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The Importance of Tubular Function in Chronic Kidney Disease

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dc.contributor.authorRisso, Maria A
dc.contributor.authorSallustio, Sofía
dc.contributor.authorSueiro, Valentin
dc.contributor.authorBertoni, Victoria
dc.contributor.authorGonzalez Torres, Henry
dc.contributor.authorMusso, Carlos G
dc.date.accessioned2019-12-13T16:32:03Z
dc.date.available2019-12-13T16:32:03Z
dc.date.issued2019
dc.description.abstractGlomerular filtration rate (GFR) and proteinuria-albuminuria are the renal functional parameters currently used to evaluate chronic kidney disease (CKD) severity. However, tubular secretion is another important renal functional parameter to be taken into account since proximal tubule (PT) secretion, in particular, is a crucial renal mechanism for endogenous organic cations, anions and drug elimination. The residual diuresis is a relevant survival predictor in patients on dialysis, since their urine is produced by the glomerular and tubular functions. It has been hypothesized that drugs which up-regulate some renal tubular transporters could contribute to uremic toxin excretion, and nephroprevention. However, if tubular transporters' down-regulation observed in CKD patients and experimental models is a PT adaptation to avoid intracellular accumulation and damage from uremic toxins, consequently the increase of toxin removal by inducing tubular transporters' up-regulation could be deleterious to the kidney. Therefore, a deeper understanding of this phenomenon is currently needed. In conclusion, tubular function has an important role for endogenous organic cations, anions and drug excretion in CKD patients, and a deeper understanding of its multiple mechanisms could provide new therapeutic alternatives in this population.eng
dc.identifier.issn11787058
dc.identifier.urihttps://hdl.handle.net/20.500.12442/4461
dc.language.isoengeng
dc.publisherDove Presseng
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internacional
dc.rights.accessrightsinfo:eu-repo/semantics/openAccesseng
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.sourceInternational Journal of Nephrology and Renovascular Diseaseeng
dc.sourceVol. 12 (2019)
dc.source.urihttps://doi.org/10.2147/IJNRD.S216673
dc.subjectTubular functioneng
dc.subjectChronic kidney diseaseeng
dc.subjectDrugseng
dc.titleThe Importance of Tubular Function in Chronic Kidney Diseaseeng
dc.typearticleeng
dcterms.referencesSuchy-Dicey AM, Laha T, Hoofnagle A, et al. Tubular secretion in CKD. J Am Soc Nephrol. 2016;27(7):2148–2155. doi:10.1681/ASN. 2014121193eng
dcterms.referencesMusso CG, Gavrilovici C, Covic A. Tubular secretion in chronic kidney disease staging: a new proposal. Int Urol Nephrol. 2017;49 (11):2087–2089. doi:10.1007/s11255-017-1673-0eng
dcterms.referencesMasereeuw R, Mutsaers HA, Toyohara T, et al. The kidney and uremic toxin removal: glomerulus or tubule? Semin Nephrol. 2014;34 (2):191–208. doi:10.1016/j.semnephrol.2014.02.010eng
dcterms.referencesJansen J, De Napoli IE, Fedecostante M, et al. Human proximal tubule epithelial cells cultured on hollow fibers: living membranes that actively transport organic cations. Sci Rep. 2015;5:16702. doi:10. 1038/srep16702eng
dcterms.referencesNigam SK, Bush KT, Martovetsky G, et al. The organic anion transporter (OAT) family: a systems biology perspective. Physiol Rev. 2015;95(1):83–123. doi:10.1152/physrev.00025.2013eng
dcterms.referencesVallon V, Eraly SA, Rao SR, et al. A role for the organic anion transporter OAT3 in renal creatinine secretion in mice. Am J Physiol Renal Physiol. 2012;302(10):F1293–9. doi:10.1152/ajprenal.00013. 2012eng
dcterms.referencesSuzuki T, Toyohara T, Akiyama Y, et al. Transcriptional regulation of organic anion transporting polypeptide SLCO4C1 as a new therapeutic modality to prevent chronic kidney disease. J Pharm Sci. 2011;100(9):3696–3707. doi:10.1002/jps.22641eng
dcterms.referencesShen H, Liu T, Morse BL, et al. Characterization of organic anion transporter 2 (SLC22A7): a highly efficient transporter for creatinine and species-dependent renal tubular expression. Drug Metab Dispos. 2015;43(7):984–993. doi:10.1124/dmd.114.062364eng
dcterms.referencesXu L, Shi Y, Zhuang S, Liu N. Recent advances on uric acid transporters. Oncotarget. 2017;8(59):100852–100862. doi:10.18632/ oncotarget.20135eng
dcterms.referencesDousdampanis P, Trigka K, Musso CG, Fourtounas C. Hyperuricemia and chronic kidney disease: an enigma yet to be solved. Ren Fail. 2014;36(9):1351–1359. doi:10.3109/0886022X.2014.947516eng
dcterms.referencesMusso CG, Alvarez Gregori J, Jauregui JR, Macías Núñez JF. Creatinine, urea, uric acid, water and electrolytes renal handling in the healthy oldest old. World J Nephrol. 2012;1(5):123–126. doi:10.5527/wjn.v1.i5.123eng
