Ureteral complications in renal transplantation with more than one donor ureter.
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BACKGROUND: The purpose of this study was to evaluate the ureteral complications of renal transplant recipients with more than one donor ureter METHODS: Between 1967 and 1997, 19 patients (median age 34 years, range 6-62 years) received renal transplants from donors with more than one ureter. There were 18 donor organs with two ureters, and one patient underwent en bloc renal transplantation with four donor ureters. In nine patients, the ureters were implanted separately at the bladder dome according to the extravesical technique of Witzel, Sampson, Lich and Rohl. In 10 patients, we performed a modification of this extravesical technique according to Nghiem with a side-to-side anastomosis of the ureters before completing the ureteroneocystostomy. RESULTS: After a median follow-up of 55 months (range 2-218 months), no graft loss due to ureteral complications was noted. One patient died due to myocardial infarction, seven patients returned to dialysis without ureteral complications. There were two patients (one patient after side-to-side ureteral anastomosis, one patient with separate implantation of the two ureters) with ureteral obstruction of one donor ureter. Both patients underwent open surgical revision with temporarily placement of internal ureteral stents. CONCLUSIONS: The presence of multiple ureters from donor kidneys is associated with a higher complication rate in our patient population compared with donor kidneys with one ureter. There was no difference in the long-term outcome between the two implantation techniques used. (+info)
The value of intra-operative cystoscopy at the time of laparoscopic hysterectomy.
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The aim of this study was to determine the usefulness of routine intra-operative cystoscopy in documenting ureteral injury during total laparoscopic hysterectomy with vault suspension and to document the incidence of this complication in a large series. The charts of 118 patients who underwent laparoscopic hysterectomy with vault suspension from January 1992 to January 1998 were retrospectively reviewed. The patients underwent intra-operative cystoscopic evaluation to verify ureteral permeability and bladder integrity. Intra-operative ureteral obstruction occurred in four patients (3.4%). All complications were immediately fixed and there were no postoperative ureteral problems. No late ureteral complications were observed. Intra-operative cystoscopy allows for early recognition and treatment of obstructive ureteral injuries and may reduce the rate of late postoperative complications during advanced laparoscopic procedures. (+info)
Epithelial cell morphology and cytoskeletal organization are determined by interactions, with both adjacent cells and the extracellular matrix, which are mediated by integrins and cadherins. Little is known, however, of the relative contributions of integrins and cadherins to maintaining the sub-cortical cytoskeleton characteristic of epithelial cells. Since most studies that utilize integrin-blocking antibodies result in a loss of both cell-cell adhesion and sub-cortical cytoskeletal organization, it has been difficult to distinguish whether integrins and cadherins both mediate cytoskeletal assembly in epithelial cells. Therefore, cells derived from kidney collecting ducts of (alpha)3(beta)1 integrin-deficient mice were used to examine the role of integrins in epithelial cell morphology and cytoskeletal organization. In primary cell culture, (alpha)3(beta)1 integrin-deficient kidney collecting duct cells maintain cadherin-mediated cell-cell adhesions but fail to form the sub-cortical cytoskeleton that is characteristic of epithelial cells, and instead assemble actin stress fibers. Moreover, the cell-cell junctions in mutant cells were irregular, rather than being uniformly oriented perpendicular to the culture substrate. These results demonstrated that integrins have an primary and essential function in establishing and maintaining the sub-cortical cytoskeleton that is characteristic of epithelial cells. To further study the role of (alpha)3(beta)1 integrin in establishing and maintaining cytoskeletal organization in tubular epithelial cells, we derived immortalized cell lines from wild-type and (alpha)3(beta)1 integrin-deficient kidney collecting ducts that duplicated the cytoskeletal and cadherin organization observed in primary cells. E-cadherin and (alpha)- and (beta)-catenin were complexed together in equal amounts in membranes of wild-type and (alpha)3(beta)1 integrin-deficient cells. However, association of the cadherin:catenin complex with (alpha)-actinin was greatly decreased in mutant cells, indicating that integrin-mediated assembly of the sub-cortical cytoskeleton is essential for subsequent association of the cytoskeleton with the cadherin:catenin complex. These results present direct evidence for integrin:cadherin cross-regulation in which cadherin function is dependent on the presence of an integrin. (+info)
How they begin and how they end: classic and new theories for the development and deterioration of congenital anomalies of the kidney and urinary tract, CAKUT.
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CAKUT are problems that often require surgical intervention or, in the worst case, lead to renal failure and the need for dialysis and/or renal transplantation. It is believed that these anomalies share a common genetic cause and to date there has been no good animal model with which to study these abnormalities. Although the abnormal interaction between the ureteral bud and metanephric blastema leads to renal hypodysplasia, vesicoureteral reflux, and ectopic ureters to name a few, the genetic and biochemical modulation of urinary tract development is not understood. Studies using the mouse strain mutant for angiotensin type 2 (AT2) receptors have given new insight into this mystery. The animals show defective apoptosis of undifferentiated mesenchymal cells in the area surrounding the developing kidney and urinary tract. This abnormal apoptosis may well interfere with the normal interaction between the ureteral bud and metanephric blastema resulting in CAKUT. This abnormal interaction would theoretically lead to preexisting intrinsic abnormalities of the kidney, which are programmed and take effect early in embryonic development. In the worst cases, the renal abnormalities would lead to progressive deterioration of renal function. Undoubtedly, there are more genes and biochemical modulators involved in this process other than the RAS and AT2 receptors. Our current animal model gives new and unique possibilities with which to study development of the kidney and urinary tract and ultimately seek ways of preventing an often debilitating disease process. (+info)
Sonographic diagnosis of ureteral tumors.
