Behzad Einollahi

Hossein Kachuee

Javad Ameli

Kazem Ghoddusi

Vahid Poorfarziani

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Urology JournalUNRC/IUA122Subacute Polyneuropathy after Initiation of PeritonealDialysis, Improved Following Kidney TransplantationJavad Ameli,* Kazem Ghoddusi, Hossein Kachuee, Vahid Poorfarziani, Behzad EinollahiDepartment of Internal Medicine, Bagiatallah Medical University, Tehran, IranKEY WORDS: polyneuropathy, peritoneal dialysis, kidney transplantation, immunomodulatory therapy,inflammatory demyelinating neuropathyVol. 2, No. 2, 122-124 Spring 2005Printed in IRANIntroductionUremic neuropathy is the most commonneurologic complication of uremia, and it affectsmore than 60% of patients with end-stage renaldisease (ESRD) who undergo dialysis.(1) This typeof neuropathy symmetrically involves the distalextremities, especially the lower limbs. Onelectrophysiological assessment, an axonalpattern is dominant. The clinical course and theintensity of uremic neuropathy vary from oneindividual to another. Coexisting chronicconditions such as diabetes mellitus canaggravate the symptoms,(2) while dialysis canstop or delay progression of chronic uremicneuropathy.(3) Complete improvement occursafter kidney transplantation.(4)Recently, acute and subacute neuropathies inESRD patients have also been reported.(5-8) Theseconditions have a demyelinating feature anddevelop after the initiation of continuousambulatory peritoneal dialysis (CAPD). Thepathogenesis of these nonchronic forms ofneuropathy remains unclear. We report 2 cases ofsubacute uremic polyneuropathy that improvedfollowing kidney transplantation.Case ReportCase 1. A 54-year-old man presented withprogressive weakness of the extremities of 5months' duration. He had been diagnosed withESRD for 13 years and with diabetes mellitus for25 years. He had been receiving peritonealdialysis for 6 months, and his current symptomshad appeared after 3 to 4 weeks.  Within2 months, he had lost the ability to walk. Resultsof a neurologic examination of the cranial nerveswere normal. Atrophy of the calf and thighmuscles, loss of hair in legs, and pseudomotorchanges in the skin of the calf were apparent.Muscle strength of the wrist extensors andflexors, the elbow extensors, and shoulderabductors was 4/5. Muscle strength of the hipextensors and flexors, knee flexors, and knee andankle extensors was 3/5, 2/5, and 1/5,respectively. Tendon reflexes were diminished.Pain and heat senses in the distal lowerextremities were disrupted up to the knees, andthe proprioceptive sense in the feet wasdisturbed. Electrophysiological assessmentshowed demyelinating peripheral neuropathy.CAPD was continued, and 2 courses ofintravenous immunoglobulin therapy (20 mgdaily) were initiated but had no positive effect.Subsequently, plasma exchange was attempted at2 liters daily for 5 consecutive days and thenweekly for 2 months. Considerable improvementwas achieved, and the patient was able to do finehandwork and walk with the help of a cane. Thepatient underwent kidney transplantation, andimmunomodulatory treatment was discontinued.Neurologic symptoms and signs persisted butbegan to improve gradually after 4 months. Bythe first posttransplant year, the patient was ableto do fine movements with his hands and walk onhis own. However, diminished reflexes and mildmuscular atrophy of the lower extremitiespersisted.Case 2. A 55-year-old man presented in whomESRD had been diagnosed following admissionfor acute pulmonary edema 6 months earlier. Hehad a 5-year history of diabetes mellitus and a2-year history of uncontrolled hypertension.Received July 2004Accepted November 2004*Corresponding author: Department of InternalMedicine, Baqiatallah hospital, Mollasadra St,Vanak Sq, Tehran, Iran. Tel: ++98 912 154 2560E-mail: j.ameli@bmsu.ac.irAmeli et al 123Following a few hemodialysis sessions, peritonealdialysis was begun. Within 2 months, weaknessof the extremities developed and previous tinglingand numbness in the distal extremities becameaggravated. He was not able to walk on his ownafter 1 month. Results of a physical examinationof the 12 cranial nerves were normal. Atrophywas present in the interosseous muscles of thefingers and the muscles of forearms, thighs,calves, and feet. Muscle strength was about 4/5in the upper and 3/5 in the low extremities.Tendon reflexes were completely diminished.Pain, heat, and positional senses in the lowerextremities were abnormal. Without furthertreatment, the patient underwent kidneytransplantation.On electrophysiological assessment, peripheralneuropathy with a predominant demyelinationpattern was detected. On follow-up, movementpower in the extremities returned, and sensorydisorders were alleviated. He was able to walk onhis own after 6 months. The ability to do finemovements, however, remained mildly impaired.Atrophy of the calf and interosseous muscles ofthe hand persisted. On 1-year follow-up, norecurrence or aggravation of symptoms was seen.DiscussionAcute and subacute forms of uremicneuropathy in ESRD patients have been reportedin few studies. These forms, which aredemyelinating peripheral neuropathies, becomesymptomatic within a few weeks after the start ofCAPD and cause severe disability in the patientswithin 1 to 3 months.