Whether Renal Injury is Aggravated in the Overlapping Syndrome of Chronic Obstructive Pulmonary Disease-Obstructive Sleep Apnoea

Abstract

Objectives: Chronic obstructive pulmonary disease-obstructive sleep apnoea (COPD-OSA) syndrome is an overlapping respiratory disease characterised by hypoxia and inflammation. This study aimed to explore the degree of renal injury in COPD-OSA syndrome. Methods: The COPD-OSA rat model was established through exposure to cigarette smoke (CS) combined with chronic intermittent hypoxia (IH). Rats were randomly divided into six groups, including the normal control, CS, 5% IH, 10% IH, CS + 5%IH, and CS + 10% IH. Serum levels of creatinine (Cr), cystatin C (Cys-C), and blood urea nitrogen (Bun) were measured using an enzyme-linked immunosorbent assay. The histopathological injury was evaluated by haematoxylin-eosin staining and transmission electron microscopy. In renal tissues, apoptotic cells were detected by Terminal deoxynucleotidyl transferase-mediated dUTP in situ nick end labelling (TUNEL) staining, and the protein expression of B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) was measured by western blot. Results: The serum level of Cys-C was increased by CS and IH. However, Cr and Bun levels were only significantly increased by 5% IH and CS, respectively. Histopathological injury in rats exposed to CS or IH mainly included tubular epithelial cell oedema, inflammatory cell infiltration, and collagen fibre deposition. Compared with the controls, CS and IH induced more TUNEL-positive cells, upregulated Bax, and downregulated Bcl-2 in renal tissues. In addition, IH had a stronger effect on inducing histopathological injury and apoptosis than CS. CS + IH had an additive effect on aggravating the renal injury in COPD-OSA rats. Conclusions: Renal injury was aggravated in COPD-OSA rats, mainly presenting as serum Cys-C elevation, tubular epithelial cell oedema, inflammatory cell infiltration, collagen fibre deposition, and cell apoptosis.