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Journals / Turkish Journal of Medical Sciences / 2018 / Cilt: 48 - Sayı: 3

Serum vasohibin-1 and suppression of tumorigenicity-2 levels in children with predialysis chronic kidney disease

Nuran ÇETİN
Nadide Melike SAV
Pages
576–583
Publication Date
2022-11-03
DOI
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⚡ TL;DR(Too Long; Didn't Read)

The measurement of serum sST2 levels might contributeto early detection of hypertension in patients.

📌 3 Key Takeaways

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Objective & Hypothesis:Background/aim: Chronic kidney disease (CKD), which is one of the most important health problems worldwide, could be consideredas an immune inflammatory disease.
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Key Findings & Data:A prognostic biomarker may be helpful in determining the progression of CKD in children.We aimed to investigate the serum vasohibin-1 and soluble suppression of tumorigenicity-2 (sST2) levels as potential biomarkers inchildren with predialysis CKD.Materials and methods: Forty-seven children with stage 2–4 CKD and 20 healthy controls were included in this cross-sectional study.Glomerular filtration rate (GFR) and urinary excretion of protein were measured in 24-h urine samples.
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Conclusion & Impact:The measurement of serum sST2 levels might contributeto early detection of hypertension in patients.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Abstract

Background/aim: Chronic kidney disease (CKD), which is one of the most important health problems worldwide, could be consideredas an immune inflammatory disease. A prognostic biomarker may be helpful in determining the progression of CKD in children.We aimed to investigate the serum vasohibin-1 and soluble suppression of tumorigenicity-2 (sST2) levels as potential biomarkers inchildren with predialysis CKD.Materials and methods: Forty-seven children with stage 2–4 CKD and 20 healthy controls were included in this cross-sectional study.Glomerular filtration rate (GFR) and urinary excretion of protein were measured in 24-h urine samples. Serum vasohibin-1 levels andsST2 were measured. The results were expressed as pg/mL and ng/mL, respectively.Results: Serum vasohibin-1 levels were similar between the patients and the control group (P > 0.05), but serum vasohibin-1 levels werehigher in patients with proteinuria than in nonproteinuric patients (2574.5 ± 701.60 vs. 1822.4 ± 300.32 pg/mL, P = 0.001). A positivecorrelation was found between serum vasohibin-1 levels and 24-h urine protein values in patients (P = 0.036). Serum sST2 levels werehigher in patients than the control group (P = 0.013). The patients with hypertension had higher sST2 levels than normotensive patients(P = 0.015). Serum vasohibin-1 and sST2 levels were not correlated with age, GFR, albumin, hemoglobin, or PTH levels.Conclusion: Serum vasohibin-1 and sST2 levels were not associated with decline in renal function. Elevated serum vasohibin levels maybe a compensatory response to proteinuria in patients with predialysis CKD. The measurement of serum sST2 levels might contributeto early detection of hypertension in patients.

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Cite This Article

ÇETİN, N., SAV, N. M. (2022). Serum vasohibin-1 and suppression of tumorigenicity-2 levels in children with predialysis chronic kidney disease. Turkish Journal of Medical Sciences, Cilt: 48 - Sayı: 3, 576–583. https://ajindex.com/articles/610226

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References (9)

  1. Collins AJ, Foley RN, Chavers B, Gilbertson D, Herzog C, Johansen K, Kasiske B, Kutner N, Liu J, St Peter W et al. United States Renal Data System 2011 annual data report: Atlas of chronic kidney disease & end-stage renal disease in the United States. Am J Kidney Dis 2012; 59: e1-420. Fogo AB. Mechanisms of progression of chronic kidney disease. Pediatr Nephrol 2007; 22: 2011-2022.
  2. Hung AM, Crawford DC, Griffin MR, Brown-Gentry K, Lipkowitz MS, Siew ED, Cavanaugh K, Lewis JB, Ikizler TA. CRP polymorphisms and progression of chronic kidney disease in African Americans. Clin J Am Soc Nephrol 2010; 5: 24-33.
  3. Tonelli M, Sacks F, Pfeffer M, Jhangri GS, Curhan G. Biomarkers of inflammation and progression of chronic kidney disease. Kidney Int 2005; 68: 237-245.
  4. Lv W, Booz GW, Wang Y, Fan F, Roman RJ. Inflammation and renal fibrosis: Recent developments on key signaling molecules as potential therapeutic targets. Eur J Pharmacol 2018: 5; 820: 65-76.
  5. Kakkar R, Lee RT. The IL-33/ST2 pathway: therapeutic target and novel biomarker. Nat Rev Drug Discov 2008; 7: 827-840.
  6. Schmitz J, Owyang A, Oldham E, Song Y, Murphy E, McClanahan TK, Zurawski G, Moshrefi M, Qin J, Li X et al. IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines. Immunity 2005; 23: 479-490.
  7. Mildner M, Storka A, Lichtenauer M, Mlitz V, Ghannadan M, Hoetzenecker K, Nickl S, Dome B, Tschachler E, Ankersmit HJ. Primary sources and immunological prerequisites for sST2 secretion in humans. Cardiovasc Res 2010; 87: 769-777.
  8. Buckley JM, Liu JH, Li CH, Blankson S, Wu QD, Jiang Y, Redmond HP, Wang JH. Increased susceptibility of ST2- deficient mice to polymicrobial sepsis is associated with an impaired bactericidal function. J Immunol 2011; 187: 4293- 4299. Griesenauer B, Paczesny S. The ST2/iL-33 Axis in immune cells during inflammatory diseases. Front Immunol 2017; 8: 475. Liang H, Xu F, Wen XJ, Liu HZ, Wang HB, Zhong JY, Yang CX, Zhang B. Interleukin-33 signaling contributes to renal fibrosis following ischemia reperfusion. Eur J Pharmacol 2017; 812: 18-27. Folkman J. Angiogenesis in cancer, vascular, rheumatoid and other disease. Nat Med 1995; 1: 27-31.
  9. Tufro A, Norwood VF, Carey RM, Gomez RA. Vascular endothelial growth factor induces nephrogenesis and vasculogenesis. J Am Soc Nephrol 1999; 10: 2125-2134. Sato Y. Novel link between inhibition of angiogenesis and tolerance to vascular stress. J Atheroscler Thromb 2015; 2