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We present our experience with transabdominal ultrasonographic diagnosis of ureteral tumors. During the years 1989 to 1998, 16 patients were diagnosed as having ureteral tumors. These patients were referred for sonographic examination for evaluation of hematuria (seven patients) or flank pain (four patients) or for follow-up screening in patients who were asymptomatic but at high risk for transitional cell carcinoma because of known past bladder tumor (five patients). Ten of these patients underwent intravenous urography examination, three patients had retrograde pyelography, and 11 patients underwent CT scanning. Ultrasonography revealed the ureteral tumors in all 16 patients, which appeared as hypoechoic intraluminal soft tissue. Three tumors were localized in the upper ureter, four in the middle ureter, and nine in the distal ureter. The degree of ureterohydronephrosis was minimal (two cases), mild (five cases), moderate (eight cases), or severe (one case). Eleven tumors caused local widening of the ureteral diameter. On intravenous urography, four patients had a nonfunctioning kidney, three patients had unexplained ureterohydronephrosis, and three patients showed ureteral filling defects, of which only two had irregular contours. On retrograde pyelography, two patients had filling defects (one of which with smooth margins), and one had a truncated ureter. On CT the tumor was clearly demonstrated in only seven patients. We found that ultrasonography can be a useful diagnostic tool in the workup of ureteral tumors. (+info)
The Wilms tumor suppressor WT1 encodes a transcriptional activator of amphiregulin.
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WT1 encodes a zinc finger transcription factor implicated in kidney differentiation and tumorigenesis. In reporter assays, WT1 represses transcription from GC- and TC-rich promoters, but its physiological targets remain uncertain. We used hybridization to high-density oligonucleotide arrays to search for native genes whose expression is altered following inducible expression of WT1. The major target of WT1 was amphiregulin, a member of the epidermal growth factor family. The WT1(-KTS) isoform binds directly to the amphiregulin promoter, resulting in potent transcriptional activation. The in vivo expression profile of amphiregulin during fetal kidney development mirrors the highly specific pattern of WT1 itself, and recombinant Amphiregulin stimulates epithelial branching in organ cultures of embryonic mouse kidney. These observations suggest a model for WT1 as a transcriptional regulator during kidney differentiation. (+info)
Evolution of gene expression patterns in a model of branching morphogenesis.
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Branching morphogenesis of the ureteric bud in response to unknown signals from the metanephric mesenchyme gives rise to the urinary collecting system and, via inductive signals from the ureteric bud, to recruitment of nephrons from undifferentiated mesenchyme. An established cell culture model for this process employs cells of ureteric bud origin (UB) cultured in extracellular matrix and stimulated with conditioned media (BSN-CM) from a metanephric mesenchymal cell line (H. Sakurai, E. J. Barros, T. Tsukamoto, J. Barasch, and S. K. Nigam. Proc. Natl. Acad. Sci. USA 94: 6279-6284, 1997.). In the presence of BSN-CM, the UB cells form branching tubular structures reminiscent of the branching ureteric bud. The pattern of gene regulation in this model of branching morphogenesis of the kidney collecting system was investigated using high-density cDNA arrays. Software and analytical methods were developed for the quantification and clustering of genes. With the use of a computational method termed "vector analysis," genes were clustered according to the direction and magnitude of differential expression in n-dimensional log-space. Changes in gene expression in response to the BSN-CM consisted primarily of differential expression of transcription factors with previously described roles in morphogenesis, downregulation of pro-apoptotic genes accompanied by upregulation of anti-apoptotic genes, and upregulation of a small group of secreted products including growth factors, cytokines, and extracellular proteinases. Changes in expression are discussed in the context of a general model for epithelial branching morphogenesis. In addition, the cDNA arrays were used to survey expression of epithelial markers and secreted factors in UB and BSN cells, confirming the largely epithelial character of the former and largely mesenchymal character of the later. Specific morphologies (cellular processes, branching multicellular cords, etc.) were shown to correlate with the expression of different, but overlapping, genomic subsets, suggesting differences in morphogenetic mechanisms at these various steps in the evolution of branching tubules. (+info)
GDNF and its receptors in the regulation of the ureteric branching.
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Recent transgenic and organ culture experiments have inevitably shown that glial cell line-derived neurotrophic factor (GDNF) is a mesenchyme-derived signal for ureteric budding and branching. The signalling receptor complex for GDNF includes a dimer of Ret receptor tyrosine kinase and two molecules of GDNF family receptor alpha1. Alpha-receptors are not only needed for the ligand binding and Ret activation, but they might mediate signals without Ret. While GDNF is clearly required for ureteric branching, tissue recombination studies have shown that it is not sufficient for the completion of ureteric morphogenesis, and other signalling molecules are needed. Different experimental models have resulted in somewhat contradictory results on their molecular identity, but transforming growth factor-beta1, -beta2, fibroblast growth factor-7 and hepatocyte growth factor form, obviously among others, a redundant set of growth factors in ureteric differentiation. Three other members of the GDNF family, neurturin, artemin and persephin, are also expressed in the developing kidney, and at least neurturin and persephin promote ureteric branching in vitro, but their true in vivo roles are still unclear. (+info)