Peripheral neuropathy in uremic patients and in renal transplant recipients.
Eighteen patients, ten with clinical uremia and eight with functioning kidney transplants, were studied clinically for neuropathy and were subsequently subjected to a sural nerve biopsy. The biopsy specimens were studied using light and electron microscopic and morphometric methods. The clinical polyneuropathy was qualitatively and quantitatively most severe in the hemodialysis group. These results conformed with the light and electron microscopic observations. Clinical, morphological and morphometric indications of recovery from uremic neuropathy were observed in the transplant recipients. The pathophysiology of uremic peripheral neuropathy was marked axonal degeneration. Pathologic Schwann cells were also frequently found. Axonal degeneration and Schwann cell damage seemed to exist independently of each other. In morphometric analysis, axonal atrophy and abnormal myelin sheath thickness were observed in all patient groups. A closs relationship was found between axonal atrophy and low conduction velocity. Unexpectedly low nerve conduction velocities were also observed, which cannot be explained by either loss of nerve fibers or demyelination. The findings of damaged endoneural blood capillaries supported the ischemic theory as one mechanism in the pathogenesis of uremic neuropathy.
D000328:Adult; D001369:Axons / Q000648:ultrastructure; D001706:Biopsy; D005260:Female; D006801:Humans; D016030:Kidney Transplantation; D008297:Male; D008854:Microscopy, Electron; D008875:Middle Aged; D009186:Myelin Sheath / Q000648:ultrastructure; D009431:Neural Conduction; D010523:Peripheral Nervous System Diseases / Q000473:pathology*; D006435:Renal Dialysis; D012583:Schwann Cells / Q000648:ultrastructure; D013497:Sural Nerve / Q000473:pathology; D014511:Uremia / Q000473:pathology*