Jsmc-10287

USING CYSTATIN C TO ASSESS KIDNEY DAMAGE IN BETA THALASSEMIC PATIENTS RESIDING IN SULAIMANI CITY

Dereen Najat a and Lana Karim b

a Chemistry Department, University of Sulaimani, Kurdistan Region/ Iraq.

b Pharmacy School, University of Sulaimani, Kurdistan Region/ Iraq.

Submitted: 23/2/2020; Accepted: 9/6/2020; Published: 21/3/2021

DOI Link: https://doi.org/10.17656/jsmc.10287

ABSTRACT

Background

In beta-thalassemia, major patients usually have anemia and iron overload which affects the function of many organs such as the heart, liver, and kidneys. Many previous studies concentrated on heart and liver complications, but fewer researches have focused on kidney dysfunction.

Objectives

Our main aim was to study renal dysfunction in BTM patients in the Sulaimani thalassemia center, using both novel urinary dysfunction markers (cystatin C) and traditional urine biomarkers.

Methods

This study was a case-control study (101 thalassemic patients and 97 controls). We studied the hematological parameters of the patients; we also assessed kidney function using cystatin c, serum creatinine, and blood urea and albumin creatinine ratio. T-test was used to assess the difference between study and control groups.

Results

Our results for the thalassemic group were as follow; serum iron levels were 240.27 (std.= ±80.80) µg/dl, mean serum ferritin was 1559.32 (std= ±1066.02) ng/ml; mean haemoglobin levels were 7.99 (std=± 1.14). The mean blood urea was 26.13 mg/dl (std.= ±7.38), serum creatinine was 0.43 mg/dl (std.=±0.16). The mean urinary albumin creatinine ratio was 271.14 mg/g (std=±131.23); mean eGFR (creatinine) was 170.0 (std.=101.1); mean eGFR (cystatin c) was 76.7 ml/min/1.73 (std.=±39.5).

Conclusion

Our results showed the majority of BTM were anaemic and suffered from iron overload despite the use of iron chelating agents. Our kidney function tests showed that although traditional urinary markers doesn’t show kidney damage, the novel biomarker cystatin C showed BTM might have early kidney damage.

KEYWORDS

ICystatin C; Beta thalassemia major; Kidney dysfunction; eGFR; Biomarker.

References

1. Origa R. β-Thalassemia. Genet Med [Internet]. 2017 Jun 3;19(6):609–19.

2. WHO-TIF. Management of hemoglobin disorders. Rep a Jt WHO-TIF Meet Nicosia, Cyprus. 2008;

3. Abolghasemi H, Amid A, Zeinali S, Radfar MH, Eshghi P, Rahiminejad MS, et al. Thalassemia in Iran: Epidemiology, prevention, and management. J PediatrHematolOncol. 2007;

4. Kadhim KA, Baldawi KH, Lami FH. Prevalence, Incidence, Trend, and Complications of Thalassemia in Iraq.Hemoglobin. 2017;

5. Sabzghabaei F, Darnahal M, Azarkeivan A. Renal function in β-thalassemia major receiving desferal versus deferasirox. J RenInj Prev. 2018;

6.Musallam KM, Taher AT. Mechanisms of renal disease in β-thalassemia. J Am SocNephrol. 2012;

7. Galanello R, Origa R. Beta-thalassemia. Orphanet Journal of Rare Diseases. 2010.

8. Moukalled NM, Bou-Fakhredin R, Taher AT. Deferasirox: Over a decade of experience in thalassemia. Mediterranean Journal of Hematology and Infectious Diseases. 2018.

9. Voskaridou E, Terpos E, Michail S, Hantzi E, Anagnostopoulos A, Margeli A, et al. Early markers of renal dysfunction in patients with sickle cell/β-thalassemia. Kidney Int. 2006;

10. Badeli H, Baghersalimi A, Eslami S, Saadat F, Rad AH, Basavand R, et al. Early Kidney Damage Markers after Deferasirox Treatment in Patients with Thalassemia Major: A Case-Control Study. Oxid Med Cell Longev [Internet]. 2019 Apr 21; 2019:1–8.

11. Perrone RD, Madias NE, Levey AS. Serum creatinine as an index of renal function: New insights into old concepts. Clinical Chemistry. 1992.

12. Economou M, Printza N, Teli A, Tzimouli V, Tsatra I, Papachristou F, et al. Renal dysfunction in patients with beta-thalassemia major receiving iron chelation therapy either with deferoxamine and deferiprone or with deferasirox. Acta Haematol. 2010;

13. Díaz-García JD, Gallegos-Villalobos A, Gonzalez-Espinoza L, Sanchez-Niño MD, Villarrubia J, Ortiz A. Deferasirox nephrotoxicity - The knowns and unknowns. Nature Reviews Nephrology. 2014.

14. Shemesh O, Golbetz H, Kriss JP, Myers BD. Limitations of creatinine as a filtration marker in glomerulopathic patients. Kidney Int. 1985;

15. Samra M, Abcar AC. False estimates of elevated creatinine. Perm J. 2012;

16. Şen V, Ece A, Uluca Ü, Söker M, Güneş A, Kaplan I, et al. Urinary early kidney injury molecules in children with beta-thalassemia major. Ren Fail. 2015;

17. Mohkam M, Shamsian BS, Gharib A, Nariman S, Arzanian MT. Early markers of renal dysfunction in patients with beta-thalassemia major.Pediatr Nephrol. 2008;

18. Aldudak B, Bayazit AK, Noyan A, Özel A, Anarat A, Sasmaz I, et al. Renal function in pediatric patients with β-thalassemia major. PediatrNephrol. 2000;

19. Kassab-Chekir A, Laradi S, Ferchichi S, Haj Khelil A, Feki M, Amri F, et al. Oxidant, antioxidant status and metabolic data in patients with beta-thalassemia. Clin Chim Acta. 2003;

20. Milo G, Nevo RFG, Pazgal I, Gafter-Gvili A, Shpilberg O, Gafter U, et al. GFR in patients with β-thalassemia major. Clin J Am SocNephrol. 2015;

21. Smolkin V, Halevy R, Levin C, Mines M, Sakran W, Ilia K, et al. Renal function in children with β-thalassemia major and thalassemia intermedia. Pediatr Nephrol. 2008;

22.Murray P. Fundamental issues in questionnaire design. AccidEmergNurs. 1999;

23.Groenwold RHH, Van Smeden M. Efficient sampling in unmatched case-control studies when the total number of cases and controls is fixed. Epidemiology. 2017;

24. Houlihan CA, Tsalamandris C, Akdeniz A, Jerums G. Albumin to creatinine ratio: A screening test with limitations. Am J Kidney Dis. 2002;

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