We read with interest the article by Nishimura et al. [1], reporting an association between parasympathetic neuropathy and left ventricular hypertrophy (LVH) in diabetic patients on haemodialysis. We are pleased to see that the results of this study extend to the population of diabetic uraemic patients, observations that we made 4 years ago and reported in this journal [2]. The study by Nishimura et al. makes even more compelling the need to establish whether the link between autonomic neuropathy and LVH found in our study and now confirmed in diabetic-uraemics is causal or non-causal. The authors speculate at length on the nature of this link, but miss the most likely mechanism explaining this intriguing association. In our study, which the authors may not have noticed (not quoted), we provided circumstantial evidence that nocturnal hypoxaemia may explain both dysautonomia and LVH, a pathogenetic possibility which appears even more likely in diabetics, a population at high risk for sleep apnoea as well as dysautonomia [3]. It would be of interest for Nishimura et al. to reanalyse their data taking into account heart geometry, because we found that concentric hypertrophy is very frequent in patients with nocturnal hypoxaemia [4]. Considering sleep apnoea as a potential mechanism mediating dysautonomia and LVH is important because sleep apnoea is a modifiable, though systematically neglected, cardiovascular risk factor in end-stage renal disease patients.
Conflict of interest statement. None declared.
Ospedali Riuniti UO Nefrologia and CNR-IBIM 89124 Reggio Calabria Italy Email: carmine.zoccali{at}ibim.cnr.it
References
|