Kidney Transplantation Using Gonadal Vein for Venous Anastomosis in Patients With Iliac Vein Thrombosis or Stenosis: A Series of Cases.

BACKGROUND: Kidney transplantation is the treatment of choice for patients with end-stage renal disease. The standard surgery uses the recipient's iliac vessels for vascular anastomosis. Thrombosis and/or stenosis of the iliac vein, which are possible complications of multiple vascular access points for dialysis, can be detected intraoperatively, constituting a surgical challenge. An infrequently reported option is the use of the gonadal vein. OBJECTIVES: This study aims to evaluate the outcomes of venous anastomosis in the gonadal vein in patients with iliac vein thrombosis and/or stenosis submitted to kidney transplantation. METHODS: We reviewed the records of five adult recipients with iliac vein thrombosis and/or stenosis detected intraoperatively during emergency kidney transplantation with deceased donor due to vascular access failure from February 2013 to December 2014. Antithrombotic prophylaxis was not performed. We evaluated the postoperative complications, length of stay, early graft echo-Doppler, and renal function during the first year postoperatively. RESULTS: Delayed graft function occurred in three cases. Two patients developed postoperative infection requiring antibiotics. One patient required reoperation due to post-renal biopsy complications. The mean length of stay was 31.2 days and the mean serum creatinine levels at discharge, at 6 months, and at 12 months postoperatively were 1.42 mg/dL, 0.86 mg/dL, and 0.82 mg/dL, respectively. All patients had normal ultrasonography. There were no losses of graft or deaths during follow-up. CONCLUSION: Venous anastomosis using the gonadal vein in kidney transplantation for patients with iliac vein thrombosis and/or stenosis showed good clinical and surgical results, showing this method to be a viable alternative to venous drainage in these complex patients.

Artery Stenosis of the Renal Graft: Experience of a Center of Northeastern Brazil.

BACKGROUND: Transplant renal artery stenosis (TRAS), the most common vascular complication after transplant (Tx), leads to resistant hypertension, impaired renal function, and even loss of the graft. The purpose of the study was to investigate the prevalence and factors associated with TRAS in northeastern Brazil. METHODS: The study was conducted as a retrospective case-control study in a population of Tx recipients in a renal Tx center in northeastern Brazil. Demographic and clinical characteristics of the recipients and donors, data related to the surgery, laboratory data, and number of anti-hypertensive drugs were assessed. Statistical analysis was performed with the use of SPSS 17.0. RESULTS: A total of 494 of 529 recipients were assessed, of which 24 had TRAS. The prevalence of TRAS was 4.8%. Twelve patients (50%) were men with a mean age of 46.7 ± 13.5 years. The mean time of diagnosis was 89.9 days after Tx. The risk factors associated with TRAS were number of anti-hypertensive drugs ≥2 (odds ratio, 17.0; confidence interval, 4.1 to 70.4; P = .001) and grafting with 2 or more arteries (odds ratio, 8.9; confidence interval, 1.4 to 56.6; P = .021). There was a significant reduction in mean systolic blood pressure (147.1 ± 23.7 to 127.8 ± 15.2 mm Hg, P = .001) and diastolic blood pressure (86.6 ± 13.0 to 77.6 ± 9.4 mm Hg, P = .001) after TRAS repair and in serum creatinine (2.8 ± 2.4 to 1.9 ± 1.8 mg/dL, P = .04). CONCLUSIONS: Grafts with 2 or more arteries are associated with TRAS, as well as patients who use a higher number of anti-hypertensive drugs. TRAS repair was associated with improved blood pressure control and renal function.

Relaxant effect of a metal-based drug in human corpora cavernosa and its mechanism of action.

We studied the mechanisms involved in the human corpora cavernosa (HCC) relaxation induced by a new metal-based nitric oxide (NO) donor, the ruthenium complex cis-[Ru(bpy)2Imn(NO)](+3) (FOR0811). FOR0811 produced relaxation in phenylephrine (PE)-precontracted HCC with a maximal response that achieved 112.9 ± 10.6%. There was no difference between the maximal relaxation induced by FOR0811 when compared with sodium nitroprusside (SNP) (106.8 ± 7.3%), BAY41-2272 (107.6 ± 4.1%) or vardenafil (103.4 ± 3.8%), however, FOR0811 was less potent than SNP and vardenafil. L-N(G)-nitroarginine methyl ester (L-NAME), a NO synthase inhibitor, had no effect in the concentration-response curve elicited by FOR0811. 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), a heme-site inhibitor of soluble guanylyl cyclase (sGC) was able to either block or reverse the relaxation induced by FOR0811. On the other hand, the relaxation induced by FOR0811 was not affected by glibenclamide, a blocker of ATP-sensitive potassium channels. FOR0811 (10 µM) was able to increase cyclic guanosine monophosphate (cGMP) levels in corpora cavernosa strips. FOR0811 completely relaxes HCC by a sGC-cGMP-dependent mechanism and can be a lead compound in the development of new stable NO donors.

Yohimbine relaxes the human corpus cavernosum through a non-adrenergic mechanism involving the activation of K+ATP-dependent channels.

The mechanism by which yohimbine relaxes the human corpus cavernosum remains unclear. Using the human corpus cavernosum strips immersed in isometric baths containing Krebs-Henseleit solution, this study investigates the effect of yohimbine on the relaxation of the human corpus cavernosum through nitrergic pathways involving the activation of ATP-dependent potassium channels (K(ATP)). The maximal relaxation induced by yohimbine in the human corpus cavernosum strips pre-contracted with phenylephrine was 100+/-0% and only 30.5+/-5.0% when they were pre-contracted with 60-mM potassium (K(+)) solution. The maximal relaxation induced by yohimbine in phenylephrine pre-contracted tissues was significantly inhibited by tetrodotoxin, 1H-[1,2,4] oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) or 7-nitroindazole (43.6, 36.1 and 42.6%, respectively). Neither the combination charybdotoxin-apamin nor tetraethylammonium altered the response of the human corpora cavernosa strips to yohimbine. Nevertheless, glibenclamide decreased the maximum relaxant response to yohimbine by 29.8% (P<0.05; n=12). The results suggest that yohimbine relaxes the human corpus cavernosum by a non-adrenergic, non-cholinergic mechanism, probably activating the nitrergic-soluble guanylate cyclase (NO-sGc) pathway and K(ATP).