Relationship between serum myo-inositol and peripheral neuropathy in patients with chronic renal failure

Myo-inositol is a precursor and component of phosphoinositides which is involved in propagation and generation of action potentials as the nerve function. The first stage of catabolism of serum myo-inositol is performed by an oxidase in the renal cortex. During renal insufficiency, the activities of...

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Published inNihon Jinzo Gakkai shi Vol. 28; no. 6; pp. 739 - 747
Main Authors TSUJI, HIROYUKI, KANIU, HITOSHI, MIURA, MASAHIRO, NIHEI, HIROSHI, FURUKAWA, KEIICHI, KUZUHARA, KEIHACHIRO, MIMURA, NOBUHIDE, AKAGI, KUNIHIKO, SUZUKI, YOSHIO, UCHIGATA, MASANOBU, HARA, SHIGEKO
Format Journal Article
LanguageJapanese
Published Japan Japanese Society of Nephrology 01.06.1986
Subjects
Creatinine - blood
Humans
Inositol - blood
Kidney Failure, Chronic - blood
Kidney Failure, Chronic - complications
myo-inositol
Neural Conduction
Peripheral Nervous System Diseases - blood
Peripheral Nervous System Diseases - complications
Peripheral Nervous System Diseases - physiopathology
uremic neuropathy
uremic toxin
Online AccessGet full text
ISSN0385-2385
1884-0728
DOI10.14842/jpnjnephrol1959.28.739

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Abstract Myo-inositol is a precursor and component of phosphoinositides which is involved in propagation and generation of action potentials as the nerve function. The first stage of catabolism of serum myo-inositol is performed by an oxidase in the renal cortex. During renal insufficiency, the activities of the oxidase decrease to cause retention of myo-inositol in the blood. Experimental rats of hypermyoinositolemia showed delayed MCV in the sciatic nerve. In this study, serum free myo-inositol (S, fm-I) and serum creatinine (S-Cr) levels as well as peripheral nerve conduction velocity (NCV) were measured prior to dialysis in the patients for whom dialysis therapy has recently been instituted or who have been on dialysis for no less than 10-years. As a result, S. fm-I level was clearly high in those with abnormal NCV compared with those with normal NCV in both groups of patients. In the patients for whom dialysis was recently instituted, there was clealy an inverse correlation between S. fm-I and all of NCV measured in both upper and lower extremities. Based on the above, it will not be unreasonable to consider myo-inositol as a metabolic factor in uremic neuropathy and a uremic toxin.
AbstractList Myo-inositol is a precursor and component of phosphoinositides which is involved in propagation and generation of action potentials as the nerve function. The first stage of catabolism of serum myo-inositol is performed by an oxidase in the renal cortex. During renal insufficiency, the activities of the oxidase decrease to cause retention of myo-inositol in the blood. Experimental rats of hypermyoinositolemia showed delayed MCV in the sciatic nerve. In this study, serum free myo-inositol (S, fm-I) and serum creatinine (S-Cr) levels as well as peripheral nerve conduction velocity (NCV) were measured prior to dialysis in the patients for whom dialysis therapy has recently been instituted or who have been on dialysis for no less than 10-years. As a result, S. fm-I level was clearly high in those with abnormal NCV compared with those with normal NCV in both groups of patients. In the patients for whom dialysis was recently instituted, there was clealy an inverse correlation between S. fm-I and all of NCV measured in both upper and lower extremities. Based on the above, it will not be unreasonable to consider myo-inositol as a metabolic factor in uremic neuropathy and a uremic toxin.
Author NIHEI, HIROSHI
TSUJI, HIROYUKI
HARA, SHIGEKO
MIURA, MASAHIRO
UCHIGATA, MASANOBU
KANIU, HITOSHI
MIMURA, NOBUHIDE
KUZUHARA, KEIHACHIRO
FURUKAWA, KEIICHI
SUZUKI, YOSHIO
AKAGI, KUNIHIKO
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References 1)　原茂子,葛原敬八郎,鈴木好夫,二瓶宏,三村信英:慢性腎不全の脳・神経系合併症とその対策透析会誌15: 207-218, 1982.
6) Scribner, B. H. & Babb, A. L.: Evidence for toxins of middle molecular weight. Kidney. Intern., 7: supp 349-351, 1975.
