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Biomedical subjects

H Holdaas

Publications and source records attributed to H Holdaas.

At least 55 records · Page 3Linked to original sources
PubMed1991

Rehabilitation and quality of life in diabetic patients after successful pancreas-kidney transplantation.

Twenty-seven Type I diabetic patients in end-stage renal failure were followed after combined pancreas-kidney transplantation. All patients received duct-occluded segmental pancreas grafts. Clinical progression of extrarenal diabetic complications was studied in 11 patients with long-term functioning pancreatic and renal transplants (Group 1), and in 16 patients who had lost pancreatic graft function, but retained renal graft function (Group 2). Pretransplant, extrarenal diabetic complications were equally distributed in the two groups. In the follow-up period, however, the progress of these complications was less severe in patients with functioning pancreatic transplants. No differences were found between the groups concerning rehabilitation, working capacity, need of help or hospital admittance. It is suggested that pancreas transplantation performed in an earlier stage of diabetes before serious complications have developed, would probably improve rehabilitation and quality of life in these patients.

Adult↗
PubMed1991

Effects of isradipine on renal function in cyclosporin-treated renal transplanted patients.

The renal effects of the calcium-channel antagonist isradipine were evaluated in cyclosporin A (CsA)-treated renal allografted patients more than 5 months after transplantation. Twelve patients with stable renal function were given placebo for 2 weeks and then isradipine 1.25 mg x 2 for 1 week and 2.5 mg x 2 for the next 3 weeks in an open trial. The CsA dose was unchanged during the study. Isradipine did not interfere with the pharmacokinetics of CsA as both whole blood trough and peak levels were unchanged. Isradipine reduced mean arterial blood pressure (MAP) from 117.0 +/- 1.8 to 106.3 +/- 1.9 mmHg (P less than 0.01). The renal effects were studied during water diuresis 1-3 h after drug intake. Para-aminohippurate clearance (CPAH) increased from 256.4 +/- 21.5 to 291.5 +/- 26.3 ml/min (P less than 0.05), renal vascular resistance was reduced by 21.5% (P less than 0.01) and inulin clearance (CIn) was unchanged. Fractional proximal reabsorption, calculated from lithium clearance (CLi), was reduced by 11.9% (P less than 0.01) by isradipine. Isradipine also reduced proximal reabsorption of sodium (APRNa) and increased distal sodium delivery (DDNa). Distal sodium reabsorption (ADRNa) and free-water clearance (CH2O) were significantly increased. Urinary excretion of enzymes and proteins was unchanged by isradipine.

Adult↗
PubMed1991

Lack of effect of the calcium antagonist isradipine on cyclosporine pharmacokinetics in renal transplant patients.

Hypertension has emerged as a frequent side effect in transplant recipients on effective doses of cyclosporine (CsA). To control hypertension in renal transplant patients, calcium channel blockers have been used; some of these, however, have been shown to cause significant increases in CsA levels. These findings point out that possible interactions of each calcium antagonist with CsA deserve investigation. We performed an open, placebo-controlled study in 12 stable renal transplant recipients to determine whether short-term isradipine influences CsA pharmacokinetics. All patients had mild to moderate hypertension and received triple immunosuppressive therapy with CsA, azathioprine, and prednisolone. Throughout a 4-week period of isradipine treatment, blood CsA levels (specific and nonspecific monoclonal antibodies) remained stable. The mean trough specific level was 121 +/- 14 micrograms/L following placebo, compared to 120 +/- 14 micrograms/L during isradipine. Corresponding non-specific values were 465 +/- 68 and 474 +/- 63 micrograms/L. Also, values for Cmax, AUC, and t1/2 were not significantly changed following 4 weeks of isradipine. Mean arterial pressure was significantly reduced at the end of the study. This study implies that isradipine does not influence CsA metabolism. Further studies should be carried out to determine its long-term effects on CsA pharmacokinetics and renal function in transplanted patients.

Adult↗
PubMed1991

Contrasting effects of lisinopril and nifedipine on albuminuria and tubular transport functions in insulin dependent diabetics with nephropathy.

An open, randomized, cross-over study was undertaken to assess the effects of lisinopril and nifedipine on albumin excretion, renal haemodynamics and segmental tubular reabsorption in overt diabetic nephropathy. The study consisted of a 4-week run-in period, a 3-week active treatment period, a 4-week wash-out period and a second 3-week active treatment period. Twelve patients with type 1 diabetes with albuminuria, mild to moderate hypertension and a serum creatinine level of less than 200 mumol l-1 were included. Lisinopril reduced albumin excretion from 1343 +/- 337 micrograms min-1 to 879 +/- 299 micrograms min-1 (P less than 0.01), whereas nifedipine was without effect, 1436 +/- 336 micrograms min-1 vs. 1319 +/- 342 micrograms min-1. Glomerular filtration rate (GFR) was unchanged by either drug. Both drugs increased effective renal plasma flow (ERPF) by about 20%. No differences between the drugs were observed with regard to their effect on renal haemodynamic parameters. By contrast, nifedipine exerted an inhibitory effect on several proximal tubular transport markers, whereas lisinopril was without effect. The different actions on tubular transport mechanisms exerted by lisinopril and nifedipine may contribute to the observed effect on albumin excretion.

