Search

Uremic encephalopathy is a well-known disease with typical MR findings including bilateral vasogenic or cytotoxic edema at the cerebral cortex or basal ganglia. Involvement of the basal ganglia has been very rarely reported, typically occurring in uremic-diabetic patients. We recently treated a patient who had non-diabetic uremic encephalopathy with an atypical lesion distribution involving the supratentorial white matter, without cortical or basal ganglia involvement. To the best of our knowledge, this is only the second reported case of non-diabetic uremic encephalopathy with atypical MR findings.

The interesting article by Vikrant and colleagues1 prompts us to contribute our recent experience. Herein we report a case in which profound hypothyroidism was the trigger for severe rhabdomyolysis...

Uremic encephalopathy (UE) is a clinical syndrome that was frequently seen in patients with end stage renal disease. Pathophysiology is multifactorial and partially characterised. Patients may have symptoms ranging from mild sensorial clouding to coma. Because of those, clinical symptoms like disorder of consantration, decrease in attention span, unwillingness and debility which may be seen on early stage couldn't realised by the patient's family or the clinician or was thought to be the clinical features of the primary disease. With renal transplantation and advanced dialysis techniques UE becomes less frequent but also different clinical features present as a problem. For these reasons, good cooperation between nephrologists and neurologists who care for these patients are important. This article consantrates on recent developments in pathophisyology, clinics, diagnosis and differential diagnosis of UE.

Dr. Willem J. Kolff's imaginative venturesomeness in adopting "new ways of thinking" has served as an encouraging model for this author's research career. In appreciation of his leadership and beginning with the favorable results that attended the initial use of the Brigham-Kolff artificial kidney at a renal center in the Korean war, this presentation summarizes four experiences to illustrate how "new ways of thinking" produced new results and new research, namely, the concept and use of prophylactic daily hemodialysis; the use of a model of acute renal failure in rats to examine mechanisms of pathogenesis and means of prevention; the recognition of patients' uremic illness as an encephalopathy that can be quantified by appropriate measures; and the use of daily peritoneal dialysis and quantified EEGs in rats to explore relationships between dialysis-induced concentrations of potentially toxic solutes, quantified indices of symptomatic uremic encephalopathy, and concurrent, localized metabolic abnormalities in the brain. The results of these "new ways of thinking" suggest that we may ultimately come to understand the clinical uremic illness and its response to dialysis.

The central nervous system disorders associated with untreated renal failure are referred to as uremic encephalopathy. Patients with renal failure are also at risk to develop organic brain disease and metabolic encephalopathy, which can afflict the general population. Therefore, when a patient with end-stage kidney disease presents with altered mental status, a thorough and complete evaluation is necessary.

A síndrome hemolítico-urêmica é patologia caracterizada pela tríade insuficiência renal aguda, anemia hemolítica microangiopática e trombocitopenia, apresentando complicações no sistema nervoso central em número considerável de casos. As alterações observadas na tomografia computadorizada são, geralmente, infartos. Os autores apresentam dois casos nos quais, além dos infartos, é vista hipodensidade difusa na substância branca, reversível com a resolução da fase aguda da doença, à semelhança de alterações descritas em casos de encefalopatia urêmica e de encefalopatia hipertensiva de outras etiologias. The hemolytic-uremic syndrome is a pathology characterized by a triad consisting of acute renal failure, microangiopathic hemolytic anemia and thrombocytopenia, with complications of the central nervous system arising in a considerable number of cases. Altered cranial computerized tomography examinations usually reveal cerebral infarctions. We present here two cases in which diffuse hypodensity was observed in the white matter in addition to the infarcts. This hypodensity was reversible after resolution of the acute phase of the disease, as is also the case for the alterations described in uremic encephalopathy and in hypertensive encephalopathy of other etiologies.

Much of the history of acute renal failure and its managment is derived from wartime experience. The phenomenon of acute post-traumatic renal failure was recognized by Bywaters and Beall [1] in military and civilian casualties during World War II; unfortunately, hemodialysis was not yet available at that time. Conventional hemodialysis was first used in chnical practice in 1944, when Kolff [2] successfully dialyzed a 45-year-old woman with drug-induced oliguric acute renal failure and uremic encephalopathy. By the early 1950s, Swan and Merrill [3] were able to achieve a survival rate of 54% in 85 acute renal failure patients, using the Kolff-Brigham coil hemodialyzer [4]. These techniques were later applied successfully during the Korean War.