24)　黒田満彦:ミオイノシトール臨床医3: 633, 1977.
2) Hegstrom, R. M., Murray, J. S., Pendras, J. P., Burnell, J. M. & Scribner, B. H.: Two years experience with periodic hemodialysis in the treatment of chronic uremia, Trans. Amer. Soc. Artif. Int. Organs, 8 : 266-230, 1962.
28)　広瀬源二郎,小副川寛,高堂松平,山本悌司,篠田晤:尿毒症ニューロパチーと血漿ミオイノシトール臨床神経学21: 443-447, 1981.
23) Hawthorne, J. N. & Kai, M.: Metabolism of phosphoinositides. In handbook of neurochemistry 491-508, Edited by A. Lajtha. Plenum. Press, New York, 1970.
30)　島田幸彦,大坪修,重富伸一,室崎恵子,大谷克子,渡辺信行,横田一憲,植田修逸,白石喜久,大坪公子:慢性腎不全における末梢神経障害,電気生理学的検討最新医学33: 1734-1742, 1978.
8) Howard, C. F. Jr. and Anderson, L.: Metabolism of myoinositol in animals, part 2. Arch. Biochem. Biophys., 118: 332-339, 1967.
13) Kuzuhara, K., Uchima, T., Sugimoto, T., Otsubo, O. & Inou, T.: A new method for evaluating the viability of preserved kidney by determing for myoinositol levels in the early effluent perfusate. Transplantation. Proc., 14: 231-237, 1982
9) Clements, R. S. Jr., DeJesus, P. V. Jr. & Winegrad, A.I.: Raised plasma myoinositol levels in uremia and experimental neuropathy. Lancet, 1: 1137-1141, 1973.
17) Preswick, G. & Jeremy, D.: Subclinical polyneuropathy in renal insufficiency. Lancet, 2: 731-732, 1964.
11) DeJesus, P. V. Jr., Clements, R. S. Jr. & Winegrad, A. I.: J. Neurol. Sci., 21; 237-249, 1974.
12)　立花新太郎,飛松好子,藤原稔泰,桃井康晴,長野昭,二瓶宏,葛原敬八郎,内潟雅信:長期血液透析患老に発生した手根管症候群について.日本手の外科学会誌1: 129-134, 1984.
25) Greene, D. A., Dejesus, P. V. & Winegrad, A.I.: Effects of insulin and dietary myoinositol on impaired peripheral moter nerve conductionn velocity in acute streptozotocin diabetes. J. Clini. Invest., 55: 1326-1336, 1975.
21)　堀田饒,坂本信夫:糖尿病性神経障害―病態生化学的考察最近医学39: 445-453, 1984.
16) Hegstrom, R. M., Murray, J. S., Pendras, J. P., Burnell, J. M. & Scribner, B. H.: Hemodialysis in the treatment of chronic uremia. Trans. Amer. Soc. Artif. Int. Organs., 7: 136-149, 1961.
15)　筒井高紀,森脇モト,岡山幸恵: ラウリル硫酸ソーダを利用した血清アレアチニン直接測定法臨床病理19:総会号324, 1971.
4) Thomas, P. K.: Metabolic neuropathy, J. roy. coll. Phycns, Lond., 7: 154-160, 1973.
7) Kai, M. & Hawthorne, J.N.: Physiological significanece gnificance of polyphosphoinositides in brain. Ann. NY. acad. Sci. 165: 761-773, 1969.
18) Delmez, J. A., Holtmann, B., Sicard, G. A., Goldberg, A. P. & Harter, H. R.: Peripheral nerve entrapment syndromes in chronic hemodialysis patients. Nephron., 30: 118-123, 1982.
3) Lasker, N., Harvey, A. & Baker, H.: Vitamin levels in hemodialysis and intermittent peritoneal dial ysis, Trans. Amer. Soc. Artif. Int. Organs, 9; 51-56, ,1930
27) Jefferys, J. G. R., Palmano, K. P., Sharma, A. K. & Thomas, P. K.: Influence of dietary myoinositol on nerve conduction and inositol phospho lipids in normal and diabetic rats. J. Neural, Neurosurg. Psychiat. 41: 333-339, 1978.
