The Experts below are selected from a list of 96 Experts worldwide ranked by ideXlab platform

Hannsjörg W. Seyberth - One of the best experts on this subject based on the ideXlab platform.

  • The role of prostanoids in pediatric diseases employing mass spectrometric techniques
    1992
    Co-Authors: Hannsjörg W. Seyberth, Horst Schweer, Burkhard Tönshoff, Andreas Leonhardt
    Abstract:

    Urinary excretion rates of primary prostanoids and their metabolites are useful parameters to assess as well Renal as systemic prostanoid activity under clinical conditions. Children with Renal diseases with systemic involvement, such as Bartter syndrome, Renal Diabetes insipidus, postobstructive hydronephrosis, and acute Renal allograft rejection, have exclusively elevated excretion rates of primary prostanoids. In patients with systemic diseases and additional Renal involvement, such as hyperprostaglandin E syndrome and hemolytic uremic syndrome, rates of primary prostanoids and of their metabolites are elevated

  • The role of prostanoids in pediatric diseases employing mass spectrometric techniques.
    Eicosanoids, 1992
    Co-Authors: Hannsjörg W. Seyberth, Horst Schweer, Burkhard Tönshoff, Andreas Leonhardt
    Abstract:

    Urinary excretion rates of primary prostanoids and their metabolites are useful parameters to assess as well Renal as systemic prostanoid activity under clinical conditions. Children with Renal diseases with systemic involvement, such as Bartter syndrome, Renal Diabetes insipidus, postobstructive hydronephrosis, and acute Renal allograft rejection, have exclusively elevated excretion rates of primary prostanoids. In patients with systemic diseases and additional Renal involvement, such as hyperprostaglandin E syndrome and hemolytic uremic syndrome, rates of primary prostanoids and of their metabolites are elevated. In contrast, systemic vascular diseases without Renal involvement, such as Henoch-Schönlein purpura and persistent pulmonary hypertension in the newborn, are associated only with increased systemic prostanoid activity indicated by elevated excretion rates of prostanoid metabolites, whereas excretion rates of primary metabolites are in the normal range.

  • Prostanoids in paediatric kidney diseases
    Pediatric Nephrology, 1991
    Co-Authors: Hannsjörg W. Seyberth, Burkhard Tönshoff, Andreas Leonhardt, Nader Gordjani
    Abstract:

    Prostanoids belong to the growing family of eicosanoids, which are all derived from arachidonic acid. Prostanoids act as modulators and mediators in a large spectrum of physiological and pathophysiological processes within the kidney. On the one hand, the potent vasoconstrictor and platelet-aggregating thromboxane (TX) A_2 is involved in the pathophysiology of a variety of glomerular diseases, such as haemolytic-uraemic syndrome and immune-mediated glomerulopathies. Prostaglandin (PG) E_2, on the other hand, interferes with tubular electrolyte and water handling. Clinical data support the hypothesis that this member of the prostanoid family contributes to the pathophysiology of Bartter's syndrome, hyperprostaglandin E syndrome, idiopathic hypercalciuria and Renal Diabetes insipidus. Both prostanoids, TXA_2 and PGE_2, are involved in the pathophysiology of obstructive uropathies. The physiological and protective role of Renal vasodilator prostanoids (PGI_2 and PGE_2) has been studied during treatment with non-steroidal anti-inflammatory drugs. Part of the pharmacological effects of frusemide and converting enzyme inhibitors is mediated by PGI_2 and PGE_2. The role of Renal prostanoids in cyclosporine toxicity is still equivocal. Future investigations on the physiological and pathophysiological role of Renal prostanoids will have to consider the multiple interactions between prostanoids on the one hand, and classical hormones and other mediators (e. g. cytokines) on the other hand.

Andreas Leonhardt - One of the best experts on this subject based on the ideXlab platform.

  • The role of prostanoids in pediatric diseases employing mass spectrometric techniques
    1992
    Co-Authors: Hannsjörg W. Seyberth, Horst Schweer, Burkhard Tönshoff, Andreas Leonhardt
    Abstract:

    Urinary excretion rates of primary prostanoids and their metabolites are useful parameters to assess as well Renal as systemic prostanoid activity under clinical conditions. Children with Renal diseases with systemic involvement, such as Bartter syndrome, Renal Diabetes insipidus, postobstructive hydronephrosis, and acute Renal allograft rejection, have exclusively elevated excretion rates of primary prostanoids. In patients with systemic diseases and additional Renal involvement, such as hyperprostaglandin E syndrome and hemolytic uremic syndrome, rates of primary prostanoids and of their metabolites are elevated

