Abstract
Chronic progressive nephropathy (CPN) is a commonly encountered lesion in aging laboratory rats. CPN has been given a variety of names, based upon its complex nature. It is a lesion that occurs primarily in albino strains and is influenced not only by genetics but also by sex, age, hormones, diet, and microflora, among other factors. Affected kidneys are enlarged, pale and finely indented. The lesion begins with progressive thickening of glomerular, Bowman's capsular and proximal tubular basement membranes. Mesangial matrix increases with deposition of IgM and, to a lesser extent, other serum components. Tubular atrophy and degenerative changes occur as the lesion progresses. The disease is manifested by increasingly non-selective proteinuria, consisting mainly of albumin. Serum chemical changes include elevations in α globulins and cholesterol and a decrease in albumin. Creatinine and urea remain unchanged until late in the course of CPN. Renal secondary hyperparathyroidism may occasionally be seen.
