COVID-19 hastalığı böbrek taşı olan hastaları nasıl etkiledi?

Öz

Amaç: Böbrek taşı varlığı ile COVID-19 hastalığı arasındaki ilişkinin değerlendirilmesi
Gereç ve yöntem: COVID-19 tanısı ile 15 Kasım-31 Aralık 2020 tarihleri arasında 2. ve 3. basamak 2 farklı merkezde ayaktan, servis ve/veya yoğun bakımda tedavi uygulanan hastalar retrospektif olarak tarandı. Öncelikle hastalar böbrek taşı varlığına göre alt gruplara ayrıldı ve daha sonra böbrek taşı olan olgular, ayaktan tedavi gören hastalar Grup 1, serviste yatarak tedavi gören hastalar Grup 2 ve yoğun bakımda tedavi ihtiyacı doğan olgular ise Grup 3 olarak kategorize edildi.
Bulgular: Çalışmaya toplam 1335 COVID-19 hastası dahil edildi. Ayaktan tedavi edilen 450 hastanın 31'inde (%6,9), serviste yatan 460 hastanın 41'inde (%8,9) ve yoğun bakımda yatan 425 hastanın 60'ında (%14,1) böbrek taşı mevcuttu. Grup 1'de, böbrek taşı olan hastalarda COVID-19 tedavi süresi böbrek taşı olmayan hastalara göre anlamlı olarak daha uzundu (8,1±1,7 ve 6,8±2,2 gün, p=0,01). Grup 2 ve Grup 3'te ortalama hastanede kalış süresi böbrek taşı olan hastalarda böbrek taşı olmayanlara göre anlamlı olarak daha uzundu (sırasıyla 9,1±3,7 ve 6,2±2,1 gün, p=0,007; 19,1±8,1 ve 11,3±6,2 gün, p=0,001).
Sonuç: Böbrek taşı olanlarda COVID-19 tedavi süresinin daha fazla ve COVID-19 enfeksiyonunun daha şiddetli olduğu saptandı.

Anahtar Kelimeler

• COVID-19
• Böbrek taşı
• nefrolitiazis
• pandemi

How has the COVID-19 disease affected patients with kidney stones?

Öz

Purpose: To evaluate the relationship between the presence of kidney stones and COVID-19.
Materials and methods: Patients, who were treated for COVID-19 as outpatients as well as inpatients in the ward and/or ICU of two different secondary and tertiary care centers between July 15, 2020, and December 31, 2020, and aged ≥18 years were retrospectively evaluated. The patients were divided into two subgroups based on the presence of kidney stones, and then the patients with kidney stone were categorized into three groups: those who were treated in an outpatient setting (Group 1), those who were treated in the ward (Group 2), and those who were treated in the intensive care unit (Group 3).
Results: The total of 1,335 COVID-19 patients included in the study. Kidney stone was present in 31 (6.9%) of 450 outpatients, 41 (8.9%) of 460 inpatients treated in the ward, and 60 (14.1%) of 425 inpatients treated in the intensive care unit. In Group 1, the duration of COVID-19 treatment was significantly longer in patients with kidney stone than patients without kidney stone (8.1±1.7 vs. 6.8±2.2 days, p=0.01). In Group 2 and in Group 3, the mean hospitalization duration was significantly longer in patients with kidney stone than in those without kidney stone (9.1±3.7 vs. 6.2±2.1 days, p=0.007; 19.1±8.1 vs. 11.3±6.2 days, p=0.001, respectively).
Conclusion: The duration of COVID-19 treatment was longer and the COVID-19 infection was more severe in those with kidney stones.

Anahtar Kelimeler

• COVID-19
• kidney stone
• nephrolithiasis
• pandemic

Kaynakça

1. 1. Erensoy, S., SARS-CoV-2 and Microbiological Diagnostic Dynamics in COVID-19 Pandemic. Mikrobiyoloji bulteni, 2020. 54(3): p. 497-509.
2. 2. Krishnan, A., et al., A narrative review of coronavirus disease 2019 (COVID-19): clinical, epidemiological characteristics, and systemic manifestations. Intern Emerg Med, 2021: p. 1-16.
3. 3. Mehta, P., et al., COVID-19: consider cytokine storm syndromes and immunosuppression. Lancet, 2020. 395(10229): p. 1033-1034.
4. 4. Yoshikawa, T., et al., Severe acute respiratory syndrome (SARS) coronavirus-induced lung epithelial cytokines exacerbate SARS pathogenesis by modulating intrinsic functions of monocyte-derived macrophages and dendritic cells. J Virol, 2009. 83(7): p. 3039-48.
5. 5. Yuki, K., M. Fujiogi, and S. Koutsogiannaki, COVID-19 pathophysiology: A review. Clin Immunol, 2020. 215: p. 108427.
6. 6. Pirola, C.J. and S. Sookoian, Age but not sex may explain the negative effect of arterial hypertension and diabetes on COVID-19 prognosis. J Infect, 2020. 81(4): p. 647-679.
7. 7. Ragab, D., et al., The COVID-19 Cytokine Storm; What We Know So Far. Front Immunol, 2020. 11: p. 1446.
8. 8. López-Lluch, G., et al., Mitochondrial responsibility in ageing process: innocent, suspect or guilty. Biogerontology, 2015. 16(5): p. 599-620.

