Trends in Body-Mass Index After Donor Nephrectomy.

The link between obesity and diabetes, hypertension, and eventual kidney dysfunction is well recognized. To evaluate trends in the body-mass index (BMI) of donor nephrectomy patients, the BMI was evaluated in 532 donors over 11 years from 2002 to 2012. Measurements were made preoperatively, at 1 year, and at the present time. The follow-up range varied from 12 months to 11 years dependent on the date of donation. Of the 532 patients queried, 100 patients had long-term results. At 1 year, there was an overall decrease in BMI, however, at anytime after the first year, postoperative BMI trended upward, with more than half of the overweight patients (BMI 25-30), at the time of donation, dipping into the obese range (BMI >30). Given these results and recognizing the attendant risks-especially with the background of a single kidney-we have initiated further lifestyle and nutrition counseling at our center and are considering a more stringent preoperative weight control policy.

Surgical flow disruptions during robotic-assisted radical prostatectomy.

INTRODUCTION: We sought to apply the principles of human factors research to robotic-assisted radical prostatectomy to understand where training and integration challenges lead to suboptimal and inefficient care. MATERIALS AND METHODS: Thirty-four robotic-assisted radical prostatectomy and bilateral pelvic lymph node dissections over a 20 week period were observed for flow disruptions (FD) - deviations from optimal care that can compromise safety or efficiency. Other variables - physician experience, trainee involvement, robot model (S versus Si), age, body mass index (BMI), and American Society of Anesthesiologists (ASA) physical status - were used to stratify the data and understand the effect of context. Effects were studied across four operative phases - entry to insufflations, robot docking, surgical intervention, and undocking. FDs were classified into one of nine categories. RESULTS: An average of 9.2 (SD = 3.7) FD/hr were recorded, with the highest rates during robot docking (14.7 [SD = 4.3] FDs/hr). The three most common flow disruptions were disruptions of communication, coordination, and equipment. Physicians with more robotic experience were faster during docking (p < 0.003). Training cases had a greater FD rate (8.5 versus 10.6, p < 0.001), as did the Si model robot (8.2 versus 9.8, p = 0.002). Patient BMI and ASA classification yielded no difference in operative duration, but had phase-specific differences in FD. CONCLUSIONS: Our data reflects the demands placed on the OR team by the patient, equipment, environment and context of a robotic surgical intervention, and suggests opportunities to enhance safety, quality, efficiency, and learning in robotic surgery.

Long-Term Body Mass Index Trends After Living-Donor Nephrectomy.

OBJECTIVES: As the demand for kidney transplant allografts has increased, many centers are expanding the upper limit of acceptable body mass index for kidney donors. However, obesity is a risk factor for developing renal disease. Our goal was to quantify body mass index trends in donor nephrectomy patients and to institute nutrition counseling to promote sustainable weight loss to reduce the risk of metabolic syndrome-derived renal dysfunction. MATERIALS AND METHODS: Ninety patients who underwent donor nephrectomy between 2007 and 2012 consented to having height and weight data collected at multiple time points. After data collection, each patient underwent a standardized nutrition counseling session. One year later, body mass index was reassessed. RESULTS: Preoperatively, 52% of the patients were overweight or obese. The percentage of overweight and obese patients remained stable for 2 years after surgery. However, at 3, 4, and 5 years after surgery, these rates increased to 59%, 69%, and 91%. Each patient was counseled about obesity-related comorbidities and provided information about lifestyle modification. One year later, 94% of previously overweight patients and 82% of previously obese patients had a decrease in mean body mass index from 27.2 ± 4.0 kg/m2 to 25.1 ± 3.6 kg/m2. CONCLUSIONS: Living-donor nephrectomy patients are at risk of developing obesity, similar to the adult population. Nutrition counseling may be beneficial to help normalize body mass index in patients who have become overweight or obese to potentially prevent obesity-related comorbidities. All patients were evaluated by a nutrition specialist after surgery to review our donor nephrectomy nutrition brochure. Body mass index monitoring and primary care follow-up appear to be appropriate surveillance methods.

Histone deacetylase inhibitors mediate DNA damage repair in ameliorating hemorrhagic cystitis.

Hemorrhagic cystitis is an inflammatory and ulcerative bladder condition associated with systemic chemotherapeutics, like cyclophosphomide. Earlier, we reported reactive oxygen species resulting from cyclophosphamide metabolite, acrolein, causes global methylation followed by silencing of DNA damage repair genes. Ogg1 (8-oxoguanine DNA glycosylase) is one such silenced base excision repair enzyme that can restore DNA integrity. The accumulation of DNA damage results in subsequent inflammation associated with pyroptotic death of bladder smooth muscle cells. We hypothesized that reversing inflammasome-induced imprinting in the bladder smooth muscle could prevent the inflammatory phenotype. Elevated recruitment of Dnmt1 and Dnmt3b to the Ogg1 promoter in acrolein treated bladder muscle cells was validated by the pattern of CpG methylation revealed by bisulfite sequencing. Knockout of Ogg1 in detrusor cells resulted in accumulation of reactive oxygen mediated 8-Oxo-dG and spontaneous pyroptotic signaling. Histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA), restored Ogg1 expression in cells treated with acrolein and mice treated with cyclophosphamide superior to the standard of care, mesna or nicotinamide-induced DNA demethylation. SAHA restored cyclophosphamide-induced bladder pathology to that of untreated control mice. The observed epigenetic imprinting induced by inflammation suggests a new therapeutic target for the treatment of hemorrhagic cystitis.

