The purpose of this study was to explore risk factors affecting the incidence of chronic kidney disease (CKD) in general population. We conducted a 10-year follow-up study with 123 764 (male: 41 012, female: 82 752) adults aged 40 years and over who received community-based annual examinations. The primary outcome for the analysis was the development of CKD during the follow-up period. Predictors for the development of CKD were obtained by the significant hazard ratios (HR) in Cox regression model by sex. During the follow-up period, 4307 subjects (male: 2048, female: 2259) developed CKD stage I or II, and 19 411 subjects (male: 4257, female: 15 154) developed CKD stage III or higher. The baseline-adjusted predictor of developing CKD included age, glomerular filtration rate, hematuria, hypertension, diabetes, serum lipids, obesity, smoking status, and consumption of alcohol. Treated diabetes in male subjects, and treated hypertension, systolic blood pressure >160 mm Hg and/or diastolic blood pressure >100 mm Hg, diabetes, and treated diabetes in female subjects were associated with more than a doubling of the HR. For the development of CKD stage III or higher, proteinuria of >or= + +, and proteinuria and hematuria were associated with more than a doubling of the HR in male subjects. The prevalence of newly developed CKD over 10 years was 23 718 subjects (19.2%) in adults. This study suggested that not only hypertension and diabetes but also several metabolic abnormalities were independent risk factors for developing CKD.

This article represents the update of ‘European Stroke Initiative Recommendations for Stroke Management’, first published in this Journal in 2000. The recommendations are endorsed by the 3 European societies which are represented in the European Stroke Initiative: the European Stroke Council, the European Neurological Society and the European Federation of Neurological Societies.

Background and Purpose: This study was conducted to evaluate the role of high serum lipoprotein(a) levels in a group of patients with a relatively early onset of cerebral infarction as a whole and in a subgroup with the perforating artery occlusion subtype of cerebral infarction.Methods: Fifty-four patients with cerebral infarction, the onset of which was before age 65 years (37 men, 17 women; mean age, 61.9±7.7 years) were examined in this study. When patients with atrial fibrillation were excluded to omit cardiac embolic strokes from analysis, the group consisted of 45 patients. The patients were classified into two subtype groups, the perforating artery occlusion group and the cortical artery occlusion group, by using magnetic resonance imaging. Lipoprotein(a) levels were measured by an enzyme-linked immunosorbent assay. Four biochemical variables (serum levels of lipoprotein(a),

This study was designed to examine the effects of oral adsorbent AST-120 on the progression of CRF in patients on strict LPD. Thirteen patients with CRF (serum creatinine: 1.8-8.2 mg/ dl) that had been kept on LPD (0.4-0.7 g/kg/day) were enrolled in this study. After LPD alone for 5-24 months, AST-120 (3-6 g/day) was administered concurrently with the LPD for an additional 5-13 months. In 9 of the 13 patients, the slopes of reciprocal creatinine (Cr) vs. time plot linearly declined before AST-120 treatment. After treatment, the slopes of these patients lessened from -0.01 ± 0.001 to -0.003 ± 0.001 dl/mg/month (p < 0.01). Because reciprocal Cr did not decline linearly with time before AST-120 treatment in the remaining 4 patients, the slopes of reciprocal Cr could not be compared before and after treatment with AST-120. Seven of the 9 patients had sufficient creatinine clearance (C_cr) data after treatment with AST-120. The decline of C_cr decreased from -0.59 ± 0.13 to -0.12 ± 0.12 ml/min/ month in these patients. This study has clearly demonstrated that AST-120 compounds the effects of well-controlled LPD on retarding the progression of CRF. AST-120 may remove some uremic metabolite(s) which promote the progression of CRF.

Background/Aims: Non-volatile acid is produced by metabolism of organic sulfur in dietary protein, and promotes kidney damage. We investigated the role of dietary acid load, in terms of net endogenous acid production (NEAP), in chronic kidney disease (CKD) progression. Methods: 217 CKD patients on low-protein diet with a normal serum bicarbonate level were enrolled in this retrospective cohort study in Japan. The primary outcome was 25% decline in estimated glomerular filtration rate (eGFR) or start of dialysis. Their NEAP was measured every 3 months. The patients were categorized into four groups on the basis of quartiles of NEAP every 3 months. The groups were treated as time-dependent variables. Results: The average age (SD) was 70.6 (7.1) years; eGFR 23.5 (14.2) ml/min/1.73 m². Analysis using extended Cox models for the NEAP groups adjusted for baseline characteristics (referring to group 1 showing the lowest NEAP) showed that high NEAP was associated with a high risk of CKD progression; group 2, adjusted hazard ratio (HR) 3.930 (95% confidence interval (CI) 1.914, 8.072); group 3, adjusted HR 4.740 (95% CI 2.196, 10.288); group 4, adjusted HR 4.303 (95% CI 2.103, 8.805). Logistic regression analysis adjusted for baseline characteristics showed that the occurrence of hypoalbuminemia or hyperkalemia was associated with low serum bicarbonate level and the presence of complications at baseline, but not with NEAP. Conclusion: In elderly CKD patients, our findings suggest that high NEAP is independently associated with CKD progression. The decrease in NEAP may be an effective kidney-protective therapy.