We analyzed the frequency of vesicoureteral reflux and the factors that favor its appearance after kidney transplantation in pediatric patients. This retrospective analysis examined the prevalence of post-transplant vesicoureteral reflux in a total of 181 kidney transplants performed in children at our center between 1978 and 2004. In patients who required corrective surgery for this problem, we analyzed pretransplant residual diuresis, pretransplant pathology and post-transplant problems related to vesicoureteral reflux. We also analyzed form of presentation, whether reflux was to the graft or to the native kidney, degree of reflux, and surgical technique used to correct reflux. Ten patients (5.5%) needed surgery to correct reflux to the graft (nine children) or to the native kidney (one child). Reflux was manifested as urinary tract infection in six children and progressive graft failure in one. Urethrovesical disorders that favored vesicoureteral reflux were present in eight patients (non-compliance bladder, detrusor overactivity, posterior urethral valves, urethral stenosis). Lengthening the submucosal tunnel stopped urinary tract infections in all 10 patients, whereas six-month voiding cystourethrograms showed resolution in 8 patients and (only) reduction in the degree of reflux in two. The high percentage of post-transplant vesicoureteral reflux in pediatric patients were related with higher frequencies of ureterovesical pathology in children who received the transplant. Lengthening the submucosal ureteral tunnel vesicoureteral reflux was corrected in 80%. We recommend during implantation in children with pretransplant urethrovesical abnormality an initial technique, which utilizes a longer submucosal tunnel such as the Lich-Gregoir.
PTPL1 is a non-receptor protein tyrosine phosphatase involved in apoptosis regulation, although controversial findings have been reported in different cancer types. We report here a proapoptotic role for PTPL1 in PC3 and LNCaP prostate cancer cells, as its absence induces apoptosis resistance upon treatment with different drugs. In PC3 cells, PTPL1 silencing by small interfering RNA influences the expression levels of Bcl-xL and Mcl-1S proteins as well as final events in the apoptotic process such as activation of caspases and caspase-mediated cleavage of proteins like Mcl-1 or poly (ADP-ribose) polymerase. We have identified PKCδ as an intermediary of PTPL1-mediated apoptotic signalling and that phosphorylation status of NF-κB and IκBα is influenced by PTPL1 and PKCδ. Furthermore, the loss of PTPL1 and PKCδ expression in poorly differentiated, more aggressive human prostate cancers also indicate that their absence could be related to apoptosis resistance and tumour progression.
Abstract: We analyzed the frequency of vesicoureteral reflux and the factors that favor its appearance after kidney transplantation in pediatric patients. This retrospective analysis examined the prevalence of post-transplant vesicoureteral reflux in a total of 181 kidney transplants performed in children at our center between 1978 and 2004. In patients who required corrective surgery for this problem, we analyzed pretransplant residual diuresis, pretransplant pathology and post-transplant problems related to vesicoureteral reflux. We also analyzed form of presentation, whether reflux was to the graft or to the native kidney, degree of reflux, and surgical technique used to correct reflux. Ten patients (5.5%) needed surgery to correct reflux to the graft (nine children) or to the native kidney (one child). Reflux was manifested as urinary tract infection in six children and progressive graft failure in one. Urethrovesical disorders that favored vesicoureteral reflux were present in eight patients (non-compliance bladder, detrusor overactivity, posterior urethral valves, urethral stenosis). Lengthening the submucosal tunnel stopped urinary tract infections in all 10 patients, whereas six-month voiding cystourethrograms showed resolution in 8 patients and (only) reduction in the degree of reflux in two. The high percentage of post-transplant vesicoureteral reflux in pediatric patients were related with higher frequencies of ureterovesical pathology in children who received the transplant. Lengthening the submucosal ureteral tunnel vesicoureteral reflux was corrected in 80%. We recommend during implantation in children with pretransplant urethrovesical abnormality an initial technique, which utilizes a longer submucosal tunnel such as the Lich–Gregoir.
