Factors affecting hemostasis in the control of iatrogenic renal hemorrhage.

PURPOSE: To investigate factors affecting hemostasis in iatrogenic renal hemorrhage. METHODS: Seventy-three patients with iatrogenic renal hemorrhage experiencing selective renal artery angiography between Jan 2015 and Dec 2020 were enrolled in this study. The clinical features, treatment modalities and outcomes were reviewed. Factors affecting hemostasis were analyzed by univariate and multivariate models using linear regression techniques. The optimum values of the independent factors to predict postangiographic hemostasis were conducted by receiver operating characteristic (ROC) curve analysis. RESULTS: Of the 73 iatrogenic renal hemorrhage patients, 47 (64.4%) patients had positive angiographic findings and received therapeutic embolization. Of the patients with negative angiographic findings, 20 (76.9%) and 6 (23.1%) received conservative therapy and prophylactic embolization, respectively. The red blood cell (RBC) count (OR = 0.61, P = 0.04), the hematuria time before angiography (OR = - 0.19, P < 0.01) and treatment modality were independent factors affecting hemostasis time. The ROC curve analysis showed that the RBC count of 3.5 × 109/L and the hematuria time before angiography of 7 days were the optimum indicators. Therapeutic embolization and prophylactic embolization were protective factors affecting hemostasis time compared with conservative treatment (OR = - 1.59, P = 0.02; OR = - 3.31, P < 0.01). CONCLUSIONS: The hematuria time before selective renal artery angiography, the RBC count, and embolization treatment are associated with rapid hemostasis. Embolization is an effective strategy for iatrogenic renal hemorrhage, and also enables rapid hemostasis in patients with negative angiographic findings.

Roles of sphingosine-1-phosphate signaling in cancer.

The potent pleiotropic lipid mediator sphingosine-1-phosphate (S1P) participates in numerous cellular processes, including angiogenesis and cell survival, proliferation, and migration. It is formed by one of two sphingosine kinases (SphKs), SphK1 and SphK2. These enzymes largely exert their various biological and pathophysiological actions through one of five G protein-coupled receptors (S1PR1-5), with receptor activation setting in motion various signaling cascades. Considerable evidence has been accumulated on S1P signaling and its pathogenic roles in diseases, as well as on novel modulators of S1P signaling, such as SphK inhibitors and S1P agonists and antagonists. S1P and ceramide, composed of sphingosine and a fatty acid, are reciprocal cell fate regulators, and S1P signaling plays essential roles in several diseases, including inflammation, cancer, and autoimmune disorders. Thus, targeting of S1P signaling may be one way to block the pathogenesis and may be a therapeutic target in these conditions. Increasingly strong evidence indicates a role for the S1P signaling pathway in the progression of cancer and its effects. In the present review, we discuss recent progress in our understanding of S1P and its related proteins in cancer progression. Also described is the therapeutic potential of S1P receptors and their downstream signaling cascades as targets for cancer treatment.