Pub Date : 2004-02-01DOI: 10.1016/j.emcnep.2003.10.001
C. Combe (Professeur des Universités, praticien hospitalier) , B. Vendrely (Chef de clinique des Universités, assistant des Hôpitaux) , I. Dubus (Maître de Conférences des Universités) , K. Moreau (Chef de clinique des Universités, assistant des Hôpitaux) , C. Lasseur (Praticien hospitalier) , P. Chauveau (Médecin attaché) , M. Aparicio (Professeur des Universités)
Protein metabolism is modified in the course of chronic renal failure, whatever its stage or the type of renal replacement therapy, haemodialysis, peritoneal dialysis or renal transplantation. Protein catabolism results, rather than chronic renal failure per se, from associated conditions such as chronic inflammation, metabolic acidosis and peripheral resistance to insulin. Nutritional parameters reflecting body-protein stores are frequently altered in patients with chronic renal failure, with deleterious consequences on morbidity and mortality. Correction of these different abnormalities may maintain nutritional status and improve the outcome of patients with chronic renal failure.
{"title":"Métabolisme protéique et insuffisance rénale chronique","authors":"C. Combe (Professeur des Universités, praticien hospitalier) , B. Vendrely (Chef de clinique des Universités, assistant des Hôpitaux) , I. Dubus (Maître de Conférences des Universités) , K. Moreau (Chef de clinique des Universités, assistant des Hôpitaux) , C. Lasseur (Praticien hospitalier) , P. Chauveau (Médecin attaché) , M. Aparicio (Professeur des Universités)","doi":"10.1016/j.emcnep.2003.10.001","DOIUrl":"https://doi.org/10.1016/j.emcnep.2003.10.001","url":null,"abstract":"<div><p>Protein metabolism is modified in the course of chronic renal failure, whatever its stage or the type of renal replacement therapy, haemodialysis, peritoneal dialysis or renal transplantation. Protein catabolism results, rather than chronic renal failure per se, from associated conditions such as chronic inflammation, metabolic acidosis and peripheral resistance to insulin. Nutritional parameters reflecting body-protein stores are frequently altered in patients with chronic renal failure, with deleterious consequences on morbidity and mortality. Correction of these different abnormalities may maintain nutritional status and improve the outcome of patients with chronic renal failure.</p></div>","PeriodicalId":100433,"journal":{"name":"EMC - Néphrologie","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.emcnep.2003.10.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91594641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2004-02-01DOI: 10.1016/j.emcnep.2003.11.001
D.-G Bichet (M.-D., professeur titulaire) , M Zellweger (moniteur clinique)
Nephrogenic diabetes insipidus (NDI) which can be inherited or acquired, is characterized by an inhability to concentrate urine despite normal or elevated plasma concentrations of the antidiuretic hormone, arginine-vasopressine (AVP). Polyuria, with hyposthenuria and polydipsia are the cardinal clinical manifestations of the disease. Hypercalcemia, hypokaliemia, lithium administration and chronic renal failure are the principal causes of acquired NDI. About 90 percent of patients with congenital NDI are males with X-linked recessive NDI who have mutations in the arginine-vasopressin receptor 2 (AVPR2) gene that codes for the vasopressin V2 receptor. The gene is located in chromosome region Xq28. In less than 10 percent of the families studied, congenital NDI has an autosomal recessive or autosomal dominant mode of inheritance. In these cases, mutations have been identified in the aquaporin-2 gene (AQP2), which is located in chromosome region 12q13 and codes for the vasopressin-sensitive water channel. Other inherited disorders with mild, moderate or severe inhability to concentrate urine include Bartter’s syndrome and cystinosis. Identification of the molecular defect underlying congenital NDI is of immediate clinical significance because early diagnosis and treatment of affected infants can avert the physical and mental retardation associated with episodes of dehydration.
{"title":"Diabètes insipides néphrogéniques","authors":"D.-G Bichet (M.-D., professeur titulaire) , M Zellweger (moniteur clinique)","doi":"10.1016/j.emcnep.2003.11.001","DOIUrl":"https://doi.org/10.1016/j.emcnep.2003.11.001","url":null,"abstract":"<div><p>Nephrogenic diabetes insipidus (NDI) which can be inherited or acquired, is characterized by an inhability to concentrate urine despite normal or elevated plasma concentrations of the antidiuretic hormone, arginine-vasopressine (AVP). Polyuria, with hyposthenuria and polydipsia are the cardinal clinical manifestations of the disease. Hypercalcemia, hypokaliemia, lithium administration and chronic renal failure are the principal causes of acquired NDI. About 90 percent of patients with congenital NDI are males with X-linked recessive NDI who have mutations in the arginine-vasopressin receptor 2 (<em>AVPR2</em>) gene that codes for the vasopressin V2 receptor. The gene is located in chromosome region Xq28. In less than 10 percent of the families studied, congenital NDI has an autosomal recessive or autosomal dominant mode of inheritance. In these cases, mutations have been identified in the aquaporin-2 gene (<em>AQP2</em>), which is located in chromosome region 12q13 and codes for the vasopressin-sensitive water channel. Other inherited disorders with mild, moderate or severe inhability to concentrate urine include Bartter’s syndrome and cystinosis. Identification of the molecular defect underlying congenital NDI is of immediate clinical significance because early diagnosis and treatment of affected infants can avert the physical and mental retardation associated with episodes of dehydration.</p></div>","PeriodicalId":100433,"journal":{"name":"EMC - Néphrologie","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.emcnep.2003.11.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91594639","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2004-02-01DOI: 10.1016/J.EMCNEP.2003.10.001
C. Combe, B. Vendrely, I. Dubus, K. Moreau, C. Lasseur, P. Chauveau, M. Aparicio
{"title":"Métabolisme protéique et insuffisance rénale chronique","authors":"C. Combe, B. Vendrely, I. Dubus, K. Moreau, C. Lasseur, P. Chauveau, M. Aparicio","doi":"10.1016/J.EMCNEP.2003.10.001","DOIUrl":"https://doi.org/10.1016/J.EMCNEP.2003.10.001","url":null,"abstract":"","PeriodicalId":100433,"journal":{"name":"EMC - Néphrologie","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2004-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77818900","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1900-01-01DOI: 10.1016/S1762-0945(06)75774-6
J. Cledes, C. Hanrotel-Saliou, R. Perrichot, Bernard Strullu, T. Tanquerel
{"title":"Néphropathies glomérulaires et interstitielles chez les sujets âgés","authors":"J. Cledes, C. Hanrotel-Saliou, R. Perrichot, Bernard Strullu, T. Tanquerel","doi":"10.1016/S1762-0945(06)75774-6","DOIUrl":"https://doi.org/10.1016/S1762-0945(06)75774-6","url":null,"abstract":"","PeriodicalId":100433,"journal":{"name":"EMC - Néphrologie","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76115821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1900-01-01DOI: 10.1016/J.EMCNEP.2005.09.003
L. Frimat, C. Loos-Ayav, S. Briançon, M. Kessler
{"title":"Épidémiologie des maladies rénales chroniques","authors":"L. Frimat, C. Loos-Ayav, S. Briançon, M. Kessler","doi":"10.1016/J.EMCNEP.2005.09.003","DOIUrl":"https://doi.org/10.1016/J.EMCNEP.2005.09.003","url":null,"abstract":"","PeriodicalId":100433,"journal":{"name":"EMC - Néphrologie","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1900-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74482265","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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