20) Rex. S. & Clements, Jr.: Diabetic neuropathy. "new concepts of its etiology". Diabetes 28: 604-611, 1979.
26) Reznek, R. H., Salway, J. G. & Thomas, P. K.: Plasma-myoinositol concentrations in uremic neuropathy. Lancet, I: 675-676, 1977.
29) V. Kamp. Nielsen.: The peripheral nerve function in chronic renal failure. Acta. Med. Scand., 194: 455-462, 1973.
5) Giovannetti, S., Biagini, M. & Cioni, L.: Evidence that methylguanidine is retained in chronic renal failure. Experientia, 24: 341-342, 1963.
14) Sweeley, C. C., Bentley, R., Makita, M. & Wells, W. W.: Gas-liquid chromatography of trimethylsilyl derivatives of sugers and related substances. J. Amen. Chem. Soci., 85: 2497-2507, 1963.
22)　葛原敬八郎:ミオイノシトールによる摘出腎Viability判定法の開発に関する研究日泌誌73: 411-431, 1982.
19) Thomas, P. K., Hollinrake, K., Lascelles, R. G., Osullivan, D. J., Baillod, R. A., Moorhead, J. F. and Mackenzie, J. C.: The polyneuropathy of chronic renal failure. Brain, 94: 761-780, 1971.
10)　葛原敬八郎,稲生綱政,和田栄子,積田亨:血中FREE MYO-INOSITOLと腎機能について日本腎臓学会誌22: 385-392, 1980.
References_xml – reference: 12)　立花新太郎,飛松好子,藤原稔泰,桃井康晴,長野昭,二瓶宏,葛原敬八郎,内潟雅信:長期血液透析患老に発生した手根管症候群について.日本手の外科学会誌1: 129-134, 1984.
– reference: 21)　堀田饒,坂本信夫:糖尿病性神経障害―病態生化学的考察最近医学39: 445-453, 1984.
– reference: 16) Hegstrom, R. M., Murray, J. S., Pendras, J. P., Burnell, J. M. & Scribner, B. H.: Hemodialysis in the treatment of chronic uremia. Trans. Amer. Soc. Artif. Int. Organs., 7: 136-149, 1961.
– reference: 15)　筒井高紀,森脇モト,岡山幸恵: ラウリル硫酸ソーダを利用した血清アレアチニン直接測定法臨床病理19:総会号324, 1971.
– reference: 28)　広瀬源二郎,小副川寛,高堂松平,山本悌司,篠田晤:尿毒症ニューロパチーと血漿ミオイノシトール臨床神経学21: 443-447, 1981.
– reference: 2) Hegstrom, R. M., Murray, J. S., Pendras, J. P., Burnell, J. M. & Scribner, B. H.: Two years experience with periodic hemodialysis in the treatment of chronic uremia, Trans. Amer. Soc. Artif. Int. Organs, 8 : 266-230, 1962.
– reference: 11) DeJesus, P. V. Jr., Clements, R. S. Jr. & Winegrad, A. I.: J. Neurol. Sci., 21; 237-249, 1974.
– reference: 13) Kuzuhara, K., Uchima, T., Sugimoto, T., Otsubo, O. & Inou, T.: A new method for evaluating the viability of preserved kidney by determing for myoinositol levels in the early effluent perfusate. Transplantation. Proc., 14: 231-237, 1982
– reference: 25) Greene, D. A., Dejesus, P. V. & Winegrad, A.I.: Effects of insulin and dietary myoinositol on impaired peripheral moter nerve conductionn velocity in acute streptozotocin diabetes. J. Clini. Invest., 55: 1326-1336, 1975.
– reference: 26) Reznek, R. H., Salway, J. G. & Thomas, P. K.: Plasma-myoinositol concentrations in uremic neuropathy. Lancet, I: 675-676, 1977.
– reference: 19) Thomas, P. K., Hollinrake, K., Lascelles, R. G., Osullivan, D. J., Baillod, R. A., Moorhead, J. F. and Mackenzie, J. C.: The polyneuropathy of chronic renal failure. Brain, 94: 761-780, 1971.
– reference: 6) Scribner, B. H. & Babb, A. L.: Evidence for toxins of middle molecular weight. Kidney. Intern., 7: supp 349-351, 1975.
