Pathology of the urinary system

21

 

RENAL FIBROSIS AND END-STAGE KIDNEY

 

 

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chronic renal failure tends to be progressive, once the glomerular filtration rate of the kidneys has 

decreased to 30-50% of normal; some of the factors involved in this vicious cycle include: 

   - 

compensatory capillary hypertension in, and hyperfiltration by, surviving glomeruli, which 

can lead to endothelial and epithelial injury and excess production of mesengial matrix → 

glomerulosclerosis; 

   - 

compensatory hyperfunction of surviving tubules: 

    * 

excessive and persistent traffic through the proximal tubular epithelial cells of protein 

lost through damaged glomeruli (proteinuria) can up-regulate vasoactive and pro-

inflammatory molecules normally produced by these cells and thus lead to further 

renal injury; 

    * 

hyperfunction of distal convoluted tubules and collecting tubules can lead to increased 

production of ammonia which, in turn, can cause tubular injury; 

   - 

injury of surviving nephrons as a result of: altered phosphate metabolism; altered lipid 

composition; and increased activity of the complement and coagulation systems associated 

with inflammation; 

   - 

accumulation of fibrous tissue of repair, resulting in interference with adequate blood 

perfusion (at a level appropriate to supply energy to the highly demanding nephrons); possibly 

also resulting in compression atrophy of the parenchyma. 

 

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renal fibrosis is a common sequel to chronic inflammation. 

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primary renal fibrosis also occurs as a familial renal disease in some breeds of dogs. 

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clinical signs can be very varied (see: Renal Failure). 

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grossly:  kidneys with fibrosis appear pale, shrunken, firm; distribution of the fibrosis more or less 

corresponds to the distribution of the preceding lesions. 

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microscopically:  fibrosis and tubular atrophy are the predominant changes. 

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