Dear Editor,
We read the recently published article by Bulcun et al. with a keen interest (Citation1). These researchers recruited 66 patients with chronic obstructive pulmonary disease (COPD) and 40 controls to study the impact of COPD on microalbuminuria. All of the enrolled subjects at inclusion were free of diabetes mellitus (DM), severe congestive heart failure, obstructive sleep apnea and history of overt renal disease or macroalbuminuria. The results of the study demonstrated that the partial pressure of oxygen and BODE index were independently related to the presence of microalbuminuria. Given the methodology of the study (cross-sectional), it is impossible to draw any causality. Nevertheless, we believe that this study further supports the notion that COPD is a systemic disorder, rather than purely a process limited to the lungs. We believe that some issues should be mentioned briefly, which may supplement the above findings.
First, a recent study by Chen et al. (Citation2) published in the same issue of this journal showed that patients with COPD have impaired renal functional reserve. Another finding was that COPD associated inflammation and greater airflow obstruction correlated with decreased renal reserve. Second, chronic kidney disease (CKD) was shown to be common in patients with COPD (Citation3, 4), and the presence of COPD is associated with a greater mortality among patients with CKD (Citation4).
So, what are the mechanisms of COPD related renal dysfunction? It is essential to note that kidneys may be intrinsically prone to cellular hypoxia, because of decreased oxygen consumption (Citation5). On a molecular level, hypoxia can upregulate the activity of hypoxia inducible factor-1 (HIF-1), which in turn leads to enhanced inflammation and oxidative stress (Citation6–8). On a kidney level, hypoxia can lead to propagated inflammatory response and fibrotic changes (Citation9, 10).
On the other hand, it is essential to keep in mind the association between COPD and other medical conditions, which are known to be established risk factors for renal disease. One of such co-morbid conditions is DM. Indeed, scientific evidence suggests that COPD may increase the risk for the development of type 2 DM (Citation11). COPD-related systemic inflammation and oxidative stress may mediate the relationship between COPD and type 2 DM (Citation12). On the other hand, the development of albuminuria may partly explain the increased risk of cardiovascular disease in patients with COPD (Citation13–15).
In conclusion, it is important to note that prospective studies with a large population sample size are urgently needed to answer the questions whether COPD is indeed a risk factor for kidney disease. We are grateful to Bulcun et al. for their dedication to studying the association between COPD and renal dysfunction, which further support the link between hypoxia, systemic inflammation and renal damage.
Declaration of Interest Statement
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.
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