The Role of Interleukin-6 and Procalcitonin in Kidney Patients have Bacterial and Viral Infection

Abstract

Background: IL-6 is one of the most studied cytokines in kidney disease. It is making inflammation worse by activating B cells that affect the production of hepatic acute phase proteins. It is also involved in metabolic, regenerative, and neurological processes Procalcitonin (PCT) is a typical biomarker for bacterial infections. since it increases in response to bacterial infections but not to other inflammatory reactions such as viral infections. Aim: study the role of IL-6 and PCT on renal failure that is affected by bacterial and viral infection. Methods: Between January and April 2023, 120 patients were confirmed to have chronic renal failure with or without diabetes mellitus who were affected or not via bacterial or viral infections based on previous medical reports and were divided into six groups; each of them included 20 patients. IL-6 and PCT levels were assayed and compared among groups. Different groups had very significantly different levels of IL-6 (90.40±25.77 for patients in G1, 42.33±17.32 for patients in G2, 84.95±19.80 for patients in G3, and 36.68±15.10 for patients in G4). The levels were 2.44±0.79 for patients in G5 and 2.26±0.59 for the control group, respectively (p<0.0001). The levels of PCT were also significantly different between groups (4.77±1.86 for patients in G1; 0.31±0.09 for patients in G2; 4.41±1.43 for patients in G3; 0.28±0.09 for patients in G4). The levels were 0.04±0.01 for patients in G5 and 0.03±0.01 for the control group, respectively (p<0.0001). Results: The findings demonstrated significant in levels of interleukin-6, urea, and creatinine in all patients except diabetic patients and significant increase in the level of procalcitonin in patients who have a bacterial infection, not a viral infection. Conclusion: The level of IL-6 increases in renal failure in both bacterial and viral infection states, but the Procalcitonin level increases in bacterial infection only.