Hepatic encephalopathy is ameliorated by drugs acting on the central GABAA-benzodiazepine receptor complex. To investigate whether these effects are specific for hepatic encephalopathy or just reflect a nonspecific arousal reaction, various benzodiazepine antagonists like flumazenil or with inverse agonistic properties (Ro 15-4513, Ro 15-3505) were studied in uremic encephalopathy in rats after bilateral ureteral ligation (n = 20) and compared with hepatic encephalopathy caused by thioacetamide-induced acute liver failure (n = 33). As soon as the animals developed clear signs of metabolic encephalopathy, their motor activity was recorded in an animal activity meter for 10 min. Furthermore, a composite score was calculated by grading various behavioral signs from 0 = absent to 3 = apparently normal. Rats were then injected with coded preparations of Ro 15-4513 (0.5, 2.5 and 5 mg/kg body wt intraperitoneally), flumazenil (2.5, 10, 25 and 40 mg/kg), Ro 15-3505 (10 mg/kg) or vehicle, and the measurements were repeated. The code was broken after the completion of the study. Pretreatment motor activity was decreased both in hepatic and uremic encephalopathy (20.7 ± 6.4 [S.E.M.] and 41.3 ± 37.1 movements/10 min). In hepatic encephalopathy motor activity and the composite score were improved both by 5 mg/kg Ro 15-4513 (by 293%, p 0.01), whereas vehicle and flumazenil had no effects. In uremic encephalopathy neither drug was effective in improving the neurobehavioral status. These results indicate that the amelioration of neurobehavioral symptoms both by Ro 15-4513 and Ro 15-3505 seems to be specific for hepatic encephalopathy and is consistent with the hypothesis that hepatic encephalopathy is associated with an increased GABA-ergic tone. (HEPATOLOGY 1991;14:963–968.)

Twenty-seven children, ages 6 months - 13 years, with encephalopathy complicating hemolytic-uremic syndrome are reported from The University of British Columbia, Vancouver, Canada.

The symptoms which develop in well-managed patients with acute or chronic progressive renal failure comprise the neurobehavioral syndrome, uremic encephalopathy. Interfering with vigilance, cognitive functions, and ultimately consciousness, these symptoms impose significant disability unless dialysis treatment can reverse and suppress them or a successful renal transplant provides the patient with virtually normal renal function, and, consequently, complete symptomatic recovery. This apparent connection between disability as a neurobeha-vioral “encephalic” disorder and its response to dialysis prompted our attempts to apply quantitative electroencephalogram (EEG) measures as indices of the “toxic encephalopathy” of renal failure and of its response to “standard” dialysis regimens and to transplantation. Subsequent work indicates that EEG measures are sensitive to varying amounts or intensity of maintenance dialysis, to changes in modality of dialysis, for example, the shift from conventional prescriptions of maintenance hemodialysis to peritoneal dialysis, CAPD, CCPD, and so forth, or to effects within individual dialysis sessions in cases of dialysis disequilibrium.These findings invite the prospect that one may objectively assess at least the relative adequacy of different levels and modalities of dialysis in individual patients using objective indices which are particularly relevant both to the symptomatic disability of renal failure on one hand, and to the symptomatic improvement evoked by dialysis on the other.Therefore, in this article we describe the use of computer-based methods for the evaluation of uremic encephalopathy and its response to treatment. Examples are given in which such computerized evaluations have guided decisions about treatment, particularly to assure sufficient dialysis to suppress even the milder manifestations of the dialysis-responses, clinical uremic syndrome. The purpose of the article is to dispel the mystique that has surrounded the use of the computer for evaluation of EEGs recorded from renal patients.The methods described below were designed specifically for use with EEGs recorded from renal patients and should not be considered as a replacement for a trained EEG scorer. Visual scoring of the EEG provides a comprehensive examination of an EEG record that is unlikely ever to be matched by any computer program. Hence, the methods described should be viewed simply as a quantitative evaluation tool for a limited range of significant features in EEGs secured from a rather select population.We hope the practical information given can be used to guide physicians as they begin to incorporate the methods described into their everyday practice. A survey of the history of the use of computers in the evaluation of electroencephalograms recorded from patients with renal disorders is given as well as a critical evaluation of computer methods employed in past approaches. The practical consequences of a decision to utilize computerized testing methods will be examined. A prospectus that attempts to highlight possible future directions in this area completes the paper.

It has been demonstrated that anesthesia primarily affects the reticular activating system and psychological studies on patients undergoing anesthesia demonstrated a verbal memory defect. This study was performed in order to determine whether metabolic (uremic) encephalopathy follows the Jacksonian dissolution hypothesis and disrupts cortical function or whether it acts like an anesthetic, causes dysfunction in phylogenetically older systems and thereby produces a memory defect. Twenty-four uremic subjects were tested for memory function, language function, and intellectual function, and compared to 12 control subjects. The greatest difference between the groups was in immediate memory function suggesting that uremia probably acts in a manner similar to anesthesia (by causing dysfunction in the reticular activating system). It is postulated that poor arousal interferes with rehearsal and rehearsal is probably an important component of immediate memory.

