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Biomedical subjects

A Innes

Publications and source records attributed to A Innes.

At least 37 records · Page 2Linked to original sources
PubMed1992

The short term effects of oral labetalol in patients with chronic renal disease and hypertension.

This double-blind, controlled, crossover study compared the effects on blood pressure control, glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) of labetalol, methyldopa and placebo in patients with chronic renal disease and hypertension. When compared with placebo, BP was significantly lower during treatment with both labetalol and methyldopa (P greater than 0.05) but did not differ significantly between the two active treatment periods; post-exercise heart rates were also significantly lower on labetalol than placebo (P less than 0.05). After treatment with labetalol, ERPF was significantly greater than with the placebo (P less than 0.05) but did not differ significantly between the active treatments. GFR did not differ significantly between the three groups. No significant differences were observed in haematology or liver function test results on labetalol compared with placebo. Labetalol is a safe and effective antihypertensive in patients with hypertension associated with chronic renal disease. In the short term it leads to an increase in ERPF which may be beneficial for such patients.

Administration, Oral↗
PubMed1991

Post-transplant erythrocytosis and immunosuppression with cyclosporin: a case-control study.

Review of 142 renal transplant recipients treated with cyclosporin and prednisolone revealed 23 patients with post-transplant erythrocytosis. The clinical characteristics of these patients were compared with 23 cyclosporin/prednisolone-treated control subjects matched for age, sex, and duration of transplant. Erythrocytosis developed between 6 weeks and 30 months (median 12 months) after transplant. It persisted in 16 patients and resolved spontaneously in five. In two patients the decrease in haematocrit was associated with acute leukaemia in one and sudden deterioration of renal function in the other. In the study group there were fewer HLA (A, B and DR) mismatches (P less than 0.05) and greater pretransplant haematocrit (P less than 0.01) than in the control group. Other clinical factors--previous allografts, panel reactive cytotoxic antibodies, duration and type of dialysis, transplant function, pre- and post-transplant blood pressure, number of rejection episodes, cyclosporin concentration and dose, smoking habits and use of diuretics--did not differ significantly between the two groups. In our experience, erythrocytosis in cyclosporin-treated patients is a relatively common phenomenon and does not, in general, resolve spontaneously. It is unrelated to transplant function or rejection episodes but affects patients with well-matched kidneys and elevated pretransplant haematocrit values.

Adult↗
PubMed1991

Very late recurrence of renal vasculitis.

We report a case of renal vasculitis with a relapse occurring 9 and a half years after the original presentation. The plasma creatinine six months before relapse was only 118 mumol/l. During the initial illness there was histological evidence of glomerular damage but at the time of relapse renal biopsy showed the remaining glomeruli to be normal with the destructive process causing fibrinoid necrosis of arteries.

Biopsy↗
PubMed1990

The detection of antibodies in pregnancy: a comparison of two assay systems.

In this study we have compared the ability of two assay systems, erythrocyte antibody rosette inhibition (EAI) and cellular enzyme-linked immunospecific assay (CELISA) to detect maternal alloantibody activity during pregnancy. Antibody activity to antigens on paternal lymphocytes was present in nine of 23 primigravid sera tested by EAI and in seven of 23 by CELISA. In multiparous sera, antibodies directed to paternal lymphocytes were detected in 11 of 15 individuals by EAI and in six of 15 by CELISA. The techniques correlated significantly when assaying the humoral response in sera from multiparous women. The lack of correlation when assaying primigravid sera suggests that both assays encounter difficulty in detecting the low titres of antibodies present.

Enzyme-Linked Immunosorbent Assay↗
PubMed1989

Renal transplantation: cyclosporin A and antibody development after donor-specific transfusion.

The survival of a one haplotype, mismatched living-related renal allograft is improved by donor specific transfusion (DST) before transplantation although the mechanism is unclear. The major risk of DST is sensitization of the recipient to donor lymphocytes precluding transplantation. Fifty prospective recipients of a living related transplant received either DST with cyclosporin A (group I) or DST alone (group II). Persistent donor sensitization precluding transplantation occurred in no patients in group I but in six in group II (P less than 0.05). Ten of 14 of those who developed donor cytotoxicity had previously been pregnant or received greater than or equal to 10 third party transfusions compared with 11 of 36 without such a history (P less than 0.05). Alloantibodies detected by a cellular ELISA developed following DST in 29% patients and antiidiotypic antibodies detected by the short antiidiotypic assay (SAA) in 36%; antiidiotypic activity occurred more frequently in those given cyclosporin A (P less than 0.02). Potentiating activity in the SAA which occurred in sera from six patients after DST had no influence on transplant outcome. Persistent sensitization, particularly in potential transplant recipients who have been pregnant or received many transfusions, can be prevented by giving cyclosporin A with DST; the mechanisms of this effect may be the induction of antiidiotypic antibodies. Both alloantibodies and antiidiotypic antibodies are induced by DST and may protect a subsequent renal allograft from the specific donor.

