Abstract
Certain data support the notion that chronic exposure to excess parathyroid hormone (PTH) is associated with decreased motor nerve conduction velocity, while other studies failed to confirm such an effect. Also, chronic renal failure of 4 months duration in dogs did not elicit changes in MNCV or calcium content of nerve. These discrepancies may be due to differences in other metabolic parameters, such as degree of uremia, serum levels of calcium, phosphorus, or magnesium, and acid-base parameters, or in duration of chronic renal failure. To examine the effect of PTH on peripheral nerve function in renal failure in a more defined biochemical setting, we studied the changes in MNCV and nerve calcium content in dogs with and without excess PTH and with prolonged and similar duration of chronic renal failure (57 +/- 1.7 weeks) and comparable biochemical parameters. Dogs with chronic renal failure displayed a significant (P less than 0.01) decrease in MNCV (before renal failure, 65 +/- 1.5 m/sec; after renal failure, 49 +/- 3.5 m/sec) and marked elevation in calcium content of peripheral nerve (444 +/- 45 mg/kg dry wt). These derangements were not observed in parathyroidectomized chronic renal failure animals; MNCV before renal failure was 66 +/- 1.5 m/sec and after renal failure was 65 +/- 1.5 m/sec, and nerve calcium content after renal failure was 229 +/- 3 mg/kg dry wt. Also, parathyroidectomy of three dogs with preexisting chronic renal failure of 52 weeks was associated with reversal of the abnormalities in MNCV and calcium content of nerve despite an additional period of renal failure of 52 weeks in two of the dogs and 40 weeks in the third. Our data are consistent with the proposition that excess PTH plays a major role in the genesis of peripheral nerve dysfunction in chronic renal failure. This adverse effect of the hormone is most likely mediated by the PTH-induced accumulation of calcium in peripheral nerve.
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