  • The role of prostanoids in pediatric diseases employing mass spectrometric techniques.
    Eicosanoids, 1992
    Co-Authors: Hannsjörg W. Seyberth, Horst Schweer, Burkhard Tönshoff, Andreas Leonhardt
    Abstract:

    Urinary excretion rates of primary prostanoids and their metabolites are useful parameters to assess as well Renal as systemic prostanoid activity under clinical conditions. Children with Renal diseases with systemic involvement, such as Bartter syndrome, Renal Diabetes insipidus, postobstructive hydronephrosis, and acute Renal allograft rejection, have exclusively elevated excretion rates of primary prostanoids. In patients with systemic diseases and additional Renal involvement, such as hyperprostaglandin E syndrome and hemolytic uremic syndrome, rates of primary prostanoids and of their metabolites are elevated. In contrast, systemic vascular diseases without Renal involvement, such as Henoch-Schönlein purpura and persistent pulmonary hypertension in the newborn, are associated only with increased systemic prostanoid activity indicated by elevated excretion rates of prostanoid metabolites, whereas excretion rates of primary metabolites are in the normal range.

  • Prostanoids in paediatric kidney diseases
    Pediatric Nephrology, 1991
    Co-Authors: Hannsjörg W. Seyberth, Burkhard Tönshoff, Andreas Leonhardt, Nader Gordjani
    Abstract:

    Prostanoids belong to the growing family of eicosanoids, which are all derived from arachidonic acid. Prostanoids act as modulators and mediators in a large spectrum of physiological and pathophysiological processes within the kidney. On the one hand, the potent vasoconstrictor and platelet-aggregating thromboxane (TX) A_2 is involved in the pathophysiology of a variety of glomerular diseases, such as haemolytic-uraemic syndrome and immune-mediated glomerulopathies. Prostaglandin (PG) E_2, on the other hand, interferes with tubular electrolyte and water handling. Clinical data support the hypothesis that this member of the prostanoid family contributes to the pathophysiology of Bartter's syndrome, hyperprostaglandin E syndrome, idiopathic hypercalciuria and Renal Diabetes insipidus. Both prostanoids, TXA_2 and PGE_2, are involved in the pathophysiology of obstructive uropathies. The physiological and protective role of Renal vasodilator prostanoids (PGI_2 and PGE_2) has been studied during treatment with non-steroidal anti-inflammatory drugs. Part of the pharmacological effects of frusemide and converting enzyme inhibitors is mediated by PGI_2 and PGE_2. The role of Renal prostanoids in cyclosporine toxicity is still equivocal. Future investigations on the physiological and pathophysiological role of Renal prostanoids will have to consider the multiple interactions between prostanoids on the one hand, and classical hormones and other mediators (e. g. cytokines) on the other hand.

Burkhard Tönshoff - One of the best experts on this subject based on the ideXlab platform.

  • The role of prostanoids in pediatric diseases employing mass spectrometric techniques
    1992
    Co-Authors: Hannsjörg W. Seyberth, Horst Schweer, Burkhard Tönshoff, Andreas Leonhardt
    Abstract:

    Urinary excretion rates of primary prostanoids and their metabolites are useful parameters to assess as well Renal as systemic prostanoid activity under clinical conditions. Children with Renal diseases with systemic involvement, such as Bartter syndrome, Renal Diabetes insipidus, postobstructive hydronephrosis, and acute Renal allograft rejection, have exclusively elevated excretion rates of primary prostanoids. In patients with systemic diseases and additional Renal involvement, such as hyperprostaglandin E syndrome and hemolytic uremic syndrome, rates of primary prostanoids and of their metabolites are elevated

  • The role of prostanoids in pediatric diseases employing mass spectrometric techniques.
    Eicosanoids, 1992
    Co-Authors: Hannsjörg W. Seyberth, Horst Schweer, Burkhard Tönshoff, Andreas Leonhardt
    Abstract:

    Urinary excretion rates of primary prostanoids and their metabolites are useful parameters to assess as well Renal as systemic prostanoid activity under clinical conditions. Children with Renal diseases with systemic involvement, such as Bartter syndrome, Renal Diabetes insipidus, postobstructive hydronephrosis, and acute Renal allograft rejection, have exclusively elevated excretion rates of primary prostanoids. In patients with systemic diseases and additional Renal involvement, such as hyperprostaglandin E syndrome and hemolytic uremic syndrome, rates of primary prostanoids and of their metabolites are elevated. In contrast, systemic vascular diseases without Renal involvement, such as Henoch-Schönlein purpura and persistent pulmonary hypertension in the newborn, are associated only with increased systemic prostanoid activity indicated by elevated excretion rates of prostanoid metabolites, whereas excretion rates of primary metabolites are in the normal range.

