Pogglitsch H, Wawschinek O, Holzer H, Petek W, Ladurner G, Katschnig H, Korthals C
Acta Med Austriaca. 1980;7(3):71-6.
18 data with etiopathogenetic relations to the dialysis encephalopathy, such as plasma aluminum levels, parameters of azotemia and parathyroid function, blood pressure, IQ, and EEG-findings, were compared between 5 patients suffering with encephalopathy and 54 dialysis-patients without neurological symptoms. The investigations, including statistical computations (variance analysis, multiple linear regression, multivariate analysis) elicited the following results: 1. All patients suffering from encephalopathy showed higher plasma aluminum concentrations (505 +/- 58 microgram/L : 228.9 +/- 213 microgram/L, p = greater than 0.01), higher serum calcium levels (2.48 +/- 0.15 mmol/L : 2.35 +/- 0.11 mmol/L, p = less than 0.001), higher rates of osteopathy and abnormal EEG's (5 of 5 : 7 in 41 patients). 2. Age, duration of dialysis treatment, quality of dialysis treatment, blood pressure, did not show any pathogenetic influence. 3. Hyperaluminemia was caused by the oral administration of aluminum hydroxide. After reduction of the daily dose from originally 6.18 +/- 3.24 gm to 1.52 +/- 0.45 gm, the plasma aluminum levels decreased to 54.05 +/- 34.59 microgram/L without any adverse effects on the serum phosphate levels. The results suggest that dialysis-patients need less AI-OH than is usually indicated. 4. Encephalopathy did not occur after normalisation of plasma aluminum levels. 5. With respect to the aluminum toxicity in dialysis-patients, dialysis encephalopathy should not be classified as a complication of multifactorial etiology. Only hyperparathyroidism seems to be an additional risk factor.