Abstract: Vascular complications represent a significant cause of morbidity and mortality following a kidney transplant. Pseudoaneurysms are rare, occurring in approximately 1% of cases. We present a 15‐yr‐old patient who received a kidney transplant in the right iliac fossa. Thirty‐six days following the transplant, the patient was admitted to the hospital because of a marked increase in serum creatinine levels, arterial hypertension, scrotal edema, and lower right limb pain. The patient did not present fever or raised inflammatory markers. A pseudoaneurysm was diagnosed by means of a Doppler echography and a CT. By a selective arteriography of the right iliac artery, we placed a 8 × 5 cm stent to isolate the pseudoaneurysm, due to the high risk of an extensive defect occurring in the arterial wall. Forty‐eight h later the patient underwent transplant nephrectomy. Seven days following surgery, the patient experienced febrile syndrome and therefore another CT was carried out which showed a large abscess around the stent. So we decided to perform another intervention in order to drain this abscess. Due to the extensive loss of the arterial wall where the prosthesis was largely exposed, we ligated the common iliac and external iliac arteries, removed the prosthesis and performed a femoro‐femoral bypass with the usual subcutaneous positioning of the prosthesis (separate from surgical site). The stent and mural thrombus were sent for culture analysis and Candida albicans was observed. The diagnosis of a pseudoaneurysm in these types of patients continues to be considered as a surgical emergency by the majority of authors. Transplantectomy is the most frequently used treatment technique. Positioning a stent prior to transplantectomy avoids ligature of the iliac artery in the majority of cases.
The development of benign prostatic hyperplasia (BPH) is an androgen-dependent process which may be mediated by a number of locally produced growth factors. One of these, the basic fibroblast growth factor (bFGF or FGF2), has a mitogenic effect on prostatic stroma. High expression levels of bFGF have been reported in BPH. FGFR1 and FGFR2 receptors, that exhibit affinity for bFGF, have been identified in normal and hyperplastic prostate. Finasteride, a 5alpha-reductase inhibitor, is an effective drug in the treatment of BPH, inducing regressive changes in the prostate of treated patients, even though its mechanisms of action are not yet completely elucidated. This study was designed to assess the effects of finasteride on the expression levels of bFGF, FGFR1, and FGFR2 in patients with BPH.The expression levels of bFGF, FGFR1, and FGFR2 in 9 patients with prostatic hyperplasia treated with finasteride were assessed by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) analysis of mRNA expression and were compared with those of 9 control patients with untreated BPH.Immunohistochemistry showed strong bFGF immunoreactivity in the prostatic stroma of untreated patients, this being somewhat weaker in the epithelium. In treated patients, epithelial immunoreactivity was practically negative, and a considerable reduction in stromal immunoreactivity was seen. These findings were also confirmed by RT-PCR. FGFR1 showed a weak immunoreactivity in the stroma and in basal epithelial cells. FGFR1 showed a weak immunoreactivity in the stroma and in basal epithelial cells. FGFR2 exhibited strong stromal immunoreactivity, becoming weaker in the basal epithelium. No differences were seen in the expression of both receptors between the groups of treated and untreated patients.A marked reduction in bFGF levels is seen in BPH treated with finasteride in comparison to untreated BPH. In our opinion, finasteride may act as a negative regulator of bFGF expression, counteracting the role of bFGF in the development of BPH.
Prostatic atrophy has been documented histologically as a consequence of finasteride action on human hyperplastic prostates. An increase in apoptotic rates has also been reported in androgen-deprived hyperplastic prostates. Transforming growth factor beta (TGF-beta) signaling is implicated in apoptotic cell death. TGF-betas have been detected in normal and diseased human prostate. In the normal prostate, TGF-beta acts as a predominantly negative growth regulator. TGF-beta signaling receptors TbetaRI and TbetaRII have been shown to be negatively regulated by androgens.We studied the histological changes in 9 selected finasteride-treated patients with benign prostatic hyperplasia (BPH), and analyzed the levels of expression and localization of TGF-beta receptor types TbetaRI and TbetaRII in these patients as compared to selected BPH controls.The prostatic epithelial compartment seemed to be a primary target site for finasteride action, since we observed moderate to severe glandular atrophy after 4-6 months of treatment. TGF-beta receptors were upregulated in treated cases. We assessed a twofold increase in TbetaRII mRNA levels in treated cases as compared to controls. An increase in both TbetaRI and TbetaRII at the protein level by immunostaining was observed, which also provided a helpful means for detecting glands undergoing regression.We conclude that finasteride may modulate the TGF-beta signaling system to promote changes leading to apoptosis of epithelial cells and prostatic glandular atrophy.