Angiotensin-converting enzyme gene polymorphism in IgA nephropathy (abstract) Korea J Int Med. preliminary serum creatinine level, the real amount of patients with initial azotemia( 1.4mg/dL) and with preliminary 24-hr proteinuria quantity more than 2.0 g. Significant anti-proteinuric aftereffect of ACE inhibitor was within IgAN(p =0.001), but zero factor was found among genotypes. Factor (p =0.011) was noticed between II type and DD enter the slope of reciprocal variant of the serum creatinine against follow-up length. In conclusion, efficiency of ACE inhibitors on renal function preservation in IgAN was even more pronounced in DD genotype than II genotype. 0.001, Fig. 2). Open up in another home window Fig. 2. Adjustments of 24-hr proteinuria quantity in each affected person regarding to ACE genotypes (I: Preliminary, 1 yr: 12 months after ACE inhibitor treatment) Dialogue We demonstrated that ACE inhibitors efficiency on renal function preservation in IgAN was even more pronounced in DD genotype than II genotype whenever we likened the slopes of reciprocal variant of the serum creatinine against follow-up duration. Also, the significant antiproteinuric response to ACE inhibitors was within IgAN, but no factor Rabbit Polyclonal to CCBP2 was discovered among three ACE genotypes. Due to the relatively lengthy observation period (mean 44.6, median 44.5 months, range 5 to 113 months) of the study, we expected the fact that long-term renal protective ramifications of ACE inhibitors in IgAN will be variable according to ACE gene polymorphism. Nevertheless, with regard towards the antiproteinuric responsiveness, we’re able to not look for a factor among the three genotypes. This shows that other mechanisms by ACE inhibitor besides antiproteinuric effect might contribute in preserving the renal function in IgAN. It’s been reported the fact that distribution of ACE genotypes in IgAN is comparable to that in the overall inhabitants7,8,9). The association between DD genotype as well as the renal disease development was questionable. Some reported the fact that genotypes with D allele weren’t linked to the development of glomerulonephritis including IgAN9,10). Alternatively, others reported the development of IgAN may be inspired with the genotypes with D allele8,11,12). Dissimilar towards the above research which noticed the natural span of IgAN, we noticed the span of IgAN after healing involvement with ACE inhibitors. ACE has an integral enzyme in the renin-angiotensin and kallikrein-kinin program by activating angiotensin I into angiotensin II and by inactivating bradykinin13,14,15). The renin-angiotensin program is thought to play a significant pathophysiologic function in the development of persistent renal disease. ACE inhibitors have already been reported to attenuate the development of persistent renal disease such as for example major glomerulonephritis or diabetic nephropathy16,17,18). An ACE gene polymorphism continues to be called an essential genetic aspect influencing the plasma and mobile ACE amounts; ACE activity may be higher in the region of DD, Identification, II4,5). As a result, actions of neighborhood angiotensin bradykinin and II could be linked to ACE gene polymorphism. Most likely because II genotype was connected with lower angiotensin II level in the kidney than DD genotype, ACE inhibition in II genotype could be much less effective on renal function preservation weighed against that in DD genotype11). We also discovered that ACE inhibitors had been better in DD genotype in protecting renal function in IgAN when you compare the slope of creatinine variant against follow-up length. Compared to various other research, we observed much longer intervals(median 44 relatively.5 months, range 5 to 113 months). We noticed the span Fluorocurarine chloride of six IgA sufferers for under twelve months; the distribution of II, DD and ID genotypes was 3, 1, 2, respectively. Nevertheless, because of little sample size, another large-scale study ought to be completed to generalize and confirm our positive results. Antiproteinuric aftereffect of ACE inhibitors was Fluorocurarine chloride first of all reported by de Jong et al19). Some reported ACE inhibitors had been far better in antiproteinuric effect than any other antihypertensive drugs20,21). Also, some reported antiproteinuric effects of ACE inhibitors were more pronounced in DD genotype than II or ID genotype of IgAN patients at 1 year after prescription of ACE inhibitors6,11,12). However, we found that antiproteinuric effect of ACE inhibitors in IgAN was not different among the three genotypes. This discrepancy may be related to the small sample size of this study and the abrupt antiproteinuric response to ACE inhibitors in a few patients with II and ID genotype. Antiproteinuric effect of ACE inhibition is now widely accepted through the hemodynamic effect of ACE inhibitor besides reducing systemic blood.[PubMed] [Google Scholar] 3. respectively. There were no differences among three genotypes in age, sex, the number of patients with initial blood pressure over 140/90 mmHg, initial serum creatinine level, the number of patients with initial azotemia( 1.4mg/dL) and with initial 24-hr proteinuria amount over 2.0 g. Significant anti-proteinuric effect of ACE inhibitor was found in IgAN(p =0.001), but no significant difference was found among genotypes. Significant difference (p =0.011) was noticed between II type and DD type in the slope of reciprocal variation of the serum creatinine against follow-up duration. In conclusion, efficacy of ACE inhibitors on renal function preservation in IgAN was more pronounced in DD genotype than II genotype. 