Kidney Circulation

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Rajkumar Jalan - One of the best experts on this subject based on the ideXlab platform.

  • The role of the Molecular Adsorbents Recirculating System (MARS) in the management of liver failure.
    Perfusion, 2020
    Co-Authors: Rajkumar Jalan
    Abstract:

    Albumin-bound toxins accumulate in liver failure, and are believed to contribute to the development of the associated end-organ dysfunctions (Kidney, Circulation, brain). The scavenging functions of albumin are utilized in albumin dialysis for toxin removal. The Molecular Adsorbents Recirculating System (MARS) is an extracorporeal liver support device based on dialysis across an albumin-impregnated membrane, using 20% albumin as dialysate. Charcoal and anion exchange resin columns in the circuit help cleanse and regenerate the dialysate. Clinical studies over the last decade have demonstrated proven reduction in hyperbilirubinaemia, along with an improvement in hepatic encephalopathy, systemic haemodynamics and renal function in liver failure patients, as well as apparent improvement in survival. However, the specific mechanisms underlying these observed clinical changes are as yet unclear. The results of larger controlled clinical trials, as well as studies investigating the pathophysiological basis of its effect, are awaited.

  • The role of the Molecular Adsorbents Recirculating System (MARS) in the management of liver failure
    Perfusion, 2016
    Co-Authors: Rajkumar Jalan
    Abstract:

    Albumin-bound toxins accumulate in liver failure, and are believed to contribute to the development of the associated end-organ dysfunctions (Kidney, Circulation, brain). The scavenging functions of albumin are utilized in albumin dialysis for toxin removal. The Molecular Adsorbents Recirculating System (MARS) is an extracorporeal liver support device based on dialysis across an albumin-impregnated membrane, using 20% albumin as dialysate. Charcoal and anion exchange resin columns in the circuit help cleanse and regenerate the dialysate. Clinical studies over the last decade have demonstrated proven reduction in hyperbilirubinaemia, along with an improvement in hepatic encephalopathy, systemic haemodynamics and renal function in liver failure patients, as well as apparent improvement in survival. However, the specific mechanisms underlying these observed clinical changes are as yet unclear. The results of larger controlled clinical trials, as well as studies investigating the pathophysiological basis of i...

  • Emerging indications for albumin dialysis
    AM J GASTROENTEROL, 2005
    Co-Authors: Rajkumar Jalan
    Abstract:

    The accumulation of albumin-bound toxins in liver failure is believed to be responsible for the development of associated end-organ dysfunctions (Kidney, Circulation, brain). Albumin dialysis utilizes the scavenging functions of albumin for the removal of toxins. The Molecular Adsorbents Recirculating System (MARS) is one such extracorporeal liver support device where blood is dialyzed across an albumin-impregnated membrane against 20% albumin. Charcoal and anion exchange resin columns in the circuit cleanse and regenerate the albumin dialysate. Clinical studies in the last decade have demonstrated proven reduction in hyperbilirubinemia, along with an improvement in encephalopathy in liver failure patients, as well as apparent improvement in survival. Some studies have also reported improvement of systemic hemodynamics and renal function in these patients. Amelioration of intractable pruritus and treatment of toxicities with albumin-bound substances are some of the newer indications emerging. However, the specific underlying pathophysiological mechanisms are still not clear. Two other systems based on the removal of albumin-bound toxins, the Prometheus (using the principle of fractionated plasma separation and adsorption [FPSA]), and the single pass albumin dialysis (SPAD) are also currently under development but available clinical data are limited.

  • Liver failure: basis of benefit of therapy with the molecular adsorbents recirculating system
    The International Journal of Biochemistry & Cell Biology, 2003
    Co-Authors: Rajkumar Jalan, Roger Williams
    Abstract:

    Accumulation of albumin-bound toxins is known to occur in liver failure, and to variable extents is responsible for the associated end-organ dysfunctions (Kidney, Circulation, brain). The toxin-binding and scavenging functions of albumin are exploited in albumin dialysis for removal of these toxins. The extracorporeal liver support device known as molecular adsorbents recirculating system (MARS) is based on dialysis across an albumin-impregnated membrane, using 20% albumin as dialysate. Charcoal and anion exchange resin columns in the circuit help cleanse and regenerate the dialysate. Clinical studies over the last few years have demonstrated proven reduction in hyperbilirubinaemia, along with an improvement in encephalopathy, systemic haemodynamics and renal function in liver failure patients, as well as apparent improvement in survival. The results of larger controlled clinical trials, as well as studies investigating the pathophysiological basis of its effect, are awaited.

Nilesh J Samani - One of the best experts on this subject based on the ideXlab platform.

