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Biomedical subjects

C Grönhagen-Riska

Publications and source records attributed to C Grönhagen-Riska.

At least 91 records · Page 5Linked to original sources
PubMed1989

Clinical testing of a new, low-flux polysulfone membrane. Results of a 26-week study.

In a 6-month study, a new hollow-fiber (HF) dialyzer with a modified polysulfone (PS) membrane was evaluated in 12 hemodialysis patients. Seven of them had previously used a cuprophane (CU) HF and five a polymethylmethacrylate (PMMA) HF dialyzer. The PS dialyzer reduced the concentration of serum creatinine by 54 +/- 5% (SD), that of urea by 59 +/- 5%, that of urate by 62 +/- 6% and that of phosphate by 40 +/- 12%; the mean urea index (Kt/V) was 0.9. Heparin consumption diminished with the PS dialyzer compared with the PMMA dialyzer. The serum predialysis beta-2-microglobulin (beta 2M) concentrations rose by 5.4 mg/l (mean). The intradialytic beta 2M measurements showed insignificant changes in all the membranes studied. Eosinophilia was initially observed in 4/12 (33%) of the patients, all using an ethylene oxide (ETO)-sterilized CU dialyzer. At the end of the study this figure had decreased to 1/12 (8%). The serum IgE concentrations also decreased significantly. IgE class antibodies to ETO were initially detected in 2 patients. The level decreased clearly in 1 of them after switching to the PS dialyzer. The new PS dialyzer was found to be effective, possibly less allergenic and, owing to its moderate hydraulic permeability, suitable for routine dialyses.

Adult↗
PubMed1989

Mechanisms of insulin resistance after kidney transplantation.

In order to study the effect of corticosteroids on energy metabolism in immunosuppressed patients after kidney transplantation, we have examined glucose utilization, energy expenditure, and lean body mass in 10 kidney-transplanted patients receiving steroids (methylprednisolone 8.2 +/- 1.5 mg/day) and in 10 healthy age- and weight-matched control subjects. Glucose utilization was measured during euglycemic insulin clamp in combination with indirect calorimetry and infusion of [3H-3]-glucose, while beta-cell function was measured during a hyperglycemic clamp. The kidney-transplanted patients were resistant to the glucoregulatory effect of insulin, as demonstrated by a 25% reduction in total glucose disposal compared to control subjects. This defect was almost completely accounted for by a defect in storage of glucose as glycogen (3.3 +/- 0.5 vs. 5.0 +/- 0.5 mg/kg LBM min; P less than 0.05). The reduction in nonoxidative glucose disposal was associated with reduced lean body mass and incapacity to release energy as heat after infusion of insulin, i.e. thermogenic defect. In contrast, oxidation of glucose and lipids was not influenced by steroid therapy. Furthermore, suppression of hepatic glucose production was normal, and insulin secretion was normally enhanced in relation to the degree of insulin resistance in the steroid-treated patients. In conclusion, steroid-induced insulin resistance in kidney-transplanted patients is due to alterations in the nonoxidative pathway of glucose metabolism. These findings raise the question of whether steroid therapy directly influences glycogen synthase in man.

Adrenal Cortex Hormones↗
PubMed1988

Increased levels of immunoreactive plasma renin substrate during infectious peritonitis in patients on continuous ambulatory peritoneal dialysis.

1. Renin substrate (RS) and certain serine protease inhibitors share structural homology. Previous studies have shown that RS may be an acute-phase protein. 2. This prospective study was carried out to monitor plasma RS and other components of the renin-angiotensin system and acute-phase proteins during infectious peritonitis in patients on continuous ambulatory peritoneal dialysis. 3. RS was measured by both an enzymatic assay and a direct radioimmunoassay. An enzymatic assay measures intact RS only, whereas a direct radioimmunoassay measures both intact RS, capable of releasing angiotensin I and des-(angiotensin I)-RS, the residue of RS after cleavage of angiotensin I. 4. RS determined by direct radioimmunoassay increased (P less than 0.001) during acute inflammation (peritonitis), whereas neither RS measured enzymatically nor plasma renin activity changed significantly. 5. Our observation points to RS being an acute-phase protein in man. 6. Serum angiotensin-converting enzyme was measured by both an enzymatic and an inhibitor-binding assay. Both assays showed decreased levels of angiotensin-converting enzyme during acute inflammation.

Acute-Phase Proteins↗
PubMed1988

Direct radio-immunoassay of renin substrate: effect of converting enzyme inhibition.

