Ficolin B in Diabetic Kidney Disease in a Mouse Model of Type 1 Diabetes

Abstract EN

Background.

The innate immune system may have adverse effects in diabetes and cardiovascular disease.

The complement system seems to play a key role through erroneous complement activation via hyperglycaemia-induced neoepitopes.

Recently mannan-binding lectin (MBL) was shown to worsen diabetic kidney changes.

We hypothesize that mouse ficolin B exerts detrimental effects in the diabetic kidney as seen for MBL.

Methods.

We induced diabetes with streptozotocin in female wild-type mice and ficolin B knockout mice and included two similar nondiabetic groups.

Renal hypertrophy and excretion of urinary albumin and creatinine were quantified to assess diabetic kidney damage.

Results.

In the wild-type groups, the kidney weighed 24% more in the diabetic mice compared to the controls.

The diabetes-induced increase in kidney weight was 29% in the ficolin B knockout mice, that is, equal to wild-type animals (two-way ANOVA, P=0.60).

In the wild-type mice the albumin-to-creatinine ratio (ACR) was 32.5 mg/g higher in the diabetic mice compared to the controls.

The difference was 62.5 mg/g in the ficolin B knockout mice, but this was not significantly different from the wild-type animals (two-way ANOVA, P=0.21).

Conclusions.

In conclusion, the diabetes-induced effects on kidney weight and ACR were not modified by the presence or absence of ficolin B.