Faculty Bibliography

OBJECTIVES/OBJECTIVE:Venous invasion is common in advanced renal cell carcinoma (RCC) due to the unique biology of this cancer. The presence of a tumor thrombus often makes clinical management challenging. In this review, we detail specific preoperative, perioperative, and surgical strategies involving the care of the complex kidney cancer patient with venous tumor involvement. METHODS:We performed a comprehensive review of selected peer-reviewed publications regarding RCC tumor thrombus biology, medical and surgical management techniques, and immediate and long-term outcomes. RESULTS:The perioperative management may require special imaging techniques, preoperative testing, very recent imaging, and consultation with other surgical services. There are various approaches to these patients as the clinical presentation, stage of disease, primary tumor size, level of thrombus, degree of venous occlusion, presence of bland thrombus, and primary tumor laterality influence management. Select patients with metastatic disease can do well with cytoreductive nephrectomy and thrombectomy. Those with localized disease have a high risk of recurrence; however, some patients can exhibit durable survival with surgery alone. The evolving surgical and medical treatments are discussed. CONCLUSIONS:Even when these surgeries are performed in high volume centers, significant perioperative complications are common and greater complications are seen with higher thrombus extent. If surgery is attempted, it is important for urologic oncologists to follow strict attention to specific surgical principles. These general principles include complete vascular control, avoidance of thrombus embolization, close hemodynamic monitoring, and institutional resources for caval resection/replacement and venous bypass if necessary.

PURPOSE/OBJECTIVE:Despite the high morbidity of repeat renal surgery in patients with multifocal recurrent renal carcinoma, in most patients adequate renal function is preserved to obviate the need for dialysis. To our knowledge the economic burden of repeat renal surgery has not been evaluated. We provide a cost analysis for patients requiring repeat renal surgery on a solitary kidney. MATERIALS AND METHODS/METHODS:We reviewed the charts of patients treated at the National Cancer Institute who required repeat renal surgery from 1989 to 2010. Functional, oncological and surgical outcomes were evaluated and the costs of repeat renal surgery were calculated. We then compared costs in a cohort of 33 patients who underwent repeat renal surgery on a solitary kidney and in a hypothetical patient cohort treated with uncomplicated nephrectomy, fistula placement and dialysis. All costs were calculated based on Medicare reimbursement rates derived from CPT codes. Cost analysis was performed. RESULTS:Despite a high 45% complication rate, 87% of patients maintained renal function that was adequate to avoid dialysis and 96% remained metastasis free at an average followup of 3.12 years (range 0.3 to 16.4). Compared to the hypothetical dialysis cohort, the financial benefit of repeat renal surgery was reached at 0.68 years. CONCLUSIONS:Repeat renal surgery is a viable alternative for patients with multifocal renal cell carcinoma requiring multiple surgical interventions, especially when left with a solitary kidney. Despite the high complication rate, renal function is preserved in most patients and they have an excellent oncological outcome. The financial benefit of repeat renal surgery is reached at less than 1 year.

Chronic granulomatous disease (CGD) is a rare hereditary disease in which phagocytes have difficulty forming the superoxide radical required to kill certain pathogens. Individuals with CGD are susceptible to a specific set of infections and granulomatous lesions. We present the case of a 15-year-old boy with X-linked CGD who presented with unremitting cough and fevers. He had a left-sided pneumonia that persisted despite home intravenous antibiotics. He was admitted to an outside facility for bronchoalveolar lavage to obtain cultures and polymerase chain reaction. Computed tomography of chest, abdomen, and pelvis was done for baseline evaluation of extent of disease. Computed tomography revealed a fluid collection in the prostatic fossa, later determined to be a prostatic abscess. To our knowledge, this is the first reported case of a prostatic abscess in a pediatric patient with CGD.

Microsporidians are a group of emerging pathogens typically associated with chronic diarrhea in immunocompromised individuals. The number of reports of infections with these organisms and the disseminated pathology is growing as diagnostic tools become more readily available. However, little is known about the innate immune response induced by and generated against these parasites. Using a coculture chemotaxis system, primary human macrophages were infected with Encephalitozoon cuniculi or Encephalitozoon intestinalis, and the recruitment of naïve monocytes was monitored. Encephalitozoon spp. induced an average threefold increase in migration of naïve cells 48 h postinfection, which corresponded to optimal infection of monocyte-derived-macrophages. A limited microarray analysis of infected macrophages revealed several chemokines involved in the inflammatory responses whose expression was upregulated, including CCL1, CCL2, CCL3, CCL4, CCL7, CCL15, CCL20, CXCL1, CXCL2, CXCL3, CXCL5, and CXCL8. The levels of 6 of 11 chemokines also present in the microarray were confirmed to be elevated by protein profiling. Kinetic studies confirmed that secreted CCL2, CCL3, and CCL4 were expressed as early as 6 h postinfection, with peak expression at 12 to 24 h and expression remaining until 48 h postinfection. Neutralization of these chemokines, specifically CCL4, significantly reduced the number of migrating cells in vitro, indicating their role in the induction of monocyte migration. This mechanism of recruitment not only supports the evidence that in vivo cellular infiltration occurs but also provides new hosts for the parasites, which escape macrophages by rupturing the host cell. To our knowledge, this is the first documentation that chemokine production is induced by microsporidian infections in human macrophages.