How to Trip Rapid Review

Step 1: Select articles relevant to your search (remember the system is only optimised for single intervention studies)

Step 2: press

Step 3: review the result, and maybe amend the or if you know better! If we're unsure of the overall sentiment of the trial we will display the conclusion under the article title. We then require you to tell us what the correct sentiment is.

1,215 results for

Renal Tubular Acidosis

by
...
Latest & greatest
Alerts

Export results

Use check boxes to select individual results below

SmartSearch available

Trip's SmartSearch engine has discovered connected searches & results. Click to show

2. Renal tubular acidosis

Renal tubular acidosis Renal tubular acidosis - Symptoms, diagnosis and treatment | BMJ Best Practice You'll need a subscription to access all of BMJ Best Practice Search  Renal tubular acidosis Last reviewed: February 2019 Last updated: October 2017 Summary Patients with renal tubular acidosis (RTA) are often asymptomatic but may present with complaints of muscular weakness related to associated hypokalaemia. Patients with severe acidaemia can show hyperventilation or Kussmaul's breathing due (...) metabolic acidosis. Adult cases exhibit similar urinary losses, but the clinical impact is largely restricted to metabolic acidosis. Fanconi's syndrome is marked by the appearance in the urine of all amino acids. Specific amino aciduria as seen in isolated cystinuria, glucose loss in isolated glycosuria, and isolated phosphaturia do not constitute Fanconi's syndrome. Definition The term renal tubular acidosis (RTA) describes any one of a number of disorders, in which the excretion of fixed acid (distal

2017 BMJ Best Practice

3. Ibuprofen Abuse—A Case of Rhabdomyolysis, Hypokalemia, and Hypophosphatemia With Drug-Induced Mixed Renal Tubular Acidosis Full Text available with Trip Pro

Ibuprofen Abuse—A Case of Rhabdomyolysis, Hypokalemia, and Hypophosphatemia With Drug-Induced Mixed Renal Tubular Acidosis 30197993 2019 02 26 2468-0249 3 5 2018 Sep Kidney international reports Kidney Int Rep Ibuprofen Abuse-A Case of Rhabdomyolysis, Hypokalemia, and Hypophosphatemia With Drug-Induced Mixed Renal Tubular Acidosis. 1237-1238 10.1016/j.ekir.2018.05.014 Patil Shakuntala S Department of Nephrology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA (...) Department of Nephrology, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA. eng Case Reports 2018 06 08 United States Kidney Int Rep 101684752 2468-0249 2018 9 11 6 0 2018 9 11 6 0 2018 9 11 6 1 epublish 30197993 10.1016/j.ekir.2018.05.014 S2468-0249(18)30125-6 PMC6127439 Med J Aust. 2011 Mar 21;194(6):313-6 21426288 Case Rep Crit Care. 2012;2012:141505 24826329 Case Rep Crit Care. 2013;2013:875857 24829833 NDT Plus. 2008 Aug;1(4):270-1 25983902

2018 Kidney international reports

4. Changes in V-ATPase subunits of human urinary exosomes reflect the renal response to acute acid/alkali loading and the defects in distal renal tubular acidosis. Full Text available with Trip Pro

Changes in V-ATPase subunits of human urinary exosomes reflect the renal response to acute acid/alkali loading and the defects in distal renal tubular acidosis. In the kidney, final urinary acidification is achieved by V-ATPases expressed in type A intercalated cells. The B1 subunit of the V-ATPase is required for maximal urinary acidification, while the role of the homologous B2 subunit is less clear. Here we examined the effect of acute acid/alkali loading in humans on B1 and B2 subunit (...) abundance in urinary exosomes in normal individuals and of acid loading in patients with distal renal tubular acidosis (dRTA). Specificities of B1 and B2 subunit antibodies were verified by yeast heterologously expressing human B1 and B2 subunits, and murine wild-type and B1-deleted kidney lysates. Acute ammonium chloride loading elicited systemic acidemia, a drop in urinary pH, and increased urinary ammonium excretion. Nadir urinary pH was achieved at four to five hours, and exosomal B1 abundance

