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PubMed1986

Distal renal tubular acidosis and hepatic lipidosis in a cat.

Clinical and laboratory evidence of hepatic failure was found in a chronically anorectic cat. Simultaneous blood and urine pH determinations established a diagnosis of distal renal tubular acidosis. The cat did not respond to treatment. Necropsy revealed distal tubular nephrosis and hepatic lipidosis. The finding of distal renal tubular acidosis in a cat with hepatic lipidosis emphasizes the importance of complete evaluation of acid-base disorders in patients.

Acidosis, Renal Tubular↗
PubMed1998

Hyperkalemic renal tubular acidosis induced by trimethoprim/sulfamethoxazole in an AIDS patient.

A patient with the acquired immunodeficiency syndrome (AIDS) and sickle cell anemia presented to the University of Wisconsin Hospital on two separate occasions with pneumocystis carinii pneumonia (PCP). On both occasions he was treated with high-dose intravenous trimethoprim/sulfamethoxazole (TMP/SMX). Several days into each treatment course he developed hyperkalemia and systemic acidosis consistent with hyperkalemic renal tubular acidosis (RTA). The abnormalities resolved in the first instance with the addition of amphotericin B while continuing TMP/SMX, and in the second upon discontinuation of the TMP/SMX. While an increasing number of cases with TMP/SMX-induced hyperkalemia have been reported, hyperkalemic RTA is an uncommon complication of TMP/SMX therapy, occurring in patients with predisposing factors for acidosis such as aldosterone defects, medullary dysfunction and renal insufficiency.

AIDS-Related Opportunistic Infections↗
PubMed2000

New insights into the pathogenesis of renal tubular acidosis--from functional to molecular studies.

The diagnosis and classification of renal tubular acidosis (RTA) have traditionally been made on the basis of functional studies. On these grounds, RTA has been separated into three main categories: (1) proximal RTA, or type 2; (2) distal RTA, or type 1; and (3) hyperkalemic RTA, or type 4. In recent years significant advances have been made in our understanding of the subcellular mechanisms involved in renal bicarbonate (HCO3-) and H+ transport. Application of molecular biology techniques has also opened a completely new perspective to the understanding of the pathophysiology of inherited cases of RTA. Mutations in the gene SLC4A4, encoding Na+-HCO3- cotransporter (NBC-1), have been found in proximal RTA with ocular abnormalities; in the gene SLC4A1, encoding Cl(-)-HCO3- exchanger (AE1), in autosomal dominant distal RTA; in the gene ATP6B1, encoding B1 subunit of H+-ATPase, in autosomal recessive distal RTA with sensorineural deafness; and in the gene CA2, encoding carbonic anhydrase II, in autosomal recessive osteopetrosis. Syndromes of aldosterone resistance have been also characterized molecularly and mutations in the gene MLR, encoding mineralocorticoid receptor, and in the genes SNCC1A, SNCC1B, and SCNN1G, encoding subunits of the epithelial Na+ channel, have been found in dominant and recessive forms of pseudohypoaldosteronism type 1, respectively. It can be concluded that, although functional studies are still necessary, a new molecular era in the understanding of disorders of renal acidification has arrived.

Acidosis, Renal Tubular↗
PubMed2007

Renal tubular acidosis after kidney transplantation--incidence, risk factors and clinical implications.

BACKGROUND: Renal tubular acidosis (RTA) is a non-anion gap metabolic acidosis and is generally mild and asymptomatic in kidney recipients. Although calcineurin inhibitors, suboptimal allograft function, donor age and acute rejection have been associated with RTA, no detailed study has been conducted to investigate the prevalence and clinical implications of RTA in long-term kidney recipients. METHODS: In this cross-sectional study, we enrolled 109 patients (74 males, 35 females) for the study [patients with glomerular filtration rate (GFR) <30 ml/min/1.73 m(2), unstable allograft function, diarrhoea, and respiratory disease were excluded]. Thirty-six patients (33%) were found to have RTA on the basis of plasma bicarbonate, arterial pH, urine and serum anion gap measurements. RESULTS: Deceased donor transplantation [P = 0.034, 95% confidence interval (CI): 1.10-13.27], female gender (P = 0.017, 95% CI: 1.23-8.50), and lower GFR (55.8 +/- 19.4 in RTA and 66.1 +/- 15.9 ml/min/1.73 m(2) in non-RTA, P = 0.002, 95% CI: 1.10-13.27) were independent risk factors for RTA. Also, C-reactive protein was found to be higher in the RTA group (2.7 +/- 1.5 vs 2.0 +/- 1.5 mg/dl, P = 0.03), while no difference was noticed in body mass index or serum albumin. Analysis of the prevalence of osteoporosis and osteopenia in patients with RTA and without RTA, respectively, revealed no difference in frequency of osteoporosis (33% vs 31%) or osteopenia (33% vs 47%). CONCLUSION: Although long-term kidney recipients have a relatively high prevalence of RTA, it is usually mild and subclinical. Further studies are needed to clarify long-term effects of RTA in kidney recipients.

