Treatment of anastomotic leaks with metallic stent after esophagectomies.

The diagnosis and the treatment of anastomotic leak after esophagectomy are the keys to reduce the morbidity and mortality after this surgery. The stent plays an important role in the treatment of the leakage and in the prevention of reoperation. We have analyzed the database of the section of the esophagogastric surgery of Donostia University Hospital from June 2003 to May 2012. It is a retrospective study of 113 patients with esophagectomy resulting from tumor, and 24 (21.13%) of these patients developed anastomotic leak. Of these 24 patients, 13 (54.16%) have been treated with a metallic stent and 11 (45.84%) without a stent. The average age of the patients was 55.69 and 62.45 years, respectively. All patients treated with and without a stent have been males. Eight (61.5%) stents were placed in the neck and five (38.5%) in the chest. However, among the 11 fistulas treated without a stent, 9 patients had cervical anastomosis (81.81%) and 2 patients (18.18%) had anastomosis in the chest. Twelve patients (92.30%) with a stent preserve digestive continuity, and 10 patients (90.90%) were treated without a stent. One patient died in the stent group and one in the nonstent group. The treatment with metallic stent of the anastomotic leak after esophagectomy is an option that can prevent reoperation in these patients, but it does not decrease the average of the hospital stay. The stent may be more useful in thoracic anastomotic leaks.

Modulation of renal kallikrein by a high potassium diet in rats with intense proteinuria.

Injury of the renal tubulointerstitial compartment is recognized to play an important role in hypertension. Its damage may in turn, impair the activity of vasodepressor systems, like the kallikrein-kinin, in blood pressure regulation. The overload proteinuria model induces tubulointerstitial injury with activation of the renin-angiotensin system, but renal kallikrein and the development of hypertension have not received special attention. Sprague-Dawley rats received seven intraperitoneal doses of bovine serum albumin (BSA) 2 g/day under normosodic diet and were hydrated ad libitum. A second group received a high potassium diet to stimulate kallikrein production during the previous four weeks and while under BSA administration. A third one received potassium and BSA in the same schedule, but with the kinin B2 receptor antagonist, HOE140, added during the protein load phase. A control group received seven saline injections. Kallikrein protein was detected by immune labeling on renal sections and enzymatic activity in the urine. The BSA group showed massive proteinuria followed by intense tubulointerstitial damage. Blood pressure increased after the third dose in BSA animals, remaining elevated throughout the experiment, associated with significant reductions in renal expression and urinary activity of kallikrein, compared with controls. An inverse correlation was found between blood pressure and immunohistochemistry and urinary activity of kallikrein. Potassium induced a significant increase in both urinary activity and renal kallikrein expression, associated with significant reduction in blood pressure. The HOE140 antagonist blunted the antihypertensive effect of kallikrein stimulation in proteinuric rats. Loss of renal kallikrein, produced by tubulointerstitial injury, may participate in the pathogenesis of the hypertension observed in this model.