  • 058 fibroblast growth factor binding protein 1 gene fgfbp1 and hypertension from pathway analysis to renal glomerulus
    Heart, 2010
    Co-Authors: Maciej Tomaszewski, Fadi J Charchar, Timothy A Barnes, Christine Maric, E Zukowskaszczechowska, Nilesh J Samani
    Abstract:

    Essential hypertension is a complex, multifactorial disease with a strong genetic component. Fibroblast growth factor 1 gene (FGF1) is one of the most relevant candidates having been associated not only with familial susceptibility to hypertension but also with up-regulation within the glomerulus of the human hypertensive Kidney/Circulation 2007;116:1915–24/. We have hypothesised that systematic analysis of genes interacting with FGF1 may uncover novel variants underlying essential hypertension. Seventy-nine common (minor allele frequency≥0.1) tagging (r2≥0.8) and functional single nucleotide polymorphisms (SNPs) spanning eight critical components of the FGF (fibroblast growth factor) pathway (FGF2, FGFR1, FGFR2, FGFR3, FGFR4, FGFBP1, FIBP, SPRY1) were genotyped by MALDI-TOF mass spectrometry in 629 subjects from 207 Polish hypertensive families (Silesian Hypertension Study — SHS). 83.5% of genotyped SNPs that passed quality control filters provided 92.9% genetic coverage of FGF pathway loci. Family-based analysis in SHS revealed that alleles of three SNPs (rs2956724, rs2245964 and rs16892645) in two loci (FGFR1 and FGFBP1) were transmitted to hypertensive offspring more frequently than expected by chance. However, only one association survived correction for multiple testing – major allele of rs16892645 in FGFBP1 was over-transmitted from heterozygous parents to hypertensive offspring more frequently than expected by chance(p=0.0048, false discovery rate

  • 058 Fibroblast growth factor binding protein 1 gene (FGFBP1) and hypertension — from pathway analysis to renal glomerulus
    Heart, 2010
    Co-Authors: Maciej Tomaszewski, Fadi J Charchar, Timothy A Barnes, Christine Maric, Ewa Zukowska-szczechowska, Nilesh J Samani
    Abstract:

    Essential hypertension is a complex, multifactorial disease with a strong genetic component. Fibroblast growth factor 1 gene (FGF1) is one of the most relevant candidates having been associated not only with familial susceptibility to hypertension but also with up-regulation within the glomerulus of the human hypertensive Kidney/Circulation 2007;116:1915–24/. We have hypothesised that systematic analysis of genes interacting with FGF1 may uncover novel variants underlying essential hypertension. Seventy-nine common (minor allele frequency≥0.1) tagging (r2≥0.8) and functional single nucleotide polymorphisms (SNPs) spanning eight critical components of the FGF (fibroblast growth factor) pathway (FGF2, FGFR1, FGFR2, FGFR3, FGFR4, FGFBP1, FIBP, SPRY1) were genotyped by MALDI-TOF mass spectrometry in 629 subjects from 207 Polish hypertensive families (Silesian Hypertension Study — SHS). 83.5% of genotyped SNPs that passed quality control filters provided 92.9% genetic coverage of FGF pathway loci. Family-based analysis in SHS revealed that alleles of three SNPs (rs2956724, rs2245964 and rs16892645) in two loci (FGFR1 and FGFBP1) were transmitted to hypertensive offspring more frequently than expected by chance. However, only one association survived correction for multiple testing – major allele of rs16892645 in FGFBP1 was over-transmitted from heterozygous parents to hypertensive offspring more frequently than expected by chance(p=0.0048, false discovery rate

Maciej Tomaszewski - One of the best experts on this subject based on the ideXlab platform.

  • 058 fibroblast growth factor binding protein 1 gene fgfbp1 and hypertension from pathway analysis to renal glomerulus
    Heart, 2010
    Co-Authors: Maciej Tomaszewski, Fadi J Charchar, Timothy A Barnes, Christine Maric, E Zukowskaszczechowska, Nilesh J Samani
    Abstract:

    Essential hypertension is a complex, multifactorial disease with a strong genetic component. Fibroblast growth factor 1 gene (FGF1) is one of the most relevant candidates having been associated not only with familial susceptibility to hypertension but also with up-regulation within the glomerulus of the human hypertensive Kidney/Circulation 2007;116:1915–24/. We have hypothesised that systematic analysis of genes interacting with FGF1 may uncover novel variants underlying essential hypertension. Seventy-nine common (minor allele frequency≥0.1) tagging (r2≥0.8) and functional single nucleotide polymorphisms (SNPs) spanning eight critical components of the FGF (fibroblast growth factor) pathway (FGF2, FGFR1, FGFR2, FGFR3, FGFR4, FGFBP1, FIBP, SPRY1) were genotyped by MALDI-TOF mass spectrometry in 629 subjects from 207 Polish hypertensive families (Silesian Hypertension Study — SHS). 83.5% of genotyped SNPs that passed quality control filters provided 92.9% genetic coverage of FGF pathway loci. Family-based analysis in SHS revealed that alleles of three SNPs (rs2956724, rs2245964 and rs16892645) in two loci (FGFR1 and FGFBP1) were transmitted to hypertensive offspring more frequently than expected by chance. However, only one association survived correction for multiple testing – major allele of rs16892645 in FGFBP1 was over-transmitted from heterozygous parents to hypertensive offspring more frequently than expected by chance(p=0.0048, false discovery rate

