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  • 1
    Electronic Resource
    Electronic Resource
    Hyperhomocysteinemia and other thrombotic risk factors in women with placental vasculopathy (2000)
    Oxford, UK : Blackwell Publishing Ltd
    BJOG 107 (2000), S. 0 
    Details
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective To investigate coagulation inhibitors and abnormalities of the homocysteine metabolism, which are related to an increased thrombotic risk, as risk factors for placental vasculopathy.Design A case-control study comparing nonpregnant women with an obstetric history of placental vasculopathy (study group) with nonpregnant women (control group) matched for age and occupation.Setting Obstetric outpatient clinic in the University Hospital Nijmegen.Sample One hundred and one women in the study group and 92 women in a control group.Methods Determinations in blood samples of homocysteine concentrations; the occurrence of 677 C→T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene; protein C activities; activated protein C resistance ratios; concentrations of free protein S antigen; antithrombin III activities; and the occurrence of factor V Leiden mutation.Results Increased risk for placental vasculopathy was found in the study group with elevated homocysteine (odds ratio 2.28, 95% CI 1.18–4.39), MTHFR mutation (odds ratio 3.29, 95% CI 1.03–10.5), decreased activated protein C resistance ratio (odds ratio 2.46, 95% CI 1.06–5.72) and protein C (odds ratio 2.01, 95% CI 1.11–3.65). Any combination of two risk factors in the same individual resulted in a 3.40 (95% CI 1.80–6.42) higher relative risk for placental vasculopathy; combinations of three risk factors in a 6.83 (95% CI 1.52–30.7) higher risk.Conclusions The thrombotic risk factors decreased levels of activated protein C resistance ratios and protein C, elevated homocysteine and the MTHFR 677 C→T mutation are likely risk factors for placental vasculopathy. Combinations of these risk factors in one individual resulted in synergistic increase of risk.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-0528.2000.tb13341.x
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  • 2
    Electronic Resource
    Electronic Resource
    Nephrogenic diabetes insipidus: identification of the genetic defect (1993)
    Springer
    Pediatric nephrology 7 (1993), S. 685-688 
    Details
    ISSN: 1432-198X
    Keywords: Nephrogenic diabetes insipidus ; V2 receptor gene ; Point mutations
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Congenital nephrogenic diabetes insipidus (NDI) is an X-linked inherited disorder characterized by renal resistance to the antidiuretic hormonal action of arginine vasopressin. The disease gene has been assigned to the subtelomeric region of the X chromosome long arm by demonstrating close linkage between NDI and several X-chromosomal DNA markers. The finding of closely linked genetic markers is useful in the diagnosis of NDI. Receptor studies in patients have indicated that NDI might be due to the absence or an abnormality of the adenylate cyclase-bound vasopressin type 2 receptor. This assumption was supported by the discovery of functional vasopressin V2 receptor activity in somatic cell hybrid cell lines that carried at least the distal part of the human X chromosome long arm. Definite evidence for a V2 receptor defect being the cause of NDI was found in a recent study demonstrating point mutations in the V2 receptor gene from affected individuals. Direct mutation analysis is now applicable for accurate carrier detection and early (prenatal) diagnosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00852579
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  • 3
    Electronic Resource
    Electronic Resource
    The glycosaminoglycan content of renal basement membranes in the congenital nephrotic syndrome of the Finnish type (1992)
    Springer
    Pediatric nephrology 6 (1992), S. 10-15 
    Details
    ISSN: 1432-198X
    Keywords: Congenital nephrotic syndrome ; Finnish type ; Glomerular basement membrane ; Heparan sulphate ; Heparan sulphate proteoglycan
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A decrease in the concentration of heparan sulphate proteoglycan (HSPG) in the glomerular basement membrane (GBM) is supposed to cause the increased GBM permeability in the congenital nephrotic syndrome (CNS). Therefore, we analysed the glycosaminoglycan (GAG) content and composition of the GBM and tubular basement membrane (TBM) from 3 patients with CNS of the Finnish type (FCNS) and 16 control infants. The GAG content, determined by spectrophotometric assay after papain digestion, was not significantly different in FCNS patients compared with controls. In addition, the GAG composition was comparable in the two groups, with heparan sulphate (HS) constituting at least 75% of the total GAG content. The urinary GAG content (expressed as mg GAG/mmol creatinine) was age dependent, but similar in both groups. Indirect immunofluorescence studies on kidney tissue from normal human infants, using monoclonal or polyclonal antibodies against the core protein of human GBM HSPG, showed linear staining of almost all renal basement membranes. A monoclonal antibody directed against the HS chain of HSPG showed strong GBM and a weak TBM staining. Kidney tissue from three patients with FCNS displayed no discernible differences in the distribution or quality of staining with the same antibodies. These biochemical and immunohistochemical results are in contrast to the decrease in anionic sites (by polyethyleneimine staining) and the replacement of GBM HS by chondroitin sulphate, observed by others in CNS of the diffuse mesangial sclerosis type.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00856820
