Structures already discussed alongside proximal renal tubular acidosis in the retrieved literature, rendered from public PubChem SMILES. Which drugs appear here reflects the evidence found, not a ranked prediction.
RCSB Protein Data Bank · entry 6CAA · 3.9 Å · ligand none (apo structure). Experimental structure, not a prediction.
In type I (distal) renal tubular acidosis nephrolithiasis is the main source of morbidity in adults and adolescents. A 1989 review of 21 per cent of patients with type I renal tubular acidosis and nephrolithiasis had hyperuricosuria. The most frequent risk factor was hypocitraturia, which occurred even in incomplete (non-acidotic) forms of the disease. Alkali therapy with bicarbonate or citrate salts increased citrate excretion in both complete and incomplete type I renal tubular acidosis, suggesting the hypocitraturia may stem from a proximal tubule defect. Hypercalciuria had two proposed causes: metabolic acidosis, usually in children with hereditary acidification defects, or familial idiopathic hypercalciuria leading to nephrocalcinosis and distal tubular damage. Potassium citrate appeared to reduce calcium excretion in both hypercalciuric subtypes.
A 2011 protocol for a prospective, multicentre, randomised controlled study (the UBI Study) noted that a Cochrane review had found no evidence that sodium bicarbonate corrected acidosis in pre-end-stage renal disease patients and concluded that randomised trials were needed. The protocol proposed randomising 600 patients with chronic kidney disease stages 3b and 4, keeping serum bicarbonate above 24 mEq/L in the treatment group with sodium bicarbonate or another alkalinising agent such as sodium citrate. The aim was to see whether optimal correction of uraemic acidosis reduced renal and cardiovascular mortality. The paper reported no results; it was only a study design.
Earlier literature from 1961 and 1980 described renal tubular acidosis as a set of disorders defined by impaired urinary acidification, with variable mechanisms and clinical severity. The 1961 paper reviewed familial cases and the then-known biochemistry, while the 1980 review stated that differential diagnosis was straightforward and treatment effective, without giving specific outcome data. A 1995 article and a 2010 nursing review added no new quantitative evidence on treatment efficacy.
What is missing are completed randomised controlled trials that test alkali therapy specifically in proximal renal tubular acidosis, with hard endpoints such as stone recurrence, kidney function decline, or mortality. The existing data are limited to observational reports, small case series, and one trial protocol that has not reported results. Patient stratification by underlying cause (hereditary, autoimmune, idiopathic) and by baseline acid-base status is also lacking in most studies. Funding for adequately powered, long-term trials in this rare disease remains absent.
Retrieved by DeepSearch across 234,678,978 indexed works and resolved on OpenAlex — ranked by citations, including the results that did not work.
The Journal of Urology · 1989 · 93 citations
Nephrolithiasis in Renal Tubular Acidosis
AbstractRenal tubular acidosis is a term applied to several conditions in which metabolic acidosis is caused by specific defects in renal tubular hydrogen ion secretion. Three types of renal tubular acidosis generally are recognized based on the nature of the tubular defect. Nephrolithiasis occurs only in type I renal tubular acidosis, a condition marked by an abnormality in the generation and maintenance of a hydrogen ion gradient by the distal tubule. A forme fruste of type I renal tubular acidosis has been described in which the characteristic defect in distal hydrogen ion secretion occurs in the absence of metabolic acidosis (incomplete renal tubular acidosis). Type I renal tubular acidosis is a heterogeneous disorder that may be hereditary, idiopathic or secondary to a variety of conditions. Secondary type I renal tubular acidosis in sporadic cases is associated most commonly with autoimmune diseases, such as Sjögren's syndrome and systemic lupus erythematosus, and it occurs more frequently in women than men. Nephrolithiasis, which