Hemofiltration, in contrast to hemodialysis or peritoneal dialysis, eliminates toxic substances accumulated in uremia by a process that is independent of molecular weight. By means of a special device, the ultrafiltrate of blood is replaced, up to the desired amount, by a modified Ringer's lactate solution. The application of this new method results in better control of severe hypertension, and controls calcium phosphate and lipid metabolism in a more physiologic manner than dialysis does, without additional drug therapy being necessary. Smaller amounts of fluid and a simplification of devices improve hygienic conditions and patient mobility.
Elimination by hemofiltration of gentamicin, doxycylin, ampicillin, sulfamethoxazole and clofibrate was measured in patients with chronic renal insufficiency. Clearance values of ampicillin and clofibrate were roughly in the range that might be expected according to the reported protein binding values of these drugs, whereas doxycyclin and sulfamethoxazole were eliminated to a much higher degree. Gentamicin clearances during a 6-hour hemofiltration treatment were lower than should be expected from reported protein binding values. For gentamicin and doxycyclin the filtered fraction linearly increased with time, a phenomenon which may be explained by membrane polarization.
The acute changes in calcium, phosphate and parathyroid hormone have been examined in chronic renal failure patients under-going hemofiltration therapy and the results compared to a similar group treated by hemodialysis. In both groups there was a significant increase in Catot (0.32 mEq/1 for hemodialysis; 0.56 m Eq/1 for hemofiltration) with Ca++ remaining constant. Plasma phosphate and parathyroid hormone decreased during hemofiltration. Calcium balances were slightly positive and phosphate balances distinctly negative in all cases. To date there is no indication of induced osteodystrophy during hemofiltration therapy, although long-term studies are needed. However, the present results indicate, that hemofiltration more closely approaches the physiological situation than conventional hemodialysis.
In seven patients with chronic renal failure in an advanced stage 17 episodes of upper abdominal pain, hypertension, vomiting and (in some of them) coma occurred during peritoneal dialysis with sorbitol-containing dialysate. The signs recurred in some of the patients but did not when glucose-containing dialysate of otherwise identical composition was used. Very high levels of sorbitol in CSF and serum were measured in the comatose patients. The precipitating factor is probably a reduced metabolic breakdown of sorbitol in renal failure with preferential intracellular deposition of sorbitol and subsequent cellular oedema. To avoid this dangerous reaction it is necessary to use glucose instead of sorbitol in peritoneal dialysates, despite the technical problems of sterilisation. Where this is not possible, glucose should be added in order to reduce the sorbitol concentration in the dialysate to less than 15g/l.
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