Acidosis, Renal Tubular↗
PubMed2005

Long-term outcome in children with primary distal renal tubular acidosis.

OBJECTIVE: To evaluate complications in adequately treated children with distal renal tubular acidosis (RTA) and to identify factors influencing their development. DESIGN: Records of patients with primary distal RTA followed for 2 or more years at this hospital were reviewed. Case records were examined for age at onset of symptoms and at initiation of treatment, treatment details, follow-up and complications. Height, weight and growth velocity were expressed as standard deviation score (SDS) during different periods of follow-up. Regression analysis was performed to evaluate factors influencing increase in height and weight SDS. P value of less than 0.05 was considered significant. RESULTS: Of 18 patients (eleven boys), the diagnosis was established at the median (range) age of 6 yr (1.5-13 yr). These patients were followed up for a median (range) period of 4 yr (2-18.5 yr). Short stature (height SDS <-2) was noted in all patients at the time of diagnosis with median (range) height SDS of -5.2(-7.5 - -0.4). All patients had failure to thrive with median (range) weight SDS of -3(-5.7 - -1.5). Height SDS increased by median (range) of 2 (1.2-5.5) to become -2.7(-4.8 - -1.1) at last follow-up. Weight SDS increased by median (range) of 0.9 (-0.6 - 2.8) to become -2.4 (-4 - -0.5). Median (range) growth velocity SDS decreased from 3 (1-16) during first year of treatment to 1(-0.3 - 7) at four years with an increase in mean height SDS by 1.3 during the first two years of treatment. Height SDS at last follow-up was not influenced by the age at initiation of treatment, follow-up duration, initial height SDS or severity of acidosis at diagnosis. Increase in height SDS correlated negatively with base excess and height SDS at diagnosis, and positively with follow-up duration on univariate analyses. Initial height SDS was the only factor that influenced increase in height SDS on multivariate analyses. Increase in weight SDS was negatively correlated with base excess and initial weight SDS with significant association with initial weight SDS, on multivariate analyses. All patients had rickets at the time of diagnosis with pathological fractures in four. Rickets resolved without treatment with vitamin D in seventeen patients after a median (range) period of 4 mo (1-12 mo). Eight patients (44.4%) had nephrocalcinosis at diagnosis. Twenty-four hour urine calcium excretion was higher in those with nephrocalcinosis (p = 0.01). Creatinine clearance remained normal in all except one who progressed to renal failure. CONCLUSION: There is a need for early diagnosis, appropriate treatment and regular follow-up of patients with distal RTA for improving outcome.

Acidosis, Renal Tubular↗
PubMed2004

Alteration of noncollagenous bone matrix proteins in distal renal tubular acidosis.

Our previous report on bone histomorphometry in patients with distal renal tubular acidosis (dRTA) revealed decreased bone formation rate (BFR) when compared to healthy subjects. The abnormality improved significantly after alkaline therapy. The modest increase in osteoblastic surface, after correction of metabolic acidosis, could not explain the striking improvement in bone formation, suggesting additional influence of metabolic acidosis on osteoblast function and/or bone matrix mineralization. Osteoblasts and, to a lesser extent, osteoclasts synthesize and secrete bone matrix including type I collagen and various noncollagenous proteins (NCPs). Substantial evidence suggested diverse functions of NCPs related to bone formation, resorption, and mineralization. Metabolic acidosis, through its effect on bone cells, may result in an alteration in the production of NCPs. Our study examined bone histomorphometry with detailed analysis on the mineralization parameters and NCPs expression within the bone matrix of patients with dRTA before and after treatment with alkaline. Seven dRTA patients underwent bone biopsy at their initial diagnosis and again 12 months after alkaline therapy. Bone mineral density (BMD) and bone histomorphometry were obtained at baseline and after the treatment. The expression of NCPs was examined by immunohistochemistry, quantitated by digital image analysis, and reported as a percentage of area of positive staining or mineralized trabecular bone area. Alkaline therapy normalized the low serum phosphate and PTH during acidosis. The reduction in BMD at baseline improved significantly by the treatment. Bone histomorphometry demonstrated the increase in osteoid surface and volume without significant alteration after acidosis correction. In comparison to the normal subjects, osteoid thickness was slightly but insignificantly elevated. Osteoblast and osteoclast populations and their activities were suppressed. The reduction in mineral apposition rate and adjusted apposition rate were observed in conjunction with the prolongation of mineralization lag time. Alkaline therapy improved the mineralization parameters considerably. In addition to the increase in BFR relative osteoblast number after acidosis correction, osteocalcin expression in the bone matrix increased significantly from 16.7% to 22.3%. Six of seven patients had decreased osteopontin expression. In conclusion, the abnormal bone remodeling in dRTA is characterized by low turnover bone disease with some degree of defective mineralization. Alteration of NCPs expression suggested the effect of metabolic acidosis on bone cells. Alkaline therapy increased bone mass through the restoration of bone mineral balance and, perhaps, improved osteoblast function.

