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Genetic modulation of diabetic nephropathy among mouse strains with Ins2 Akita mutation.

Wu X, Davis RC, McMillen TS, Schaeffer V, Zhou Z, Qi H, Mazandarani PN, Alialy R, Hudkins KL, Lusis AJ, LeBoeuf RC - Physiol Rep (2014)

Bottom Line: Urine albumin-to-creatinine ratios (ACRs), volume and cystatin C as well as blood urea nitrogen and lipoprotein levels varied significantly among the diabetic strains.ACRs correlated with cystatin C (P = 0.0286), a measure of hyperfiltration and an interstitial tubular marker associated with DN onset in humans suggesting that tubule damage as well as podocyte-stress contributed to reduced kidney function assessed by ACR.However, glomerular hypertrophy and collagen IV content were found to vary significantly among strains suggesting a genetic basis for early onset features of DN.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.

No MeSH data available.


Related in: MedlinePlus

Impact of genetic background on (A) Left kidney weight (g) among nondiabetic and diabetic mice. *P < 0.05 (n = 3–17 mice/group). (B) Urine cystatin C to creatinine ratio (CCR; Cystatin C (μg/mL)/Creatinine (μg/mL)) and (C) urine nephrin to creatinine ratio among mice carrying the Akita mutation. *P < 0.05 for (n = 3–4 mice/group). For each graph, the maternal strain is indicated on the horizontal axis and strains are in rank order based on the average level observed in diabetic mice. To facilitate comparisons among strains, these data are presented in alphabetical strain order in Figure 7‐4A, 4B, and 4C at the end of the manuscript.
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fig04: Impact of genetic background on (A) Left kidney weight (g) among nondiabetic and diabetic mice. *P < 0.05 (n = 3–17 mice/group). (B) Urine cystatin C to creatinine ratio (CCR; Cystatin C (μg/mL)/Creatinine (μg/mL)) and (C) urine nephrin to creatinine ratio among mice carrying the Akita mutation. *P < 0.05 for (n = 3–4 mice/group). For each graph, the maternal strain is indicated on the horizontal axis and strains are in rank order based on the average level observed in diabetic mice. To facilitate comparisons among strains, these data are presented in alphabetical strain order in Figure 7‐4A, 4B, and 4C at the end of the manuscript.

Mentions: Tissue weights were also assessed as additional reflections of diabetic complications. Absolute kidney weights were significantly greater for most diabetic mice compared to nondiabetic controls (Fig. 4A). Increased kidney weight is one feature of DN often seen in type 1 diabetic humans (Mogensen and Andersen 1973; Bogdanovic 2008) and is associated with hyperfiltration, a predecessor to microalbuminuria. Heart to tibia ratios, a measure of heart hypertrophy and heart failure, showed reduced values for diabetic as compared to nondiabetic mice (data not shown).


Genetic modulation of diabetic nephropathy among mouse strains with Ins2 Akita mutation.

Wu X, Davis RC, McMillen TS, Schaeffer V, Zhou Z, Qi H, Mazandarani PN, Alialy R, Hudkins KL, Lusis AJ, LeBoeuf RC - Physiol Rep (2014)

Impact of genetic background on (A) Left kidney weight (g) among nondiabetic and diabetic mice. *P < 0.05 (n = 3–17 mice/group). (B) Urine cystatin C to creatinine ratio (CCR; Cystatin C (μg/mL)/Creatinine (μg/mL)) and (C) urine nephrin to creatinine ratio among mice carrying the Akita mutation. *P < 0.05 for (n = 3–4 mice/group). For each graph, the maternal strain is indicated on the horizontal axis and strains are in rank order based on the average level observed in diabetic mice. To facilitate comparisons among strains, these data are presented in alphabetical strain order in Figure 7‐4A, 4B, and 4C at the end of the manuscript.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255814&req=5

fig04: Impact of genetic background on (A) Left kidney weight (g) among nondiabetic and diabetic mice. *P < 0.05 (n = 3–17 mice/group). (B) Urine cystatin C to creatinine ratio (CCR; Cystatin C (μg/mL)/Creatinine (μg/mL)) and (C) urine nephrin to creatinine ratio among mice carrying the Akita mutation. *P < 0.05 for (n = 3–4 mice/group). For each graph, the maternal strain is indicated on the horizontal axis and strains are in rank order based on the average level observed in diabetic mice. To facilitate comparisons among strains, these data are presented in alphabetical strain order in Figure 7‐4A, 4B, and 4C at the end of the manuscript.
Mentions: Tissue weights were also assessed as additional reflections of diabetic complications. Absolute kidney weights were significantly greater for most diabetic mice compared to nondiabetic controls (Fig. 4A). Increased kidney weight is one feature of DN often seen in type 1 diabetic humans (Mogensen and Andersen 1973; Bogdanovic 2008) and is associated with hyperfiltration, a predecessor to microalbuminuria. Heart to tibia ratios, a measure of heart hypertrophy and heart failure, showed reduced values for diabetic as compared to nondiabetic mice (data not shown).

Bottom Line: Urine albumin-to-creatinine ratios (ACRs), volume and cystatin C as well as blood urea nitrogen and lipoprotein levels varied significantly among the diabetic strains.ACRs correlated with cystatin C (P = 0.0286), a measure of hyperfiltration and an interstitial tubular marker associated with DN onset in humans suggesting that tubule damage as well as podocyte-stress contributed to reduced kidney function assessed by ACR.However, glomerular hypertrophy and collagen IV content were found to vary significantly among strains suggesting a genetic basis for early onset features of DN.

View Article: PubMed Central - PubMed

Affiliation: Division of Cardiology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, California, USA.

No MeSH data available.


Related in: MedlinePlus