may occur in any of the subsets of type I renal tubular acidosis, accounts for most of the morbidity in adults and adolescents. Major risk factors for nephrolithiasis include alkaline urine, hypercalciuria and hypocitraturia. In addition, we found hyperuricosuria in 21 per cent of the patients with type I renal tubular acidosis with nephrolithiasis. The most frequently occurring risk factor, hypocitraturia, is due to decreased filtered load and/or to increased tubular reabsorption of filtered citrate. While increased tubular reabsorption may be due to systemic acidosis, hypocitraturia occurs in incomplete renal tubular acidosis. Furthermore, alkali therapy (either bicarbonate or citrate salts) increases citrate excretion in complete and incomplete type I renal tubular acidosis. These data suggest that hypocitraturia in type I renal tubular acidosis may be due to a defect in proximal tubule function. Hypercalciuria appears to have 2 causes. It may be due to metabolic acidosis, usually in children with a hereditary defect in urine acidification. In other cases familial idiopathic hypercalciuria causes nephrocalcinosis and nephrolithiasis resulting in distal tubular damage and type I renal tubular acidosis. In these latter cases hypercalciuria is present in complete and incomplete type I renal tubular acidosis. Potassium citrate appears to reduce calcium excretion in both types of hypercalciuric type I renal tubular acidosis.(ABSTRACT TRUNCATED AT 400 WORDS)
https://doi.org/10.1016/s0022-5347(17)40997-9Annals of Pharmacotherapy · 2004 · 42 citations
Antimicrobial-Associated Renal Tubular Acidosis
AbstractOBJECTIVE: To review the literature documenting the association of various antimicrobial medications with the development of renal tubular acidosis (RTA). DATA SOURCES: A search of the English literature via MEDLINE (1966-November 2003) and International Pharmaceutical Abstracts (1970-November 2003) was conducted to identify human reports of RTA associated with various drugs from all available classes of antimicrobial agents. Major search terms included renal tubular acidosis, acidosis, antibiotics, and antimicrobials. Bibliographies of selected articles were also searched to identify additional reports of RTA. STUDY SELECTION AND DATA EXTRACTION: Case reports, observational studies, and experimental studies documenting the association of any antimicrobial agent with the development of RTA were included. DATA SYNTHESIS: Antimicrobial-associated RTA is a relatively uncommon adverse effect, with most reports involving amphotericin B, trimethoprim/sulfamethoxazole, and outdated tetracycline. These agents may induce RTA either through direct tubular toxicity or as a function of their pharmacologic action. The time course for the development of RTA varies depending on the antimicrobial utilized. In most instances, RTA is reversible; however, some patients may experience prolonged recovery after the offending agent is removed. CONCLUSIONS: Given that antimicrobial-associated RTA is a relatively uncommon adverse effect, review of the patient's drug regimen may reveal these agents as otherwise unrecognized causes of RTA. Likewise, underlying causes of RTA other than medications must be ruled out. Diagnosing antimicrobial-induced RTA may be difficult, given many of these agents may be used in combination and some are intrinsically nephrotoxic.
https://doi.org/10.1345/aph.1d573Clinical Pediatrics · 2001 · 30 citations
Renal Tubular Acidosis: A New Look at an Old Problem
AbstractAlthough the definition of renal tubular acidosis (RTA) is simple, understanding the physiologic basis underlying the various types of this clinical entity is much more difficult. The pathophysiology of this disorder is reviewed using the normal acid-base functions of the involved segments of the nephron as a guide to understanding. Clinical and laboratory features of the subtypes of RTA are addressed, and diagnosis and treatment discussed. New developments in the knowledge and understanding of the associated growth disturbances, mineral metabolism, and molecular biology of RTA are also reviewed to provide the most current view of this relatively common pediatric entity.
