Blood pressure management and progression of chronic kidney disease in a canine remnant kidney model.

The canine remnant kidney model is fundamental to understanding the relationship between hypertension and chronic kidney disease (CKD). This study aimed to create a 1/16 remnant kidney model and to determine whether blood pressure (BP) control affects the progression of CKD. A group of dogs received BP treatment (group A) and another received BP treatment except for the first 2 weeks (group B). The remnant kidney model was induced using a two-step subtotal nephrectomy method; dogs received antihypertensive therapy. Systolic BP, blood urea nitrogen, serum creatinine, urinary protein, and creatinine levels were measured weekly. Kidney tissues were obtained at the conclusion of the study. Systolic BP was controlled to <160 mmHg in both groups for 18 weeks, except for the first 2 weeks in group B. Proteinuria was elevated after renal ligation in both groups, but gradually increased in group B and decreased in group A (p = 0.009). Blood urea nitrogen (p = 0.014) and creatinine (p = 0.020) levels were higher in group B than in group A. More histological damage was observed in group B than in group A. Induction of 1/16 nephrectomy successfully established CKD. Control of BP may be important to prevent or control the progression of CKD in dogs.

Circulating TNF receptors predict cardiovascular disease in patients with chronic kidney disease.

Cardiovascular disease (CVD) is the main public health problem in patients with chronic kidney disease (CKD); however, there is no established biomarker for predicting CVD morbidity and mortality in CKD. The aim of this study was to evaluate the role of circulating tumor necrosis factor receptors (cTNFRs) in predicting CVD risk in CKD patients.We prospectively recruited 984 patients with CKD from 11 centers between 2006 and 2012. The levels of cTNFR1 and cTNFR2 were determined by performing an enzyme-linked immunosorbent assay. During the mean follow-up period of 4 years, 36 patients experienced a CVD event. The median serum concentrations of cTNFR1 and cTNFR2 were 2703.4 (225.6-13,057.7) and 5661.0 (634.9-30,599.6) pg/mL, respectively, and the cTNFR1 level was closely correlated with the cTNFR2 level (r = 0.86, P < .0001). The urinary protein-to-creatinine ratio (UPCR) and estimated glomerular filtration rate (eGFR) were significantly correlated with the cTNFR2 level (r = 0.21 for UPCR, r = -0.67 for eGFR; P < .001 for all). Similar correlations were observed for serum cTNFR1 (r = 0.21 for UPCR, r = -0.75 for eGFR; P < .001 for all). In the Cox proportional hazard analyses, cTNFR1 (hazard ratio [HR] 2.506, 95% confidence interval [CI] 1.186-5.295, P = .016) and cTNFR2 (HR 4.156, 95% CI 1.913-9.030, P < .001) predicted CVD risk even after adjustment for clinical covariates, such as UPCR, eGFR, and high-sensitivity C-reactive protein. cTNFR1 and 2 are associated with CVD and other risk factors in CKD, independently of eGFR and UPCR. Furthermore, cTNFRs could be relevant predictors of CVD in CKD patients.