Chronic Renal Failure Subjects Research Articles

Promotion of lymphocyte blastogenesis by hemodialysate of chronic renal failure.

Effects of hemodialysate of patients with chronic renal failure (CRF) on blastogenesis of human peripheral blood lymphocytes in the presence of concanavalin A or phytohemagglutinin was investigated. Hemodialysates from 11 CRF patients significantly promoted lymphocyte blastogenesis when compared with control dialysis fluids (p less than 0.01). The strongest activity (39% promotion of the lymphocyte blastogenesis) was observed with a hemodialysate obtained at 0.5 h after beginning dialysis. The activity decreased thereafter. On the contrary, the blastogenesis-promoting activity in plasma decreased significantly after hemodialysis (p less than 0.01, n = 11). To further confirm the presence of low-molecular-weight factor(s) in CRF, ultrafiltration of plasma obtained from CRF and healthy subjects was conducted using a membrane filter with a molecular cutoff of 3,000 D. The filtrate of CRF plasma significantly promoted lymphocyte blastogenesis when compared to that of healthy subjects (p less than 0.01). Heat treatment (100 degrees C, 40 min) did not abolish the activity of the hemodialysate. None of the drugs taken by the patients nor creatinine accumulated in CRF promoted the lymphocyte blastogenesis. Chromatographic analysis of a hemodialysate demonstrated several peaks which were absent in the control dialysis fluid. These results showed the presence of a novel lymphocyte-stimulating factor(s) in CRF, which is heat stable and has a low molecular weight (less than 3,000 D).

Role of altered prednisolone-specific lymphocyte sensitivity in chronic renal failure as a pharmacodynamic marker of acute allograft rejection after kidney transplantation

The effects of four immunosuppressive agents on the in vitro blastogenesis of peripheral blood lymphocytes activated by concanavalin A have been studied using cells from 26 healthy subjects, 34 patients with chronic renal failure (CRF) and 30 kidney transplant recipients. Differences in lymphocyte sensitivity to prednisolone between the healthy subjects and the CRF patients were statistically significant (P less than 0.0002), with impaired sensitivity in CRF. Impaired lymphocyte sensitivity occurred in 3.8% and 52.9% of the healthy and CRF subjects, respectively. Lymphocyte sensitivity to prednisolone, both preoperatively and 3 months post-operatively, was strongly correlated with early allograft rejection during co-administration of prednisolone with cyclosporin or azathioprine. Lymphocyte sensitivity to cyclosporin, azathioprine, and mizoribine in CRF was not significantly less than that in healthy subjects. Since the pharmacokinetics of prednisolone are little altered in renal transplantation, it is concluded that lymphocyte sensitivity specific to prednisolone may be a pharmacodynamic marker characteristic of successful graft survival in patients with histo-incompatibility and/or drug resistance.

Vitamin D3 Metabolites in Chronic Renal Failure and After Renal Transplantation

Circulating vitamin D3 metabolites were measured in 31 adult patients with chronic renal failure and 31 adults between 3 and 30 months after renal transplantation. No subject excreted over 1 g urinary protein daily nor received vitamin D or its metabolites. There was a positive correlation between 1,25(OH)2D3 and GFR between 15 and 90 ml/min in both chronic renal failure (r = 0.60, P less than 0.001) and transplant subjects (r = 0.49, P less than 0.01) and between 1,25(OH)2D3 and 25(OH)D3 after transplant (r = 0.69, P less than 0.001), but not in chronic renal failure (r = 0.22, P = ns). There was a weak inverse correlation between 1,25(OH)2D3 and serum phosphate in chronic renal failure (r = 0.36, P less than 0.05) but not post transplant (r = 0.03, P = ns). Compared with 1,25(OH)2D3 concentrations in 16 normal subjects (mean +/- SEM: 39.5 +/- 1.9 pg/ml), chronic renal failure subjects with mild renal impairment (GFR 45-90 ml/min, mean: 61.5 +/- 3.3 ml/min, n = 17) had reduced 1,25(OH)2D3 (28.9 +/- 2.7 pg/ml, P less than 0.01). In transplant subjects with mild impairment (GFR 45-90 ml/min, mean: 61.4 +/- 3.7), 1,25(OH)2D3 was positively (r = 0.79, P less than 0.001) and iPTH inversely correlated (r = 0.51, P less than 0.05) with 25(OH)D3. In each of nine such subjects studied, seasonal variations in 1,25(OH)2D3 (P less than 0.001) and PTH (P less than 0.05, 1-tailed test), as well as in 25(OH)D3 and 24,25(OH)2D3, were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Gastric secretion kinetics in chronic renal failure.

A dose-response gastric secretion test was performed in 87 nondialyzed patients with chronic renal failure (CRF) and in 87 age- and sex-matched controls without renal disease. Twenty-six of the CRF patients were reexamined, 18 undergoing regular hemodialysis and 8 after successful transplantation. The gastric acidity, acid output, and volume output of the nondialyzed CRF subjects were decreased when compared with those of the controls or of patients in the posttransplant phase. This decrease was more marked with low than with high stimulant doses. The decrease in acid output was significantly greater than that in volume output. Moreover, when compared with the dialysis phase the nondialyzed patients had lowered gastric acidity and acid output, but no decrease in volume output was evident. The results indicate that there is an inhibition of gastric secretion in CRF. This inhibition is dependent on strength of stimulation and is abolished by active treatment of CRF, more clearly by transplantation than by maintenance dialysis. In addition, the inhibition is predominantly on the secretion of acid, the output of gastric juice being less affected.

Caries resistance in children with chronic renal failure: plaque pH, salivary pH, and salivary composition.

We studied properties of saliva and of dental plaque which affect the caries process in an effort to understand the low prevalence of caries in patients with chronic renal failure. Plaque pH, before and following carbohydrate exposure, saliva pH, and saliva composition were evaluated in children and adolescents with chronic renal failure (n = 10) and successful renal transplantation (n = 11), and in two comparison groups of healthy children with few caries (n = 15) and numerous caries (n = 15). Salivary urea nitrogen concentration was elevated in all subjects with elevated serum urea nitrogen concentration. Chronic renal failure subjects had significantly higher salivary urea nitrogen concentration than transplanted subjects. Plaque pH correlated directly with salivary urea nitrogen concentration and was significantly more alkaline in chronic renal failure than transplant or comparison groups. Salivary urea nitrogen concentration accounted for the majority of variability in plaque pH; salivary pH and salivary phosphorous contributed negligibly. Absolute pH drop following carbohydrate exposure did not differ among groups, but because baseline plaque pH was elevated for chronic renal failure subjects, minimum pH did not attain cariogenic levels. Our data support the hypothesis that the relative paucity of caries in patients with chronic renal failure results from alteration of plaque by metabolic end products of urea metabolism. Our data further suggest that transplanted patients whose renal function is normal may be at increased risk of caries, especially if enamel hypoplasia is present and oral hygiene is poor.