Disease may affect any of the four major structural components of the kidney (glomerulus, tubules, interstitial tissue and blood vessels) separately. The anatomic interdependence of structures implies that disease in one functional unit almost always will affect neighboring structures as well. For example, glomerular disease alters the blood flow as well as the flow through the tubules and the composition of the filtrate, thus affecting the tubular epithelium. Occlusion of the tubular lumen may increase the pressure in Bowman's space, thereby causing glomerular atrophy. As a consequence, disorder in one component of the kidney will sooner or later also have severe implications for other renal components as well.

Even in severe cases of extensive destruction of renal tissue, the fish seem to do amazingly well. The explanation to this is the large functional reserve of this organ and the fact that other organs (gills and intestines) may take over some of the excretory function of the kidney. Because of its double blood supply and the trapping abilities of the phagocytes that line the peritubular capillaries and sinusoids, pathogens are readily trapped in the kidney. Disease may initially be restricted to the nephron (or only parts of it), to the interstitial hemopoietic tissue, or both. As already mentioned, there is a tendency in chronic disease, however, towards involvement of all renal components.

1 SOME USEFUL DEFINITIONS (FROM STEDMAN's MEDICAL DICTIONARY, 25th EDITION, Williams & Wilkins, Baltimore, 1990):

  • Nephropathy: any disorder of the kidney
  • Nephrosis: a nephropathy or degeneration of tubular epithelium
  • Nephritis: inflammation of the kidney
  • Nephrocalcinosis: the formation of calcium deposits in the kidney
  • Nephrocystosis: the formation of renal cysts
  • Nephromegaly: extreme hypertrophy of the kidney
  • Glomerulonephritis: glomerular changes that are the result infection
    elsewhere in the kidney

Glomerular disease is not as common in fish as in higher vertebrates. Nevertheless, knowledge of normal structure and basic pathology is important for the understanding of glomerular lesions in renal disease. Glomerulonephritis is typically characterized by at least one of the following histologic alterations: 1) hypercellularity, 2) thickening of the basement membrane, 3) hyalinization and 4) sclerosis.

1) Hypercellularity of the glomerulus may be caused by:

1: proliferation of mesangial, endothelial or parietal epithelial cells.
2: infiltration with inflammatory cells
3: a combination of 1) and 2).

2) Thickening of the basement membrane (usually seen as thickening of the capillary wall in PAS-stained sections). This is usually the result of depositions of immune complexes or fibrin.

4) Sclerosis of the glomerular tuft is usually preceded by accumulation of a homogenous, eosinophilic material (3) hyalinization) and loss of structural detail. Fibrin, let or amyloid depositions plus thrombosis may accompany sclerosis of the glomerulus.

The end result of such changes may be shrinkage or complete loss of the glomerular tuft. Extensive haemorrhage into Bowman's space due to destruction of capillary endothelium may lead to pressure atrophy of the glomerular tuft.

Most diseases will to a variable degree affect the different parts of the kidney. In this overview, only the more important and the specific kidney disorders have been listed.


Nephrosis: a nephropathy or degeneration of tubular epithelium.