Source:http://linkedlifedata.com/resource/pubmed/id/14569094
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
11
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| pubmed:dateCreated |
2003-10-21
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| pubmed:abstractText |
The impact of polymorphisms in the genes coding for angiotensinogen (M235T), ACE (ID), and angiotensin II type 1 receptor (A(1166)-->C) on decline in GFR and doubling of s-creatinine or development of ESRD in patients with type 1 diabetes and diabetic nephropathy (DN) was tested. From 1985, all patients (n = 169) who had established diabetic nephropathy and were treated with angiotensin-converting enzyme inhibition (ACE-I) were identified consecutively at Steno Diabetes Center. Patients were followed for a median of 6 yr (range, 3 to 15 yr), with nine (range, three to 29) measurements of GFR ((51)Cr-EDTA). In a Cox proportional hazards model corrected for other risk factors, the D allele (ACE/ID) was associated with time to doubling of s-creatinine/ESRD (rate ratio, 1.81 per allele; 95% confidence interval, 1.09 to 3.03; P = 0.02). A new interaction hypothesis was generated demonstrating that the following variables were associated with accelerated decline in GFR: albuminuria (estimate, 2.12 ml/min per yr per 10-fold increase in albuminuria; P < 0.001), mean BP (estimate, 0.88 ml/min per yr per 10 mmHg; P = 0.02), hemoglobin A(1c) (estimate, 0.54 min/min per yr per 1%; P = 0.02), and number of M (M235T)/D (ID)/A (A(1166)-->C) alleles (estimate, 0.45 ml/min per yr per allele; P = 0.049). Number of M/D/A alleles also influenced time to doubling of s-creatinine or ESRD. In this study of patients with type 1 diabetes, the D allele of the ACE/ID polymorphism in addition to nongenetic risk factors independently accelerated progression of DN during ACE-I. Interaction between polymorphisms in the renin-angiotensin system also influenced the loss of kidney function. This new genetic interaction model needs to be confirmed in future studies.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin-Converting Enzyme...,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensinogen,
http://linkedlifedata.com/resource/pubmed/chemical/Creatinine,
http://linkedlifedata.com/resource/pubmed/chemical/Peptidyl-Dipeptidase A,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1
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| pubmed:status |
MEDLINE
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| pubmed:month |
Nov
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| pubmed:issn |
1046-6673
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
14
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2843-50
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:14569094-Adult,
pubmed-meshheading:14569094-Angiotensin-Converting Enzyme Inhibitors,
pubmed-meshheading:14569094-Angiotensinogen,
pubmed-meshheading:14569094-Creatinine,
pubmed-meshheading:14569094-Diabetes Mellitus, Type 1,
pubmed-meshheading:14569094-Diabetic Nephropathies,
pubmed-meshheading:14569094-Female,
pubmed-meshheading:14569094-Follow-Up Studies,
pubmed-meshheading:14569094-Glomerular Filtration Rate,
pubmed-meshheading:14569094-Humans,
pubmed-meshheading:14569094-Kidney Failure, Chronic,
pubmed-meshheading:14569094-Male,
pubmed-meshheading:14569094-Middle Aged,
pubmed-meshheading:14569094-Peptidyl-Dipeptidase A,
pubmed-meshheading:14569094-Polymorphism, Genetic,
pubmed-meshheading:14569094-Receptor, Angiotensin, Type 1,
pubmed-meshheading:14569094-Renin-Angiotensin System,
pubmed-meshheading:14569094-Time Factors
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| pubmed:year |
2003
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| pubmed:articleTitle |
Genetic variation in the Renin-Angiotensin system and progression of diabetic nephropathy.
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| pubmed:affiliation |
Steno Diabetes Center, Gentofte, Denmark. pkjacobsen@dadlnet.dk
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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