A direct radio-immunoassay (RIA) for renin substrate (RS) was compared to the enzymatic (indirect) assay, which measures intact RS only, whereas a direct assay measures both intact RS and des-angiotensin I-RS. In normal subjects, a significant, albeit weak, correlation between the methods was noticed. In hypertensive patients with different levels of plasma renin activity (PRA), RS concentration measured by both assays increased with increasing PRA, and for patients with PRA greater than 10 micrograms AI/l/h, the direct assay gave significantly higher RS values (55%), compared to the enzymatic assay. This indicates consumption of RS by increasing plasma renin and increasing production rate of RS with increasing PRA, of potential importance in the pathogenesis of hypertension. In 11 patients with renovascular hypertension, treatment with the angiotensin-converting enzyme (ACE) inhibitor, lisinopril, resulted in a significant increase in PRA, accompanied by a decrease in RS measured by the enzymatic assay. Lowered plasma RS concentration, by reduction of the velocity of the renin-RS reaction, will distort and invalidate results of PRA determination during treatment with ACE inhibitory compounds. No change in RS measured by direct RIA was noticed, however. The results suggest that ACE inhibition may not have an effect upon RS production and that its effect on plasma RS is limited to a reduction of intact RS measured by the enzymatic assay.

Angiotensin I↗
PubMed1987

Competitive inhibitor binding assay (CIBA) of captopril and other ACE inhibitors.

We describe a new principle for measuring concentrations of pharmacologically active captopril or other angiotensin-converting enzyme (ACE) inhibitors in blood. Serum is incubated with 125I-labelled ACE inhibitor (351A, a p-hydroxy-benzamidine derivative of N-(1-carboxy-3-phenylpropyl)-L-lysyl-L-proline) in a nonequilibrated system, in which label and ACE inhibitor compete for binding to added serum ACE. Free label is separated by adsorption to coated charcoal. Sensitivity for captopril is 2 ng/ml, and for other tested ACE inhibitors 0.25-5 ng/ml. Results in healthy volunteers showed rapid absorption of captopril with maximal concentration of active drug within 1 h, and fast disappearance within 2.5 h. Stability of captopril was improved by immediate 1:100 dilution of blood samples with assay buffer. In spite of this precaution, analysis should be performed within two days to avoid loss of active drug due to polymerization and protein binding. Samples of other tested ACE inhibitors can be frozen and later analyzed at convenience. The new principle is simple, sensitive, and specific.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1987

Long-term monotherapy with lisinopril in renovascular hypertension.

Eleven patients (five women and six men), aged 24-60 years, were treated with the angiotensin-converting enzyme (ACE) inhibitor, lisinopril, with a once-daily dose as the only antihypertensive treatment. Renal artery stenosis was unilateral in eight patients and bilateral in the remaining three. Fibromuscular dysplasia was present in seven patients, and renal arteriosclerotic narrowing was present in the remaining four. All completed a 6-month treatment and went on to a long-term treatment program for a final 24 months, now completed by five patients. Mean pretreatment blood pressure, 187 +/- 19/112 +/- 5 mm Hg (systolic/diastolic; mean +/- SD), was reduced to 148/87 following the drug titration period (1 week), and the same antihypertensive control was maintained throughout the study. Plasma concentration of angiotensin II, aldosterone, and serum ACE activity were effectively reduced for at least 24 h following drug administration. Serum concentrations of lisinopril varied individually and rose in two patients with moderate renal failure. Renal function was well maintained, and control renography revealed no worsening of renal artery stenosis or renal function. The drug was well tolerated without side effects other than cough in one patient. We conclude that lisinopril monotherapy is highly effective in renovascular hypertension. Drug safety was demonstrated by the lack of serious side effects.

Adult↗
PubMed1987

Outcome of patients with diabetic nephropathy after kidney transplantation.

During the period 1973-1983, 1,014 patients with end stage renal failure received a kidney graft at the Helsinki University Central Hospital. As a consequence of diabetic nephropathy, 163 of them (16%) developed renal failure. Ten diabetic (6%) and 72 non-diabetic (9%) patients received grafts from a living donor. One-year patient survival did not differ between diabetic and non-diabetic patients (76% and 79%, respectively). From the second post-transplant year onwards patient survival was worse in diabetic than in non-diabetic patients. The two groups did not differ with respect to graft survival. Sixty-two diabetic patients (38%) died during the follow-up period, with myocardial infarction as the most common cause of death (31%), followed by infection (15%) and cerebral stroke (13%). Seven myocardial infarctions out of 19 occurred within three months of transplantation. However, significantly more fatal and non-fatal myocardial infarctions were observed in post-transplant patients who had returned to dialysis therapy than in patients with a functioning kidney graft. Blindness did not influence the outcome of transplantation. Nor did the transplantation significantly affect the course of this diabetic complication. In conclusion, although the early success rate of kidney transplantation in our study population was acceptable, the later outcome was poor, mainly due to advanced disease-related complications.

Cardiovascular Diseases↗
PubMed1987

Interstitial mononuclear cell infiltration in Heymann nephritis.

