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

Year 2022, , 203 - 210, 30.08.2022

Hasan Esat Yücel , Naime Meric Konar

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

Abstract

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. 

Keywords

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

Thanks

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

Abstract

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.

Keywords

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

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