https://doi.org/10.1177/000992280104001001Journal of Nephrology · 2011 · 27 citations
A prospective, multicenter, randomized, controlled study: the Correction of Metabolic Acidosis with Use of Bicarbonate in Chronic Renal Insufficiency (UBI) Study
AbstractBACKGROUND: A Cochrane Collaboration review (Roderick, Cochrane Data base of systemic reviews 2007, DOI 10.1002/14651858.CD0018.90.pub3) reported that there was no evidence for correction of acidosis by sodium bicarbonate in pre-end-stage renal disease (ESRD) patients, and concluded that randomized controlled trials (RCTs) are necessary to evaluate the benefits and harms of correcting metabolic acidosis in pre-ESRD patients. We wanted to evaluate if the administration of alcaly (mainly sodium bicarbonate) is able to significantly modify renal death and to reduce mortality due to cardiovascular events. METHODS: This is a proposal for a multicenter, prospective, cohort, randomized and controlled study. We will randomize 600 patients with chronic kidney disease (CKD) stages 3b and 4; 300 of these patients will be included in the bicarbonate study group (Bic), in which levels of bicarbonate should be kept >24 mEq/L; the other 300 patients will be included in the usual-treatment group (no-Bic). RESULTS: The aim of the research protocol is to demonstrate whether the optimal correction of uremic acidosis (with administration of sodium bicarbonate or of any other alkalinizing agent - e.g., sodium citrate) reduces renal and cardiovascular mortality. CONCLUSIONS: In conclusion, the Work Group on Conservative Therapy for Chronic Renal Insufficiency proposes this prospective, multicenter, cohort, randomized, controlled study to evaluate the effects of correction of acidosis on the progression of the kidney disease evaluated as renal death in ESRD patients.
https://doi.org/10.5301/jn.5000014Annals of Internal Medicine · 1961 · 24 citations
FAMILIAL RENAL TUBULAR ACIDOSIS
AbstractArticle1 June 1961FAMILIAL RENAL TUBULAR ACIDOSISRUSSELL E. RANDALL JR., WILLIAM H. TARGGART, M.D.RUSSELL E. RANDALL JR.Search for more papers by this author, WILLIAM H. TARGGART, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-54-6-1108 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAcidosis of renal origin is an increased hydrogen ion concentration due to an impairment in the excretion of titratable acid and/or ammonium ion, to an excessive excretion of bicarbonate, or to a combination of these two defects.1-4While all renal acidosis is presumably tubular in origin, the term "renal tubular acidosis" has come to represent (and will be so used in this text) that syndrome characterized by a hyperchloremic acidosis resulting from marked impairment in the ability to excrete an acid urine.3-15The latter is significantly out of proportion to any impairment in glomerular filtration, and hence is not associated...Bibliography1. SchwartzRelman WBAS: Acidosis in renal disease. New Engl. J. Med. 256: 1184, 1957. CrossrefMedlineGoogle Scholar2. SchwartzHallHaysRelman WBPWRMAS: On the mechanism of acidosis in chronic renal disease. J. Clin. Invest. 38: 39, 1959. CrossrefMedlineGoogle Scholar3. WrongDavies OHE: The excretion of acid in renal disease. Quart. J. Med. 28: 259, 1959. MedlineGoogle Scholar4. Elkinton JR: Renal acidosis. Amer. J. Med. 28: 165, 1960. CrossrefMedlineGoogle Scholar5. AlbrightBurnettParsonReifensteinRoos FCHWECA: Osteomalacia and late rickets: the various etiologies met in the United States with emphasis on those resulting from a specific form of renal acidosis, the therapeutic indications for each etiological sub-group, and the relationship between osteomalacia and Milkman's syndrome. Medicine 25: 399, 1946. CrossrefMedlineGoogle Scholar6. PinesMudge KLGH: Renal tubular acidosis with osteomalacia. Report of three cases. Amer. J. Med. 11: 302, 1951. CrossrefMedlineGoogle Scholar7. SmithSchreiner LHGE: Studies on renal hyperchloremic acidosis. J. Lab. 