0.001, Fig. 2). Open in a separate window Fig. 2. Changes of 24-hr proteinuria amount in each patient according to ACE genotypes (I: Initial, 1 yr: 1 year after ACE inhibitor treatment) DISCUSSION We showed that ACE inhibitors efficacy on renal function preservation in IgAN was more pronounced in DD genotype than II genotype when we compared the slopes of reciprocal variation of the serum creatinine against follow-up duration. Also, the significant antiproteinuric response to ACE inhibitors was found in IgAN, but no significant difference was found among three ACE genotypes. Because of the relatively long observation period (mean 44.6, median 44.5 months, range 5 to 113 months) of this study, we expected that the long-term renal protective effects of ACE inhibitors in IgAN would be variable according to ACE gene polymorphism. However, with regard to the antiproteinuric responsiveness, we could not find a significant difference among the three genotypes. This suggests that other mechanisms by ACE inhibitor besides antiproteinuric effect may contribute in preserving the renal function in IgAN. It has been reported that the distribution of ACE genotypes in IgAN is similar to that in the general population7,8,9). The association between DD genotype and the renal disease progression was controversial. Some reported that the genotypes with D allele were not related to the progression of glomerulonephritis including IgAN9,10). On the other hand, others reported the progression of IgAN may be influenced by the genotypes with D allele8,11,12). Dissimilar to the above studies which observed the natural course of IgAN, we observed the course of IgAN after therapeutic intervention with ACE inhibitors. ACE plays a key enzyme in the renin-angiotensin and kallikrein-kinin system by activating angiotensin I into angiotensin II and by inactivating bradykinin13,14,15). The renin-angiotensin system is believed to play an important pathophysiologic role in the progression of chronic renal disease. ACE inhibitors have been reported to attenuate the progression of chronic renal disease such as primary glomerulonephritis or diabetic nephropathy16,17,18). An ACE gene polymorphism has been known as an important genetic factor influencing the plasma and cellular ACE levels; ACE activity is known to be higher in the order of DD, ID, II4,5). Therefore, activities of local angiotensin II and bradykinin may be related to ACE gene polymorphism. Probably because II genotype was associated with lower angiotensin II level in the kidney than DD genotype, ACE inhibition in II genotype may be less efficient on renal function preservation compared with that in DD genotype11). We also found that ACE inhibitors were more efficient in DD genotype in preserving renal function in IgAN when comparing the slope of creatinine variation against follow-up duration. In comparison to other studies, we observed relatively longer periods(median 44.5 months, range 5 to 113 months). We observed the course of six IgA patients for less than one year; the distribution of II, ID and DD genotypes was 3, 1, 2, respectively. However, because of small sample size, a future large-scale study should be done to generalize and confirm our positive findings. Antiproteinuric effect of ACE inhibitors was firstly reported by de Jong et al19). Some reported ACE inhibitors.1994;23:247C257. of patients with initial azotemia( 1.4mg/dL) and with initial 24-hr proteinuria amount over 2.0 g. Significant anti-proteinuric effect of ACE inhibitor was found in IgAN(p =0.001), but no significant difference was found among genotypes. Significant difference (p =0.011) was noticed between II type and DD type in the slope of reciprocal variation of the serum creatinine against follow-up duration. In conclusion, efficacy of ACE inhibitors on renal function preservation in IgAN was more pronounced in DD genotype than II genotype. 0.001, Fig. 2). Open in a separate window Fig. 2. Changes of 24-hr proteinuria amount in each patient according to ACE genotypes (I: Initial, 1 yr: 1 year after ACE inhibitor treatment) DISCUSSION We showed that ACE inhibitors efficacy on renal function preservation in IgAN was more pronounced in DD genotype than II genotype when we compared the Fluorocurarine chloride slopes of reciprocal variation of the serum creatinine against follow-up duration. Also, the significant antiproteinuric response to ACE inhibitors was found in IgAN, but no significant difference was found among three ACE genotypes. Because of the relatively long observation period (mean 44.6, median 44.5 months, range 5 to 113 months) of this study, we expected that the long-term renal protective effects of ACE inhibitors in IgAN would be variable according to ACE gene polymorphism. However, with regard to the antiproteinuric responsiveness, we could not find a significant difference among the three genotypes. This suggests that other mechanisms by ACE inhibitor besides antiproteinuric effect may contribute in preserving the renal function in IgAN. It has been reported that the distribution of ACE genotypes in IgAN is similar to that in the general population7,8,9). The association between DD genotype and the renal disease progression was controversial. Some reported that the genotypes with D allele were not related to the progression of glomerulonephritis including IgAN9,10). On the other hand, others reported the progression of IgAN may be influenced by the genotypes with D allele8,11,12). Dissimilar to the above studies which observed the natural course of IgAN, we observed the course of IgAN after therapeutic intervention with ACE inhibitors. ACE plays a key enzyme in the renin-angiotensin and kallikrein-kinin system by activating angiotensin I into angiotensin II and by inactivating bradykinin13,14,15). The renin-angiotensin system is believed to play an important pathophysiologic role in the progression of chronic renal disease. ACE inhibitors have been reported to attenuate the progression of chronic renal disease such as primary glomerulonephritis or diabetic nephropathy16,17,18). An ACE gene polymorphism has been known as an important genetic factor influencing the plasma and cellular ACE levels; ACE activity is known to be higher in the order of DD, ID, II4,5). Therefore, activities of local angiotensin II and bradykinin may be related to ACE gene polymorphism. Probably because II genotype was associated with lower angiotensin II level in the kidney than DD genotype, ACE inhibition in II genotype may be less efficient on renal function preservation compared with that in DD genotype11). We also found that ACE inhibitors were more efficient in DD genotype in preserving renal function in IgAN when comparing the slope of creatinine variation against follow-up duration. In comparison to other studies, we observed relatively longer periods(median 44.5 months, range 5 to 113 months). We observed the course of six IgA patients for less than one year; the distribution of II, ID and DD genotypes was 3, 1, 2, respectively. However, because of small sample size, a future large-scale study should be carried out to generalize and confirm our positive findings. Antiproteinuric effect of ACE inhibitors was firstly reported by de Jong et al19). Some reported ACE inhibitors were more effective in antiproteinuric effect than some other antihypertensive medicines20,21). Also, some reported antiproteinuric effects of ACE inhibitors were.
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