Major Cause Of Chronic Kidney Disease Research Articles

Nicorandil Improves Glomerular Injury in Rats With Mesangioproliferative Glomerulonephritis via Inhibition of Proproliferative and Profibrotic Growth Factors

Recent clinical studies on chronic kidney disease (CKD) reported that renal dysfunction was a critical risk factor for cardiovascular events (CVE), which lead us to reconsider the effect of cardioprotective agents on the kidney. Glomerulonephritis, which is the major cause of CKD, is characterized by mesangial cell proliferation and extracellular matrix deposition. Nicorandil, a therapeutic drug for angina and acute heart failure, have been reported to show antiproliferative activity in mesangial cells. In this study, we first investigated the in vivo effects of nicorandil in anti-Thy1 nephritis rats. In male F344 rats, anti-Thy1 nephritis was induced by the injection of an anti-Thy1 antibody. From three days before induction, nicorandil (10, 30 mg/kg per day) was administered in the drinking water for 12 consecutive days. Anti-Thy1 nephritis resulted in a significant increase in proteinuria and glomerular mesangial cell proliferation. In nephritis rats, nicorandil (30 mg/kg per day) significantly suppressed increase in proteinuria, mesangial cell proliferation (the number of glomerular cell and glomerular area), and renal hypertrophy without affecting blood pressure. Nicorandil significantly prevented the overexpression of type I collagen, fibronectin, transforming growth factor (TGF)-β, and platelet-derived growth factor (PDGF) mRNA. These results suggest that nicorandil may have renoprotective effects in mesangioproliferative glomerulonephritis.

Childhood chronic kidney disease in a developing country

We have retrospectively reviewed the records of children aged >1 month to 16 years who had been referred to the Department of Pediatrics of Prince of Songkla University's Faculty of Medicine, a tertiary referral center in Thailand, between 1982 and 2005 and subsequently diagnosed with chronic kidney disease (CKD). Our aim was to evaluate the prevalence and etiology of CKD in southern Thailand. There were 101 cases of CKD, with one case each diagnosed in 1988, 1989 and 1993, respectively, and 98 cases diagnosed between 1994 and 2005. These latter cases were divided into two 6-year periods: an early period (1994-1999), with 32 cases, and a later period (2000-2005), with 66 cases. The majority of this pediatric population with CKD were male (62/101, 61.4%). The etiologies of CKD were 35 cases of chronic glomerulonephritis (CGN) (34.7%), 29 of genitourinary tract (GU) anomalies (28.7%), nine of systemic lupus erythematosus (SLE) (8.9%), four malignancies (4.0%), four miscellaneous (4.0%) and 19 of unknown causes (18.8%). The patients were divided into age groups of <2 years (20 CKD patients), 2-6 years (15), >6-10 years (22), >10-13 years (20) and >13 years (24). The etiologies of CKD were significantly different in each age group, with GU anomalies and glomerulonephritis being the major causes of CKD in children aged <or=6 years (20/36, 55.6%) and >6 years (40/65, 61.5%), respectively. In conclusion, the incidence of CKD in our university hospital situation was not rare, with the prevalence doubling during the past 6 years, and the etiologies varying by age group.

Intérêt d’une collection tissulaire ciblée dans le programme de recherche des tumorothèques : l’exemple des carcinomes pulmonaires

Hyperuricemia and gout are common in chronic kidney disease (CKD) patients. This relationship has been noted since the 1800s. Over the years there has been great controversy over the biologic significance of hyperuricemia, with some individuals arguing it is a major cause of CKD, and others viewing the rise in serum urate concentration (S[Ur]) as strictly an epiphenomenon. During the last 10–15 years, interest in uric acid has reawakened with the realization that an elevated S[Ur] can predict the development of CKD and by experimental studies that document a causal role for uric acid in both the development and progression of CKD. Today there is great interest in the potential that uric acid may represent a remediable risk factor for CKD. We provide an update on uric acid and the kidney, focusing both on uric acid metabolism and a critical evaluation of the current evidence base for uric acid as a risk factor for CKD.