(5-8) Ropper, in 1994,described 4 cases of subacute and acuteneuropathy following CAPD. The patientsdeveloped generalized limb weakness over days orweeks, severe imbalance, diminished reflexes,and numbness within a few weeks after theinitiation of CAPD. Spinal fluid protein levelswere elevated, and some demyelinating featureswere noted on electrophysiological testing. In 1patient, neuropathy was alleviated by morefrequent peritoneal dialysis and improved afterkidney transplantation. But in 2 patients withdiabetes mellitus, the neuropathy progressed.(5)Toepfer and colleagues reported 3 patients withacute inflammatory demyelinating neuropathy,which developed 4 to 10 weeks following theinitiation of CAPD. They also detected elevatedspinal fluid protein and signs of demyelinatingneuropathy. None of the patients improvementwith intensified peritoneal dialysis, butimmunomodulatory treatments were effective.One patient responded to hemodialysis andimproved completely after receiving a kidneyallograft.(6) Lui and coworkers have described2 cases of acute neuropathy, occurring 6 to 10weeks after peritoneal dialysis. The diseaseresolved after kidney transplantation in 1 andwith immunomodulatory therapies in another.(8)In all reported acute and subacute uremicneuropathy cases, the patients have had ESRDand a history of prolonged diabetes mellitus. Itseems that the combination of ESRD anddiabetes predisposes patients to this type ofneuropathy. Acute and subacute forms of nerveinvolvement (eg, plexopathy and radiculopathy)are common,(9,10) but they affect the extremitiesasymmetrically, while uremic neuropathy has asymmetric pattern and affects both upper andlower limbs at the same time.Another pathologic cause of neuropathy inthese patients can be acute inflammatorypolyneuropathy. This condition, namely Guillain-Barre syndrome, develops over a period of lessthan 1 month and results in severe disability.High-dose intravenous immunoglobulin therapyand plasma exchange can aid a more rapidremission of patients.(11,12) A relativeimprovement with immunomodulatorytreatments in some patients, as was true in oursecond patient, suggests a role for aninflammatory process and the coincidentaloccurrence of subacute inflammatory neuropathyin ESRD patients. Nonetheless, evidence existsagainst this explanation for subacute neuropathyin ESRD patients. First, immunomodulatorytreatments are not always effective in these cases,and second, resolution of disease after kidneytransplantation can provide reason to reject thishypothesis. In agreement with other studies,(5-8) ourpatients were involved with polyneuropathy whenthey received peritoneal dialysis. This indicates acausal relationship, probably due to a metabolicdisturbance, between acute and subacutepolyneuropathy and CAPD. However, furtherstudies are warranted to ellucidate thepathogenesis of this disease.Subacute Polyneuropathy, Improved Following Kidney Transplantation124References1. Asbury AK. Uremic neuropathy. In: Dyck PJ, ThomasPK, Lambert EH, Bunge R, editors. Peripheralneuropathy. 2nd ed. Philadelphia: WB Saunders; 1984. p.1811.2. Tyler HR. Neurologic disorders in renal failure. Am JMed. 1968;44:734-48.3. Nielsen VK. The peripheral nerve function in chronicrenal failure. VII. Longitudinal course during terminalrenal failure and regular hemodialysis. Acta Med Scand.1974;195:155-62.4. Bolton CF, Baltzan MA, Baltzan RB. Effects of renaltransplantation on uremic neuropathy. A clinical andelectrophysiologic study. N Engl J Med. 1971;284:1170-5.5. Ropper AH. Accelerated neuropathy of renal failure.Arch Neurol. 1993;50:536-9.6. Toepfer M, Schiffl H, Fricke H, et al. Inflammatorydemyelinating neuropathy in patients with end-stagerenal disease receiving continuous ambulatory peritonealdialysis (CAPD). Perit Dial Int. 1998;18:172-6.7. Chen J, Guest S. Inflammatory demyelinatingneuropathy presenting in a temporal relationship withthe initiation of peritoneal dialysis. Perit Dial Int.1998;18:542-3.8. Lui SL, Hui CK, Chan TM, Lo WK, Lai KN. Progressivedemyelinating neuropathy after initiation of continuousambulatory peritoneal dialysis--report of two cases. ClinNephrol. 2001;56:407-10.9. Bastron JA, Thomas JE. Diabetic polyradiculopathy:clinical and electromyographic findings in 105 patients.Mayo Clin Proc. 1981;56:725-32.10. Garland H. Diabetic amyotrophy. Br Med J.1955;(4951):1287-90.11. Hughes RA, Rees JH. Clinical and epidemiologic featuresof Guillain-Barre syndrome. J Infect Dis. 1997;176 Suppl2:S92-8.12. Kuwabara S. Guillain-Barre syndrome: epidemiology,pathophysiology and management. Drugs. 2004;64:597-610.

Subacute Polyneuropathy after Initiation of Peritoneal Dialysis, Improved Following Kidney Transplantation

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Subacute Polyneuropathy after Initiation of Peritoneal Dialysis, Improved Following Kidney Transplantation

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