Interstitial mononuclear cell infiltration in rats during the development of autoimmune Heymann nephritis (HN) was studied using the fine-needle aspiration biopsy (FNAB) technique. The results were compared with those obtained by immunohistochemical studies of infiltrating T helper (T-h) and T suppressor/cytotoxic (T-s) cells, and with traditional histopathological and immunofluorescence examinations. Three weeks after initial immunization with isolated tubular brush border antigen, when the histopathological finding was quite normal, FNAB revealed increased numbers of interstitial blast cells, large granular lymphocytes and activated lymphocytes. These increases reached significant levels 2 weeks after a booster injection and were still prominent in a few rats with manifest membranous glomerulonephritis (MGN) and proteinuria 14 weeks after initial immunization. Immunohistochemical staining 3 weeks after immunization showed a significant increase in T-h cells in peritubular regions. Infiltration decreased successively 2 weeks after the booster and during manifest MGN. On the other hand, the mean number of cortically infiltrating T-s cells successively increased during the course of the study and this increase had reached a statistically significant level 2 weeks after the booster. Prominent T-s infiltration appeared in a few rats 2 weeks after the booster and when MGN was histopathologically manifest, and it was then associated with histopathologically detectable interstitial mononuclear infiltration and also with blast cell infiltration in FNAB. Our results suggest linkage between tubulointerstitial lesions in HN and cell-mediated immunoreactivity, and that severe interstitial inflammation is associated with T-s cell infiltration. Cytological interpretation indicated that infiltrating blast cells were plasmablasts, which may imply local antibody production, especially since anti-brush border antibody titres and blast cell infiltration simultaneously reached maximum levels 2 weeks after the booster.

Animals↗
PubMed1987

Renal mononuclear inflammatory cell populations in membranous glomerulonephritis: a fine-needle aspiration biopsy study.

Fine-needle aspiration biopsy (FNAB) technique was applied to the detection of alterations in renal inflammatory cell subsets in seven healthy control persons and 24 patients with membranous glomerulonephritis (MGN). Eighteen of the patients had nephrotic syndrome, and the rest had either persistent proteinuria or remission of the disease. Only one patient showed impaired renal function. Compared with the controls, FNAB revealed a significantly (p less than 0.01) increased number of mononuclear inflammatory cells (MIC, the sum in increment percentages of lymphocytes and monocytes) in MGN. This was mainly due to relative lymphocytosis; the number of monocytes was high particularly in patients with daily urine protein excretion in excess of 5 g. The duration of the disease did not clearly correlate with the degree of lympho- or monocytosis. In nine patients the results of the renal needle biopsy and FNAB could be compared. Biopsy revealed signs of MIC infiltration in 5/9 patients and FNAB in 7/9 patients. T-lymphocyte subsets in FNAB and peripheral blood were analyzed using monoclonal antibodies and indirect immunoperoxidase technique. The OKT4/OKT8 ratio in FNAB was 0.96 +/- 0.07 (s.e.m.) in patients and 1.49 +/- 0.12 in controls (p less than 0.01). In peripheral blood these ratios were 0.8 +/- 0.07 and 1.43 +/- 0.13 (p less than 0.001), respectively. The alterations were due to a decreased number of OKT4 positive lymphocytes. These studies suggest an associated interstitial accumulation of MIC and an imbalance between T helper/inducer and T suppressor/cytotoxic cells in MGN.

Adult↗
PubMed1986

Cerebrospinal fluid lysozyme and beta 2-microglobulin in neurosarcoidosis.

The levels of lysozyme (LZM) and beta 2-microglobulin (beta 2m) were measured in the cerebrospinal fluid (CSF) and serum of 32 patients with sarcoidosis, 20 of whom had neurosarcoidosis. LZM was analyzed by a new radioimmunoassay (RIA) modification. CSF LZM was elevated in 15 of 20 patients with neurosarcoidosis but in only 4 of 12 patients with extraneural sarcoidosis. CSF beta 2m values were elevated in 13 of 19 and in one of 11 patients, respectively. In neurosarcoidosis, both CSF LZM and beta 2m correlated to CSF leucocytes but not significantly to CSF albumin thus suggesting that LZM and beta 2m were secreted from cells within the central nervous system (CNS). In patients with sarcoidosis, elevations of CSF LZM and beta 2m revealed disease activity in the CNS. Both analyses were also useful in the follow-up of neurosarcoidosis.

Adult↗
PubMed1986

Competitive inhibitor binding assay (CIBA) of ACE inhibitors.

We describe a new principle for measuring concentrations of pharmacologically active captopril or other angiotensin-converting enzyme (ACE) inhibitors in blood. Serum is incubated with 125-I-labeled ACE inhibitor (substance 351A, a lisinopril analogue, Merck Sharp & Dohme) in a nonequilibrated system, in which label and ACE inhibitor compete for binding to added serum ACE. Free label is separated by adsorption to coated charcoal. Concentration of captopril or other ACE inhibitor is calculated from a standard curve. Results in healthy volunteers showed rapid absorption of captopril with maximal concentration of active drug within 1 h, and fast disappearance within 2.5 h. Stability of captopril was improved by immediate 1:100 dilution of blood samples with assay buffer. In spite of this precaution, analysis should be performed within two days to avoid loss of active drug due to polymerization and protein binding. Samples of other tested ACE inhibitors can be frozen and later analyzed at convenience. The new principle is simple, sensitive, and specific.

Angiotensin-Converting Enzyme Inhibitors↗