9. 9. Moreno Fernández-Ayala, D.J., P. Navas, and G. López-Lluch, Age-related mitochondrial dysfunction as a key factor in COVID-19 disease. Exp Gerontol, 2020. 142: p. 111147.
10. 10. Sorokin, I., et al., Epidemiology of stone disease across the world. World Journal of Urology, 2017. 35(9): p. 1301-1320.
11. 11. Scales, C.D., Jr., et al., Prevalence of kidney stones in the United States. Eur Urol, 2012. 62(1): p. 160-5.
12. 12. Patel, M., et al., Oxalate induces mitochondrial dysfunction and disrupts redox homeostasis in a human monocyte derived cell line. Redox Biol, 2018. 15: p. 207-215.
13. 13. de Lucena, T.M.C., et al., Mechanism of inflammatory response in associated comorbidities in COVID-19. Diabetes Metab Syndr, 2020. 14(4): p. 597-600.
14. 14. Zhu, N., et al., A Novel Coronavirus from Patients with Pneumonia in China, 2019. N Engl J Med, 2020. 382(8): p. 727-733.
15. 15. Darisipudi, M.N. and F. Knauf, An update on the role of the inflammasomes in the pathogenesis of kidney diseases. Pediatr Nephrol, 2016. 31(4): p. 535-44.
16. 16. Joosten, L.A.B., et al., Asymptomatic hyperuricaemia: a silent activator of the innate immune system. Nat Rev Rheumatol, 2020. 16(2): p. 75-86.
17. 17. Mulay, S.R., A. Evan, and H.J. Anders, Molecular mechanisms of crystal-related kidney inflammation and injury. Implications for cholesterol embolism, crystalline nephropathies and kidney stone disease. Nephrol Dial Transplant, 2014. 29(3): p. 507-14.
18. 18. Zeng, G., et al., Prevalence of kidney stones in China: an ultrasonography based cross-sectional study. BJU Int, 2017. 120(1): p. 109-116.
19. 19. Fu, Y., Y. Cheng, and Y. Wu, Understanding SARS-CoV-2-Mediated Inflammatory Responses: From Mechanisms to Potential Therapeutic Tools. Virol Sin, 2020. 35(3): p. 266-271.
20. 20. Favalli, E.G., et al., COVID-19 infection and rheumatoid arthritis: Faraway, so close! Autoimmun Rev, 2020. 19(5): p. 102523.
21. 21. Ferri, C., et al., COVID-19 and rheumatic autoimmune systemic diseases: report of a large Italian patients series. Clin Rheumatol, 2020. 39(11): p. 3195-3204.
22. 22. Popa, I.V., et al., COVID-19 and Inflammatory Bowel Diseases: Risk Assessment, Shared Molecular Pathways, and Therapeutic Challenges. Gastroenterol Res Pract, 2020. 2020: p. 1918035.
23. 23. Doran, M.F., et al., Frequency of infection in patients with rheumatoid arthritis compared with controls: a population-based study. Arthritis Rheum, 2002. 46(9): p. 2287-93.
24. 24. Franklin, J., et al., Risk and predictors of infection leading to hospitalisation in a large primary-care-derived cohort of patients with inflammatory polyarthritis. Ann Rheum Dis, 2007. 66(3): p. 308-12.
25. 25. Fink, H.A., et al., Medical management to prevent recurrent nephrolithiasis in adults: a systematic review for an American College of Physicians Clinical Guideline. Ann Intern Med, 2013. 158(7): p. 535-43.
26. 26. Holmes, R.P. and D.G. Assimos, The impact of dietary oxalate on kidney stone formation. Urol Res, 2004. 32(5): p. 311-6.
27. 27. Nunnari, J. and A. Suomalainen, Mitochondria: in sickness and in health. Cell, 2012. 148(6): p. 1145-59.
28. 28. Khan, S.R., Reactive oxygen species, inflammation and calcium oxalate nephrolithiasis. Transl Androl Urol, 2014. 3(3): p. 256-276.
29. 29. Williams, J., et al., Monocyte Mitochondrial Function in Calcium Oxalate Stone Formers. Urology, 2016. 93: p. 224.e1-6.
30. 30. Meftahi, G.H., et al., The possible pathophysiology mechanism of cytokine storm in elderly adults with COVID-19 infection: the contribution of "inflame-aging". Inflamm Res, 2020. 69(9): p. 825-839.