The renin-angiotensin-aldosterone system (RAAS) has pivotal roles in the pathogenesis of hypertension in hemodialysisdependent chronic kidney disease (HDD-CKD) patients. Activated RAAS also increases inflammatory mediators by directly increasing proinflammatory gene expression and by putting oxidative stress on the vascular endothelium. Both hypertension and inflammation are major risk factors for cardiovascular disease (CVD) in HDD-CKD patients. In this study, we assessed the efficacy of a direct renin inhibitor, aliskiren, on blood pressure (BP) and CVD predictive biomarkers, such as brain natriuretic peptide (BNP), high-sensitivity C-reactive protein (hs-CRP) and diacron-reactive oxygen metabolite (d-ROM). A total of 30 hypertensive HDD-CKD patients were assigned to receive aliskiren (150 mg) orally once daily with their existing antihypertensives. After 8 weeks, aliskiren treatments reduced systolic blood pressure (SBP) from 169.0 ± 20.1 to 153.7 ± 19.6 mm Hg (Po0.001) and diastolic blood pressure (DBP) from 78.1 ± 12.0 to 73.0 ± 13.6 mm Hg (P¼0.048). RAAS was suppressed by aliskiren treatment as follows: PRA (from 3.6±4.0 to 1.0±1.5 ng ml -1 h -1 (P¼0.004)), angiotensin I (from 1704.0 ± 2580.9 to 233.7 ± 181.0 pg ml -1 (P¼0.009)), angiotensin II (from 70.2 ± 121.5 to 12.4 ± 11.5 pg ml -1 (P¼0.022)) and aldosterone (from 107.9 ± 148.0 to 73.1 ± 34.6 pg ml -1 (NS)). The biomarkers for CVD were inhibited by aliskiren: BNP (from 362.5±262.1 to 300.0±232.0 pg ml -1 (P¼0.043)), hS-CRP (from 6.2±8.1 to 3.5±3.7 mg l -1 (P¼0.022)) and d-ROM (from 367.0 ± 89.8 to 328.3 ± 70.9 U.CARR (P¼0.022)). The inhibition levels of biomarkers for CVD by aliskiren did not correlate with the decreased levels of SBP and DBP. These results suggested that aliskiren was effective for BP control and may have cardiovascular protective effects in hypertensive HDD-CKD patients.

Chronic kidney disease (CKD) is associated with an increased risk of cardiovascular disease, and thus is

The tumor-bearing rats developed features of glomerulopathy, as expected from the clinical perspective, and this animal model may provide new insights into the development of paraneoplastic glomerulopathies.

Objective Patients with chronic kidney disease (CKD) are at a high risk for cardiovascular diseases including stroke. However, the characteristics of the stroke subtypes in patients with CKD remain to be determined. Methods We investigated the associations between stroke subtypes and estimated glomerular filtration rate (eGFR), and traditional risk factors in 451 (males, 239; mean age, 71.1 y) acute stroke patients at our hospital between 2006 and 2010. Results The stroke subtype was cardiogenic cerebral embolism in 129 (29%), cerebral hemorrhage in 104 (23%), unclassified cerebral infarction in 65 (14%), lacunar infarction in 65 (14%), subarachnoid hemorrhage in 41 (9%), atherothrombosis in 30 (7%), and transient ischemic attacks in 17 (4%). Among the 451 patients, 134 (30%) had CKD with eGFR <60 mL/min/1.73 m 2 . Compared with a group without CKD, mean age (75.9 vs. 69.0 years, p<0.05), the prevalence of atrial fibrillation (AF) (44% vs. 21%, p<0.01) and a history of cardiovascular disease (37% vs. 19%, p<0.01) were significantly higher in that with CKD. A comparison of stroke subtypes revealed a significantly higher incidence of cardiogenic cerebral embolism (36% vs. 26%, p<0.05) in the group with, than without CKD. Conclusion We showed the prevalence of CKD in about 30% of acute stroke patients, and those patients were older, had a significantly higher prevalence of AF and a higher rate of cardiogenic cerebral embolism compared with patients without CKD. Thus, strict control of blood pressure and management of AF should be important to prevent stroke among patients with CKD.

Minimal change nephrotic syndrome (MCNS) is a common form of nephrotic syndrome (NS). We herein present the case of a 57-year-old woman with advanced lung adenocarcinoma treated with the tyrosine kinase inhibitor (TKI) gefitinib who developed NS. A renal biopsy revealed minor glomerular abnormalities, and the patient's symptoms improved exclusively with the discontinuation of gefitinib. Therefore, we diagnosed her with MCNS associated with gefitinib treatment. A few months later, however, she developed recurrent lung tumors. Following the challenging initiation of the TKI erlotinib, she achieved remission without proteinuria. We thus conclude that erlotinib is a potential treatment option in patients with NS associated with gefitinib therapy.