Acta neurol. scandinav. 58, 280-287, 1978 Copenhagen County Holspital in Glostrup, Department of Neurology and Delpartment of Medicine, B., Glostrup, Denmark

Grand mal-provoked hyperuricemia K. LUHDORF, H. PETERSSON AND K. PEDERSEN A significant increase in S-urate was found postictally in 17 patients with two or more grand ma1 seizures within 24 h. In six patients S-urate was above the level at which hyperuricemic renal failure may develop. Impaired renal function was observed in two patients who had extremely high S-urates. It is proposed that prophylactic procedures against hyperuricemic renal failure should be carried out in all patients with repetitive convulsions. Key words: Grand ma1 - hyperuricemia - renal failure

-

urate.

Hyperuricemic renal failure (HRF) caused by repetitive convulsions was described by Warren et al. (1975), who reported seven patients with recurrent convulsions followed by extremely high S-urate levels. Two of these patients had to be hemodialyzed because of renal failure. As the authors within half a year have observed grand mal-provoked transient renal failure in two patients and renal failure in one patient in whom hemodialysis had to be performed, it is suggested that H R F is a much more common phenomenon as hitherto recognized. Nausea and lethargy are early symptoms of H R F (Kjellstrand & Campbell 1974) but may easily be overlooked in grand ma1 patients and ascribed to postictal mental clouding. Furthermore as untreated H R F may be fatal (Lilje 1970) it seems obvious that prospective studies concerning grand mal-provoked H R F are required. MATERIAL AND METHODS In the study are included consecutive patients admitted to the neurological department at Glostrup Hospital meeting the criterium of two or more grand ma1 seizures within 24 h. 17 patients, four women and 13 men, with a median age of 37 years (17-66 years), were examined. All patients but one had had only two seizures within 24 h. Patient 15 experienced three seizures, the last of which occurred at the time of admission. All seizures but one occurred before admission and measurements of the duration of seizures were thus not possible. All patients were admitted to the hospital within 1 h after the last seizure. The median interval between seizures was 20 min (range 5-240 min). Epilepsy had previolusly been diagnosed in 12 patients. In one of these patients antiepileptic

28 1 treatment had been withdrawn half a year previously as the patient had been free from seizures for more than 2 years. The etiology as to seizures in the remaining five patients was alcohol abstinence in two, while one patient half a year previously had been treated for an intracerebral abscess. In the last two patients epilepsy was diagnosed as idiopathic. At the time of admission blood was drawn for measurement of S-urate, -creatinine, -carbamide and -electrolytes (potassium, sodium and chloride). S-urate, -creatinine, -carbamide and -electrolytes were measured daily during the following 4 days. Urine sampling was started on the morning of the first day and carried out for 3 days. 24-h diuresis was measured together with U-creatinine, -potassium and -sodium. Urine sampling was started also on the fourth day, but was not completed if creatinine clearance the second and third day were both within normal limits, when they became available during the fourth day. S-glutamic oxaloacetic transaminasis (SCOT) was measured the first and third days, and hence every second day if the study was prolonged for reasons indicated below. If S-urate was above the normal on the fourth day measurements were carried out daily until two consecutive measurements were within normal limits. If creatinine clearance was not normal on both the second and third days the study was prolonged until normal values were found. Blood pressure was measured hourly during the first 24 h and hence once daily. In six patients 24-h urine sampling succeeded less than three times. These patients have been excluded from the presented results in regard to creatinine clearance and urinary electrolyte output. Creatinine clearance calculated from the obtained 24-h urine samples in these patients was all normal.

MEDIAN S-Ura t e

s/r 120-

10080-

60N=17

4 0-

204

I

I

A

j

I

i

I

3

I

i

pc0.01 p.0.01 pc0.05 NS.

OUYS

I 95% CONFIDENCE LIMITS Figure I.

Table 1 . Variables measured during the trial

Acute

S-K meq/l S-Na meq/l S-Creat. mg/l S-Carb. g/l SGOT u/1 U-K* meql24 h U-Na meq/24 h RCC ml/min

3.8 (3.5-4.2) 138 (137-140) 9 (8-10) 0.26 (0.22-0.32)

Day 1 3.7 (3.5-4.0) 139 (138-141) 10 (8-11) 0.28 (0.23-0.31) 0.9 (0.7-1.2) 37 (18-43) 62 (33-189) 104 (45-220)

Day 2

Day 3

4.0 (3.8-4.2) 139 (137-140) 9 (7-10) 0.25 (0.22-0.30)

4.2 4.3 (3.8-4.4) (3.8-4.4) 140 140 (139-141) (138-141) 8 9 (7-10) (7-10) 0.24 0.26 (0.22-0.3 1) (0.20-0.34) 1.0 (0.6-1.8) 53 (35-93) 102 (89-166) 128 (85-164)

41 (27-56) 84 (36-284) 92 (80-175)

Day 4

N 17 17 17 17 17

11 11

11

Carb.: Carbamid. Creat.: Creatinine. SGOT: S-glutamic oxaloacetic transaminase. RCC: Renal creatinine clearance$. 95 % confidence limits indicated in parenthesis. * U-K excretion increases significantly from day 1 t o day 2 ( P 0.01) and from day 2 to day 3 ( P < 0.01).

Grand mal-provoked hyperuricemia.

Acta neurol. scandinav. 58, 280-287, 1978 Copenhagen County Holspital in Glostrup, Department of Neurology and Delpartment of Medicine, B., Glostrup,...
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