Acidosis, Renal Tubular↗
PubMed2007

Inadequate dietary intake but not renal tubular acidosis is associated with bone demineralization in primary biliary cirrhosis.

BACKGROUND: Metabolic bone disease associated with primary biliary cirrhosis (PBC) is inadequately characterized. Renal tubular acidosis (RTA) may lead to bone loss through chronic mobilization of skeletal calcium salts to buffer increased acid load. AIM: To evaluate the prevalence of RTA in PBC and establish the relationships among bone mineral density (BMD), renal function and nutritional status. METHODS: We enrolled 69 female patients with compensated PBC and 35 control patients with chronic hepatitis C. RTA was searched in all patients, and 24-h dietary recalls were collected at enrolment. BMD was measured by dual-energy X-ray absorptiometry at the femur neck, lumbar spine and radius ultradistalis sites. RESULTS: No patients received a diagnosis of RTA. BMD values (Z-scores) showed only little deviation from normal population with no difference between PBC and controls. Osteopoenic PBC patients (T-score < 1) showed significantly lower daily phosphorus intake [median: 672 (288-1374) vs. 921 (253-1923) mg/day; P = 0.037], with a trend towards lower caloric intake than their nonosteopoenic counterparts. CONCLUSIONS: Renal tubular acidosis is uncommon in compensated PBC. Cholestasis is not associated with an increased risk of bone demineralization. Inadequate dietary intake may be a preventable factor contributing to bone loss in PBC.

Acidosis, Renal Tubular↗
PubMed1994

Acquired nephrogenic diabetes insipidus secondary to distal renal tubular acidosis and nephrocalcinosis associated with Sjögren's syndrome.

A 52-year-old woman was referred to our hospital because of 16-year history of polyuria and polydipsia. Hyposthenuria, hyperchloremic metabolic acidosis and the inabilities to acidify the urine after acid-loading test and to concentrate the urine in responses to water-deprivation and antidiuretic hormone administration allowed us to diagnose renal tubular acidosis and nephrogenic diabetes insipidus. Radiographic examinations revealed bilateral nephrocalcinosis. The patient was also found to have clinical and laboratory findings characteristic for Sjögren's syndrome. Thus the longstanding, poorly monitored distal renal tubular acidosis associated with Sjögren's syndrome was considered to result in very rare renal complications-nephrocalcinosis and nephrogenic diabetes insipidus. In patients with renal tubular acidosis and/or nephrogenic diabetes insipidus of unknown etiology, therefore, Sjögren's syndrome should be considered as one of primary disorders.

Acidosis, Renal Tubular↗
PubMed1991

[Renal tubular acidosis in primary Sjogren's syndrome: study on the immunology and ultrastructure of EBV].

The related antigens of EBV were examined by McAB against Epstein-Barr virus EAp 138. The related antibody of serous EBV VCA and EBNA of Sjogren's syndrome (SS) patients was examined by indirect immunofluorescence and immunoenzyme methods. EBV was found in the tubular epithelial cells by EM and the relationship between EBV and SS was studied. The results showed that (1) Around the nuclei and basement membrane of the proximal tubular epithelial cells there were positively reacting granules but not in the control group. (2) The related antibody of serous EBV VCA and EBNA showed positive reaction, and the highest titre was VCA-IgA 1:80, VCA-IgM 1:40, VCA-IgG 1:320 and EBNA-IgG 1:320 respectively. In addition, mature granules were found in the cytoplasm of the renal tubular epithelial cells.

Acidosis, Renal Tubular↗