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In the past 15 years, there has been an increased understanding of the tumor biology of renal cell carcinoma (RCC). The identification of vascular endothelial growth factor (VEGF), its related receptor (VEGFR), and the mammalian target of rapamycin as dysregulated signaling pathways in the development and progression of RCC has resulted in the rational development of pharmaceutical agents capable of specifically targeting key steps in these pathways. Clinical trials have demonstrated survival benefit with these agents, particularly in clear cell RCC patients. However, metastatic RCC will progress in all patients, resulting in a critical need to determine patient risk and optimize treatment. The goal of this article is to highlight the significant breakthroughs made in understanding the critical genetic alterations and signaling pathways underlying the pathogenesis of RCC. The discovery of prognostic factors and development of comprehensive nomograms to stratify patient risk and predictive biomarkers to facilitate individualized treatment selection and predict patient response to therapy also are reviewed.

Aim: Whether or not sacrificing accessory pudendal arteries (APAs) during radical prostatectomy affects potency has been an ongoing source of concern. Herein, we present our potency results relative to sacrificing APAs in normally pre-potent men following robot-assisted radical prostatectomy (RARP)., Methods: The distribution of APAs and clinical characteristics were prospectively recorded in 200 consecutive patients undergoing RARP with a cautery-free technique. Sexual function was assessed using the International Index of Erectile Function 5-item questionnaire (IIEF-5). All APAs were sacrificed due to stapling the dorsal vein complex., Main Outcome Measures: Postoperatively, potency was defined by an affirmative answer to the following two questions: "Were erections adequate for penetration?" and "were the erections satisfactory?" Postoperative IIEF-5 scores and quality of erections (% of preoperative firmness: 0%, 25%, 50%, 75%, 100%) were also obtained. Subgroup analysis of patients age < or =65 years with IIEF-5 score of 22-25 was performed., Results: Eighty patients (40%) had APAs. Preoperatively, there was no association with having an APA and normal/abnormal sexual function. Preoperatively, 58/200 were < or =65 years with self-administered IIEF-5 scores of 22-25. Postoperatively, 53/58 (91%) were potent at 24 months follow-up. Nineteen of 58 patients had a sacrificed APA; 39 patients had no APA. Eighteen of 19 (95%) patients with sacrificed APAs were potent vs. 35/39 (90%) with no APA present (P = 0.53). Multivariate analysis showed no significant correlation between sacrificing an APA and time of potency recovery, quality of postoperative erections (94% vs. 90% P = 0.80) or mean IIEF-5 score (22.4 vs. 20.8, P = 0.13)., Conclusion: We found no correlation between the presence or absence of APAs and preoperative sexual function. Furthermore, after sacrificing all APAs, we found no correlation with potency return, time to return of potency, quality of erections, or mean IIEF-5 scores at 24 months.

Aim: Stuttering priapism is an uncommon form of recurrent priapism whose etiology if often unknown. To date, there has been one report of a patient with stuttering priapism and glucose-6-phosphate dehydrogenase (G6PD) deficiency. Herein we describe the second-known case of recurrent priapism in a patient with G6PD deficiency. The pathophysiology of G6PD deficiency and its potential to cause priapism is reviewed., Methods: A case report is described of a 29-year-old African-American man with G6PD deficiency who presented with numerous episodes of recurrent ischemic priapism. Clinical data was reviewed., Results: Despite medical management with gonadotropin-releasing hormone (GnRH) agonist, an antiandrogen, and baclofen, he required several surgical procedures which also ultimately failed. A continuous phosphodiesterase type-5 inhibitor (PDE5) was started and the patient had no recurrences at 3-month follow-up., Conclusion: Idiopathic recurrent priapism may be explained by underlying hemolytic anemia associated with G6PD deficiency. Several possible mechanisms exist to explain this association, including hyperviscosity, direct endothelial dysfunction secondary to bare hemoglobin vasculotoxicity, and relative nitric oxide deficiency causing vasoconstriction and vascular smooth muscle proliferation.