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  • 4
    Electronic Resource
    Electronic Resource
    Nephrogenic diabetes insipidus: clinical symptoms, pathogenesis, genetics and treatment (1992)
    Springer
    Pediatric nephrology 6 (1992), S. 476-482 
    Details
    ISSN: 1432-198X
    Keywords: Nephrogenic diabetes inspidus ; V2 receptor ; X chromosomal localization ; Amiloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This review summarizes various aspects of the inherited kidney disorder nephrogenic diabetes insipidus (NDI). The clinical manifestations of the disease are presented. The important role of the genetic localization of the NDI gene to the X-chromosome long arm, in region Xq28, for carrier detection and early (prenatal) diagnosis of the disorder is emphasized. Following an overview of the cellular physiology involved in the antidiuretic action of vasopressin, possible mechanisms in the pathogenesis of NDI are discussed. We hypothesize that NDI is most probably due to the absence or abnormality of the renal V2 receptor. This assumption is strengthened by recent findings in receptor studies, which indicate a general V2 receptor defect in NDI, and in experiments with somatic cell hybrid cell lines, which are consistent with a co-localization of the genes for NDI and for the V2 receptor in the Xq28 region. Finally, the efficacy of the combination amiloride-hydrochlorothiazide, compared with the indomethacin-hydrochlorothiazide regimen, in the treatment of NDI is presented and the advantages of the former combination are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00874020
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  • 5
    Electronic Resource
    Electronic Resource
    Hereditary disorders of the glomerular basement membrane (1996)
    Springer
    Pediatric nephrology 10 (1996), S. 779-788 
    Details
    ISSN: 1432-198X
    Keywords: Key words: Glomerular basement membrane ; Hereditary disorders
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Increased knowledge of the biochemical composition of the glomerular basement membrane (GBM) and the introduction of molecular genetics has shed new light on the hereditary disorders of the GBM. In this review three disorders are highlighted. About 85% of the cases reported as Alport syndrome are transmitted as the X-linked form and are due to mutations of the COl4A5 chain localized at Xq22. The autosomal recessive form can be explained by mutations in the COl4A3 and COl4A4 gene. Anti-GBM nephritis leading to loss of the renal allograft in about 1% – 5% of transplanted Alport patients can be the tragic consequence of this disorder. Some patients with familial benign hematuria have an abnormality of COl4A4. The nail-patella syndrome is a rare autosomal dominant disorder defined by the association of nail dysplasia, bone abnormalities, and frequently renal disease. The gene is localized in region 9q34.1, COl5A1 is not involved. The Finnish type is the best known of the different forms of congenital nephrotic syndrome. The gene has been mapped to the long arm of chromosome 19. Diffuse mesangial sclerosis occurs in the isolated form and as part of the Denys Drash syndrome. Disturbances of the WT1 function in the epithelial cells can have a role in the renal abnormalities of the Denys Drash syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670050217
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  • 6
    Electronic Resource
    Electronic Resource
    Intraperitoneal hypercoagulation and hypofibrinolysis is present in childhood peritonitis (1999)
    Springer
    Pediatric nephrology 13 (1999), S. 284-287 
    Details
    ISSN: 1432-198X
    Keywords: Key words Fibrinolysis ; Peritonitis ; Peritoneal dialysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  An increased rate of obstruction of peritoneal dialysis catheters is observed during peritonitis. Hypercoagulation and hypofibrinolysis may explain this increased occurrence. We studied plasminogen activator inhibitor type 1 antigen (PAI-1), tissue-type plasminogen activator antigen (t-PA), D-dimer (DD), plasmin-α2-antiplasmin complexes (PAP), and thrombin-antithrombin III complexes (TAT) in 7 children with peritonitis (group A) and 12 children during stable peritoneal dialysis (group B). Albumin, β2-microglobulin, IgG, and α2-macroglobulin were measured for baseline transperitoneal protein transport. After a dwell of 6 h with 1.36% Dianeal, dialysate and serum samples were collected. Dialysate to plasma ratios of all proteins were calculated. During peritonitis (group A) TAT was higher: 34.7 versus 22.0 (P=0.01). PAI-1 was increased in group A: 76.5 versus 22.9 (P=0.004). PAP was decreased during peritonitis (group A): 24.9 versus 39.3 (P=0.01). In group A, DD were decreased. 10.8 versus 26.7 (P=0.002). t-PA was similar in both groups (23.7 in group A vs. 27.7 in group B; P=0.26). In both groups TAT, PAI-1, t-PA, PAP, and DD were significantly higher than in baseline transperitoneal transport, suggesting intraperitoneal production. Hypercoagulability and hypofibrinolysis were present during peritonitis compared with the control situation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670050609
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  • 7
    Electronic Resource
    Electronic Resource
    Clinical experience with icodextrin in children: ultrafiltration profiles and metabolism (2000)
    Springer
    Pediatric nephrology 15 (2000), S. 21-24 
    Details
    ISSN: 1432-198X
