Evaluation The role of Trefoil Factor1 as early stage biomarker in patients with Nephrolithiasis
Article Sidebar
Main Article Content
Abstract
Nephrolithiasis is a public health problem that affect large scale of
peoples around the world. naturally, there are many substances ,proteins,
lipids, glycosaminoglycans and inorganic compounds, work as kidney
stone inhibitors in the normal renal tubular fluid that inhibit crystal
growth, aggregation, and/or adhesion to renal surfaces, among this
inhibitors we investigate the concentration of trefoil factor 1 (TFF1) as a
stone formation inhibitor and kidney injury biomarker in serum of 75
kidney stone patients and 15 healthy subjects using ELISA technique.
The results shows no significant changes within patients groups while
shows that TFF1 levels were significantly increased in stone patients
when compared with the healthy controls (P≤0.05), which support the
fact that it could use as early marker of kidney injury (KI) .The results
also revealed no significant changes within patients groups while there
was a significant changes between patients and controls for both blood
urea and serum creatinine levels in renal stone patients in comparison to
the apparently healthy control subjects (P ≤0.05). Further investigation
are needed to show the inhibitory effect of TFF1 in urine of kidney stone
patients.
Article Details
This work is licensed under a Creative Commons Attribution 4.0 International License.
Tikrit Journal of Pure Science is licensed under the Creative Commons Attribution 4.0 International License, which allows users to copy, create extracts, abstracts, and new works from the article, alter and revise the article, and make commercial use of the article (including reuse and/or resale of the article by commercial entities), provided the user gives appropriate credit (with a link to the formal publication through the relevant DOI), provides a link to the license, indicates if changes were made, and the licensor is not represented as endorsing the use made of the work. The authors hold the copyright for their published work on the Tikrit J. Pure Sci. website, while Tikrit J. Pure Sci. is responsible for appreciate citation of their work, which is released under CC-BY-4.0, enabling the unrestricted use, distribution, and reproduction of an article in any medium, provided that the original work is properly cited.
References
[1] Alelign, T. and Petros, B. (2018). Kidney Stone Disease: An Update on Current Concepts. Advances in Urology. 2018. 10.1-12.
[2] Sofia, H.N.; Manickavasakam, K. and Walter, T. M. (2016). Prevalence and Risk Factors of Kidney Stone. Global journal for Research Analysis. 5. 183-187.
[3] Lieske, J.C. and Deganello, S. (1999). Nucleation, adhesion, and internalization of calcium-containing urinary crystals by renal cells. J. Am. Soc. Nephrol.10(Suppl. 14):S422–S429.
[4] Parks, J.H.; Coward, M. and Coe, F.L. (1997). Correspondence
between stone composition and urine supersaturation in nephrolithiasis. Kidney Int. 51:894–900.
[5] Mandel, N. (1996). Mechanism of stone formation. Semin. Nephrol. 16:364–374.
[6] Kok, D.J.; Papapoulos, S.E.; and Bijvoet, O.L. (1990). Crystal agglomeration is a major element in calcium oxalate urinary stone formation. Kidney Int. 37:51–56.
[7] Lieske, J.C.; Swift, H.; Martin, T.; Patterson, B. and Toback, F.G. (1994). Renal epithelial cells rapidly bind and internalize calcium oxalate monohydrate crystals. Proc. Natl. Acad. Sci. U. S. A. 91:6987–6991.
[8] Lieske, J.C.; Deganello, S. and Toback, F.G. (1999). Cell-crystal interactions and kidney stone formation. Nephron. 81(Suppl. 1):8–17.
[9] Ramegowda, B.D.; Biyani, C.; Browning, J.A. and Cartledge, J. (2007). The Role of Urinary Kidney Stone Inhibitors and Promoters in the Pathogenesis of Calcium Containing Renal Stones. EAU-EBU Update Series. 5. 126-136.
[10] Kok, D.J.; and Khan, S.R.(1994). Calcium oxalate nephrolithiasis, a free or fixed particle disease. Kidney Int. 46:847–854.
