The Effects of COVID-19 in Chronic Kidney Disease: Progression and Increased Severity of Chronic Inflammatory

Yıl 2022, Cilt: 6 Sayı: 2, 203 - 210, 30.08.2022

Hasan Esat Yücel , Naime Meric Konar

https://doi.org/10.46332/aemj.1124062

Öz

Purpose: SARS-COV-2 (Severe acute Respiratory Syndrome Virus) has a wide organotropism. Although it predominantly affects the pulmonary system, it is commonly involved in the kidneys. Studies have shown that it increases acute kidney injury and mortality in patients with chronic kidney disease (CKD). However, its effects on the progression and severity of chronic inflammation in patients who survived and were followed up without dialysis are not yet known. Our aim in the study is to investigate kidney functions and the severity of chronic inflammation in post-COVID CKD.

Materials and Methods: The study was carried out retrospectively. Two groups were created as COVID-CKD(n=54) and NONCOVID CKD (control group)(n=60). Basal Blood Urea Nitrogen (BUN), Urea, Creatinine (Cre), Glomerular Filtration Rate (GFR), White Blood Cell (WBC), Neutrophil (Neu), Lymphocyte (Ly), Platelet (Plt), Plt/Ly ratio (PLR), and Neu/Ly Ratio (NLR) levels were analyzed and compared. Changes in the same parameters were analyzed in the groups, 6 months after the acute infection.

Results: An increase in Cre (p=0.002) and PLR (p=0.02) and a decrease in Ly (p=0.037) and GFR (p=0.001) were observed 6 months after acute infection in the COVID-CKD group. No changes were detected in the NON-COVID group. A positive correlation was found between PLR-NLR and BUN, Cre, and Urea, whilst a negative correlation was detected between PLR-NLR and GFR.

Conclusions: Progression and severity of chronic inflammation increased in SARS-COV-2 infected-survivor, non-dialysis followedup CKD patients. 

Anahtar Kelimeler

chronic inflammation severity, chronic kidney disease, progression, SARS-COV-2

Teşekkür

We would like to thank the information processing team of Kirsehir Ahi Evran University Training and Research Hospital, who contributed to the collection of data, the medical secretaries who recorded the diagnosis, examination, and treatment of the patients in the service and intensive care units, and all the health workers who provided treatment services.

COVID-19 Enfeksiyonunun Kronik Böbrek Hastalığında Progresyon ve Kronik İnflamasyon Şiddetine Etkileri

Öz

Amaç: SARS-COV-2 (Şiddetli akut Solunum Sendromu Virüsü), geniş bir organotropizme sahiptir. Baskın olarak pulmoner sistemi tutsa da, böbreklerde yaygın olarak tutulmaktadır. Kronik böbrek hastalarında (KBH), akut böbrek hasarını ve mortaliteyi artırdığı çalışmalarla gösterilmiştir. Ancak hayatta kalan ve diyalizsiz takipte olan hastalarda progresyon ve kronik inflamasyon şiddetine etkileri henüz bilinmemektedir. Çalışmadaki amacımız post-COVID KBH’da böbrek fonksiyonlarını ve kronik inflamasyon şiddetini araştırmaktır.

Araçlar ve Yöntem: Çalışma retrospektif olarak gerçekleştirildi. COVID-KBH(n=54) ve NON-COVID KBH (kontrol grubu) (n=60) olmak üzere, iki grup oluşturuldu. Grupların bazal Kan Üre Azotu (BUN), Üre, Kreatin (Cre), Glomerüler filtrasyon hızı (GFR), Beyaz kan hücresi (WBC), Nötrofil (Neu), Lenfosit (Ly), Trombosit (Plt), Trombosit/Lenfosit Oranı (PLR) ve Nötrofil/Lenfosit Oranı (NLR) seviyeleri incelendi ve karşılaştırıldı. Akut enfeksiyondan 6 ay sonra olmak üzere, gruplarda aynı parametrelerin değişimleri incelendi. 

