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  1. Article ; Online: Cardiovascular disease in childhood and adolescence: Lessons from children with chronic kidney disease.

    Querfeld, Uwe

    Acta paediatrica (Oslo, Norway : 1992)

    2020  Volume 110, Issue 4, Page(s) 1125–1131

    Abstract: Children suffering from chronic kidney disease (CKD) have the apparent highest risk for the development of cardiovascular disease (CVD) at a young age. While symptoms of CVD are characteristically absent in childhood and adolescence, remodelling of the ... ...

    Abstract Children suffering from chronic kidney disease (CKD) have the apparent highest risk for the development of cardiovascular disease (CVD) at a young age. While symptoms of CVD are characteristically absent in childhood and adolescence, remodelling of the myocardium, medium and large-sized arteries and of the microcirculation is clinically significant and can be assessed with non-invasive technology. Kidney disease and its progression are the driver of CVD, mediated by an unparalleled accumulation of risk factors converging on several comorbid conditions including hypertension, anaemia, dyslipidaemia, disturbed mineral metabolism and chronic persistent inflammation. Large prospective paediatric cohorts studies have provided valuable insights into the pathogenesis and the progression of CKD-induced cardiovascular comorbidity and have characterised the cardiovascular phenotype in young patients. They have also provided the rationale for close monitoring of risk factors and have defined therapeutic targets. Recently discovered new biomarkers could help identify the individual risk for CVD. Prevention of CVD by aggressive therapy of modifiable risk factors is essential to enable long-term survival of young patients with CKD.
    MeSH term(s) Adolescent ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/etiology ; Child ; Humans ; Hypertension ; Prospective Studies ; Renal Insufficiency, Chronic/epidemiology ; Risk Factors
    Language English
    Publishing date 2020-11-05
    Publishing country Norway
    Document type Journal Article
    ZDB-ID 203487-6
    ISSN 1651-2227 ; 0365-1436 ; 0803-5253
    ISSN (online) 1651-2227
    ISSN 0365-1436 ; 0803-5253
    DOI 10.1111/apa.15630
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Aortic dilatation in children with chronic kidney disease.

    Querfeld, Uwe / Haffner, Dieter

    Pediatric nephrology (Berlin, Germany)

    2020  Volume 35, Issue 10, Page(s) 2011

    MeSH term(s) Aortic Diseases ; Child ; Dilatation ; Humans ; Renal Insufficiency, Chronic
    Language English
    Publishing date 2020-05-29
    Publishing country Germany
    Document type Letter ; Comment
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-020-04620-5
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  3. Book ; Thesis: Störungen des Fettstoffwechsels bei Kindern mit chronischen Nierenerkrankungen und ihre Bedeutung für die Pathogenese der Arteriosklerose

    Querfeld, Uwe

    1991  

    Author's details vorgelegt von Uwe Querfeld
    Keywords Hyperlipoproteinemia / in infancy & childhood ; Hyperlipoproteinemia / complications ; Nephrotic Syndrome / in infancy & childhood ; Nephrotic Syndrome / complications ; Kidney Failure, Chronic / in infancy & childhood ; Arteriosclerosis / etiology
    Language German
    Size 165 Bl. : Ill., graph. Darst.
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Köln, Univ., Habil.-Schr., 1993
    Note ursprüngl. als Habil.-Schr. an der Univ. Heidelberg vorgelegt
    HBZ-ID HT005033865
    Database Catalogue ZB MED Medicine, Health

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  4. Article ; Online: Vitamin D and inflammation.

    Querfeld, Uwe

    Pediatric nephrology (Berlin, Germany)

    2012  Volume 28, Issue 4, Page(s) 605–610

    Abstract: Recent studies have provided evidence for an important role of vitamin D deficiency in the pathogenesis of cardiovascular disease (CVD) in the general population, and of an association with markers of inflammation. Vitamin D deficiency, defined by low ... ...

    Abstract Recent studies have provided evidence for an important role of vitamin D deficiency in the pathogenesis of cardiovascular disease (CVD) in the general population, and of an association with markers of inflammation. Vitamin D deficiency, defined by low serum levels of 25-hydroxyvitamin D, is especially prevalent in patients with chronic kidney disease (CKD). Chronic low-grade inflammation is a hallmark of CKD and has been disclosed as one important factor contributing to the progression of CKD and a high cardiovascular comorbidity. This review highlights clinical and experimental studies that could potentially explain a link between vitamin D and inflammation. Whether correction of vitamin D deficiency has beneficial effects on markers of inflammation and cardiovascular outcome should be investigated by controlled clinical trials.
    MeSH term(s) Animals ; Biomarkers/metabolism ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/metabolism ; Comorbidity ; Disease Progression ; Humans ; Inflammation/blood ; Inflammation/epidemiology ; Inflammation/metabolism ; Prognosis ; Renal Insufficiency, Chronic/blood ; Renal Insufficiency, Chronic/epidemiology ; Renal Insufficiency, Chronic/metabolism ; Risk Factors ; Vitamin D/analogs & derivatives ; Vitamin D/blood ; Vitamin D/metabolism ; Vitamin D Deficiency/epidemiology ; Vitamin D Deficiency/metabolism
    Chemical Substances Biomarkers ; Vitamin D (1406-16-2) ; 25-hydroxyvitamin D (A288AR3C9H)
    Language English
    Publishing date 2012-12-13
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-012-2377-4
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  5. Article ; Online: Cardiovascular risk factors in children on dialysis: an update.

