.

A twelve-year-old girl with persistent hyperkalemia, metabolic acidosis, normal blood pressure and glomerular filtration rate, and short stature (first percentile for height) was studied using metabolic balance techniques. Prior to therapy with hydrochlorothiazide (HCTZ), urinary potassium and acid excretion were low and urine pH was inappropriately high at 5.8. HCTZ (25 mg orally per day) (1 mg/kg) was then started and rapidly corrected her serum electrolytes. The therapy with HCTZ was associated with a diuresis, a decrease in urine pH to 4.8, and concomitant increases in potassium, titratable acid (TA) and ammonium excretion. The increase in TA excretion was explicable, in part, to the decrease in urine pH and, in part, to the considerable increase in phosphate excretion (from 56 to 81 mmol/d). Plasma renin activity and plasma aldosterone increased markedly following HCTZ but urinary prostaglandin E (PGE) excretion was unchanged. These observations suggest that administration of HCTZ in this setting increases hydrogen ion secretion. It is unclear whether this effect is a direct consequence of HCTZ at the level of the tubule or is secondary to some other action of HCTZ. However, it is clear that this effect is not related to an alteration in PGE excretion.

Acidosis, Renal Tubular↗

PubMed2004

Renal tubular acidosis, Sjögren syndrome, and bone disease.

BACKGROUND: There has been disagreement about whether osteomalacia (adult rickets) occurs in adults with type 1 (distal) renal tubular acidosis (RTA1). Therefore, after finding scapular pseudofractures in a patient with RTA1 and Sjögren syndrome, we decided to survey other patients with RTA to learn whether osteomalacia occurred in others and, if it did, whether it was necessarily associated with the presence of Sjögren syndrome. METHODS: We examined the hospital records and laboratory findings of 250 patients with codes for RTA, 124 with codes for osteomalacia, and 20 with codes for Sjögren syndrome who were seen at a university-affiliated acute care municipal hospital since 1990. Further detailed survey was then limited to patients older than 15 years and excluded those with potentially confounding causes of bone disease such as chronic renal insufficiency or sickle cell disease. Seven adults with RTA1 were thereby identified. RESULTS: Two adults with RTA1 had radiological and biochemical findings compatible with osteomalacia, and 1 had findings compatible with Sjögren syndrome. A third patient without Sjögren syndrome had biochemical findings suggestive of osteomalacia. CONCLUSIONS: Osteomalacia seems to occur in some adult patients with RTA1, and not only in association with Sjögren syndrome. We found no biochemical evidence of osteomalacia in the patients with Sjögren syndrome who did not have RTA.

Acidosis, Renal Tubular↗

PubMed1980

On the mechanism of lithium-induced renal tubular acidosis: studies in the turtle bladder.

The mechanism whereby lithium impairs urinary acidification was investigated in vitro with the bladder of the fresh water turtle. The effect of lithium was compared to that of choline or cesium. In the presence of 1% carbon dioxide, lithium (40 mM in the mucosa) failed to alter hydrogen ion secretion. Lithium also caused a significant decrease in sodium transport and in potential difference. Lithium failed to increase the passive loss of hydrogen ions from the mucosal solution, indicating that it does not affect the permeability of the mucosa to hydrogen ions. Bicarbonate secretion also was unchanged in lithium-treated hemibladders. Under open-circuit conditions, lithium caused a significant decrease in potential difference and, hence, caused a significant decrease in hydrogen ion secretion. Restoration of the potential difference, in the presence of lithium, to control levels caused a return of hydrogen ion secretion to the original value. These data demonstrate that in the turtle baldder lithium inhibits hydrogen ion secretion solely by reducing the potential difference and suggest that in vivo lithium causes an acidification defect not by directly inhibiting the hydrogen ion pump or causing a hydrogen ion backleak but by inhibiting sodium transport, thereby decreasing the favorable electric gradient for hydrogen ion secretion.

Acidosis, Renal Tubular↗

PubMed1995

Light-chain-induced renal tubular acidosis: effect of sodium bicarbonate on sodium-proton exchange.

We measured sodium-proton (Na+/H+) exchange in lymphocytes and platelets of a 46-year-old woman with the adult Fanconi syndrome before, during, and after treatment with NaHCO3. Kappa light chains in her urine and unique but rarely observed crystalline structures confirmed the presence of light-chain nephropathy. Her glomerular filtration rate was only moderately impaired at 72 ml/min. NaHCO3 at 1, 3, and 5 mmol/kg/day for 5 days increased her serum HCO3 and pH from 17 to 21 mmol/l and 7.28 to 7.39 respectively. Plasma renin and aldosterone values were decreased by NaHCO3. Na+/H+ exchange (delta Hi/min) was measured with the fluorescent marker BCECF after acidification of lymphocytes and platelets with sodium propionate at five (10-50 mM) doses. Na+/H+ exchange was accelerated in this patient compared to normal controls. NaHCO3 treatment significantly decreased Na+/H+ exchange in lymphocytes, but not in platelets. These findings suggest that Na+/H+ exchange can be influenced by NaHCO3 ingestion at doses that only modestly affect systemic pH. Since Na+/H+ exchange is involved in stimulus response coupling, cell growth regulation, cell differentiation, and perhaps the progression of nephrosclerosis, these observations may have clinical relevance.