dcterms.referencesMusso CG, Juarez R, Vilas M, Navarro M, Rivera H, Jauregui R. Renal calcium, phosphorus, magnesium and uric acid handling: comparison between stage III chronic kidney disease patients and healthy oldest old. Int Urol Nephrol. 2012;44(5):1559–1562. doi:10.1007/ s11255-012-0230-0eng
dcterms.referencesEraly SA, Vallon V, Rieg T, et al. Multiple organic anion transporters contribute to net renal excretion of uric acid. Physiol Genomics. 2008;33(2):180–192. doi:10.1152/physiolgenomics.00207.2007eng
dcterms.referencesJing J, Ekici A, Sitter T, et al. Genetics of serum urate concentrations and gout in a highrisk population, patients with chronic kidney disease. Sci Rep. 2018;8:13184. doi:10.1038/s41598-018-31282-zeng
dcterms.referencesMandal AK, Mount DB. The molecular physiology of uric acid homeostasis. Annu Rev Physiol. 2015;77:323–345. doi:10.1146/ annurev-physiol-021113-170343eng
dcterms.referencesEmami Riedmaier A, Nies AT, Schaeffeler E, Schwab M. Organic anion transporters and their implications in pharmacotherapy. Pharmacol Rev. 2012;64(3):421–449. doi:10.1124/pr.111.004614eng
dcterms.referencesToyohara T, Suzuki T, Morimoto R, et al. SLCO4C1 transporter eliminates uremic toxins and attenuates hypertension and renal inflammation. J Am Soc Nephrol. 2009;20(12):2546–2555. doi:10.1681/ASN.2009070696eng
dcterms.referencesNigam SK, Wu W, Bush KT, Hoenig MP, Blantz RC, Bhatnagar V. Handling of drugs, metabolites,and uremic toxins by kidney proximal tubule drug transporters. Clin J Am Soc Nephrol. 2015;10 (11):2039–2049. doi:10.2215/CJN.02440314eng
dcterms.referencesBhatnagar V, Richard EL, Wu W, et al. Analysis of ABCG2 and other urate transporters in uric acid homeostasis in chronic kidney disease: potential role of remote sensing and signaling. Clin Kidney J. 2016;9 (3):444–453. doi:10.1093/ckj/sfw010eng
dcterms.referencesNigam SK. syndrome of chronic kidney disease: altered remote sensing and signalling. Nat Rev Nephrol. 2019;15(5):301–316. doi:10.1038/s41581-019-0111-1eng
dcterms.referencesWu W, Bush K, Nigam S. Key role for the Organic Anion Transporters, OAT1 and OAT3, in the in vivo handling of uremic toxins and solutes. Sci Rep. 2017;7:4939. doi:10.1038/s41598-017- 04949-2eng
dcterms.referencesWanchai K, Yasom S, Tunapong W, et al. Probiotic Lactobacillus paracasei HII01 protects rats against obese-insulin resistance induced kidney injury and impaired renal organic anion transporter 3 function. Clin Sci (Lond). 2018;132(14):1545–1563. doi:10.1042/CS20180148eng
dcterms.referencesRanganathan N, Ranganathan P, Friedman EA, et al. Pilot study of probiotic dietary supplementation for promoting healthy kidney function in patients with chronic kidney disease. Adv Ther. 2010;27 (9):634–647. doi:10.1007/s12325-010-0059-9eng
dcterms.referencesBlanco VE, Hernandorena CV, Scibona P, Belloso W, Musso CG. Acute kidney injury pharmacokinetic changes and its impact on drug prescription. Healthcare (Basel). 2019;7(1):E10. doi:10.3390/ healthcare7010010eng
dcterms.referencesSaito H. Pathophysiological regulation of renal SLC22A organic ion transporters in acute kidney injury: pharmacological and toxicological implications. Pharmacol Ther. 2010;125(1):79–91. doi:10.1016/j. pharmthera.2009.09.008eng
dcterms.referencesWatanabe H, Sakaguchi Y, Sugimoto R, et al. Human organic anion transporters function as a high-capacity transporter for p-cresyl sulfate, a uremic toxin. Clin Exp Nephrol. 2014;18(5):814–820. doi:10. 1007/s10157-013-0902-9eng
dcterms.referencesDe Broe ME, Porter GA, Bennett WM, Deray G. Clinical Nephrotoxins. Renal Injury from Drugs and Chemicals. New York: Springer; 2008.eng
dcterms.referencesTakada T, Yamamoto T, Matsuo H, et al. Identification of ABCG2 as an exporter of uremic toxin indoxyl sulfate in Mice and as a crucial factor influencing CKD progression. Sci Rep. 2018;8:11147. doi:10. 1038/s41598-018-29208-weng
dcterms.referencesWikoff WR, Nagle MA, Kouznetsova VL, Tsigelny IF, Nigam SK. Untargeted metabolomics identifies enterobiome metabolites and putative uremic toxins as substrates of organic anion transporter 1 (Oat1). J Proteome Res. 2011;10(6):2842–2851. doi:10.1021/pr20 0093weng
dcterms.referencesLowenstein J, Grantham JJ. The rebirth of interest in renal tubular function. Am J Physiol Renal Physiol. 2016;310(11):F1351–5. doi:10.1152/ajprenal.00055.2016eng
dcterms.referencesSteubl D, Block M, Herbst V, et al. Plasma uromodulin correlates with kidney function and identifies early stages in chronic kidney disease patients. Medicine (Baltimore). 2016;95(10):e3011. doi:10.10 97/MD.0000000000003011eng

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