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BearnYuGutman AJTFAB: Renal function in Wilson's disease. J. Clin. Invest. 36: 1107, 1957. CrossrefMedlineGoogle Scholar19. Lathem W: Hyperchloremic acidosis in chronic pyelonephritis. New Engl. J. Med. 258: 1031, 1958. CrossrefMedlineGoogle Scholar20. Mudge GH: Clinical patterns of tubular dysfunction. Amer. J. Med. 24: 785, 1958. CrossrefMedlineGoogle Scholar21. Stanbury SW: Some aspects of disordered renal tubular function, in Advances in internal medicine, Vol. IX, Dock, W., and Snapper, I., Eds., Year Book Publishers, Inc., 1958, pp. 231-282. Google Scholar22. HuthMayockKerr EJRLRM: Hyperthyroidism associated with renal tubular acidosis. Discussion of possible relationship. Amer. J. Med. 26: 818, 1959. CrossrefMedlineGoogle Scholar23. SchoenYoung EJG: "Lowe's syndrome." Abnormalities in renal tubular function in combination with other congenital defects. Amer. J. Med. 27: 781, 1959. CrossrefMedlineGoogle Scholar24. FourmanMcConkeySmith PBJW: Defects of water reabsorption and of hydrogen-ion excretion by the renal tubule in hyperparathyroidism. Lancet 1: 619, 1960. CrossrefMedlineGoogle Scholar25. BainesBarclayCooke GHJAWT: Nephrocalcinosis associated with hyperchloremia and low plasma-bicarbonate. Quart. J. Med. 14: 113, 1945. Google Scholar26. CookeKleeman RECR: Distal tubular dysfunction with renal calcification. Yale J. Biol. Med. 23: 199, 1950. MedlineGoogle Scholar27. Engel WJ: Nephrocalcinosis. J. A. M. A. 145: 288, 1951. CrossrefMedlineGoogle Scholar28. Rendle-Short J: Idiopathic renal acidosis in twins. Alkalosis resulting from overdosage of a citrate mixture. Arch. Dis. Child. 28: 55, 1953. CrossrefMedlineGoogle Scholar29. SchreinerSmithKyle GELHLH: Renal hyperchloremic acidosis. Familial occurrence of nephrocalcinosis with hyperchloremia and low serum bicarbonate. Amer. J. Med. 15: 122, 1953. CrossrefMedlineGoogle Scholar30. PittsSchulteSmith HHJWDR: Nephrocalcinosis in a father and three children. J. Urol. 73: 208, 1955. CrossrefMedlineGoogle Scholar31. FossPerryWood GLCBFJ: Renal tubular acidosis. Quart. J. Med. 25: 185, 1956. MedlineGoogle Scholar32. WilanskySchneiderman DLC: Renal tubular acidosis with recurrent nephrolithiasis and nephrocalcinosis. New Engl. J. Med. 257: 399, 1957. CrossrefMedlineGoogle Scholar33. RaiszMcNeelySaxon LJWFL: Studies on the renal concentrating mechanism. I. Role of vasopressin. J. Lab. Clin. Med. 52: 437, 1958. MedlineGoogle Scholar34. GordonMcNamaraBenjamin HHHHR: The response of young infants to ingestion of ammonium chloride. Pediatrics 2: 290, 1948. MedlineGoogle Scholar35. YaffeCraigFellers SJJMFE: Enzyme studies in renal tubular acidosis. J. Dis. Child. 98: 659, 1959. Google Scholar36. YaffeCraigFellers SJJMFX: Studies on renal enzymes in a patient with renal tubular acidosis. Amer. J. Med. 29: 168, 1960. CrossrefMedlineGoogle Scholar37. FourmanMcCance PRA: Tetany complicating the treatment of potassium deficiency in renal acidosis. Lancet 1: 329, 1955. CrossrefGoogle Scholar38. RiverKushnerArmstrongDubinSlodkiCutting GLDSSHASJHO: Renal tubular acidosis with hypokalemia and muscular paralysis. Metabolism 9: 1118, 1960. MedlineGoogle Scholar39. WeltHollanderBlythe LGWWB: The consequences of potassium depletion. J. Chron. Dis. 11: 213, 1960. CrossrefMedlineGoogle Scholar40. YamahiroReynolds HSTB: Potassium wasting in renal tubular acidosis: a specific tubular defect. Clin. Res. 8: 235, 1960. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: *Received for publication November 29, 1960.From the Medical Services, U. S. Air Force Hospital, Travis Air Force Base, Calif., the University of California Hospital, and the Department of Medicine, University of California, San Francisco, Calif.†Chief of Hospital Service, 1605th U. S. Air Force Hospital, APO 406, New York, N. Y.