– reference: 4) Thomas, P. K.: Metabolic neuropathy, J. roy. coll. Phycns, Lond., 7: 154-160, 1973.
– reference: 29) V. Kamp. Nielsen.: The peripheral nerve function in chronic renal failure. Acta. Med. Scand., 194: 455-462, 1973.
– reference: 7) Kai, M. & Hawthorne, J.N.: Physiological significanece gnificance of polyphosphoinositides in brain. Ann. NY. acad. Sci. 165: 761-773, 1969.
– reference: 30)　島田幸彦,大坪修,重富伸一,室崎恵子,大谷克子,渡辺信行,横田一憲,植田修逸,白石喜久,大坪公子:慢性腎不全における末梢神経障害,電気生理学的検討最新医学33: 1734-1742, 1978.
– reference: 8) Howard, C. F. Jr. and Anderson, L.: Metabolism of myoinositol in animals, part 2. Arch. Biochem. Biophys., 118: 332-339, 1967.
– reference: 14) Sweeley, C. C., Bentley, R., Makita, M. & Wells, W. W.: Gas-liquid chromatography of trimethylsilyl derivatives of sugers and related substances. J. Amen. Chem. Soci., 85: 2497-2507, 1963.
– reference: 9) Clements, R. S. Jr., DeJesus, P. V. Jr. & Winegrad, A.I.: Raised plasma myoinositol levels in uremia and experimental neuropathy. Lancet, 1: 1137-1141, 1973.
– reference: 20) Rex. S. & Clements, Jr.: Diabetic neuropathy. "new concepts of its etiology". Diabetes 28: 604-611, 1979.
– reference: 24)　黒田満彦:ミオイノシトール臨床医3: 633, 1977.
– reference: 18) Delmez, J. A., Holtmann, B., Sicard, G. A., Goldberg, A. P. & Harter, H. R.: Peripheral nerve entrapment syndromes in chronic hemodialysis patients. Nephron., 30: 118-123, 1982.
– reference: 22)　葛原敬八郎:ミオイノシトールによる摘出腎Viability判定法の開発に関する研究日泌誌73: 411-431, 1982.
– reference: 1)　原茂子,葛原敬八郎,鈴木好夫,二瓶宏,三村信英:慢性腎不全の脳・神経系合併症とその対策透析会誌15: 207-218, 1982.
– reference: 3) Lasker, N., Harvey, A. & Baker, H.: Vitamin levels in hemodialysis and intermittent peritoneal dial ysis, Trans. Amer. Soc. Artif. Int. Organs, 9; 51-56, ,1930
– reference: 27) Jefferys, J. G. R., Palmano, K. P., Sharma, A. K. & Thomas, P. K.: Influence of dietary myoinositol on nerve conduction and inositol phospho lipids in normal and diabetic rats. J. Neural, Neurosurg. Psychiat. 41: 333-339, 1978.
– reference: 10)　葛原敬八郎,稲生綱政,和田栄子,積田亨:血中FREE MYO-INOSITOLと腎機能について日本腎臓学会誌22: 385-392, 1980.
– reference: 23) Hawthorne, J. N. & Kai, M.: Metabolism of phosphoinositides. In handbook of neurochemistry 491-508, Edited by A. Lajtha. Plenum. Press, New York, 1970.
– reference: 17) Preswick, G. & Jeremy, D.: Subclinical polyneuropathy in renal insufficiency. Lancet, 2: 731-732, 1964.
– reference: 5) Giovannetti, S., Biagini, M. & Cioni, L.: Evidence that methylguanidine is retained in chronic renal failure. Experientia, 24: 341-342, 1963.
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Snippet Myo-inositol is a precursor and component of phosphoinositides which is involved in propagation and generation of action potentials as the nerve function. The...
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SubjectTerms Creatinine - blood
Humans
Inositol - blood
Kidney Failure, Chronic - blood
Kidney Failure, Chronic - complications
myo-inositol
Neural Conduction
Peripheral Nervous System Diseases - blood
Peripheral Nervous System Diseases - complications
Peripheral Nervous System Diseases - physiopathology
uremic neuropathy
uremic toxin
Title Relationship between serum myo-inositol and peripheral neuropathy in patients with chronic renal failure
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https://www.ncbi.nlm.nih.gov/pubmed/3022045
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