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O Brinkmann

Publications and source records attributed to O Brinkmann.

12 recordsLinked to original sources
PubMed2006

Reconstruction of ureteral necrosis in kidney transplantation using an ileum interposition.

PURPOSE: Ureteral necrosis is a serious problem in kidney transplantation. Sometimes re-ureterocystostomy is possible, while other cases require an elaborate reconstruction to maintain kidney function. We report our experience with ileum interposition for ureteral reconstruction. METHODS: After 9 years of dialysis treatment a 58-year-old patient was grafted using the left kidney of a 59-year-old donor with a cold ischemic time of 9.5 hours. The early postoperative course was uneventful apart from delayed graft function. Immunosuppression consisted of an IL-2-receptor antibody, calcineurin inhibitor, mycophenolate mofetil, and corticosteroids. Discharge serum creatinine was 2.3 mg/dL. In month 4 the patient showed a pararenal urinoma; cystoscopy revealed necrosis of the distal ureter. Operative revision showed urine leakage from the renal pelvis through the urinoma into the bladder. As the whole ureter was necrotic, a re-ureterocystostomy was not possible. The patient's own ureter had been extirpated, and the bladder was too small to do a direct anastomosis between it and the kidney. Consequently, an ileum interposition was performed. RESULTS: The postoperative course was uneventful. Kidney function was stable with a nadir creatinine concentration of 2.0 mg/dL 18 months' posttransplantation, and 14 months' post ileal interposition the kidney function was still satisfactory, with a creatinine level of 2.0 mg/dL. CONCLUSION: Ureteral necrosis is a serious complication following kidney transplantation. Whenever a re-ureterocystostomy or an uretero-ureterostomy is not possible, the interposition of the ileal segment represented a safe procedure to deal with this problem.

Humans↗
PubMed2005

[Fetal nephro-/uropathy: a retrospective analysis of 124 cases seen in the period from 1996 to 2002].

BACKGROUND: The embryological development of the kidneys and the urinary tract follows a complex choreography. Disorders are quite common. The incidence of disorders amounts to 0.3 - 0.8 % of live-born infants. In addition, several chromosomal anomalies are combined with renal malformations. The poor prognosis of some of these diseases is reflected in a perinatal mortality of 6.3 %. PATIENTS AND METHODS: Retrospectively 124 cases with fetal nephro-/uropathy detected by prenatal ultrasonography between 1996 and 2002 were analyzed. Features of hypo-dysplastic kidneys (uni- or bilateral) were seen in 21 cases. Multicystic kidney disease (uni- or bilateral) existed in 40 fetuses. In some cases of multicystic or dysplastic kidney diseases, extrarenal malformations were combined. 21 fetuses suffered from autosomal recessive polycystic kidney disease. 18 male unborns showed the typical picture of intravesical obstruction due to posterior uretheral valves. The prune belly syndrome was seen 4 times. Hydronephrotic kidneys with more than 5 mm pelvic dilatation were detected in 13 cases. Renal agenesis led to a lethal outcome perinatally in 5 cases. One child died of bilateral thrombosis of renal artery and venous system. RESULTS: The high incidence of diseases with a poor prognosis accounts for the high mortality of 50.8 % (intrauterine or postnatal death, induced abortion). Such a fatal outcome was observed in autosomal recessive polycystic kidney disease, bilateral multicystic dysplastic kidney disease, bilateral renal dysplasia combined with severe extrarenal malformations, intravesical obstruction, renal agenesis and bilateral thrombosis of the renal vessels. Only 60 children survived. Of these 26 needed urological surgery. 15 suffered from progressive renal insufficiency. During a follow-up of 8 - 58 months only 44 exhibited a normal renal function. CONCLUSIONS: Such complex renal and urological diseases in the fetus require an interdisciplinary management of the pregnancy.

Female↗
PubMed2001

Genotype versus phenotype in families with androgen insensitivity syndrome.

