Since metabolic acidosis in uremic patients appears to affect protein
metabolism, cardiac function and bone disease, its complete correction
seems to be necessary. CAPD enables a certain degree of correction, h
owever a substantial amount of patients still present acid base derang
ements. Several studies have dealt with acid base balance in peritonea
l dialysis reporting a considerable interpatient and intertreatment va
riability. In this study a complete analysis of factors affecting acid
base homeostasis in CAPD patients has been performed. This analysis d
emonstrated that residual renal function is not the key factor for aci
d base homeostasis, nevertheless, in patient with a high residual urin
e volume, bicarbonate loss should be taken into account. A weak but st
atistically significant negative correlation was recorded between arte
rial blood bicarbonate and the calculated metabolic acid production. B
icarbonate levels decrease with the increase of metabolic acid product
ion and patients with a higher protein intake are more prone to develo
p metabolic acidosis. Dialysate lactate concentration in spent dialysa
te was dependent on length of dwell time and did not correlate to lact
ate blood levels which were normal in all subjects. Regression analysi
s revealed that dialysate bicarbonate concentration at 4, 6 and 12 hou
rs tightly correlated to the one of arterial blood. On the contrary ul
trafiltration volume did not influence dialysate bicarbonate concentra
tion. Therefore, since bicarbonate loss depends on drained volume mult
iplied by dialysate bicarbonate concentration, it is evident that ultr
afiltration plays a key role on dialytic base gain. In conclusion, the
non adequate correction of metabolic acidosis mostly depends on high
metabolic acid production and high ultrafiltration.