  • Prostanoids in paediatric kidney diseases
    Pediatric Nephrology, 1991
    Co-Authors: Hannsjörg W. Seyberth, Burkhard Tönshoff, Andreas Leonhardt, Nader Gordjani
    Abstract:

    Prostanoids belong to the growing family of eicosanoids, which are all derived from arachidonic acid. Prostanoids act as modulators and mediators in a large spectrum of physiological and pathophysiological processes within the kidney. On the one hand, the potent vasoconstrictor and platelet-aggregating thromboxane (TX) A_2 is involved in the pathophysiology of a variety of glomerular diseases, such as haemolytic-uraemic syndrome and immune-mediated glomerulopathies. Prostaglandin (PG) E_2, on the other hand, interferes with tubular electrolyte and water handling. Clinical data support the hypothesis that this member of the prostanoid family contributes to the pathophysiology of Bartter's syndrome, hyperprostaglandin E syndrome, idiopathic hypercalciuria and Renal Diabetes insipidus. Both prostanoids, TXA_2 and PGE_2, are involved in the pathophysiology of obstructive uropathies. The physiological and protective role of Renal vasodilator prostanoids (PGI_2 and PGE_2) has been studied during treatment with non-steroidal anti-inflammatory drugs. Part of the pharmacological effects of frusemide and converting enzyme inhibitors is mediated by PGI_2 and PGE_2. The role of Renal prostanoids in cyclosporine toxicity is still equivocal. Future investigations on the physiological and pathophysiological role of Renal prostanoids will have to consider the multiple interactions between prostanoids on the one hand, and classical hormones and other mediators (e. g. cytokines) on the other hand.

Nader Gordjani - One of the best experts on this subject based on the ideXlab platform.

  • Prostanoids in paediatric kidney diseases
    Pediatric Nephrology, 1991
    Co-Authors: Hannsjörg W. Seyberth, Burkhard Tönshoff, Andreas Leonhardt, Nader Gordjani
    Abstract:

    Prostanoids belong to the growing family of eicosanoids, which are all derived from arachidonic acid. Prostanoids act as modulators and mediators in a large spectrum of physiological and pathophysiological processes within the kidney. On the one hand, the potent vasoconstrictor and platelet-aggregating thromboxane (TX) A_2 is involved in the pathophysiology of a variety of glomerular diseases, such as haemolytic-uraemic syndrome and immune-mediated glomerulopathies. Prostaglandin (PG) E_2, on the other hand, interferes with tubular electrolyte and water handling. Clinical data support the hypothesis that this member of the prostanoid family contributes to the pathophysiology of Bartter's syndrome, hyperprostaglandin E syndrome, idiopathic hypercalciuria and Renal Diabetes insipidus. Both prostanoids, TXA_2 and PGE_2, are involved in the pathophysiology of obstructive uropathies. The physiological and protective role of Renal vasodilator prostanoids (PGI_2 and PGE_2) has been studied during treatment with non-steroidal anti-inflammatory drugs. Part of the pharmacological effects of frusemide and converting enzyme inhibitors is mediated by PGI_2 and PGE_2. The role of Renal prostanoids in cyclosporine toxicity is still equivocal. Future investigations on the physiological and pathophysiological role of Renal prostanoids will have to consider the multiple interactions between prostanoids on the one hand, and classical hormones and other mediators (e. g. cytokines) on the other hand.

Siegfried Waldegger - One of the best experts on this subject based on the ideXlab platform.

  • Mechanisms of Disease: the kidney-specific chloride channels ClCKA and ClCKB, the Barttin subunit, and their clinical relevance.
    Nature Reviews Nephrology, 2020
    Co-Authors: Bernhard K Krämer, Tobias Bergler, Benjamin Stoelcker, Siegfried Waldegger
    Abstract:

