[Polymorphism studies of angiotensin converting enzyme gene in chronic glomerulonephritis].
OBJECTIVE
To investigate the relationship between polymorphism of angiotensin-converting enzyme (ACE) gene and predisposition to chronic glomerulonephritis (CGN) as well as antihypertensive and anti proteinuric response to ACE inhibitors (ACEI) treatment, therapy with angiotensin II receptor antagonists.


METHODS
Genotype was determined in 57 CGN patients and 113 subjects free of chronic diseases. Effects of ACE gene polymorphism on antihypertensive and antiproteinuric efficiency of ACEI and cozaar were studied in 35 CGN patients on monotherapy. 24-h proteinuria, levels of creatinine, potassium in the serum, arterial pressure, glomerular filtration rate were measured in all the patients.


RESULTS
No significant differences were found between incidence of ACE gene genotypes and alleles in patients with CGN and controls. Maximal antihypertensive response to therapy was observed after a month treatment in patients with genotypes II and ID. Lowering of arterial pressure in patients with genotype DD was observed on month 6-12 of continuous therapy. Proteinuria diminished on the treatment month 1-3 in patients with genotypes II and ID, in genotype DD proteinuria rose for the same period of time. Proteinuria dropped similarly in all the groups by month 6-12.


CONCLUSIONS
Relations between ACE gene polymorphism and genetic predisposition to CGN were not found. Patients with genotype II were most sensitive to IACE and cosaar treatment. Lack of an early anti proteinuric response in homozygotes DD does not determine effectiveness of long-term IACE treatment and should not be a reason for the above drug discontinuation.
I M
IM
Kutyrina
I E
IE
Tareeva
V V
VV
Nosikov
E S
ES
Kamyshova
N M
NM
Gorashko
D A
DA
Chistiakov
E B
EB
Okonova
O V
OV
Troepol'skaia
D000293:Adolescent; D000328:Adult; D000483:Alleles; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000959:Antihypertensive Agents / Q000627:therapeutic use; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001706:Biopsy; D001794:Blood Pressure / Q000187:drug effects; D002908:Chronic Disease; D004247:DNA / Q000032:analysis*; D017931:DNA Primers / Q000737:chemistry; D005260:Female; D005500:Follow-Up Studies; D020022:Genetic Predisposition to Disease; D005838:Genotype; D005919:Glomerular Filtration Rate / Q000187:drug effects; D005921:Glomerulonephritis / Q000188:drug therapy / Q000201:enzymology* / Q000235:genetics; D006801:Humans; D006977:Hypertension, Renal / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000648:ultrastructure; D019808:Losartan / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D011379:Prognosis; D011507:Proteinuria / Q000097:blood / Q000503:physiopathology / Q000652:urine
D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D015415:Biomarkers; D017931:DNA Primers; D004247:DNA; D007703:Peptidyl-Dipeptidase A; D019808:Losartan
Izuchenie polimorfizma gena angiotenzinprevrashchaiushchego fermenta pri khronicheskom glomerulonefrite.