    Querfeld, Uwe / Schaefer, Franz

    Pediatric nephrology (Berlin, Germany)

    2018  Volume 35, Issue 1, Page(s) 41–57

    Abstract: Cardiovascular disease (CVD) is a life-limiting comorbidity in patients with chronic kidney disease (CKD). In childhood, imaging studies have demonstrated early phenotypic characteristics including increases in left ventricular mass, carotid artery ... ...

    Abstract Cardiovascular disease (CVD) is a life-limiting comorbidity in patients with chronic kidney disease (CKD). In childhood, imaging studies have demonstrated early phenotypic characteristics including increases in left ventricular mass, carotid artery intima-media thickness, and pulse wave velocity, which occur even in young children with early stages of CKD. Vascular calcifications are the signature of an advanced phenotype and are mainly found in adolescents and young adults treated with dialysis. Association studies have provided valuable information regarding the significance of a multitude of risk factors in promoting CVD in children with CKD by using intermediate endpoints of measurements of surrogate parameters of CVD. Dialysis aggravates pre-existing risk factors and accelerates the progression of CVD with additional dialysis-related risk factors. Coronary artery calcifications in children and young adults with CKD accumulate in a time-dependent manner on dialysis. Identification of risk factors has led to improved understanding of principal mechanisms of CKD-induced damage to the cardiovascular system. Treatment strategies include assessment and monitoring of individual risk factor load, optimization of treatment of modifiable risk factors, and intensified hemodialysis if early transplantation is not possible.
    MeSH term(s) Cardiovascular Diseases/diagnosis ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/etiology ; Cardiovascular Diseases/prevention & control ; Carotid Intima-Media Thickness ; Child ; Coronary Vessels/diagnostic imaging ; Coronary Vessels/pathology ; Heart Disease Risk Factors ; Heart Ventricles/diagnostic imaging ; Heart Ventricles/physiopathology ; Humans ; Pulse Wave Analysis ; Renal Dialysis/adverse effects ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/physiopathology ; Renal Insufficiency, Chronic/therapy ; Time Factors
    Language English
    Publishing date 2018-10-31
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-018-4125-x
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  6. Article ; Online: Mycophenolate mofetil for sustained remission in nephrotic syndrome.

    Querfeld, Uwe / Weber, Lutz T

    Pediatric nephrology (Berlin, Germany)

    2018  Volume 33, Issue 12, Page(s) 2253–2265

    Abstract: The clinical application of mycophenolate mofetil (MMF) has significantly widened beyond the prophylaxis of acute and chronic rejections in solid organ transplantation. MMF has been recognized as an excellent treatment option in many immunologic ... ...

    Abstract The clinical application of mycophenolate mofetil (MMF) has significantly widened beyond the prophylaxis of acute and chronic rejections in solid organ transplantation. MMF has been recognized as an excellent treatment option in many immunologic glomerulopathies. For children with frequently relapsing nephrotic syndrome (FRNS) or steroid-dependent nephrotic syndrome (SDNS) experiencing steroid toxicity, MMF has been recommended as a steroid-sparing drug. Uncontrolled studies in patients with FRNS and SDSN have shown that many patients can achieve sustained remission of proteinuria with MMF monotherapy. Three randomized controlled trials have similarly demonstrated that MMF is beneficial in these patients, but less effective than the calcineurin inhibitors cyclosporin A or tacrolimus. Some, but not all, patients with steroid-resistant nephrotic syndrome (SRNS) may also respond to MMF, usually given in combination with other drugs, with partial or complete remission. There are important limitations to the interpretation and comparability of these studies including study design, sample size, patient selection, clinical endpoints, carry-over effects, and duration of follow-up. In all studies, MMF had relatively few side effects, no nephrotoxicity, or no systemic toxicity. MMF is teratogenic, and contraceptive advice is required in females. There is a poor correlation between MMF dose and mycophenolic acid (MPA) exposure and significant inter- and intra-patient variability in drug pharmacokinetics. A higher estimated MPA-AUC
    MeSH term(s) Area Under Curve ; Calcineurin Inhibitors/therapeutic use ; Child ; Dose-Response Relationship, Drug ; Drug Therapy, Combination/methods ; Glucocorticoids/therapeutic use ; Humans ; Immunosuppressive Agents/administration & dosage ; Immunosuppressive Agents/pharmacokinetics ; Mycophenolic Acid/administration & dosage ; Mycophenolic Acid/pharmacokinetics ; Nephrotic Syndrome/drug therapy ; Nephrotic Syndrome/immunology ; Nephrotic Syndrome/pathology ; Randomized Controlled Trials as Topic ; Recurrence ; Remission Induction/methods ; Secondary Prevention/methods ; Treatment Outcome
    Chemical Substances Calcineurin Inhibitors ; Glucocorticoids ; Immunosuppressive Agents ; Mycophenolic Acid (HU9DX48N0T)
    Language English
    Publishing date 2018-05-11
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-018-3970-y
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  7. Article ; Online: Treatment strategies for children with steroid-dependent nephrotic syndrome: in need of controlled studies.

