Aim To examine whether AER(albumin excretion rate) in normotensive diabeticpatients can be effectively inhibited by ACEI. Methods Literature on randomized controlled trials ofACEI for inhibiting AER in normotensive di...Aim To examine whether AER(albumin excretion rate) in normotensive diabeticpatients can be effectively inhibited by ACEI. Methods Literature on randomized controlled trials ofACEI for inhibiting AER in normotensive diabetic patients was searched. The electronic databasesretrieved were Medline (1980 ― 2003), Embase database (1980 ― 2000), Cochrane Library, CL( 1980 ―2004), CBMdisc( 1980 ― 2002), and IPA( 1980 ― 2002). Seven studies were chosen. Data werecombined by Revman 4.2. Results: The pooled effect of change in AER is - 56.31 μg·min^(-1)) [ -81.96, -30.66] (P<0.0001). According to the analysis of subgroups, the pooled effects of 1 - 5 yearsare - 11.97 μg·min^(-1)[-22.04, -1.89] (P = 0.02), -28.01 μg·min^(-1)[-34.50, -21.52](P<0.00001), -43.24 μg·min^(-1) [ -57.15, -29.32] (P< 0.00001), -61.65 μg·min^(-1)[77.77,-45.54] (P< 0.00001), and -98.41 μg·min^(-1)[-162.02,-34.79] (P = 0.002). Regarding progression toclinincal proteinuria as end-point, the pooled Peto OR =0.27 [0.18,0.40] (95% CI), P < 0.00001.According to the analysis of subgroups, the pooled effects of 2 and 5 years are Peto OR = 0.30[0.18,0.51] (P<0.00001) and Peto OR=0.25 [0.13, 0.50](P<0.0001). Publication bias is small.Conclusion In normotensive diabetic patients, ACEI inhibits AER effectively and reduces theprobability of progression of microalbuminuria to clinical proteinuria.展开更多
Objective To explore whether magnetotherapy is preventive in retarding diabetic kidney disease（DKD） progression and investigate underling molecular mechanisms related to its therapeutic efficacy. Methods Twenty-eigh...Objective To explore whether magnetotherapy is preventive in retarding diabetic kidney disease（DKD） progression and investigate underling molecular mechanisms related to its therapeutic efficacy. Methods Twenty-eight patients with type Ⅱ diabetes（T2D） were undergone pulsed electromagnetic fields（PEMF） stimulation at the acupoints of Píshū（脾俞 BL 20）, Zúsānl（足三里 ST 36）, Shènshū（肾俞 BL 23） and Yíshū（胰俞, EX-B3） for a period of 4 weeks. Urinary micro-albumin（U-m Alb） excretion, plasma methane dicarboxylic aldehyde（MDA and lipopolysaccharide（LPS） of the patients were used for evaluating therapeutic efficacies. Results After the acumagnetotherapy, U-m Alb excretion in the participated patients was markedly reduced（27.21±3.51 vs 8.51±0.95, P0.001） accompanied with decreased MDA（16.46±1.17 vs 12.40±1.86, P0.05） and LPS（37.41±3.84 vs 21.63±3.61, P0.05） levels in plasma while the metabolic control of these patients was not significantly altered. Acumagnetotherapy increased IκBα content（0.69±1.17 vs 1.30±0.29, P0.01）, an inhibitory protein of inflammatory response, and correspondingly reduced the protein levels of inflammatory activating proteins, NF-κB p65（0.98±0.42 vs 0.43±0.28, P0.05） and NF-κB p50（1.19±0.40 vs 0.76±0.30, P0.05）. The acumagnetotherapy also inhibited the oxidantproducing enzyme, Nox4 protein expression（1.32±0.40 vs 0.37±0.23, P0.05） in patient ＇s blood lymphocytes. Conclusion Short-term intervention of acumagnetotherapy in patients with T2 D mitigates DKD progress potentially by its anti-oxidative and anti-inflammatory effects.展开更多
文摘Aim To examine whether AER(albumin excretion rate) in normotensive diabeticpatients can be effectively inhibited by ACEI. Methods Literature on randomized controlled trials ofACEI for inhibiting AER in normotensive diabetic patients was searched. The electronic databasesretrieved were Medline (1980 ― 2003), Embase database (1980 ― 2000), Cochrane Library, CL( 1980 ―2004), CBMdisc( 1980 ― 2002), and IPA( 1980 ― 2002). Seven studies were chosen. Data werecombined by Revman 4.2. Results: The pooled effect of change in AER is - 56.31 μg·min^(-1)) [ -81.96, -30.66] (P<0.0001). According to the analysis of subgroups, the pooled effects of 1 - 5 yearsare - 11.97 μg·min^(-1)[-22.04, -1.89] (P = 0.02), -28.01 μg·min^(-1)[-34.50, -21.52](P<0.00001), -43.24 μg·min^(-1) [ -57.15, -29.32] (P< 0.00001), -61.65 μg·min^(-1)[77.77,-45.54] (P< 0.00001), and -98.41 μg·min^(-1)[-162.02,-34.79] (P = 0.002). Regarding progression toclinincal proteinuria as end-point, the pooled Peto OR =0.27 [0.18,0.40] (95% CI), P < 0.00001.According to the analysis of subgroups, the pooled effects of 2 and 5 years are Peto OR = 0.30[0.18,0.51] (P<0.00001) and Peto OR=0.25 [0.13, 0.50](P<0.0001). Publication bias is small.Conclusion In normotensive diabetic patients, ACEI inhibits AER effectively and reduces theprobability of progression of microalbuminuria to clinical proteinuria.
基金Supported by the Natural Science Foundation of China:81270886
文摘Objective To explore whether magnetotherapy is preventive in retarding diabetic kidney disease（DKD） progression and investigate underling molecular mechanisms related to its therapeutic efficacy. Methods Twenty-eight patients with type Ⅱ diabetes（T2D） were undergone pulsed electromagnetic fields（PEMF） stimulation at the acupoints of Píshū（脾俞 BL 20）, Zúsānl（足三里 ST 36）, Shènshū（肾俞 BL 23） and Yíshū（胰俞, EX-B3） for a period of 4 weeks. Urinary micro-albumin（U-m Alb） excretion, plasma methane dicarboxylic aldehyde（MDA and lipopolysaccharide（LPS） of the patients were used for evaluating therapeutic efficacies. Results After the acumagnetotherapy, U-m Alb excretion in the participated patients was markedly reduced（27.21±3.51 vs 8.51±0.95, P0.001） accompanied with decreased MDA（16.46±1.17 vs 12.40±1.86, P0.05） and LPS（37.41±3.84 vs 21.63±3.61, P0.05） levels in plasma while the metabolic control of these patients was not significantly altered. Acumagnetotherapy increased IκBα content（0.69±1.17 vs 1.30±0.29, P0.01）, an inhibitory protein of inflammatory response, and correspondingly reduced the protein levels of inflammatory activating proteins, NF-κB p65（0.98±0.42 vs 0.43±0.28, P0.05） and NF-κB p50（1.19±0.40 vs 0.76±0.30, P0.05）. The acumagnetotherapy also inhibited the oxidantproducing enzyme, Nox4 protein expression（1.32±0.40 vs 0.37±0.23, P0.05） in patient ＇s blood lymphocytes. Conclusion Short-term intervention of acumagnetotherapy in patients with T2 D mitigates DKD progress potentially by its anti-oxidative and anti-inflammatory effects.
