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Submitted: 14 Sep 2021
Accepted: 20 Oct 2021
ePublished: 30 Oct 2021
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J Nephropharmacol. 2023;12(1): e10437.
doi: 10.34172/npj.2022.10437

Scopus ID: 85146856831
  Abstract View: 11018
  PDF Download: 1734

Original

IL1RN VNTR Polymorphism and kidney damage in sickle cell anemia patients

LVKS Bhaskar 1* ORCID logo, Smaranika Pattnaik 2 ORCID logo

1 Department of Zoology, Guru Ghasidas Vishwavidyalaya, Bilaspur, India
2 Department of Biotechnology and Bioinformatics, Sambalpur University, India
*Corresponding Author: Corresponding author: LVKS Bhaskar, Email: , Email: lvksbhaskar@gmail.com

Abstract

Introduction: Sickle cell anemia (SCA) is a chronic illness associated with acute and chronic hemolytic anemia, recurrent vaso-occlusion episodes, intense pain, progressive multiple organ damage, and early mortality. Inflammation plays a significant role in the pathophysiology of SCA. Elevated levels of pro-inflammatory cytokines are involved in worsening the degree of kidney damage in SCA patients.

Objectives: The present study aimed to assess whether IL1RN VNTR polymorphism is associated with kidney damage in patients with SCA.

Patients and Methods: We have investigated 190 SCA patients (104 with Normal kidney function and 86 with kidney damage). Creatinine-based estimated glomerular filtration rate (eGFR) was calculated to assess kidney function. Interleukin-1 receptor antagonist gene (IL1RN) variable number tandem repeats (VNTR) genotypes were analyzed using PCR-electrophoresis. The association between IL1RN-VNTR and kidney damage was evaluated by using χ2 test. Odds ratios (OR) and 95% CI were calculated. The relationship between kidney damage and fetal hemoglobin (HbF) and their interaction with IL1RN-VNTR genotypes, was investigated using a Mantel-Haenszel (M-H) stratified analysis.

Results: There were no significant differences in genotype frequencies between SCA patients with or without kidney damage (P=0.107). Furthermore, no significant interactions between IL1RN VNTR and HbF on determining kidney damage were found.

Conclusion: These results conflict with the biological plausibility that interleukin levels modulate SCA pathophysiology and may deserve further exploration.


Implication for health policy/practice/research/medical education:

Inflammation plays a significant role in the pathophysiology of sickle cell anemia. Although there is no significant association between IL1RN-VNTR and kidney damage in this study, in vitro and in vivo data supporting the role of interleukin in pathophysiology of sickle cell anemia.

Please cite this paper as: Bhaskar LVKS, Pattnaik S. IL1RN VNTR Polymorphism and kidney damage in sickle cell anemia patients. J Nephropharmacol. 2023;12(1):e10437. DOI: 10.34172/npj.2022.10437.

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