Acidosis, Renal Tubular↗

PubMed1991

Glue-sniffing and distal renal tubular acidosis: sticking to the facts.

An index case is presented to introduce the subject of the acid-base and electrolyte abnormalities resulting from toluene abuse. These include metabolic acidosis associated with a normal anion gap and excessive loss of sodium and potassium in the urine. The major question addressed is, what is the basis for the metabolic acidosis? Overproduction of hippuric acid resulting from the metabolism of toluene plays a more important role in the genesis of the metabolic acidosis than was previously believed. This conclusion is supported by the observation that the rate of excretion of ammonium was not low during metabolic acidosis in six of eight patients, suggesting that distal renal tubular acidosis was not an important acid-base abnormality in most cases where ammonium was measured. The excretion of hippurate in the urine unmatched by ammonium also mandates an enhanced rate of excretion of the cations, sodium and potassium. The loss of sodium causes extracellular fluid volume contraction and a fall in the glomerular filtration rate, which may transform the normal anion gap type of metabolic acidosis into one with a high anion gap (accumulation of hippurate and other anions). Continuing loss of potassium in the urine leads to hypokalemia. An understanding of the metabolism of toluene provides the basis for the unusual biochemical abnormalities seen with abuse of this solvent.

Acid-Base Equilibrium↗

PubMed1997

Dimercaptosuccinic acid distribution in renal tubular acidosis.

A 99Tcm dimercaptosuccinic acid (DMSA) scan performed after a urinary tract infection demonstrated an unusual pattern of isotope uptake, promoting further investigations leading to a diagnosis of renal tubular acidosis secondary to nephropathic cystinosis. This is known to affect isotope imaging but a unique feature in this undiagnosed case was the uncorrected metabolic acidosis, which had further altered the distribution of the DMSA. It is noteworthy because other patients referred for imaging with renal disease may also have abnormalities of acid base balance.

Acidosis, Renal Tubular↗

PubMed2004

Distal renal tubular acidosis.

PURPOSE OF REVIEW: Research in the past several years has led to the understanding of numerous genetic mutations that lead to inheritable forms of distal renal tubular acidosis (dRTA). Most of these mutations affect the physiology of the A-intercalated cells of the renal cortical collecting duct. These include mutations of genes encoding carbonic anhydrase II, kidney anion exchanger 1, and different subunits of the H+-ATPase proton pump. Genetic defects in any one of these components may impair renal acidification and thereby result in persistent acidosis, failure to thrive, and nephrocalcinosis. RECENT FINDINGS: The present review provides a summary of the most recently identified genetic mutations resulting in a dRTA phenotype and, when possible, describes a mechanism. Most causes of dRTA are due to loss of function or inappropriate targeting of transporters. SUMMARY: The collaboration of clinicians, geneticists, and renal physiologists has enabled us to better understand at the cellular level the different mechanisms leading to dRTA. Such information should lead to earlier diagnosis and treatment, thereby minimizing the irreversible complications affecting patients with this or similar diseases.

Acidosis, Renal Tubular↗

PubMed2006

Hypokalemic paralysis and osteomalacia secondary to renal tubular acidosis in a case with primary Sjögren's syndrome.

A 39-year-old Japanese woman was admitted to our hospital for severe weakness owing to potassium deficiency caused by type 1 renal tubular acidosis (RTA1). Sicca complex, serological tests, and lip biopsy revealed that she had Sjögren's syndrome (SS). Acidosis was corrected by alkali supplement treatment. She also had an impaired renal function with proteinuria, and high absorbance on Ga scintigram was recognized in both kidneys. She was taking warfarin potassium after aortic valve substitution due to aortic regurgitation, therefore renal biopsy was not performed. Prednisone (20 mg/day) was administered for renal inflammation. One month later, she suffered severe chest wall pains with some local tender points over the costae of both sides, which was presumed to be due to pseudo-fractures based on osteomalacia. Hypokalemic paralysis and osteomalacia should be taken into consideration in the diagnosis of SS with RTA1.

Acidosis, Renal Tubular↗

PubMed1976