Published online Mar 15, 2017. doi: 10.4239/wjd.v8.i3.112
Peer-review started: July 14, 2016
First decision: September 12, 2016
Revised: October 6, 2016
Accepted: November 21, 2016
Article in press: November 23, 2016
Published online: March 15, 2017
Processing time: 241 Days and 23.1 Hours
To investigate the role of genetic variants of angiotensin converting enzyme (ACE) and angiotensinogen (AGT) genes in the antiproteinuric efficacy of ACE inhibitor therapy in diabetic nephropathy (DN) patients.
In the present study, 270 type 2 diabetes mellitus patients with nephropathy were enrolled and treated with ACE inhibitor (ramipril) and followed at 6 mo for renal function and albumin excretion by estimating serum creatinine, end stage renal disease, and albumin/creatinine ratio (ACR) in urine. Genotyping of ACE I/D and AGT M235T polymorphisms were performed by using primer specific polymerase chain reaction (PCR) and PCR-RFLP techniques, respectively.
Forty-eight percent of DN patients (responders) benefited with respect to proteinuria from ACE inhibitor therapy at 6 mo follow-up. A significant reduction in ACR was observed after 6 mo treatment with ACE inhibitor irrespective of whether DN patients were micro-albuminuric (≥ 30 and < 300 mg/g creatinine) or macro-albuminuric (≥ 300 mg/g creatinine) at the time of enrollment. However, macro-albuminuric patients (55%) showed better response to therapy. A reduction in urinary ACR was found independent of genotypes of ACE I/D and AGT M235T polymorphisms although macro-albuminuric patients having TT genotype showed statistically insignificant increased response (72%).
ACE inhibitor therapy reduced urinary ACR by ≥ 30% in 50% of DN patients and the response is independent of ACE I/D and AGT M235T polymorphisms.
Core tip: Angiotensin converting enzyme (ACE) inhibitors are used as standard therapy in patients with diabetic nephropathy (DN) and reported to have reno-protective effect in these patients; however, the response to ACE inhibitor therapy is not uniform in all patients. We investigated whether ACE I/D and angiotensinogen gene (AGT) M235T polymorphisms of genes of the renin-angiotensin-aldosterone system are associated with variable response to ACE inhibitors in DN patients. ACE inhibitor treatment in DN patients caused a significant reduction in urinary protein excretion and was found independent of ACE I/D and AGT M235T polymorphisms.