Medication-related factors affecting discharge to home.

To assess the reasons for barriers to home discharge by determining whether they were predicted by medication, clinical variables, and patient characteristics, the retrospective cohort study of 282 patients discharged from Kanazawa Red Cross Hospital in Kanazawa, Japan from January 2011 to December 2012 was performed. The percentage of patients discharged was 67.4%. By multivariate logistic analysis, significant differences in home discharge destination were determined by six factors: the duration of hospitalization before discharge (odds ratio (OR) 0.993; 95% 95% confidence interval (CI) 0.988-0.999), the presence of excretion assistance (OR 0.115; 95% CI 0.043-0.308), individual payment of medical expense (OR 0.344; 95% CI 0.146-0.811), the degree of independent living for the demented elderly (OR4.570; 95% CI 1.969-10.604), presence of the primary caregiver (OR 8.638; 95% CI 3.121-23.906), and admission to a hospital from home (OR 5.483; 95% CI 2.589-11.613). This study suggests that necessity of excretion assistance, long duration of hospitalization, and high individual payment of medical expense were barriers to home discharge. In contrast, three factors i.e., admission to a hospital form home, low degree of independent living for the demented elderly, and presence of the primary caregiver, favored home discharge. The relation between a patient's status (cognitive status and incontinence) and a caregiver has an important effect on the home discharge. However, medication characteristics appeared to have little effect on recuperation destination.

Vasohibin-1, a negative feedback regulator of angiogenesis, ameliorates renal alterations in a mouse model of diabetic nephropathy.

OBJECTIVE: The involvement of proangiogenic factors such as vascular endothelial growth factor as well as the therapeutic efficacy of angiogenesis inhibitors in early diabetic nephropathy has been reported. Vasohibin-1 (VASH-1) is a unique endogenous angiogenesis inhibitor that is induced in endothelial cells by proangiogenic factors. We investigated the therapeutic efficacy of VASH-1 in an early diabetic nephropathy model. RESEARCH DESIGN AND METHODS: Streptozotocin- induced type 1 diabetic mice received intravenous injections of adenoviral vectors encoding VASH-1 (AdhVASH-1) or beta-gal (AdLacZ) every other week and were killed after 28 days. RESULTS: Treatment with AdhVASH-1 resulted in sustained increase in the protein levels of VASH-1 in the liver and sera, in the absence of any inflammatory alterations. AdhVASH-1 treatment significantly suppressed renal hypertrophy, glomerular hypertrophy, glomerular hyperfiltration, albuminuria, increase of the CD31(+) glomerular endothelial area, F4/80(+) monocyte/macrophage infiltration, the accumulation of type IV collagen, and mesangial matrix compared with AdLacZ-treated diabetic mice. Increase in the renal levels of transforming growth factor-beta1, monocyte chemoattractant protein-1, and receptor for advanced glycation end products in diabetic animals was significantly suppressed by AdhVASH-1 (real-time PCR and immunoblot). VASH-1 significantly suppressed the increase of transforming growth factor-beta, monocyte chemoattractant protein-1, and receptor for advanced glycation end products, induced by high ambient glucose in cultured mouse mesangial cells. Increased phosphorylation of VEGFR2 was suppressed in AdVASH-1-treated diabetic animals and in cultured glomerular endothelial cells. Endogenous mouse VASH-1 was localized to the mesangial and endothelial area in glomeruli of diabetic mice. CONCLUSIONS: These results suggest the potential therapeutic efficacy of VASH-1 in treating early diabetic nephropathy potentially mediated via glomerular endothelial and mesangial cells.