    Querfeld, Uwe / Weber, Lutz T

    Pediatric nephrology (Berlin, Germany)

    2018  Volume 33, Issue 12, Page(s) 2391

    MeSH term(s) Child ; Cyclosporine ; Humans ; Immunosuppressive Agents ; Mycophenolic Acid ; Nephrotic Syndrome ; Steroids
    Chemical Substances Immunosuppressive Agents ; Steroids ; Cyclosporine (83HN0GTJ6D) ; Mycophenolic Acid (HU9DX48N0T)
    Language English
    Publishing date 2018-07-02
    Publishing country Germany
    Document type Letter ; Comment
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-018-4012-5
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  8. Article ; Online: Microvascular disease in chronic kidney disease: the base of the iceberg in cardiovascular comorbidity.

    Querfeld, Uwe / Mak, Robert H / Pries, Axel Radlach

    Clinical science (London, England : 1979)

    2020  Volume 134, Issue 12, Page(s) 1333–1356

    Abstract: Chronic kidney disease (CKD) is a relentlessly progressive disease with a very high mortality mainly due to cardiovascular complications. Endothelial dysfunction is well documented in CKD and permanent loss of endothelial homeostasis leads to progressive ...

    Abstract Chronic kidney disease (CKD) is a relentlessly progressive disease with a very high mortality mainly due to cardiovascular complications. Endothelial dysfunction is well documented in CKD and permanent loss of endothelial homeostasis leads to progressive organ damage. Most of the vast endothelial surface area is part of the microcirculation, but most research in CKD-related cardiovascular disease (CVD) has been devoted to macrovascular complications. We have reviewed all publications evaluating structure and function of the microcirculation in humans with CKD and animals with experimental CKD. Microvascular rarefaction, defined as a loss of perfused microvessels resulting in a significant decrease in microvascular density, is a quintessential finding in these studies. The median microvascular density was reduced by 29% in skeletal muscle and 24% in the heart in animal models of CKD and by 32% in human biopsy, autopsy and imaging studies. CKD induces rarefaction due to the loss of coherent vessel systems distal to the level of smaller arterioles, generating a typical heterogeneous pattern with avascular patches, resulting in a dysfunctional endothelium with diminished perfusion, shunting and tissue hypoxia. Endothelial cell apoptosis, hypertension, multiple metabolic, endocrine and immune disturbances of the uremic milieu and specifically, a dysregulated angiogenesis, all contribute to the multifactorial pathogenesis. By setting the stage for the development of tissue fibrosis and end organ failure, microvascular rarefaction is a principal pathogenic factor in the development of severe organ dysfunction in CKD patients, especially CVD, cerebrovascular dysfunction, muscular atrophy, cachexia, and progression of kidney disease. Treatment strategies for microvascular disease are urgently needed.
    MeSH term(s) Animals ; Cardiovascular Diseases/epidemiology ; Cardiovascular Diseases/physiopathology ; Comorbidity ; Humans ; Hypertension/epidemiology ; Hypertension/physiopathology ; Microcirculation ; Microvessels/pathology ; Microvessels/physiopathology ; Renal Insufficiency, Chronic/epidemiology ; Renal Insufficiency, Chronic/physiopathology
    Language English
    Publishing date 2020-06-15
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 206835-7
    ISSN 1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
    ISSN (online) 1470-8736
    ISSN 0301-0538 ; 0009-0360 ; 0143-5221
    DOI 10.1042/CS20200279
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  9. Article ; Online: Refractory arterial hypertension and renal failure combined with cerebral seizures and pancytopenia in a 5-year-old girl with bilateral nephromegaly: Answers.

    Hundsdoerfer, Patrick / Querfeld, Uwe

    Pediatric nephrology (Berlin, Germany)

    2016  Volume 31, Issue 10, Page(s) 1613–1614

    Language English
    Publishing date 2016-10
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-015-3183-6
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  10. Article ; Online: Refractory arterial hypertension and renal failure combined with cerebral seizures and pancytopenia in a 5-year-old girl with bilateral nephromegaly: Questions.

    Hundsdoerfer, Patrick / Querfeld, Uwe

    Pediatric nephrology (Berlin, Germany)

    2016  Volume 31, Issue 10, Page(s) 1611–1612

    Language English
    Publishing date 2016-10
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 631932-4
    ISSN 1432-198X ; 0931-041X
    ISSN (online) 1432-198X
    ISSN 0931-041X
    DOI 10.1007/s00467-015-3182-7
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