Plasma levels of interleukin-6 (IL-6), a cytokine known to be involved in lymphocyte activation and in inflammation, were studied in 10 normal volunteers, 21 continuous ambulatory peritoneal dialysis (CAPD) patients and 41 hemodialysis patients. Plasma IL-6 levels in hemodialysis patients were significantly higher than those in normal volunteers and CAPD patients (p < 0.05). The means of plasma IL-6 concentrations before and after hemodialysis did not change significantly. While IL-6 in peritoneal dialysate was detectable in only 3 of the 21 CAPD patients without peritonitis, it was extremely high in 2 patients with bacterial peritonitis. IL-6 levels decreased as peritonitis subsided.
L-threo-3,4-dihydroxyphenylserine (L-DOPS), a precursor of noradrenaline (norepinephrine), which is converted into noradrenaline when orally administered, was given orally to haemodialysed patients exhibiting dialysis-induced hypotension. In five patients given 300 mg L-DOPS plasma concentrations reached a peak of 1.43 +/- 0.59 micrograms/ml 6 h after administration and decreased slowly to disappear after 36 h. Plasma noradrenaline concentrations showed a significant increase (P < 0.05), reaching a peak of 1.28 +/- 0.64 ng/ml after 24 h and declined to 0.75 +/- 0.47 ng/ml by 48 h. Administration of L-DOPS to six patients during dialysis for 6 consecutive weeks showed no accumulation in the blood. Oral administration of 200-400 mg L-DOPS to 34 patients 1 h before dialysis prevented dialysis-induced hypotension and decreased the number of concurrent treatments required for hypotension. The signs and symptoms of hypotension were improved in 73.5% of the patients and persisted after dialysis in 64.7%. The preventive effect of L-DOPS was significantly more prominent in patients with predialysis systolic blood pressure less than 100 mmHg and in patients with non-diabetic nephropathy. L-DOPS appeared to be an effective and well-tolerated treatment for the prevention of dialysis-induced hypotension.
Human pepsinogens, the precursors of pepsin, originating from the stomach mucosa, are classified into two biochemically distinct groups, namely pepsinogen I (PG I) and pepsinogen II (PG II). We studied the serum levels of PGI and II in 51 normal volunteers, 23 chronic glomemlonephritis patients, 21 continuous ambulatory peritoneal dialysis (CAPD) patients and 40 hemodialysis patients. Serum pepsinogen levels were measured with a competitive binding double antibody radioimmunoassay. In the group of chronic glomemlonephritis patients, a positive correlation between the serum creatinine and the pepsinogen levels were found. The serum pepsinogen levels were remarkably elevated in CAPD and hemodialysis patients. The median levels of post-hemodialysis PGI(265.4 ± 165.2 ng/ml) and PG II (41.7 ± 38.0 ng/ml) were significantly higher than prehemodialysis values (PG I 207.4 ± 127.5 ng/ml, PG II 29.0 ± 16.6 ng/ml). Pepsinogen release by isolated gastric glands of guinea pigs was suppressed by guanidinosuccinic acid and was facilitated by calcium. The data suggest that both removal of guanidinosuccinic acid and infusion of calcium during hemodialysis contribute to the raised serum levels of these pepsinogens after hemodialysis.
Plasma atrial natriuretic peptide levels significantly decreased as the right and left atrial overloads decreased, and plasma brain natriuretic peptide levels did not significantly decrease after hemodialysis. Plasma brain natriuretic peptide levels were not significantly influenced by acute hemodynamic change, such as hemodialysis. However, plasma brain natriuretic peptide levels were significantly correlated with basic cardiac function.
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