  • 058 Fibroblast growth factor binding protein 1 gene (FGFBP1) and hypertension — from pathway analysis to renal glomerulus
    Heart, 2010
    Co-Authors: Maciej Tomaszewski, Fadi J Charchar, Timothy A Barnes, Christine Maric, Ewa Zukowska-szczechowska, Nilesh J Samani
    Abstract:

    Essential hypertension is a complex, multifactorial disease with a strong genetic component. Fibroblast growth factor 1 gene (FGF1) is one of the most relevant candidates having been associated not only with familial susceptibility to hypertension but also with up-regulation within the glomerulus of the human hypertensive Kidney/Circulation 2007;116:1915–24/. We have hypothesised that systematic analysis of genes interacting with FGF1 may uncover novel variants underlying essential hypertension. Seventy-nine common (minor allele frequency≥0.1) tagging (r2≥0.8) and functional single nucleotide polymorphisms (SNPs) spanning eight critical components of the FGF (fibroblast growth factor) pathway (FGF2, FGFR1, FGFR2, FGFR3, FGFR4, FGFBP1, FIBP, SPRY1) were genotyped by MALDI-TOF mass spectrometry in 629 subjects from 207 Polish hypertensive families (Silesian Hypertension Study — SHS). 83.5% of genotyped SNPs that passed quality control filters provided 92.9% genetic coverage of FGF pathway loci. Family-based analysis in SHS revealed that alleles of three SNPs (rs2956724, rs2245964 and rs16892645) in two loci (FGFR1 and FGFBP1) were transmitted to hypertensive offspring more frequently than expected by chance. However, only one association survived correction for multiple testing – major allele of rs16892645 in FGFBP1 was over-transmitted from heterozygous parents to hypertensive offspring more frequently than expected by chance(p=0.0048, false discovery rate

Christine Maric - One of the best experts on this subject based on the ideXlab platform.

  • 058 fibroblast growth factor binding protein 1 gene fgfbp1 and hypertension from pathway analysis to renal glomerulus
    Heart, 2010
    Co-Authors: Maciej Tomaszewski, Fadi J Charchar, Timothy A Barnes, Christine Maric, E Zukowskaszczechowska, Nilesh J Samani
    Abstract:

    Essential hypertension is a complex, multifactorial disease with a strong genetic component. Fibroblast growth factor 1 gene (FGF1) is one of the most relevant candidates having been associated not only with familial susceptibility to hypertension but also with up-regulation within the glomerulus of the human hypertensive Kidney/Circulation 2007;116:1915–24/. We have hypothesised that systematic analysis of genes interacting with FGF1 may uncover novel variants underlying essential hypertension. Seventy-nine common (minor allele frequency≥0.1) tagging (r2≥0.8) and functional single nucleotide polymorphisms (SNPs) spanning eight critical components of the FGF (fibroblast growth factor) pathway (FGF2, FGFR1, FGFR2, FGFR3, FGFR4, FGFBP1, FIBP, SPRY1) were genotyped by MALDI-TOF mass spectrometry in 629 subjects from 207 Polish hypertensive families (Silesian Hypertension Study — SHS). 83.5% of genotyped SNPs that passed quality control filters provided 92.9% genetic coverage of FGF pathway loci. Family-based analysis in SHS revealed that alleles of three SNPs (rs2956724, rs2245964 and rs16892645) in two loci (FGFR1 and FGFBP1) were transmitted to hypertensive offspring more frequently than expected by chance. However, only one association survived correction for multiple testing – major allele of rs16892645 in FGFBP1 was over-transmitted from heterozygous parents to hypertensive offspring more frequently than expected by chance(p=0.0048, false discovery rate

  • 058 Fibroblast growth factor binding protein 1 gene (FGFBP1) and hypertension — from pathway analysis to renal glomerulus
    Heart, 2010
    Co-Authors: Maciej Tomaszewski, Fadi J Charchar, Timothy A Barnes, Christine Maric, Ewa Zukowska-szczechowska, Nilesh J Samani
    Abstract:

