Background/Aim: The natural history of the renal microvasculature changes in PKD is not known. The aim of this study was to test the hypothesis that angiogenesis is coupled with kidney cyst expansion, and the loss of peritubular capillary networks precedes the onset of interstitial fibrosis. Methods: The renal microvasculature (RECA-1 and CD34) was evaluated in groups of Lewis polycystic kidney (LPK) rats and juvenile cystic kidney (jck) mice during the early, mid and late stage of disease. In addition, LPK rats and jck mice received sirolimus to determine if the reduction in renal cyst growth is in part mediated by the suppression of angiogenesis. Results: In LPK rats, the loss of peritubular capillaries occurred in early-stage disease and paralleled cyst formation whereas in jck mice it was delayed to the mid stage. In both models, vasa recta were displaced by growing cysts and regressed in LPK rats with disease progression but lengthened in jck mice. Cortical and medullary capillary neoangiogenesis occurred during the early stage in both models and persisted with progression. Treatment with sirolimus reduced cyst enlargement but did not alter the progression of renal microvasculature changes in either model. Conclusion: Regression of peritubular capillaries and disruption of vasa recta occur in parallel with angiogenesis and the progressive enlargement of kidney cysts. These data suggest that the regrowth of peritubular capillaries together with inhibition of angiogenesis are potential strategies to be considered in the treatment of PKD.

Introduction: Acute Ischemic Stroke (AIS) is one of the leading cause of death, premature death, and disability globally. Hemorrhagic transformation (HT) is a common complication of AIS and is related to higher mortality, early neurological deterioration, and worse long-term functional outcome. Numerous observational studies have been published but the relationship between low eGFR level and HT in AIS patients is still controversial. We sought to do a meta-analysis to determine the association between low eGFR level and HT in AIS. Methods: We searched multiple electronic databases to identify studies published from 1990 to 2018. Following the application of inclusion and exclusion criteria, the ORs and 95% CIs of all the included studies were employed to estimate the pooled OR and 95% CI using the inverse variance random-effects method. Publication bias was assessed through Egger's test and Begg test. Heterogeneity was assessed by means of the I-squared value. Results: Ten observational studies including 4,653 AIS patients contributed to the analysis. Low eGFR level significantly increased the risk of HT in AIS patients (OR=1.60, 95% CI: 1.21-2.1, P = 0.001). Significant heterogeneity was seen among studies (I 2 = 45%, p = 0.06). No evidence of publication bias was observed in this meta-analysis. The effect size was stable during sensitivity analysis. We found no subgroup difference based on study design, study population, AIS type, stroke treatment, and study site.