2018 Kidney International

5. Extrarenal Signs of Proximal Renal Tubular Acidosis Persist in Nonacidemic Nbce1b/c-Null Mice. (Abstract)

Extrarenal Signs of Proximal Renal Tubular Acidosis Persist in Nonacidemic Nbce1b/c-Null Mice. The SLC4A4 gene encodes electrogenic sodium bicarbonate cotransporter 1 (NBCe1). Inheritance of recessive mutations in SLC4A4 causes proximal renal tubular acidosis (pRTA), a disease characterized by metabolic acidosis, growth retardation, ocular abnormalities, and often dental abnormalities. Mouse models of pRTA exhibit acidemia, corneal edema, weak dental enamel, impacted colons, nutritional defects (...) insufficiency that underlies acidemia. NBCe1-B and NBCe1-C exhibit a broad extra-proximal-tubular distribution.To explore the consequences of Nbce1b/c loss in the absence of acidemia, we engineered a novel strain of Nbce1b/c-null mice and assessed them for signs of pRTA.Nbce1b/c-null mice have normal blood pH, but exhibit increased mortality, growth retardation, corneal edema, and tooth enamel defects.The correction of pRTA-related acidemia should not be considered a panacea for all signs of pRTA

2019 Journal of the American Society of Nephrology

6. Prevalence of distal renal tubular acidosis in patients with calcium phosphate stones. (Abstract)

Prevalence of distal renal tubular acidosis in patients with calcium phosphate stones. Distal renal tubular acidosis (DRTA) is a metabolic disorder that associates urolithiasis and urinary pH > 6. The prevalence of DRTA in patients with calcium phosphate stones is not well known. The objective is to determine the prevalence of DRTA in patients with calcium phosphate stones and urinary pH above 6 based on the furosemide test.A total of 54 patients with calcium phosphate stones and urinary pH

2019 World journal of urology

7. A novel homozygous deletion in ATP6V0A4 causes distal renal tubular acidosis: A case report. Full Text available with Trip Pro

A novel homozygous deletion in ATP6V0A4 causes distal renal tubular acidosis: A case report. Autosomal recessive distal renal tubular acidosis (dRTA) is a rare condition, most cases of which are caused by genetic mutations. Several loss-of-function mutations in the ATP6V0A4 gene have been recently reported.A 2-month, 24-day-old Chinese girl presenting with vomiting and diarrhea.dRTA was established by metabolic acidosis and hypokalemia. Mutational analysis of the ATP6V0A4 gene revealed

2019 Medicine

8. Novel compound heterozygous ATP6V1B1 mutations in a Chinese child patient with primary distal renal tubular acidosis: a case report. Full Text available with Trip Pro

Novel compound heterozygous ATP6V1B1 mutations in a Chinese child patient with primary distal renal tubular acidosis: a case report. Distal renal tubular acidosis (dRTA) is a heterogeneous disorder characterized by normal anion gap metabolic acidosis. Autosomal recessive dRTA is usually caused by mutations occurring in ATP6V1B1 and ATP6V0A4 genes,encoding subunits B1 and a4 of apical H+-ATPase, respectively. The heterogeneous clinical manifestations of dRTA have been described in different (...) ethnic groups harboring distinct mutations. Most of the reported cases are from Europe and Africa. At present, the prevalence of primary dRTA is still poorly elucidated in Chinese population.A 2-year and six-month-old female patient was hospitalized because of recurrent hypokalemia, hyperchloremic metabolic acidosis and growth retardation. Laboratory investigations presented a normal anion gap hyperchloremic metabolic acidosis, hypokalemia, and inappropriate alkaline urine. Renal ultrasound indicated

2018 BMC Nephrology

9. Pendred, pendrin, pseudohypoaldosteronism type II, and renal tubular acidosis. (Abstract)

Pendred, pendrin, pseudohypoaldosteronism type II, and renal tubular acidosis. The sodium chloride cotransporter is regulated by the with-no-lysine kinases 1 and 4. Mutations in these genes are responsible for Mendelian hypertension, increased sodium chloride cotransporter activity, metabolic acidosis, and hyperkalemia. Explaining metabolic acidosis and hyperkalemia has been difficult. We now learn that the versatile bicarbonate-chloride exchanger, pendrin, is important in the process (...) . As a result, we are confronted with still another mechanism causing renal tubular acidosis.Copyright © 2018. Published by Elsevier Inc.