Administered the Halstead-Reitan Battery (HRB) of neuropsychological tests to 24 patients with advanced renal failure, 24 patients with neurological disorders, and 24 patients with medical and/or non-psychotic psychiatric conditions in order to assess the effects of uremic encephalopathy on human neuropsychological functioning. The groups did not differ significantly in age, education, verbal intelligence, or level of affective disturbance. Results indicated that the uremic and neurological groups were equal in overall level of neuropsychological impairment and that both were significantly more impaired than the medical-psychiatric group. However, the uremic group showed a pattern of deficits that was qualitatively different from both the neurological and medical-psychiatric groups. Results were discussed with reference to selective cortical dysfunctions in uremia and contrasted with earlier studies that did not consider differential sparing of abilities in renal patients.

In view of the putative involvement of calcium in uremic encephalopathy and the critical importance of this element in juvenile development, we examined the effect of temporary restriction of dietary calcium intake on serum chemistry and the quantitative electroencephalogram (Q.EEG) in unilaterally 3/4 nephrectomized juvenile male Sprague-Dawley rats. Animals were renally infarcted at 22-26 days of age (50-74 g) and placed on one of two isocaloric dietary regimens: powdered normal rat diet (ND, n = 25) or low calcium diet (LCD, n = 8) for 30 days. At this time, ND animals showed normal serum chemistries, whereas LCD rats were hypocalcemic and azotemic with significantly elevated blood urea nitrogen (BUN) and serum creatinine concentrations and reduced renal creatinine clearance values. All animals thereafter received ND for 25-34 further days, during which time chronic Q.EEG electrodes were implanted. At the end of the common ND feeding period, serum chemistry values were equal and normal in both groups. The average theta/alpha ratio (TAR) of the overnight Q.EEG was assessed for 3 days. We found that the TAR of previously LCD animals was significantly elevated compared with ND rats. This indicates an encephalopathic slowing of the background rhythm of these animals. We conclude that, following restoration of a transient uremic and hypocalcemic episode induced by LCD feeding, the Q.EEG background frequency of juvenile renally impaired rats was abnormally slow after 30 days of ND feeding.

Central and peripheral neurological disturbances are often the leading symptoms in chronic renal insufficiency. Without successful treatment, loss of mental activity and finally precomatose and comatose states are the fate of these patients. The pathogenesis of this uremic encephalopathy is still obscure.

Regardless of the etiology, when acute renal failure occurs in the perioperative setting, the prognosis for survival is poor. In addition, the prognosis appears not to have changed substantially since the advent of hemodialysis 35 years ago. This presentation will explore recent data regarding prognosis and its prediction in patients who have developed renal failure.

In a prospective study, 34 patients with 41 admissions for malignant hypertension were examined by a neurologist before and after antihypertensive treatment. Neurologic examination was normal in 17 cases, and neurologic diagnoses in 19 others included acute cerebral infarction (10), uremic encephalopathy (4), dementia of uncertain etiology (3), multiple infarct dementia (1), and chronic paranoid schizophrenia (1). Five patients had a generalized neurologic syndrome consistent with hypertensive encephalopathy, characterized by altered mental function with or without generalized convulsions. In these patients, neurologic examination was normal 1 to 7 days after lowering of blood pressure, while renal function remained unchanged. Neurologic disease is therefore common in malignant hypertension, and hypertensive encephalopathy may be more frequent than previously described.

A study of nine patients, aged 23 to 67 years, showed a remarkable sequence of EEG findings in progressive uremic encephalopathy. The initial characteristics suggested a disorder of subcortical gray matter, followed by involvement of cortical gray matter and finally white matter. The same EEG findings tended to persist in the early stages of the disease and were present throughout the night and during dialysis. During dialysis, the EEG background and clinical picture between paroxysms sometimes showed deterioration. Seizures indicated a grave prognosis. Five of six patients with seizures died. In some patients, progressive uremic encephalopathy may develop without hemodialysis. Routine EEGs in dialysis units or in patients prior to admission can help uncover progressive uremic encephalopathy before the clinical emergence of this disorder.

Mental or neurobehavioral manifestations of uremia usually are the earliest and the most responsive to dialysis and to renal transplantation. An assay system relevant to uremia is capable of identifying toxic factors by quantitive neurobehavioral end points. In this system chemical composition of the body fluids is maintained by peritoneal dialysis. Mental performance by appropriately trained monkeys deteriorated following ureteral ligation when blood urea nitrogen (BUN) reached levels of 50 to 200 mg/100 ml, and was restored toward normal by peritoneal dialysis, even though BUN concentration was maintained at a high level by adding urea to the dialysate. Distribution of power in simultaneously recorded electroencephalograms favored slower frequencies as BUN level rose, with reversal following dialysis.