Abstract

This chapter discusses the changes in renal function and morphology in aging laboratory animals. The studies of the spontaneous modification in structure and function of the kidney with aging in laboratory animals are important because they serve as models of aging, leading to a more precise knowledge of the biochemical and molecular mechanism, which induces such an alteration, together with a better control of the experimental procedures than in human studies. It is also because in long-term studies on laboratory animals, the investigator must know what changes are due to the factor under study and what must be attributed to the natural senescence of the animal. Spontaneous kidney disease, such as proteinuria, increases continuously with age. There is also a reduction in the glomerular filtration rate and renal blood flow and impairment in the urinary concentrating mechanisms, although the animal generally dies of non-renal problems. Microscopically, the changes are consistent in the strains studied. In brief, the lesion is focal and segmental, affecting both glomeruli and tubules. The glomerular disease is characterized by a thickening of the capillary basement membrane and Bowman's capsule, an increase in mesangial matrix, segmental sclerosis of isolated capillary loops, and, later, segments of tufts; finally, hyalinization and sclerosis of the glomeruli are observed. Adhesion between tufts and Bowman's capsule, glomerular crescents, and protein precipitates into Bowman's space are also common findings. Tubular lesions are characterized by epithelial atrophy and secondary hyperplasia, cast formation, tubule obstruction with massive dilatation, and, finally, fibrotic degeneration. The interstitium is infiltrated with mononuclear cells and also becomes fibrotic.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call