‡Research Fellow in Gastroenterology, University of Washington School of Medicine, Seattle 5, Wash.Requests for reprints should be addressed to Major Russell E. Randall, Jr., (MC) USAF, Chief, Hospital Service, 1605th U. S. Air Force Hospital, APO 406, New York, N. Y. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRenal Tubular DisordersDistal Renal Tubular Acidosis (TYPE I, DRTA)Genetics of UrolithiasisRenal tubular acidosis : pathogenesis, diagnosis and treatmentRenal tubular acidosis — a case reportRenal tubular acidosis in childhoodClinical Utilization of Alkaline Phosphatase MeasurementsRenal tubular acidosisFamilial Renal Tubular AcidosisVARDAMAN M. BUCKALEW JR., M.D.Renal tubular acidosisThe Hereditary Renal DiseasesEhlers-Danlos syndrome with renal tuhular acidosis and medullary sponge kidneysFAMILIAL RENAL TUBULAR ACIDOSIS REVISITEDRUSSELL E. RANDALL JR., M.D.Medullary Sponge Kidney with Renal Tubular Acidosis: A Report of 3 CasesRenal Acid-Base Disorders: Pathogenesis and ManagementRenal tubular acidosis presenting with muscle weaknessThe spectrum of hereditary renal diseasesMedical genetics 1961 1 June 1961Volume 54, Issue 6Page: 1108-1116KeywordsApolipoproteinsAttentionBicarbonatesExcretionHospital medicineMedical servicesPyelonephritis Issue Published: 1 June 1961 PDF downloadLoading ...
https://doi.org/10.7326/0003-4819-54-6-1108Postgraduate Medicine · 1980 · 11 citations
Renal tubular acidosis
AbstractRenal tubular acidosis is not one entity but several. Even though all its forms are characterized by the kidney's inability to excrete an appropriately acid urine, the mechanism of the defect, its laboratory and clinical manifestations, and its management vary considerably. One type can cause disabling complications in various organ systems, while another is generally asymptomatic. Differential diagnosis is straightforward, and treatment effective.
https://doi.org/10.1080/00325481.1980.11715423Dimensions of Critical Care Nursing · 2010 · 2 citations
Renal Tubular Acidosis
AbstractIn Brief Renal tubular acidosis is a relatively uncommon clinical syndrome characterized by the inability of the kidney to adequately excrete hydrogen ions, retain adequate bicarbonate, or both. This syndrome can be categorized into 3 separate disorders, each with unique clinical characteristics. Although an uncommon finding, prompt and inexpensive tests can lead to early intervention and subsequently reduce complications from persistent renal dysfunction. The purpose of this article was to bring awareness of the clinical manifestations, diagnosis, and treatments of renal tubular acidosis to critical care nurses. Renal tubular acidosis is a relatively uncommon clinical syndrome. The purpose of this paper is to bring awareness of the clinical manifestations, diagnosis, and treatment to critical care nurses.
https://doi.org/10.1097/dcc.0b013e3181d24b62Nephrology Dialysis Transplantation · 1995 · 0 citations
Renal tubular dysfunction and acidosis
AbstractJournal Article Renal tubular dysfunction and acidosis Get access Arya M. Sharma Arya M. Sharma Department of General Internal Medicine and Nephrology, Universitätsklinikum Benjamin Franklin, Free University of BerlinGermany Hindenburgdamm 30, D-12200 Berlin Correspondence and offprint requests to: A. M. Sharma, Department of General Internal Medicine and Nephrology, Universitätsklinikum-Benjamin Franklin. Free University of Berlin, Hindenburgdamm 30, D-12200 Berlin, Germany Search for other works by this author on: Oxford Academic PubMed Google Scholar Nephrology Dialysis Transplantation, Volume 10, Issue 9, September 1995, Pages 1544–1545, https://doi.org/10.1093/ndt/10.9.1544 Published: 01 September 1995
https://doi.org/10.1093/ndt/10.9.1544Disease module: DeepOracle (Open Targets). Structures: RDKit from PubChem SMILES. Literature: retrieved by DeepSearch across 234,678,978 indexed works (targeted per-candidate search), resolved on OpenAlex.
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