Peripheral neuropathy is not an uncommon complication of chronic uremia. Because parathyroid hormone, by raising brain calcium, is partly responsible for central nervous system aberrations in uremia, we studied the relative role of uremia, per se, and(or) parathyroid hormone on peripheral nerve calcium and motor nerve conduction velocity (MNCV). Studies were made in six groups of six dogs each, as follows: (a) normal dogs, (b) thyroparathyroidectomized (T-PTX) animals, (c) dogs with 3 days of uremia produced by bilateral nephrectomy, (d) T-PTX before the induction of acute renal failure, (e) normal dogs receiving 100 U/day of parathyroid extract (PTE) for 3 days, and (f) normal animals receiving 3 days of PTE followed by 5 days without PTE. Calcium content in peripheral nerve (expressed as milligram per kilogram of dry weight) was 252±5 (SE) in normal animals and 262±4 in T-PTX dogs. It was significantly (P < 0.01) higher in dogs with acute renal failure and intact parathyroid glands (410±12) and in normal animals receiving PTE (362±7). T-PTX, before acute renal failure, prevented the rise in peripheral nerve calcium (262±4) and PTE withdrawal was followed by the return of peripheral nerve calcium to normal (261±3). The increments in peripheral nerve calcium were associated with slowing of MNCV. It decreased significantly from 70±4 to 43±1 m/s after 3 days of acute uremia in dogs with intact parathyroid glands and T-PTX before acute renal failure prevented the fall in MNCV. Administration of PTE to normal animals reduced MNCV from 63±3 to 35±3 m/s and the withdrawal of PTE restored MNCV to normal (73±2 m/s). The results show that (a) excess parathyroid hormone increases peripheral nerve calcium and slows MNCV, (b) T-PTX, previously performed, prevents these changes in acute uremia, and (c) the withdrawal of PTE administration is followed by a reversal of the abnormalities.
David A. Goldstein, Luis A. Chui, Shaul G. Massry