Antibodies↗
PubMed1989

Fetus as an allograft: noncytotoxic maternal antibodies to HLA-linked paternal antigens.

A cellular enzyme-linked immunospecific assay (CELISA) was used to monitor maternal humoral responses in human pregnancy. Non-cytotoxic IgG antibodies to paternal lymphocytes were detected in sera from 6 of 20 normal first trimester primigravidae and 6 of 13 multiparae. No antibody activity against lymphocytes from their partners was detected in sera from any of the 15 nulliparous women. The differences in antibody response between primigravidae and nulliparae (P = 0.024) and between multiparae and nulliparae (P = 0.005) were statistically significant. Lymphocytotoic antibodies to T- and B-lymphocytes were present in sera from three multiparae, but from none of the women in the other two groups. Family studies indicated that the non-cytotoxic pregnancy-associated maternal antibodies were directed to HLA-linked antigens (P less than 0.001). Evidence obtained using cell panels and platelet absorption suggested, however, that these antibodies were not directed to the currently recognized HLA specificities (HLA-A, -B, -C, or -DR).

Enzyme-Linked Immunosorbent Assay↗
PubMed1988

The alloantibody response to semiallogeneic pregnancy in the rat. I. Alloantibodies in sera and placental eluates directed to RT1A antigens.

Maternal alloantibodies to paternal cells were monitored by cellular ELISA, the indirect hemagglutination and erythrocyte antibody rosette inhibition assays in sera and placental eluates from primigravid and multigravid inbred rats. In primigravid animals, antibodies in sera were routinely detected only by the indirect hemagglutination assay and were of low titer; weak antibody activity was detectable only by indirect hemagglutination in 1 of the 8 placental eluates assayed from these animals. Alloantibodies in high titer were present in sera and placental eluates from multigravid rats and were found to be directed predominantly to the RT1A (class I MHC) antigens of the paternal strain. These data provide no support for the hypothesis that the difficulty in detecting maternal antibodies during a 1st pregnancy is due to their preferential binding to antigenic determinants expressed on the placenta.

Animals↗
PubMed1988

Human placenta--an antibody sponge?

Maternal IgG antibodies in sera and placenta eluates were studied by a cellular enzyme-linked immunosorbent assay (CELISA) method. Antibodies were not detectable in any of the serum samples obtained before or after delivery from nine normal primigravid women. Antibody activity was, however, present in five of nine placental eluates and two of nine neonatal sera tested in CELISA. Lymphocytotoxic antibodies were not detected in any of the samples tested. These results support the concept that the absence of antibody activity in maternal sera may be caused by the immunosorbent effect of the placenta.

Birth Weight↗
PubMed1988

Antiidiotypic activity in sera from sensitised potential transplant recipients.

Antiidiotypic activity was determined in non-cytotoxic sera from highly sensitised dialysis patients who previously possessed broad-spectrum lymphocytotoxic antibodies. At least four non-cytotoxic sera from six transfused patients were tested in the short antiidiotypic antibody assay against lymphocytes known to be lysed by cytotoxic sera from the same patient. Of 87 sera/cell combinations studied, antiidiotypic activity was detected in 42 (48%). Antiidiotypic activity was present in IgG fractions and F(ab')2 fragments of two active sera. These results indicate that non-cytotoxic sera from patients who were once highly sensitised possess antiidiotypic activity. Fluctuating levels of lymphocytotoxic antibodies frequently encountered in sera from dialysis patients may be explained at least in part by the development of antiidiotypic antibodies.

Adolescent↗
PubMed1988

The effect of dietary protein restriction on high dose gentamicin nephrotoxicity in rats.

Gentamicin (120 mg/kg/day) was administered for 10 days to Sprague-Dawley rats given either a low (5% w/w) or normal (18% w/w) protein diet. Serum protein concentrations remained normal in all rats during the study. Nephrotoxicity was slightly less severe in rats fed a low protein diet as shown by: (i) a mean creatinine clearance rate (14 +/- 4 ml/min) which was significantly greater than that (8 +/- 3 ml/min) recorded from the rats maintained on the normal diet (P less than 0.05); (ii) lower activities of urinary N-acetyl-beta-D glucosaminidase (NAG); and (iii) less marked histological changes. Mean tissue concentrations of gentamicin were considerably lower in both renal cortex and medulla from rats maintained on the low protein diet than from those animals on the normal diet (P less than 0.01 and P less than 0.05, respectively). These differences were, however, not reflected in the mean trough serum gentamicin concentrations which were not significantly different between the two groups. These results are discussed in relation to the proposed mechanisms involved in gentamicin-induced nephrotoxicity.

Acetylglucosaminidase↗