Androgen insensitivity syndrome encompasses a wide range of phenotypes, which are caused by numerous different mutations in the AR gene. Detailed information on the genotype/phenotype relationship in androgen insensitivity syndrome is important for sex assignment, treatment of androgen insensitivity syndrome patients, genetic counseling of their families, and insight into the functional domains of the AR. The commonly accepted concept of dependence on fetal androgens of the development of Wolffian ducts was studied in complete androgen insensitivity syndrome (CAIS) patients. In a nationwide survey in The Netherlands, all cases (n = 49) with the presumptive diagnosis androgen insensitivity syndrome known to pediatric endocrinologists and clinical geneticists were studied. After studying the clinical phenotype, mutation analysis and functional analysis of mutant receptors were performed using genital skin fibroblasts and in vitro expression studies. Here we report the findings in families with multiple affected cases. Fifty-nine percent of androgen insensitivity syndrome patients had other affected relatives. A total of 17 families were studied, seven families with CAIS (18 patients), nine families with partial androgen insensitivity (24 patients), and one family with female prepubertal phenotypes (two patients). No phenotypic variation was observed in families with CAIS. However, phenotypic variation was observed in one-third of families with partial androgen insensitivity resulting in different sex of rearing and differences in requirement of reconstructive surgery. Intrafamilial phenotypic variation was observed for mutations R846H, M771I, and deletion of amino acid N682. Four newly identified mutations were found. Follow-up in families with different AR gene mutations provided information on residual androgen action in vivo and the development of the prepubertal and adult phenotype. Patients with a functional complete defective AR had some pubic hair, Tanner stage P2, and vestigial Wolffian duct derivatives despite absence of AR expression. Vaginal length was functional in most but not all CAIS patients. The minimal incidence of androgen insensitivity syndrome in The Netherlands, based on patients with molecular proof of the diagnosis is 1:99,000. Phenotypic variation was absent in families with CAIS, but distinct phenotypic variation was observed relatively frequent in families with partial androgen insensitivity. Molecular observations suggest that phenotypic variation had different etiologies among these families. Sex assignment of patients with partial androgen insensitivity cannot be based on a specific identified AR gene mutation because distinct phenotypic variation in partial androgen insensitivity families is relatively frequent. In genetic counseling of partial androgen insensitivity families, this frequent occurrence of variable expression resulting in differences in sex of rearing and/or requirement of reconstructive surgery is important information. During puberty or normal dose androgen therapy, no or only minimal virilization may occur even in patients with significant (but still deficient) prenatal virilization. Wolffian duct remnants remain detectable but differentiation does not occur in the absence of a functional AR. In many CAIS patients, surgical elongation of the vagina is not indicated.

Adolescent↗
PubMed1999

The non-enzymatic microbicidal activity of lysozymes.

T4 lysozyme was thought to destroy bacteria by its muramidase activity. However, we demonstrate here that amphipathic helix stretches in the C-terminus of T4 lysozyme mediate its bactericidal and fungistatic activities. In heat-denatured T4 lysozyme, the enzymatic activity is completely abolished but unexpectedly, the antimicrobial functions remain preserved. Small synthetic peptides corresponding to amphipathic C-terminal domains of T4 lysozyme show a microbicidal activity. Its membrane disturbing activity was directly demonstrated for bacterial, fungal and plant cells but not in a hemolysis assay. Comparable results were obtained with hen egg white lysozyme. This opens up many new opportunities for optimization of lysozymes as antimicrobial agents in various applications by protein engineering.

Animals↗
PubMed1996

Isolation of prostate-derived single cells and cell clusters from human peripheral blood.

The detection of blood-borne prostate cancer (PCA) cells may help with clinical staging and the further understanding of PCA metastases. We discovered prostate-specific antigen (PSA)-positive stained but not PSA mRNA-expressing blood cells by means of cell sorting and PSA reverse transcription-PCR in patients. Therefore, we developed a cytokeratin immunomagnetic method to isolate PSA-positive epithelial cells from the circulating blood of PCA patients. We obtained blood-borne single cells from 6 of 10 PCA patients and clustered cells from 8 of 10 PCA patients. Patients with benign prostate hyperplasia tested negative for cell clusters. The reported isolation method yielded prostate-derived cells or clusters of them from PCA-diagnosed patients.

Humans↗
PubMedDate not supplied

[Interdisciplinary management of fetal obstructive uropathy].

The joint care of children with obstructive uropathy by perinatologists, pediatric intensivists, pediatric nephrologists and urologists can preserve as much renal function as possible. Complications such as urinary tract infections and problems with renal insufficiency can be prevented. Preterm delivery for early surgical decompression of the urinary tract postpartal should be performed only in exceptional cases. We want to underline that supporting and counselling parents in coping with severe findings and prognosis of the disease is among our main aims. We will present two selected cases to demonstrate the spectrum of methods for handling fetal obstructive uropathy.

Female↗