    Essential hypertension is a complex, multifactorial disease with a strong genetic component. Fibroblast growth factor 1 gene (FGF1) is one of the most relevant candidates having been associated not only with familial susceptibility to hypertension but also with up-regulation within the glomerulus of the human hypertensive Kidney/Circulation 2007;116:1915–24/. We have hypothesised that systematic analysis of genes interacting with FGF1 may uncover novel variants underlying essential hypertension. Seventy-nine common (minor allele frequency≥0.1) tagging (r2≥0.8) and functional single nucleotide polymorphisms (SNPs) spanning eight critical components of the FGF (fibroblast growth factor) pathway (FGF2, FGFR1, FGFR2, FGFR3, FGFR4, FGFBP1, FIBP, SPRY1) were genotyped by MALDI-TOF mass spectrometry in 629 subjects from 207 Polish hypertensive families (Silesian Hypertension Study — SHS). 83.5% of genotyped SNPs that passed quality control filters provided 92.9% genetic coverage of FGF pathway loci. Family-based analysis in SHS revealed that alleles of three SNPs (rs2956724, rs2245964 and rs16892645) in two loci (FGFR1 and FGFBP1) were transmitted to hypertensive offspring more frequently than expected by chance. However, only one association survived correction for multiple testing – major allele of rs16892645 in FGFBP1 was over-transmitted from heterozygous parents to hypertensive offspring more frequently than expected by chance(p=0.0048, false discovery rate

Timothy A Barnes - One of the best experts on this subject based on the ideXlab platform.

  • 058 fibroblast growth factor binding protein 1 gene fgfbp1 and hypertension from pathway analysis to renal glomerulus
    Heart, 2010
    Co-Authors: Maciej Tomaszewski, Fadi J Charchar, Timothy A Barnes, Christine Maric, E Zukowskaszczechowska, Nilesh J Samani
    Abstract:

    Essential hypertension is a complex, multifactorial disease with a strong genetic component. Fibroblast growth factor 1 gene (FGF1) is one of the most relevant candidates having been associated not only with familial susceptibility to hypertension but also with up-regulation within the glomerulus of the human hypertensive Kidney/Circulation 2007;116:1915–24/. We have hypothesised that systematic analysis of genes interacting with FGF1 may uncover novel variants underlying essential hypertension. Seventy-nine common (minor allele frequency≥0.1) tagging (r2≥0.8) and functional single nucleotide polymorphisms (SNPs) spanning eight critical components of the FGF (fibroblast growth factor) pathway (FGF2, FGFR1, FGFR2, FGFR3, FGFR4, FGFBP1, FIBP, SPRY1) were genotyped by MALDI-TOF mass spectrometry in 629 subjects from 207 Polish hypertensive families (Silesian Hypertension Study — SHS). 83.5% of genotyped SNPs that passed quality control filters provided 92.9% genetic coverage of FGF pathway loci. Family-based analysis in SHS revealed that alleles of three SNPs (rs2956724, rs2245964 and rs16892645) in two loci (FGFR1 and FGFBP1) were transmitted to hypertensive offspring more frequently than expected by chance. However, only one association survived correction for multiple testing – major allele of rs16892645 in FGFBP1 was over-transmitted from heterozygous parents to hypertensive offspring more frequently than expected by chance(p=0.0048, false discovery rate

  • 058 Fibroblast growth factor binding protein 1 gene (FGFBP1) and hypertension — from pathway analysis to renal glomerulus
    Heart, 2010
    Co-Authors: Maciej Tomaszewski, Fadi J Charchar, Timothy A Barnes, Christine Maric, Ewa Zukowska-szczechowska, Nilesh J Samani
    Abstract:

    Essential hypertension is a complex, multifactorial disease with a strong genetic component. Fibroblast growth factor 1 gene (FGF1) is one of the most relevant candidates having been associated not only with familial susceptibility to hypertension but also with up-regulation within the glomerulus of the human hypertensive Kidney/Circulation 2007;116:1915–24/. We have hypothesised that systematic analysis of genes interacting with FGF1 may uncover novel variants underlying essential hypertension. Seventy-nine common (minor allele frequency≥0.1) tagging (r2≥0.8) and functional single nucleotide polymorphisms (SNPs) spanning eight critical components of the FGF (fibroblast growth factor) pathway (FGF2, FGFR1, FGFR2, FGFR3, FGFR4, FGFBP1, FIBP, SPRY1) were genotyped by MALDI-TOF mass spectrometry in 629 subjects from 207 Polish hypertensive families (Silesian Hypertension Study — SHS). 83.5% of genotyped SNPs that passed quality control filters provided 92.9% genetic coverage of FGF pathway loci. Family-based analysis in SHS revealed that alleles of three SNPs (rs2956724, rs2245964 and rs16892645) in two loci (FGFR1 and FGFBP1) were transmitted to hypertensive offspring more frequently than expected by chance. However, only one association survived correction for multiple testing – major allele of rs16892645 in FGFBP1 was over-transmitted from heterozygous parents to hypertensive offspring more frequently than expected by chance(p=0.0048, false discovery rate