[11] Ryall, R.L. (1996). Glycosaminoglycans, proteins and stone formation: adult themes and child’s play. Pediatr. Nephrol. 10:656–666.
[12] Coe, F.L.; Nakagawa, Y.; Asplin, J. and Parks, J.H. (1994). Role of nephrocalcin in inhibition of calcium oxalate crystallization and nephrolithiasis. Miner. Electrolyte Metab. 20:378–384.
[13] Wesson, J.A.; et al. (2003). Osteopontin is a critical inhibitor of calcium oxalate crystal formation and retention in renal tubules. J. Am. Soc. Nephrol. 14:139–147.
[14] Hess, B. (1994). Tamm-Horsfall glycoprotein and calcium nephrolithiasis. Miner. Electrolyte Metab. 20:393–398.
[15] Kjellev, S. (2009). The trefoil factor family—small peptides with multiple functionalities. Cell Mol Life Sci, 66: 1350–69.
[16] Taupin, D. and Podolsky, D.K. (2003). Trefoil factors: initiators of mucosal healing. Nat Rev Mol Cell Biol, 4: 721–32.
[17] Rinnert, M.; Hinz, M.; Buhtz, P.; et al. (2010). Synthesis and localization of trefoil factor family (TFF) peptides in the human urinary tract and TFF2 excretion into the urine. Cell Tissue Res, 339: 639–47.
[18] Mina, C.N.; Marziyeh, H. and Roja, R. (2018). Dietary Plants for the Prevention and Management of Kidney Stones: Preclinical and Clinical Evidence and Molecular Mechanisms. Int. J. Mol. Sci.19, 765; doi:10.33-39. [19] Astor,B.C. ; Kottgen, A. ; Hwang, S. J. et al. (2011).Trefoil factor 3 predicts incident chronic kidney disease: a case-control study nested within the Atherosclerosis Risk in Communities (ARIC) study. Am. J. Nephrol, 34: 291–7.
[20] Du, T.Y.; Luo, H.M.; Qin, H.C. et al. (2014). Circulating serum trefoil factor 3 (TFF3) is dramatically increased in chronic kidney disease. PLoS One, 8: e80271.
[21] Nagmma, T.; et al. (2014). Evaluation of Oxidative Stress and Antioxidant Activity in Pre and Post Hemodialysis in Chronic Renal Failure Patients From Western Region of Nepal. Bangladesh Journal of Medical Science.13(1):183-192.
[22] Noor ul, A.; Raja, T. et al. (2014). Evaluating Urea and Creatinine Levels in Chronic Renal Failure Pre and Post Dialysis: A Prospective Study. 2(2):208-215.
[23] Jumaa, I. A .( 2013). Study of Some Biochemical Parameters in Blood Serum of Patients with Chronic Renal Failure. Journal of Basrah Researches (Sciences); 39: 4.
[24] Schoorl, M. (2014). Universities of Van Amsterdam Digital Academic Repository (UVA DARE): 176.
[25] Lebherz,E.D.; Tudor, B. J.;Ankersmit,H. et al. (2015). Trefoil Factor 1 Excretion Is Increased in Early Stages of Chronic Kidney Disease. PloS one. 10.285-291.
[26] Lopez - Novoa, J.M.; Martinez - algado, C.; Rodriguez - Pena, A.B. and Lopez - Hernandez, F.J.(2010). Common pathophysiological mechanisms of chronic kidney disease: therapeutic perspectives. Pharmacol Ther, 128: 61–81.
[27] Roth, G.A.; Lebherz - Eichinger, D.; Ankersmit, H.J. et al. (2011).Increased total cytokeratin- 18 serum and urine levels in chronic kidney disease. Clin Chim Acta, 412: 713–7.
[28] Lefebvre, O.; Chenard, M.P.; Masson, R. (1996). Gastric mucosa abnormalities and tumorigenesis in mice lacking the pS2 trefoil protein. Science, 274: 259–62.