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Acquired Renal Cysts in Five-Sixths Nephrectomized Rats: The Roles of Oxalate Deposits in Renal Tubules and a Renotropic Factor
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The present study was undertaken to see if the oxalate deposits seen in renal tubules are a causative factor in the development of acquired renal cysts in chronic renal failure. Thirty 5/<sub>6</sub> nephrectomized rats had free access to water containing 8 mg/ml of vitamin C (oxalate precursor) and 20 5/<sub>6</sub> nephrectomized rats were given tap water without vitamin C. Oxalate deposits were found on microscopy in the renal tubules of vitamin C-treated rats in the 11th and 12th postnephrectomy months; however, acquired renal cysts were noted far in advance of the appearance of oxalate crystals. It has been suggested that the tubular dilatation seen in 5/<sub>6</sub> nephrectomized rats is caused by an abrupt decrease in the functioning renal mass, leading to the production of a so-called ‘renotropic factor’. However, oxalate deposits and renal tubular dilatation in oxalate-treated 5/<sub>6</sub> nephrectomized rats preceded the renal tubular dilatation of untreated partially nephrectomized rats. In addition, these histological changes in the kidney were also seen in healthy rats which were given oxalate orally and subcutaneously. The present study suggested that the pathogenesis of acquired renal cysts is multifactorial. Renotropic factor may play an important role leading to nephron hyperplasia, but oxalate deposits in the renal tubules seem to be an important factor in the formation of these cysts.
Title: Acquired Renal Cysts in Five-Sixths Nephrectomized Rats: The Roles of Oxalate Deposits in Renal Tubules and a Renotropic Factor
Description:
The present study was undertaken to see if the oxalate deposits seen in renal tubules are a causative factor in the development of acquired renal cysts in chronic renal failure.
Thirty 5/<sub>6</sub> nephrectomized rats had free access to water containing 8 mg/ml of vitamin C (oxalate precursor) and 20 5/<sub>6</sub> nephrectomized rats were given tap water without vitamin C.
Oxalate deposits were found on microscopy in the renal tubules of vitamin C-treated rats in the 11th and 12th postnephrectomy months; however, acquired renal cysts were noted far in advance of the appearance of oxalate crystals.
It has been suggested that the tubular dilatation seen in 5/<sub>6</sub> nephrectomized rats is caused by an abrupt decrease in the functioning renal mass, leading to the production of a so-called ‘renotropic factor’.
However, oxalate deposits and renal tubular dilatation in oxalate-treated 5/<sub>6</sub> nephrectomized rats preceded the renal tubular dilatation of untreated partially nephrectomized rats.
In addition, these histological changes in the kidney were also seen in healthy rats which were given oxalate orally and subcutaneously.
The present study suggested that the pathogenesis of acquired renal cysts is multifactorial.
Renotropic factor may play an important role leading to nephron hyperplasia, but oxalate deposits in the renal tubules seem to be an important factor in the formation of these cysts.
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