    Knowledge regarding this important system of Renal chloride transporters has rapidly accumulated. A severe salt-losing tubulopathy—Bartter syndrome type III—develops when ClCKB is non-functional, whereas a common genetic variant of theCLCNKBgene results in salt-dependent hypertension. Disruption of the Barttin gene manifests as Bartter syndrome type IV with sensorineural deafness and an especially severe salt-losing phenotype. It is timely, therefore, to review the properties of these transporters. Rodent ClC-K1 and ClC-K2, and their respective human orthologs ClCKA and ClCKB, are chloride channels specific to the kidney (and inner ear); Barttin is their functionally important subunit. ClC-K1 is predominantly localized to the thin ascending limb of the loop of Henle. ClC-K2 is expressed more broadly in the distal nephron; expression levels are highest along the thick ascending limb of the loop of Henle and distal convoluted tubule. Expression of ClC-K1 is upregulated by dehydration and downregulated by the diuretic furosemide, whereas expression of ClC-K2 is upregulated by furosemide and downregulated by high salt levels. ClCKA is important for maintenance of the corticomedullary osmotic gradient and the kidney's capacity to concentrate urine. If its ortholog, ClC-K1, is nonfunctional in mice, Renal Diabetes insipidus develops. ClCKB is a key determinant of tubular reabsorption of chloride and electrolytes along the distal tubule. A severe salt-losing tubulopathy (Bartter syndrome type III) develops if ClCKB is nonfunctional, whereas a common genetic variant of the CLCNKB gene that leads to increased activity of ClCKB results in salt-dependent hypertension. Disruption of the gene encoding Barttin, BSND, results in a 'double knockout' of the functions of both ClCKA and ClCKB, manifesting as Bartter syndrome type IV with sensorineural deafness and an especially severe salt-losing phenotype.

  • Mechanisms of Disease: the kidney-specific chloride channels ClCKA and ClCKB, the Barttin subunit, and their clinical relevance
    Nature Clinical Practice Nephrology, 2008
    Co-Authors: Bernhard K Krämer, Tobias Bergler, Benjamin Stoelcker, Siegfried Waldegger
    Abstract:

    ClCKA (ClC-K1) and ClCKB (ClC-K2) are chloride channels specific to the kidney (and inner ear); Barttin is their functionally important subunit ClC-K1 is localized predominantly to the thin ascending limb of the loop of Henle; ClC-K2 is more broadly expressed along the distal nephron ClC-K1 is upregulated by dehydration and downregulated by furosemide; the channel's human ortholog, ClCKA, is activated by the cell-volume-regulated gene SGK1; ClC-K2 is upregulated by furosemide and downregulated by high salt levels ClCKA is important for maintenance of the corticomedullary osmotic gradient and for the kidney's capacity to concentrate urine; Renal Diabetes insipidus develops in mice if ClC-K1 is nonfunctional ClCKB is important for tubular chloride and electrolyte reabsorption; a severe salt-losing tubulopathy (Bartter syndrome type III) develops if ClCKB is nonfunctional, whereas a common genetic variant of the CLCNKB gene increases the activity of ClCKB, resulting in salt-dependent hypertension Dysfunction of the Barttin gene functionally corresponds to a 'double knockout' of ClCKA and ClCKB, leading to Bartter syndrome type IV with sensorineural deafness and a severe salt-losing phenotype Rodent ClC-K1 and ClC-K2, and their respective human orthologs ClCKA and ClCKB, are chloride channels specific to the kidney (and inner ear); Barttin is their functionally important subunit. ClC-K1 is predominantly localized to the thin ascending limb of the loop of Henle. ClC-K2 is expressed more broadly in the distal nephron; expression levels are highest along the thick ascending limb of the loop of Henle and distal convoluted tubule. Expression of ClC-K1 is upregulated by dehydration and downregulated by the diuretic furosemide, whereas expression of ClC-K2 is upregulated by furosemide and downregulated by high salt levels. ClCKA is important for maintenance of the corticomedullary osmotic gradient and the kidney's capacity to concentrate urine. If its ortholog, ClC-K1, is nonfunctional in mice, Renal Diabetes insipidus develops. ClCKB is a key determinant of tubular reabsorption of chloride and electrolytes along the distal tubule. A severe salt-losing tubulopathy (Bartter syndrome type III) develops if ClCKB is nonfunctional, whereas a common genetic variant of the CLCNKB gene that leads to increased activity of ClCKB results in salt-dependent hypertension. Disruption of the gene encoding Barttin, BSND , results in a 'double knockout' of the functions of both ClCKA and ClCKB, manifesting as Bartter syndrome type IV with sensorineural deafness and an especially severe salt-losing phenotype. Knowledge regarding this important system of Renal chloride transporters has rapidly accumulated. A severe salt-losing tubulopathy—Bartter syndrome type III—develops when ClCKB is non-functional, whereas a common genetic variant of the CLCNKB gene results in salt-dependent hypertension. Disruption of the Barttin gene manifests as Bartter syndrome type IV with sensorineural deafness and an especially severe salt-losing phenotype. It is timely, therefore, to review the properties of these transporters.