Issue 5, 2009June 2009

In this issue of Nephron Digest, based on papers from Nephron Clinical Practice issue 112/3/09, strong emphasis is on obesity, oxidant stress and vascular damage in CKD patients.

I would like to encourage the readers of Nephron Digest to engage in a dialogue by emailing me issues of global nephrological interest for dicussion. These would be addressed by expert members of the editorial board of Nephron.




Professor Meguid El Nahas, PhD, FRCP
Editor, Nephron Clinical Practice
nephron@sheffield.ac.uk
m.el-nahas@sheffield.ac.uk



  Digest of issue 112/3/2009
The minireview by Stephen Ting et al. (Nephron Clin Pract 2009;112:c121-c127) from Indranil Dasgupta's group in Birmingham, UK, is a timely reminder of the associations between obesity and CKD.

The global rise in overweight and obese people (more than a billion worldwide) is rapidly becoming a central focus of the global increase in chronic non-communicable disease including CVD and the associated CKD. Cardio-Kidney-Damage is a major byproduct of obesity both in affluent and deprived societies.


Kawar and colleagues (Nephron Clin Pract 2009;112:c205-c212) from the Sheffield Kidney Institute, UK, report an increasing prevalence of microalbuminuria (27%) with increasing weight in the general population of a large city in the UK (Sheffield; relative risk = 8). Microalbuminuria in obesity has been linked with systemic inflammation, endothelial dysfunction and vascular stiffness (Hermans et al, J Am Soc Nephrol 2007;18:1942-1952). Weight loss is associated with regression of microalbuminuria along with a reduction of systemic inflammation (Bello et al, Nephrol Dial Transplant 2007;22:1619-1627) and vascular stiffness (Goldberg et al, Clin Nutr 2009;28:21-25).

Eddington and co-workers (Nephron Clin Pract 2009;112:c190-c198) from Salford, UK, report data from the Chronic Renal Insufficiency Standards Implementation Study (CRISIS) showing that vascular stiffness, an early feature of CKD, is associated primarily with raised systolic blood pressure. The authors stress the importance of identifying modulators of vascular stiffness in CKD.


Wittstock and colleagues (Nephron Clin Pract 2009;112:c184-c189) from Berlin, Germany, postulate that oxidative stress plays an important role in the abnormal vascular reactivity of HD patients. They have shown, albeit in a small number of patients, that treatment with intravenous N-acetylcysteine, a potent anti-oxidant, improves such abnormal vascular response. This study supports two previous small observations that antioxidants such as N-acetylcysteine and vitamin E reduce cardiovascular events in HD patients without affecting overall survival (reviewed by Aslam, Curr Opin Nephrol Hypertens 2008;17:99-105).

I caution against the overinterpretation of studies based on a small number of patients as they can be subject to statistical bias and false positive results. On the other hand, such studies should prompt larger randomised control trials to confirm benefit.


 
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