Adult↗
PubMed1989

Long-term metabolic control in recipients of segmental-pancreas grafts with pancreaticoenterostomy or duct obstruction.

Metabolic control in recipients of segmental-pancreas grafts with pancreaticoenterostomy (performed in Stockholm) or duct obstruction by polymer injection (performed in Oslo) were compared. The recipients were uremic diabetic patients and also received a kidney from the same donor. Because the patient population in the two Scandinavian countries is very similar and the immunosuppressive protocols used are almost identical, such a comparison seemed reasonable. The number of patients available for study at 1, 2, and 3 yr was 22, 10, and 4, respectively, with duct injection and 28, 10, and 3 with pancreaticoenterostomy. The mean age of the patients was somewhat higher in the Oslo series. There were no significant differences regarding immunosuppression or kidney-graft function as estimated by serum creatinine at 1, 2, and 3 yr. No significant differences were found in fasting blood glucose, glycosylated hemoglobin, and intravenous glucose tolerance between the two groups at 1, 2, and 3 yr.

Adult↗
PubMed1986

Glomerulotubular balance during renal sympathetic stimulation.

In volume-expanded dogs receiving ethacrynic acid, a linear relationship, glomerulotubular balance (GTB), applies between the remaining sodium reabsorption and the glomerular filtration rate (GFR) during mechanical aortic constriction. To examine whether GTB applies during sympathetic stimulation, the GFR was progressively reduced by 70-75% in anaesthetized dogs by renal nerve stimulation, intrarenal norepinephrine infusion or by selective stimulation of alpha-adrenoceptors by intrarenal methoxamine infusion. Linear relationships (GTB) were obtained (r greater than 0.9). Reabsorption was not different during the various kinds of sympathetic stimulation, but less than during aortic constriction; the largest difference in NaCl reabsorption at comparable GFR amounted to 10-15% and was obtained 30-40% below control GFR, whereas inhibition of NaHCO3 reabsorption was uncertain. To inhibit NaHCO3 reabsorption and associated NaCl reabsorption in the proximal tubules, acetazolamide (30 mg kg-1) was administered instead of ethacrynic acid. No difference in reabsorption was observed at comparable GFR during norepinephrine infusion and mechanical aortic constriction. Hence, GTB applies during sympathetic stimulation. Compared with data obtained during aortic constriction, alpha-adrenergic stimulation reduces proximal reabsorption of NaCl and, possibly, NaHCO3 and exerts no effect on distal transcellular NaCl reabsorption.

Acetazolamide↗
PubMed1985

Haemodynamic conditions for renal PGE2 and renin release during alpha- and beta-adrenergic stimulation in dogs.

Constriction of the renal artery and infusion of an alpha-adrenergic agonist induce autoregulated vasodilation and increase prostaglandin E2 (PGE2) and renin release. The enhancement of renin release during autoregulated vasodilation might be mediated by prostaglandins. To examine this hypothesis, experiments were performed in three groups of anaesthetized dogs. In six dogs constriction of the renal artery to a perfusion pressure below the range of autoregulation raised renin release from 2 +/- 1 to 27 +/- 6 micrograms AI X min-1 and PGE2 release from 1 +/- 1 to 10 +/- 2 pmol X min-1. After administration of indomethacin (10 mg X kg-1 b.wt), PGE2 release was effectively blocked and constriction of the renal artery raised renin release only from 0.1 +/- 0.1 to 6 +/- 1 micrograms AI X min-1. During subsequent continuous infusion of a beta-adrenergic agonist, isoproterenol (0.2 micrograms X kg-1 X min-1), constriction of the renal artery raised renin release from 0.1 +/- 0.1 to 52 +/- 11 micrograms AI X min-1, although there was no rise in PGE2 release. In six dogs, intrarenal infusion of phenylephrine, an alpha- adrenergic agonist, increased PGE2 and renin release before, but not after, indomethacin administration. In six other dogs, phenylephrine infused during isoproterenol infusion increased renin release equally before and after indomethacin administration. Thus the enhancing effect of constricting the renal artery or infusing an alpha-adrenergic agonist is not dependent upon prostaglandins. We propose that autoregulated dilation enhances renin release whether the stimulatory agent is a prostaglandin or a beta-adrenergic agonist.

Adrenergic alpha-Agonists↗