Acute kidney injury after endovascular repair of abdominal aortic aneurysm.

Acute kidney injury (AKI) after any type of intervention negatively impacts mortality, length of hospitalization, and perhaps long-term survival. In the case of endovascular aneurysm repair (EVAR), the incidence of AKI ranges from 1% to 23% for elective and emergency procedures and is lower compared to open repair. The pathophysiology of AKI in EVAR is complex: contrast-induced nephropathy, renal microembolization, and acute tubular necrosis are all implicated. Prevention strategies include hydration, ischemic preconditioning, regional anesthesia, and pharmacological agents. There is no level I evidence regarding the prevention of AKI in EVAR, so this review sought to examine the mechanisms and prevention strategies for this potentially fatal complication.

Copy number profiling in von Hippel-Lindau disease renal cell carcinoma.

Germline mutations in the VHL tumor suppressor gene cause von Hippel-Lindau (VHL) disease and somatic VHL mutations occur in the majority of clear cell renal cell carcinoma (cRCC). To compare copy number abnormalities (CNAs) between cRCC from VHL patients and sporadic cRCC cases without detectable somatic VHL mutations, we analyzed 34 cRCC with Affymetrix 250K arrays. To increase the power of the study, we then combined our results with those of a previously published study and compared CNAs in VHL and non-VHL related cRCC using the genomic identification of significant targets in cancer (GISTIC) program. In VHL, cRCC GISTIC analysis identified four statistically significant regions of copy number gain and four statistically significant regions of deletion that occurred in >10% of tumors analyzed. Sporadic cRCC without detectable VHL mutations had, on average, more copy number abnormalities than VHL cRCC though the most common regions of loss/gain (e.g., 3p and 14q loss and 5q gain) were present in both tumor sets. However, CNAs on chromosome arms 7p (gain) and 8p (loss) were only detected in VHL RCC. Although individual copy number abnormality peaks contained clear candidate cancer genes in some cases (e.g., the 3p loss peak in VHL cRCC contained only six genes including VHL), most peaks contained many genes. To date, only a minority of the candidate genes included in these peaks have been analyzed for mutation or epigenetic inactivation in cRCC but TNFRSF10C and DUSP4 map to the 8p region deleted in VHL cRCC and TP53 and HIF2A (EPAS1) mapped to CNA loss and gain peaks (chromosomes 17 and 2, respectively) detected in sporadic VHL wild-type cRCC.

Needle tract seeding following percutaneous biopsy of renal cell carcinoma.

A 66-year-old man underwent computed tomography-guided needle biopsy of a suspicious renal mass. Two months later he underwent partial nephrectomy. Histology revealed a 30-mm clear cell renal cell carcinoma, up to Fuhrman grade 3. An area of the capsule was interrupted, which corresponded to a hemorrhagic area on the cortical surface. Under microscopy, this area showed a tongue of tumor tissue protruding through the renal capsule. A tumor deposit was found in the perinephric fat. These features suggest that tumor seeding may have occurred during the needle biopsy.

Validation of soft tissue properties in surgical simulation with haptic feedback.

Numerous experiments are being conducted to extract soft tissue values for their integration into VR surgical simulations with haptic feedback. Haptic feedback has been shown to be relevant in laparoscopic surgery, however to date no experiments have been conducted to test user sensitivity to changes in soft tissue values in surgical simulations, and how users perception of 'reality' differs from experimentally determined soft tissue values. In this study we conduct a series of experiments investigating haptic sensitivity, haptic differentiation and comparing experimental and empirical values.

Hypergonadotrophic hypogonadism due to testicular adrenal rest tumours presenting with hypogonadotrophic hypergonadism.

Primary testicular failure is characterized by low serum testosterone with appropriately high serum gonadotrophins, that is hypergonadotrophic hypogonadism. We report on a 27-year-old man with congenital adrenal hyperplasia (CAH) and infertility due to testicular adrenal rest rumours (TART) resulting in primary testicular failure but presenting with azoospermia, elevated serum testosterone and very low serum gonadotrophins. Hypergonadotrophic hypogonadism was unmasked by increasing glucocorticoid dosage. It is important to recognise the limitations of follicle-stimulating hormone, luteinising hormone and testosterone in assessing testicular function in men with CAH. Abnormal semen analysis may be the best indicator of testicular dysfunction in men with CAH.