    Keywords: Key words Icodextrin ; Peritoneal dialysis ; Ultrafiltration ; Metabolism ; Dialysis adequacy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Icodextrin use in adults provides sustained ultrafiltration (UF) in long-term dwells. No information is available on UF and metabolism in children. In 11 children, a volume of 1,049±138 ml/m2 of the study fluid (1.36% glucose, 7.5% icodextrin, 3.86% glucose) was administered for 12 h. Net UF with icodextrin (339±147 ml/1.73 m2) did not differ from UF with 3.86% glucose (450±306 ml/1.73 m2, P=0.53) and was higher than UF with 1.36% glucose (–87±239 ml/1.73 m2, P=0.003). Icodextrin added 0.52±0.07 to the weekly Kt/V. Over 6 weeks, icodextrin was used for 12-h daytime dwell. Total icodextrin reached a steady-state level of 2.91±1.22 g/l at 2 weeks. The main icodextrin metabolites were maltose, maltotriose, and maltotetraose. After 2 weeks, steady state levels were 2.02±0.66 mmol/l, 1.46±0.35 mmol/l, and 0.45±0.12 mmol/l. No icodextrin or metabolites were detectable 4 weeks after the study. We conclude that 7.5% icodextrin is capable of maintaining UF during 12-h dwell in children and is comparable to UF obtained with 3.86% glucose. Steady-state levels of icodextrin and metabolites were reached at 2 weeks and disappeared after the study.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670000406
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  • 8
    Electronic Resource
    Electronic Resource
    The development of anti-glomerular basement membrane nephritis in two children with Alport's syndrome after renal transplantation: characterization of the antibody target (1989)
    Springer
    Pediatric nephrology 3 (1989), S. 406-413 
    Details
    ISSN: 1432-198X
    Keywords: Anti-glomerular basement membrane nephritis ; Alport's syndrome ; Transplantation ; Goodpasture's syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Two children with Alport's syndrome are described, who developed anti-glomerular basement membrane (GBM) antibody-mediated nephritis after renal transplantation. The reactivity of antibodies in their serum with collagenase-solubilized normal GBM was examined by SDS-PAGE with one- and two-dimensional immunoblotting. The specificity was compared with that of antibodies present in serum from a patient with Goodpasture's syndrome, and a mouse monoclonal antibody (MCA-P1), directed against the Goodpasture antigen. All reacted in a similar way with collagenase-solubilized GBM. Since abnormalities in the composition of the GBM are present in Alport's syndrome, it is proposed that differing antigen composition of GBM in the host compared with the donor kidney, together with transplant rejection, may have provoked the development of post-transplant anti-GBM antibodies.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00850217
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  • 9
    Electronic Resource
    Electronic Resource
    Reduction of potassium in drinks by pre-treatment with calcium polystyrene sulphonate (1993)
    Springer
    European journal of pediatrics 152 (1993), S. 263-264 
    Details
    ISSN: 1432-1076
    Keywords: Potassium restriction ; Calcium polystyrene sulphonate ; Chronic renal failure
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Dietary potassium intake in patients with chronic renal failure is generally reduced by oral administration of potassium-binding resins. These drugs may cause disturbances of bowel function and have an unpleasant taste. Pre-treatment of drinks with these resins and their subsequent removal may prevent these inconveniences. In four formulas (whole milk, humanised infant formula, apple juice, and orange juice) we were able to lower the potassium content by 50% with calcium polystyrene sulphonate. No important increase of sodium content was observed, as was reported with the use of sodium polystyrene sulphonate. There was a, potentially beneficial, increase of the calcium concentration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01956159
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  • 10
    Electronic Resource
    Electronic Resource
    Pharmacokinetics of recombinant human erythropoietin in children treated with continuous ambulatory peritoneal dialysis (1994)
    Springer
    European journal of pediatrics 153 (1994), S. 850-854 
    Details
    ISSN: 1432-1076
    Keywords: CAPD ; Children Erythropoietin ; Pharmacokinetics Intraperitoneal administration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In children treated by continuous ambulatory peritoneal dialysis (CAPD) renal anaemia is preferably treated by intraperitoneal administration of erythropoietin, since subcutaneous administration is painful and frightening for the child. Pharmacokinetics of erythropoietin were studied in three groups of children treated by CAPD. In group subcutaneous (SC) (n=5) erythropoietin was administered subcutaneously, whereas in group intraperitoneal 1 (IP1) (n=8) and intraperitoneal 2 (IP2) (n=8) erythropoietin was given intraperitoneally during a 12-h dwell. Group IP1 received erythropoietin in 20 ml/kg of dialysis fluid, while in group IP2 the hormone was added to only 50 ml of dialysate, irrespective of body weight. The median area under the curve (AUC) was 4064 mU·h/ml (range 2647–24357) in group SC, 1698 (570–5514) in group IP1 and 3577 (1225–6555) in group IP2. In comparison to group SC the AUC was significantly lower in group IP1 (Wilcoxon;P=0.02). The difference between group SC and group IP2 was not statistically significant. In children on CAPD the resorption of erythropoietin after intraperitoneal administration, measured as AUC, is similar to subcutaneous administration, when erythropoietin is administered in 50 ml of dialysate. The dose needed to treat renal anaemia with erythropoietin administered intraperitoneally this way will have to be established in a therapeutic study.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01972896
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