1. Volume 76, Issue 4, Pages 395-403 (August 2009)
Kallikrein protects against microalbuminuria in experimental type I diabetes 
Sophie Bodin, Catherine Chollet, Nicolas Goncalves-Mendes, Joelle Gardes, Franck Pean, Didier Heudes, Patrick Bruneval, Michel Marre, François Alhenc-Gelas, Nadine Bouby 
Kidney International 
Volume 76, Issue 4, Pages (August 2009)
DOI: /ki
Copyright © 2009 International Society of Nephrology Terms and Conditions

2. Figure 1
Urinary albumin excretion in wild-type (WT) and tissue kallikrein–deficient (TK-null) mice 1 and 2 months after induction of diabetes (series B). Black bars: diabetic groups, white bars: control groups. Results are means±s.e.m. n=7–8/group. Analysis of variance followed by Fisher PLSD post hoc test, diabetic vs control: ***P<0.001; TK-null vs WT: ##P<0.01.
Kidney International  , DOI: ( /ki )
Copyright © 2009 International Society of Nephrology Terms and Conditions

3. Figure 2
Systolic blood pressure in wild-type (WT) and tissue kallikrein–deficient (TK-null) mice 1 and 2 months after induction of diabetes (series B). Black bars: diabetic groups, white bars: control groups. Results are means±s.e.m. n=7–8/group. Analysis of variance followed by Fisher PLSD post hoc test, diabetic vs control: ***P<0.001, TK-null vs WT: nonsignificant.
Kidney International  , DOI: ( /ki )
Copyright © 2009 International Society of Nephrology Terms and Conditions

4. Figure 3
Gene expression of the components of the renal kallikrein–kinin system in wild-type (WT) and tissue kallikrein–deficient (TK-null) mice 1 month after induction of diabetes (series A). Black bars: diabetic groups, white bars: control groups. Results are means±s.e.m. n=10–12/group. Results for each gene are expressed relative to the mean of the corresponding WT control group. Analysis of variance followed by Fisher PLSD post hoc test, diabetic vs control: ***P<0.0001, **P<0.01, TK-null vs WT: nonsignificant.
Kidney International  , DOI: ( /ki )
Copyright © 2009 International Society of Nephrology Terms and Conditions

5. Figure 4
Gene expression of ACE in kidney and lung of wild-type (WT) and tissue kallikrein–deficient (TK-null) mice 1 month after induction of diabetes (series A). Black bars: diabetic groups, white bars: control groups. Results are means±s.e.m. n=10–12/group. Results for each gene are expressed relative to the mean of the corresponding WT control group. Analysis of variance followed by Fisher PLSD post hoc test, diabetic vs control: ***P<0.0001, TK-null vs WT: nonsignificant. ACE, angiotensin I–converting enzyme.
Kidney International  , DOI: ( /ki )
Copyright © 2009 International Society of Nephrology Terms and Conditions

6. Figure 5
Gene expression of the components of the renal renin–angiotensin system in wild-type (WT) and tissue kallikrein–deficient (TK-null) mice 1 month after induction of diabetes (series A). Black bars: diabetic groups, white bars: control groups. Results are means±s.e.m. n=10–12/group. Results for each gene are expressed relative to the mean of the corresponding WT control group. Analysis of variance followed by Fisher PLSD post hoc test, diabetic vs control: ***P<0.0001, *P<0.05, TK-null vs WT; #P<0.05.
Kidney International  , DOI: ( /ki )
Copyright © 2009 International Society of Nephrology Terms and Conditions

7. Figure 6
Gene expression of precursors of the kallikrein–kinin and renin–angiotensin system in the liver of wild-type (WT) and tissue kallikrein–deficient (TK-null) mice 1 month after induction of diabetes (series A). Black bars: diabetic groups, white bars: control groups. Results are means±s.e.m. n=10–12/group. Results for each gene are expressed relative to the mean of the corresponding WT control group. Analysis of variance followed by Fisher PLSD post hoc test, diabetic vs control: ***P<0.0001, *P<0.05, TK-null vs WT; nonsignificant.
Kidney International  , DOI: ( /ki )
Copyright © 2009 International Society of Nephrology Terms and Conditions