Bulgular: COVID-KBH grubunda akut enfeksiyondan 6 ay sonra Cre (p=0.002) ve PLR'de artış(p=0.02), Ly(p=0.037) ve GFR'de (p=0.001) azalma görüldü. NON-COVID grubunda herhangi bir değişiklik tespit edilmedi. COVID grubunda PLR ve NLR ile BUN, Üre ve Cre arasında pozitif korelasyon, GFR ile negatif korelasyon izlendi. NON-COVID grubunda ise NLR ile sadece BUN arasında pozitif korelasyon izlendi.

Sonuç: SARS-COV-2 ile enfekte olup hayatta kalan ve diyalizsiz takipte olan kronik böbrek hastalarında, progresyon ve kronik inflamasyon şiddeti artmıştır.

Anahtar Kelimeler

kronik böbrek hastalığı, kronik inflamasyon şiddeti, kronik inflamasyon şiddeti, progresyon, SARS-COV-2, SARS-COV-2

Kaynakça

• 1. Wanner C, Amann K, Shoji T. The heart and vascular system in dialysis. The Lancet. 2016;388(10041):276-284.
• 2. Levin A, Tonelli M, Bonventre J, et al. Global kidney health 2017 and beyond: a roadmap for closing gaps in care, research, and policy. The Lancet. 2017;390(10105):1888-1917.
• 3. Franceschi C, Campisi J. Chronic Inflammation (Inflammaging) and its potential contribution to age-associated diseases. J Gerontol A Biol Sci Med Sci. 2014;69(Suppl_1):4-9.
• 4. Liu WC, Zheng CM, Lu CL, et al. Vitamin D and immune function in chronic kidney disease. Clin Chim Acta. 2015;450:135-144.
• 5. Kovesdy CP, Kalantar-Zadeh K. Inflammation in chronic kidney disease. In: Sayegh MH (ed), Chronic Kidney Disease, Dialysis, and Transplantation. (3rd ed). Philadelphia: WB Saunders, 2010;183-197.
• 6. Pahl MV, Vaziri ND. Immune function in chronic kidney disease. Kimmel PL, Rosenberg ME. Chronic Renal Disease. 2 nd ed. San Diego:Academic Press; 2015:285-297.
• 7. Süleymanlar G, Altıparmak MR, Seyahi N et al. Türkiye’de Nefroloji, Diyaliz ve Transplantasyon-Registry 2012. Ankara, Türk Nefroloji Derneği Yayınları;2013:743-800.
• 8. Harris MI, Flegal KM, Cowie CC, et al. Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in US adults: the Third National Health and Nutrition Examination Survey, 1988-1994. Diabetes care. 1998;21(4):518-524.
• 9. Li P,Xia C,Liu P,et al. Neutrophil-to-lymphocyte ratio and platelet-to-lymphocyte ratio in evaluation of inflammation in non-dialysis patients with end-stage renal disease (ESRD).BMC Nephrol. 2020;21(1):1-8.
• 10. Tonyali S, Ceylan C, Yahsi S, Karakan MS. Does neutrophil to lymphocyte ratio demonstrate deterioration in renal function? Ren Fail. 2018;40(1):209-212.
• 11. Zhou F, Yu T, Du R, et al. Clinicalcourseand risk factorsformortality of adultinpatientswith COVID-19 in Wuhan, China: a retrospectivecohortstudy. Lancet. 2020;395(10229):1054-1062.
• 12. Li Q, Guan X, Wu P, et al. Earlytransmissiondynamics in Wuhan, China, of novelcoronavirus-infectedpneumonia. N Engl J Med. 2020;382(13):1199-1207.
• 13. Henry BM, Lippi G. Chronickidneydisease is associatedwith severe coronavirusdisease 2019 (COVID-19) infection. Int Urol Nephrol. 2020;52(6):1193-1194.
• 14. Levey AS, Stevens LA, Schmid CH, et al. A new equation to estimate glomerular filtration rate. Ann Intern Med. 2009;150(9):604-612.
