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Seizures and Renal Failures

Acute renal failure is a potent epileptogenic state, although the specific metabolic cause is unknown. Patients with progressive uremia may develop muscle fasciculations, twitching, asterixis, tremor, myoclonus, chorea or hemiballismus, involuntary movements that reflect neuronal hyperexcitability at the level of the peripheral nerves, spinal cord, basal ganglia and cerebral cortex. Generalized tonic-clonic convulsions are most common after 8 to 11 days of untreated anuria, and often appear in the context of severe myoclonic jerks. Such convulsions are repetitive. Severe myoclonus may be repetitive and sometimes simulates ictal activity. Asterixis or termulousness, at rest or with action, can also simulate focal motor seizures. Unlike uremic seizures, myoclonus and tremors are often stimulus-sensitive, and usually move from one part of the body to another, involving the limbs or the face. An electroencephalogram is definitive in resolving any doubt, but is rarely necessary. True focal motor or other focal seizure activity is not typical of metabolically triggered seizures, and should suggest the possibility of focal cerebral lesions such as subdural hematoma, ischemic infarction, or intracerebral hematoma. Pre-existing focal cerebral lesions, particularly in the elderly, may also serve as foci for focal motor, complex partial, adversive, or aphasic seizures. Rapid increases in blood urea nitrogen (BUN) may be a potent stimulus for seizures, but the presence of so many co-variant metabolic abnormalities makes it difficult to assign causation to any single factor. The absolute BUN level is not a good predictor of seizures. The serum BUN to calcium ratio has been offered as a good predictor of convulsions (13). More specific pro-convulsant metabolites have been The International Journal of Artificial Organs I Vol. 17 I no. 5, 1994 /pp. 247-251