2018 Kidney International

10. Study Evaluating Subjects With Distal Renal Tubular Acidosis

Statement: Plan to Share IPD: No Layout table for additional information Studies a U.S. FDA-regulated Drug Product: Yes Studies a U.S. FDA-regulated Device Product: No Additional relevant MeSH terms: Layout table for MeSH terms Acidosis Acidosis, Renal Tubular Acid-Base Imbalance Metabolic Diseases Renal Tubular Transport, Inborn Errors Kidney Diseases Urologic Diseases Metabolism, Inborn Errors Genetic Diseases, Inborn Potassium Citrate Diuretics Natriuretic Agents Physiological Effects of Drugs (...) Study Evaluating Subjects With Distal Renal Tubular Acidosis Study Evaluating Subjects With Distal Renal Tubular Acidosis - Full Text View - ClinicalTrials.gov Hide glossary Glossary Study record managers: refer to the if submitting registration or results information. Search for terms x × Study Record Detail Saved Studies Save this study Warning You have reached the maximum number of saved studies (100). Please remove one or more studies before adding more. Study Evaluating Subjects

2018 Clinical Trials

11. A mouse model of pseudohypoaldosteronism type II reveals a novel mechanism of renal tubular acidosis. (Abstract)

A mouse model of pseudohypoaldosteronism type II reveals a novel mechanism of renal tubular acidosis. Pseudohypoaldosteronism type II (PHAII) is a genetic disease characterized by association of hyperkalemia, hyperchloremic metabolic acidosis, hypertension, low renin, and high sensitivity to thiazide diuretics. It is caused by mutations in the WNK1, WNK4, KLHL3 or CUL3 gene. There is strong evidence that excessive sodium chloride reabsorption by the sodium chloride cotransporter NCC (...) /bicarbonate exchanger. Here we determine whether this system is involved in the pathogenesis of PHAII. Renal pendrin activity was markedly increased in a mouse model carrying a WNK4 missense mutation (Q562E) previously identified in patients with PHAII. The upregulation of pendrin led to an increase in thiazide-sensitive sodium chloride absorption by the cortical collecting duct, and it caused metabolic acidosis. The function of apical potassium channels was altered in this model, and hyperkalemia

2018 Kidney International

12. Clinical and genetic analysis of distal renal tubular acidosis in three Chinese children Full Text available with Trip Pro

Clinical and genetic analysis of distal renal tubular acidosis in three Chinese children Primary distal renal tubular acidosis (dRTA) is a rare genetic disease characterized by distal tubular dysfunction leading to metabolic acidosis and alkaline urine. Growth retardation is a major concern in these children. The disease is caused by defects in at least three genes (SLC4A1, ATP6V0A4, and ATP6V1B1) involved in urinary distal acidification. Several series of dRTA patients from different ethnic (...) backgrounds have been genetically studied, but genetic studies regarding Chinese population is rare. Our aim was to investigate the clinical features and genetic basis of primary dRTA in Chinese children.Three unrelated patients with dRTA participated in our study. Next-generation sequencing was performed, and the findings were validated using the Sanger sequencing method.All patients exhibited hyperchloraemic metabolic acidosis, abnormally high urine pH, hypokalemia, and nephrocalcinosis. Growth

2018 Renal failure

13. Sjögren’s, Renal Tubular Acidosis and Osteomalacia - An Asian Indian Series Full Text available with Trip Pro

Sjögren’s, Renal Tubular Acidosis and Osteomalacia - An Asian Indian Series 30123372 2018 10 08 1874-3129 12 2018 The open rheumatology journal Open Rheumatol J Sjögren's, Renal Tubular Acidosis and Osteomalacia - An Asian Indian Series. 114 10.2174/1874312901812010114 Sandhya Pulukool P Department of Clinical Immunology and Rheumatology, Christian Medical College and Hospital, Vellore-632004, India. Danda Debashish D Department of Clinical Immunology and Rheumatology, Christian Medical

2018 The open rheumatology journal

14. Renal Tubular Acidosis and Hypokalemic Paralysis as a First Presentation of Primary Sjögren's Syndrome Full Text available with Trip Pro

