Pathology of the urinary system

2) Antemortem Lesions

 

 

1. 

Hyperemia and Congestion

 

        -  bright or dark red kidneys; can be physiologic or pathological (e.g. hyperemia of 

inflammation, passive congestion, hypostatic congestion); 

        -  hypostatic congestion is common with prolonged prostration and circulatory failure; 

        -  however, this change must be very marked in order to clearly distinguish it from the normal 

brown color of the kidney. 

 

 

2. 

Lipofuscinosis

 

        -  an incidental finding in adult cattle, seen as dark brown kidneys; 

        -  discoloration results from the deposition of lipofuscin ("wear and tear" pigment) in epithelial 

cells of convoluted tubules; 

        -  commonly seen at slaughter house; lipofuscinosis has no clinical or pathological significance. 

 

 

3. 

Hemoglobin (Hb)

 

        -  dark red to black kidneys, dark red discoloration of urine; 

        -  discoloration produced when there is severe intravascular hemolysis, with high amounts of 

Hb being filtered into renal tubules (hemoglobinuria); 

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        -  seen in leptospirosis, bacillary hemoglobinuria, babesiosis, chronic copper poisoning of 

sheep, etc.; 

        -  Hb is a small enough molecule to pass freely into the glomerular filtrate; when freed from 

erythrocytes, however, it is quickly bound to the plasma protein haptoglobin; the Hb-

haptoglobin complex, which is too large to pass into the glomerular filtrate, is phagocytized 

by macrophages; iron from the Hb molecule is thus recycled for further use by the body; 

        -  it is only after plasma haptoglobin has been saturated with Hb that free Hb can pass into the 

glomerular filtrate; 

        -  circulating Hb bound to haptoglobin (hemoglobinemia) imparts a port-wine color to the 

plasma. 

 

 

4. 

Myoglobin (Mb)

 

        -  dark red to black kidneys, dark red discoloration of urine; 

        -  discoloration produced when high amounts of Mb are filtered into renal tubules 

(myoglobinuria); 

        -  seen with acute and severe rhabdomyolysis, e.g. capture myopathy in wild animals, equine 

paralytic myoglobinuria (azoturia); 

        -  Mb is an even smaller molecule than Hb and therefore passes freely into the glomerular 

filtrate; 

        -  Mb does not bind to plasma haptoglobin like Hb does; therefore, it does not accumulate in 

the plasma, and the latter is of normal color.