• 15. Manabe I. Chronic inflammation links cardiovascular, metabolic and renal diseases. Circ J. 2011;75(12): 2739-2748.
• 16. Akboga MK, Canpolat U, Yuksel M, et al. Platelet to lymphocyte ratio as a novel indicator of inflammation is correlated with the severity of metabolic syndrome: A single center large-scale study. Platelets. 2016;27(2):178-183.
• 17. Iijima R, Ndrepepa G, Mehilli J, et al. Relationship between platelet count and 30-day clinical outcomes after percutaneous coronary interventions. Thromb Haemost. 2007;98(10):852-857.
• 18. Smith RA, Bosonnet L, Raraty M, et al. Preoperative platelet lymphocyte ratio is an independent significant prognostic marker in resected pancreatic ductal adenocarcinoma. Am J Surg. 2009;197(4):466-472.
• 19. Qu R, Ling Y, Zhang YH, et al. Platelet‐to‐lymphocyte ratio is associated with prognosis in patients with coronavirus disease‐19. J Med Virol. 2020;92(9):1533- 1541.
• 20. Kuppalli K, Rasmussen AL. A glimpse into the eye of the COVID-19 cytokinestorm. EBio Medicine. 2020;55(102789).
• 21. Ahbap E,Sakaci T, Kara E,et al. Neutrophil-to-lymphocyte ratio and platelet-tolymphocyte ratio in evaluation of inflammation in end-stage renal disease. Clin Nephrol. 2016;85(4):199-208.
• 22. Sarkar S, Kannan S, Khanna P, Singh AK. Role of platelet‐to‐lymphocyte count ratio (PLR), as a prognostic indicator in COVID‐19: A systematic review and meta‐analysis. J Med Virol. 2022;94(1):211-221.
• 23. Lippi G, Plebani M. The critical role of laboratory medicine during coronavirus disease 2019 (COVID19) and other viral outbreaks. Clin Chem Lab Med. 2020;58(7):1063-1069.
• 24. Qin C, Zhou L, Hu Z, et al. Dysregulation of immune response in patients with COVID-19 in Wuhan, China. Clin Infect Dis. 2020;71(15):762-768.
• 25. Tan L, Wang Q, Zhang D, et al. Lymphopenia predicts disease severity of COVID-19: a descriptive and predictive study. Signal Transduct Target Ther. 2020;5(1):33.
• 26. Dzieniszewski J, Jarosz M, Szczygieł B, et al. Nutritional status of patients hospitalised in Poland. Eur J Clin Nutr. 2005;59(4):552-560.
• 27. Kuo IC, Huang JC, Wu PY, Chen SC, Chang JM, Chen HC. A low geriatric nutrition risk index is associated with progression to dialysis in patients with chronic kidney disease. Nutrients. 2017;9(11):1228.
• 28. Carretero Gómez J, Mafé Nogueroles MC, Garrachón Vallo F, Escudero Álvarez E, Maciá Botejara E, Miramontes González JP; en representación del grupo de Diabetes, Obesidad y Nutrición de la Sociedad Española de Medicina Interna (SEMI).Inflammation, malnutrition, and SARS-CoV-2 infection: a disastrous combination. Rev Clin Esp (Barc). 2020;220(8):511- 517.
• 29. Liu Y, Du X, Chen J, et al. Neutrophil-to-lymphocyte ratio as an independent risk factor for mortalithospitalized patients with COVID-19. J Infect. 2020;81(1):6- 12.
• 30. Yoshitomi R, Nakayama M, Sakoh T, et al. High neutrophil/lymphocyte ratio is associated with poor”” outcomes in Japanese patients with chronic kidney disease. Ren Fail. 2019;41(1):238-243.