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Here, we characterize the development of hyperglycaemia-induced renal injury in the E1-DN mice. Homozygous mice showed increased albumin excretion rate (AER) at the age of 10 weeks; the albuminuria increased over time and correlated with blood glucose. Morphometric analysis of PAS-stained histological sections and electron microscopy images revealed mesangial expansion in homozygous E1-DN mice, and glomerular sclerosis was observed in the most hyperglycaemic mice. The albuminuric homozygous mice developed also other structural changes in the glomeruli, including thickening of the glomerular basement membrane and widening of podocyte foot processes that are typical for diabetic nephropathy. Increased apoptosis of podocytes was identified as one mechanism contributing to glomerular injury. In addition, nephrin expression was reduced in the podocytes of albuminuric homozygous E1-DN mice. Tubular changes included altered epithelial cell morphology and increased proliferation. In conclusion, hyperglycaemic E1-DN mice develop albuminuria and glomerular and tubular injury typical of human diabetic nephropathy and can serve as a new model to study the mechanisms leading to the development of diabetic nephropathy.<\/jats:p>","DOI":"10.1155\/2015\/102969","type":"journal-article","created":{"date-parts":[[2015,4,27]],"date-time":"2015-04-27T21:02:46Z","timestamp":1430168566000},"page":"1-11","source":"Crossref","is-referenced-by-count":11,"title":["Early-Onset Diabetic E1-DN Mice Develop Albuminuria and Glomerular Injury Typical of Diabetic Nephropathy"],"prefix":"10.1155","volume":"2015","author":[{"given":"Mervi E.","family":"Hyv\u00f6nen","sequence":"first","affiliation":[{"name":"Department of Pathology, Haartman Institute, University of Helsinki, Haartmaninkatu 3, 00290 Helsinki, Finland"},{"name":"Children\u2019s Hospital, University of Helsinki, 00290 Helsinki, 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