Issue 6, 2009July 3, 2009 This issue of Nephron Digest, based on papers from Nephron Clinical Practice issue 113/1/09, focuses on transplant glomerulopathy, obesity and CKD progression, albuminuria/microalbuminuria, and secondary hyperparathyroidism and CKD progression. 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 113/1/2009 Transplant glomerulopathy. The minireview by Fotheringham and colleagues from the Sheffield Kidney Institute (Nephron Clin Pract 2009;113:c1-c7) is a comprehensive update on transplant glomerulopathy (TG). This term has replaced that of chronic allograft nephropathy, placing more emphasis on glomerular changes. Tubular interstitial changes are labelled as Interstitial Fibrosis and Tubular Atrophy. Pathology also focuses on vascular, peritubular capillary, changes including the deposition of the complement fragment C4d suggesting a humoral, anti-donor antibody-mediated injury. Fotheringham and his colleagues review the range of available therapies for TG. Amongst the novel therapies that might prove effective in the future are anti-C5 monoclonal antibodies inducing an accommodation state in endothelial cells. Also, co-stimulation blockade with interference with the CD40-CD154 pathway may prove effective. It is likely that this area of nephrology/immunology will see major advances over the next few years (Cosio et al., Am J Transplant 2008;8:492–496). Obesity and CKD Progression. A study from the UK by Othman and his coworkers (Nephron Clin Pract 2009;113:c16-c23) reinforces the increasingly held impression that obesity is a major risk factor for CKD. A large body of evidence is now linking obesity with initiation and progression of CKD (Ting et al., Nephron Clin Pract 2009;112:c121-127). Othman and his colleagues have noted that baseline BMI at presentation to a Nephrology service is a strong and independent predictor of the rate of CKD progression. They also report that changes in BMI during the follow-up period do not affect the rate of decline in GFR. Previous observations by the same group showed that weight loss reduces microalbuminuria in a general population cohort study (Bello et al., Nephrol Dial Transplant 2007;22:1619-1627). High Normal Albuminuria and risk. Cotter and colleagues from Porto in Portugal (Nephron Clin Pract 2009;113:c8-c15) identify high normal albuminuria, poor blood pressure control as well as dyslipidemia as risk factors for the onset of microalbuminuria. This observation agrees with observations made in the general population by the PREVEND group who identified high normal albuminuria as a CVD risk marker as well as those made in people with diabetes where poor glycemia and blood pressure control, dyslipidemia and smoking have all been implicated in the onset of microalbuminuria. Of note the majority of individuals in this study (70%) were diabetics. However, this study re-emphasises that the risk associated with albuminuria is a linear one starting within the upper normal range. This observation reinforces the call for a reassessment of the artificial separation of albuminuria into high normal and microalbuminuria. Secondary Hyperparathyroidism (SHPT) and CKD progression. Schumock and associates from Chicago and Torrance (Nephron Clin Pract 2009;113:c54-c61) report the predictive value of SHPT in relation to outcomes of patients with CKD. They note that diabetic pre-dialysis CKD patients with higher levels of PTH are at increased risk of disease progression to ESRD, requiring dialysis, and also at higher risk of death. This study identifies SHPT as a CKD risk factor; future research will determine whether there is a causal link and whether control of SHPT with agents such as calcimimetics will delay CKD progression. It would also be interesting to know whether the observed association is independent of underlying changes in vitamin D levels. The latter is increasingly singled out, along with FGF-23, as a major renal and cardiovascular risk factor (Judd and Tangpricha, Am J Med Sci 2009;338:40-44).   © 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.