Document Type : Original Article
Authors
1
Department of Internal Medicine, Faculty of Medicine, Al-Azhar University, Cairo, Egypt
2
Department of Clinical Pathology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt
3
Department of Medical Physiology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt
Abstract
Background: Diabetes mellitus [DM] is growing into a global epidemic and diabetic nephropathy [DN] is one of its most feared complications. Inflammation is an important mechanism in the pathogenesis of DN and many studies have pointed to anaphylatoxins, complement 3a [C3a] and complement 5a [C5a], being involved in the pathogenesis of DN.
The aim of the work: The aim of this work was validation of C3a and C5a as biomarkers in DN.
Patients and Methods: The study included 96 participants. They were divided into three groups: Group I [32 healthy subjects], Group II [32 diabetic patients without evidence of DN] and Group III [32 diabetic patients with evidence of DN]. All were evaluated by history taking, clinical examination and laboratory tests [blood sugar, HbA1c, urea & creatinine, urine albumin to creatinine ratio, lipid profile and complete blood count]. Estimated glomerular filtration rate was calculated using Modification of Diet in Renal Disease patients’ formula. C3a and C5a levels were measured by ELISA.
Results: at C3a was significantly higher in diabetic groups than the controls. However, the difference diabetic and DN groups was non-significant. C5a was increased in both disease groups, but significantly higher in DN. At a cutoff value > 4.27 µg/ml, C3a can be a significant predictor of DM [sensitivity 75%, specificity of 96%, PPV 78.8% and NPV 95.6%]. However, C5a couldn't be a significant predictor of DM. At a cutoff value > 52.129 ng/mL, C5a can be a significant predictor of DN [sensitivity 80.65 %, specificity 73.33 %, PPV 56.4 % and NPV 89.8%].
Conclusion: The anaphylatoxins C3a and C5a, which are important effector molecules of the complement cascades, produce their effects through inducing inflammation participating in the pathogenesis of diabetic kidney disease [DKD].
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