Editor,

We read with great interest the recent publication ‘Gut microbiota and chronic kidney disease: implications for novel mechanistic insights and therapeutic strategies’ by Pan et al. [1]. Authors remarked that the intestinal microbiota plays a key role in the pathogenesis of chronic kidney disease (CKD) and CKD-associated complications. In our opinion, some additional data can be added to the pathogenesis of CKD regarding gut and renal axis.

In 1980s oxalic acid was found to be another exogenous cardiotoxic uremic retention molecule that cannot be removed effectively via hemodialysis [2]. Oxalobacter formigenes (O. formigenes) has important roles in oxalate homeostasis by providing both reduction and secretion [3]. Recently, Turkmen et al. [4] hypothesized that serum oxalic acid degradation is impaired mainly due to decreased O. formigenes colonization in hemodialysis patients and increased oxalic acid levels might be responsible for increased cardiovascular outcomes in CKD patients. In this regard, our group showed that the colonization of O. formigenes was extremely low in HD patients and furthermore we found a positive correlation between serum oxalic acid levels and pulse wave velocity, central aortic systolic/diastolic blood pressures in this population [5]. These changes might be related to the decreased consumption of dietary fiber, delayed colonic transit times, chronic constipation, and impairment of protein assimilation in the small intestine secondary to the uremic milieu in CKD patients [6]. In this context, we also hypothesized that the reduction in serum oxalic acid levels can improve cardiovascular outcomes in HD patients [3].

Therefore, replacement of O. formigenes with probiotics such as natural products might decrease serum oxalic acid levels and improve CKD-associated complications. We hope that the previously mentioned comments might add to the value of the manuscript by Pan et al.