Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031117 (peripheral neuropathy)
 10,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a series of patients with chronic renal failure managed conservatively, the rise in the plasma-myo-inositol (myoinositol) concentration has been found to be related to depression of sural-nerve conduction velocity. There was no correlation with motor-nerve conduction velocity in the peroneal nerve, or with either of these variables in a series of patients receiving chronic haemodialysis. Despite the negative correlation with sural-nerve conduction velocity, there was no correlation between the plasma-myoinositol concentration and the presence of peripheral neuropathy as assessed clinically. It is concluded that hypermyoinositolaemia may depress nerve conduction velocity, but there is no evidence that it is responsible for the development of uraemic polyneuropathy.
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PMID:Plasma-myoinositol concentrations in uraemic neuropathy. 6 75

A 61 year old man had chronic renal failure because of oxaluria and renal calculi. Two years before death, while on hemodialysis, he developed severe progressive peripheral neuropathy. At autopsy calcium oxalate crystals were found in the peripheral nerves and other tissues. Nerve lesions included segmental demyelination, axonal degeneration and crystalline deposits within the myelin sheath. Ultrastructurally there were foci of osmiophilic granular material within myelin lamellae and endoneurium, and pleomorphic lamellar bodies in the perinuclear Schwann cell cytoplasm. It is probable that chronic hemodialysis favors the deposition of oxalate in the Schwann cells and the development of neuropathy in patients with primary hyperoxaluria and renal failure.
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PMID:Peripheral neuropathy in oxalosis. A case report with electron microscopic observations. 17 8

Initial observations in adults revealed that peripheral neuropathy, as documented by reduced conduction velocity is common in chronic renal failure. Critical analysis of this problem in children on long-term dialysis is scarce, consisting of a simgle report which demonstrated that the motor nerve conduction velocities were decreased early and frequently with more severe depression in peroneal nerve velocities. This is in distinct contrast to data from adults, in whom uniform rates of deterioration are encountered. In addition, a direct correlation of the degree of nerve conduction defect with the severity of the renal failure is found in adult patients. The present study showed a relative lack of nerve conduction defects in 11 children on long-term hemodialysis. With rare exceptions, the conduction velocities were normal. To date, no clinical symptoms of neuropathy were evident in our patients. It would seem that, with the short-dialysis schedule of 12--14 h/wk over a period of up to 5 yr, there is no progressive neuropathy as quantitated by nerve conduction measurements.
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PMID:Long-term hemodialysis and nerve conduction in children. 47 89

Twelve patients with severe chronic renal failure (serum creatinine 7.0-27 mg %), and marked uremic symptoms on a 40 g protein diet, were treated with a caloric-rich diet containing 16-20 g protein, supplemented with the 8 essential amino acids (1.1-2.2 g N) and histidine (0.23-0.45 g N)in the form of tablets for periods between 3 and 34 months. During the treatment the serum urea-N fell, and the uremic symptoms subsided or diminished without the patient exhibiting signs of malnutrition. The nerve function was followed with quantitative and semiquantitative neurological tests (among others, determination of vibratory perception thresholds and nerve conduction times). Initially all patients but 2 had signs of neuropathy as measured by these methods. During the course of treatment no deterioration of peripheral nerve function was recorded in any of the patients, several of whom had had serum creatinine conceptrations above 15 mg % for long periods. We conclude that conservative treatment with N-poor diet in far advanced chronic renal failure may prevent the further development of peripheral neuropathy provided that adequatecaloried and essential amino acids (2-3 times the minimal requirements) are supplied. The results suggest that, in addition to uremic toxines, malnutrition is a factor of importance for the developments of of uremic neuropathy.
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PMID:Preservation of peripheral nerve function in severe uremia during treatment with low protein high calorie diet and surplus of essential amino acids. 111 81

A 1987 questionnaire sponsored by the Health and Welfare Ministry concerning the clinical subsets and severity of systemic lupus erythematosus (SLE) was distributed to 93 medial facilities. A clinical analysis of the outcome and treatments was accomplished on one thousand six hundred and fourteen SLE patients fulfilling ARA criteria. The outcome was evaluated into 6 categories, namely; complete remission, incomplete remission, no change, gradual worsening, rapid worsening and unknown. Treatments included (1) anti-inflammatory drugs, (2) initial dose of prednisolone (PSL) below 29 mg/day, (3) initial dose of PSL from 30 to 59 mg/day, (4) initial dose of PSL above 60 mg/day, (5) pulse therapy, (6) immunosuppressants, (7) plasmapheresis, and (8) hemodialysis. Statistical significances were determined with ridit analysis. The severity of the disease for 1,614 SLE patients was evaluated by the judgement of each medical facility independently, separating it into 3 grades. As a result, 16.8% was evaluated as severe, 54.6% was evaluated as moderate, and 28.6% was evaluated as mild. Clinical subsets were divided into 3 categories according to the outcome; (1) those with high complete remission rates (serositis, convulsion, oral ulcers, unconsciousness, hemolytic anemia and so on), (2) those with high incomplete remission rates (lupus nephritis, digital gangrene, hypertension, peripheral neuropathy, erythema, Raynaud's phenomenon and so on), and (3) those with high rates of no change or worsening (aseptic bone necrosis, pulmonary hypertension, pneumonitis, chronic renal failure and so on). SLE patients with persistent proteinuria below 3.4 g/day, pulmonary hypertension, or pneumonitis treated with large doses of PSL such as an initial dose of PSL above 60 mg/day and/or pulse therapy had a significantly higher remission rate than those treated with small dosages of PSL. Hereafter, the establishment of modes of treatments for increasing the remission rates of intractable clinical subsets in highly desired.
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PMID:[Studies on clinical subsets and severity of systemic lupus erythematosus based on a 1987 questionnaire conducted in Japan--clinical analysis of the outcome and treatments in clinical subsets]. 160 13