, who was previously diagnosed as hypokalemic periodic paralysis, presented with generalized weakness and fatigue. She was found to have severe hypokalemia with normal anion-gap metabolic acidosis consistent with distal renal tubular acidosis. Subsequent evaluation revealed Sjögren's syndrome as the cause of her problems. Kidney biopsy done to evaluate significant proteinuria revealed nonproliferative morphology with patchy acute tubular injury and significant chronic interstitial nephritis (...) Renal Tubular Acidosis and Hypokalemic Paralysis as a First Presentation of Primary Sjögren's Syndrome Sjögren's syndrome is an autoimmune disease with multisystem involvement and varying clinical presentation. We report the clinical course and outcome of a case who presented with repeated episodes of hypokalemia mimicking hypokalemic periodic paralysis and metabolic acidosis, which was later diagnosed as distal renal tubular acidosis secondary to primary Sjögren's syndrome. A 50-year-old lady

2018 Case reports in nephrology

15. Hypokalemic Paralysis Secondary to Renal Tubular Acidosis Revealing Underlying Sjogren's Syndrome Full Text available with Trip Pro

Hypokalemic Paralysis Secondary to Renal Tubular Acidosis Revealing Underlying Sjogren's Syndrome There is a well-established association of Sjogren's syndrome with renal tubular acidosis (RTA). Rarely there is a retrospective diagnosis where the patient presents with RTA and the workup reveals Sjogren's syndrome. Our case report is about a patient who presented with generalized weakness and hypokalemia, which upon further workup turned out to be RTA. Various tests were performed to find out

2018 Cureus

16. Primary Autosomal Recessive Distal Renal Tubular Acidosis Caused by a Common Homozygous SLC4A1 Mutation in Two Lao Families Full Text available with Trip Pro

Primary Autosomal Recessive Distal Renal Tubular Acidosis Caused by a Common Homozygous SLC4A1 Mutation in Two Lao Families Primary distal renal tubular acidosis (dRTA) caused by mutations of the SLC4A1 gene, which encodes for erythroid and kidney isoforms of anion exchanger, shows marked difference in inheritance patterns and clinical features in different parts of the world. While the disease shows autosomal dominant inheritance without any red cell morphological abnormalities

2018 Journal of Korean medical science

17. Bilateral Proximal Femur Fractures in a Patient with Renal Tubular Acidosis: A Case Report Full Text available with Trip Pro

Bilateral Proximal Femur Fractures in a Patient with Renal Tubular Acidosis: A Case Report The diagnosis of pathological fractures is on the rise. The morbidity involved does not only burden the patient and their families but it has a great toll on the healthcare system as well. Early identification of the patient at risk is an invaluable tool to cut cost and improve the patient's quality of life. Multiple renal pathologies have been highlighted in relation to the risk of pathological fractures (...) ; however, complications in renal tubular acidosis have been rarely documented. Nevertheless, prompt action with adequate and relevant patient education ultimately can reduce the associated morbidity. We present a case of poor control of the disease and its debilitating pathological fracture complications.

2018 Malaysian orthopaedic journal

18. Distal renal tubular acidosis caused by tryptophan-aspartate repeat domain 72 (WDR72) mutations. (Abstract)

Distal renal tubular acidosis caused by tryptophan-aspartate repeat domain 72 (WDR72) mutations. Hereditary distal renal tubular acidosis (dRTA) is a rare genetic disease that is caused by mutations in SLC4A1, ATP6V1B1, or ATP6V0A4. However, there are many families with hereditary dRTA in whom the disease-causing genes are unknown. Accordingly, we performed whole exome sequencing and genetic studies of the members of a family with autosomal recessive dRTA of an unknown genetic etiology. Here

2018 Clinical Genetics

19. Distal renal tubular acidosis. Clinical manifestations in patients with different underlying gene mutations. Full Text available with Trip Pro

Distal renal tubular acidosis. Clinical manifestations in patients with different underlying gene mutations. To evaluate whether there are differences in the phenotype of primary distal renal tubular acidosis (dRTA) patients according to the causal defective gene.Twenty-seven non-oriental patients with genetically confirmed dRTA were grouped according to the identified underlying mutations in either ATP6V1B1 (n = 10), ATP6V0A4 (n = 12), or SLC4A1 (n = 5) gene. Demographic features, growth

2018 Pediatric Nephrology

20. Primary distal renal tubular acidosis: novel findings in patients studied by next-generation sequencing. Full Text available with Trip Pro

Primary distal renal tubular acidosis: novel findings in patients studied by next-generation sequencing. This corrects the article DOI: 10.1038/pr.2015.243.

2018 Pediatric Research

To help you find the content you need quickly, you can filter your results via the categories on the right-hand side >>>>