Bochdalek-type Diaphragmatic Hernia Leading to High-grade Kidney Obstruction.

A 94-year-old female presented with sharp right flank pain. Imaging demonstrated herniation of the right renal pelvis and proximal ureter into a large diaphragmatic hernia. She underwent ureteral stent placement with resolution of her symptoms. Congenital diaphragmatic hernias can cause a variety of pulmonary, cardiac, and gastrointestinal symptoms. This is 1 of only 3 cases in the literature of unilateral kidney obstruction due to herniation of the renal pelvis and proximal ureter into a Bochdalek-type diaphragmatic hernia. Ureteral stenting is a good option to decompress the kidney. Hernia reduction and primary diaphragm repair remain the definitive treatment.

Inflammation and pyroptosis mediate muscle expansion in an interleukin-1ß (IL-1ß)-dependent manner.

Muscle inflammation is often associated with its expansion. Bladder smooth muscle inflammation-induced cell death is accompanied by hyperplasia and hypertrophy as the primary cause for poor bladder function. In mice, DNA damage initiated by chemotherapeutic drug cyclophosphamide activated caspase 1 through the formation of the NLRP3 complex resulting in detrusor hyperplasia. A cyclophosphamide metabolite, acrolein, caused global DNA methylation and accumulation of DNA damage in a mouse model of bladder inflammation and in cultured bladder muscle cells. In correlation, global DNA methylation and NLRP3 expression was up-regulated in human chronic bladder inflammatory tissues. The epigenetic silencing of DNA damage repair gene, Ogg1, could be reversed by the use of demethylating agents. In mice, demethylating agents reversed cyclophosphamide-induced bladder inflammation and detrusor expansion. The transgenic knock-out of Ogg1 in as few as 10% of the detrusor cells tripled the proliferation of the remaining wild type counterparts in an in vitro co-culture titration experiment. Antagonizing IL-1ß with Anakinra, a rheumatoid arthritis therapeutic, prevented detrusor proliferation in conditioned media experiments as well as in a mouse model of bladder inflammation. Radiation treatment validated the role of DNA damage in the NLRP3-associated caspase 1-mediated IL-1ß secretory phenotype. A protein array analysis identified IGF1 to be downstream of IL-1ß signaling. IL-1ß-induced detrusor proliferation and hypertrophy could be reversed with the use of Anakinra as well as an IGF1 neutralizing antibody. IL-1ß antagonists in current clinical practice can exploit the revealed mechanism for DNA damage-mediated muscular expansion.

Dystrophic calcification of the prostate after cryotherapy.

We present a previously undocumented complication of dystrophic calcification of the prostate after cryotherapy. An 87-year-old male presented with recurrent lower urinary tract infections and was found to have an obstructing large calcified mass in the right lobe of the prostate. Subsequently, he underwent transurethral resection of the prostate (TURP) and bladder neck with laser lithotripsy to remove the calculus. We propose that chronic inflammation and necrosis of the prostate from cryotherapy resulted in dystrophic calcification of the prostate. As the use of cryotherapy for the treatment of localized prostate cancer continues to increase, it is important that clinicians be aware of this scenario and the technical challenges it poses.

Mechanisms of hemorrhagic cystitis.

The vast majority of cases of infectious cystitis are easily treated, and most patients have no long-term complications. However, hemorrhagic cystitis is a potentially deadly complication associated with pelvic radiation therapy, chemotherapy, and stem-cell transplant therapy. The focus of current understanding, and hence therapy, is directed toward urothelial cell death. However, the primary functional ramification of inflammatory bladder disease is the loss of compliance due to muscular expansion. Recent studies on smooth muscle response in models of bladder inflammation demonstrate a process of pyroptotic cell death that potentiates further muscle hyperplasia. These findings may support alternative interventions for subjects with hemorrhagic cystitis refractive to current therapy.

Bladder perforation secondary to primary systemic amyloidosis.

Amyloidosis is a disorder of protein folding characterized by extracellular aggregation and deposition of amyloid protein fibrils. Light-chain amyloidosis, also known as primary systemic amyloidosis, is the most common form of the disease. We present a case of an 84-year-old male with a history of systemic primary amyloidosis causing genitourinary, cardiac, and autonomic dysfunction who presented with hematuria and hypotension secondary to bladder perforation. He underwent open repair of a large extraperitoneal bladder defect. He ultimately died as a result of medical complications from his disease.