Issue 7, 2009September 2009 This issue of Nephron Digest, based on papers from Nephron Clinical Practice issue 113/2/09, focuses on RAAS inhibition and the progression of CKD, endothelial dysfunction and ADPKD, arterial stiffness and fetuin A in CKD, and volume control and reduction of cardiac biomarkers. I strongly encourage the readers of Nephron Digest to engage in a dialogue by emailing me to discuss issues of global nephrological interest. 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 113/2/2009 RAAS inhibition and the progression of CKD. In this paper, Onuigbo, USA (Nephron Clin Pract 2009;113:c63-c70), critically evaluates the literature pertaining to the therapeutic advantage to the progression of CKD of the inhibition of the renin-angiotensin-aldosterone system (RAAS). He draws attention to the limitations of published evidence and stresses the risks associated with ACE inhibitors/ARBs in CKD in the elderly. This mini review should stimulate a re-evaluation of the risk/benefit ratio of inhibition of the RAAS in CKD. Endothelial dysfunction and ADPKD. Ramunni and colleagues, Italy (Nephron Clin Pract 2009;113:c71-c75), report on microvascular/endothelial dysfunction in ADPKD patients. They postulate that systemic endothelial dysfunction precedes hypertension and impaired kidney function. Nitric oxide (NO) dysfunction has been implicated in defective vascular reactivity in ADPKD. These observations are of interest as emerging data link polycystins to NO signalling (W.A. AbouAlaiwi et al., Circ Res 2009;104:860-469). Within the kidney, a defect in polycystins affects tubule cilia and may contribute to cystogenesis whilst an endothelial defect in polycystins may contribute to vascular dysfunction (S.M. Nauli et al., Circulation 2008;117:1161-1171). Polycystin abnormalities may thus underlie the systemic pathology of ADPKD. Arterial stiffness and fetuin A in CKD. Porazko and co-authors, Poland and USA, (Nephron Clin Pract 2009;113:c81-c87), attempt to link the increased arterial stiffness observed in CKD patients to decreased circulating fetuin A levels and raised CRP and IL-6. A growing body of data links fetuin deficiency to vascular, valvular and soft-tissue calcifications in CKD. In CKD, a number of bone regulatory proteins, including fetuin, are involved in both bone demineralisation and vascular calcifications (K.A. Hruska et al., Semin Nephrol 2009;29:156-165). Recognition of the links between bones and vascular calcifications in CKD should optimise management. Volume control and reduction of cardiac biomarkers. Ortega and colleagues, Spain (Nephron Clin Pract 2009;113:c96-c103), undertook a short-term prospective study that showed that strict fluid and salt restriction in HD patients may impact on biomarkers of cardiovascular prognosis such as CRP and NT-proBNP. Clearly, longer term studies are required to ascertain whether changes in biomarkers impact CVD morbidity and mortality. More emphasis should be put on the temporal evolution of key biomarkers during HD rather than on single cross-sectional values (P. Kotanko et al., Blood Purif 2009;27:38-47). This study also highlights the often overlooked importance of salt and water restriction in HD patients (F. Raimann et al., Hemodial Int 2008;12:395-405).   © S. Karger AG - Medical and Scientific Publishers Allschwilerstrasse 10, P.O. Box, CH-4009 Basel (Switzerland) Tel. +41 61 306 1200, Fax +41 61 306 1234, publications@karger.ch. Please read the Karger Privacy Policy. If you have received this email by mistake, click here and we will take you off this mailing list.