We report on 7 patients suffering from chronic renal failure (2 females, 5 males; aged 35-75 (phi 53.5) years) who showed severe neuromyeloencephalopathy (NME) after high doses of a new Henle's loop diuretic, Muzolimine. The temporal and phenomenological development of these systems was strikingly parallel. The neurological deficit was revealed on neurophysiological, neuroradiological and in 2 cases on neuropathological tests (gross demyelinisation of the posterior column, mainly of the fasciculus gracilis, less in the lateral corticospinal tract and in some spinal roots). The critical drug dose for first neurological impairment was 52 g on average; at this point the patients had been treated for 78 days. The maximal daily dose was 1.440 mg. Dominant clinical features were pallhypaesthesia, ataxia, signs of peripheral neuropathy in combination with hyperreflexia and progressive para- to tetraspastic paresis. Constellation of symptoms, course of disease and findings of additional investigations, especially those of neuropathology, very much resemble Vitamin B12 deficiency and SMON-(Subacute Myelo Optic Neuropathy) syndrome. The rare entity of Muzolimine-NME is discussed in respect to other endogenous and exotoxic neuromyelopathies. We present the hypothesis of a toxic, partially dialysable metabolite of Muzolimine.
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PMID:[Neuromyeloencephalopathy caused by high-dose muzolimine medication in patients with renal failure]. 215 46

This is the second part of a review article on metabolic neuropathies. The frequency and severity of neuropathy due to chronic renal failure have dramatically decreased during the last ten years, as a result of improvement in management of patients with renal failure, even though the mechanism leading to development of the neuropathy is not well understood. Measurement of nerve conduction velocity does not appear to be appropriate to the detection of axonal neuropathy and follow-up of patients with neuropathy associated with chronic renal failure. Peripheral neuropathy observed in association with hypoglycaemia and with hypothyroidism are briefly reviewed.
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PMID:[Acquired metabolic neuropathies (2): Kidney failure, hypothyroidism and hypoglycemia]. 283 Jun 53

In patients with end-stage renal disease, nervous system dysfunction remains a major cause of disability. Patients with chronic renal failure who have not yet received dialysis may have symptoms ranging from mild sensorial clouding to delirium and coma. Dialysis itself is associated with at least three distinct disorders of the central nervous system, including the dialysis disequilibrium syndrome, dialysis dementia, and progressive intellectual dysfunction. Peripheral neuropathy is also a major cause of disability in uremic patients. Aluminum probably contributes to the pathogenesis of dialysis dementia. Parathyroid hormone, the levels of which are elevated in patients with renal failure, also may be a uremic neurotoxin. Biochemically, brain calcium levels are elevated in renal failure, possibly because of the action of parathyroid hormone. Studies on synaptosomes have also shown that parathyroid hormone can affect calcium transport in the brain. Intellectual dysfunction, dialysis dementia, uremic neuropathy, and the dialysis disequilibrium syndrome can be diagnosed when the characteristic clinical findings are present and other causes of nervous system dysfunction have been excluded.
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PMID:Nervous system complications in uremia. 283 30

The effect of mecobalamin on autonomic neuropathy was evaluated in 20 hemodialyzed uremic patients; their mean age was 53 years and the duration of hemodialysis was 6.5 years; 14 were women. The cardiac beat-to-beat variation (BBV) was used as the measure of autonomic neuropathy. Twelve patients with normal BBV test results were either given 1,500 micrograms of mecobalamin daily for three months (six patients) or were untreated (six patients). The BBV test results did not change significantly over the three months in either the treated or untreated group, nor were there any significant between-group differences. Eight patients with abnormal results on the BBV test were given 1,500 micrograms of mecobalamin daily for six months. The mean BBV values increased significantly from 3.3 beats/min before treatment to 5.8 beats/min at six months (P less than 0.005); five of these patients (including three of the four patients with diabetes) showed normal BBV values by three months. It is concluded that mecobalamin can be used in the treatment of autonomic and peripheral neuropathy in both diabetic and nondiabetic patients with chronic renal failure.
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PMID:Improvement of autonomic neuropathy after mecobalamin treatment in uremic patients on hemodialysis. 344 Feb 72

During a study of peripheral nerve function in chronic renal failure, 11 patients who were being treated by chronic intermittent haemodialysis developed serum hepatitis. Before the infection there was a trend towards improvement in nerve conduction velocities. A pronounced deterioration in the conduction velocities in motor fibres of peripheral nerves occurred in association with hepatitis. In the months after recovery from the infection there was again a trend towards improvement in conduction velocities. We suggest that this reflects the occurrence of a peripheral neuropathy which is at least in part demyelinating. The neuropathy is related to the serum hepatitis, but its pathogenesis is indeterminate.
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PMID:Neuropathy associated with hepatitis in patients maintained on haemodialysis. 433 84


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