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Biomedical subjects

C Grönhagen-Riska

Publications and source records attributed to C Grönhagen-Riska.

At least 55 records · Page 3Linked to original sources

Serological response to Chlamydia pneumoniae in patients with sarcoidosis.

The antigen-specific serological response to Chlamydia pneumoniae was studied in 24 patients with sarcoidosis and compared to that seen in acute C. pneumoniae respiratory infection. By the micro-immunofluorescence test, five sarcoidosis patients had acute antibody, 15 had chronic antibody and four had no antibody against C. pneumoniae. By enzyme immunoassay, 20 sarcoidosis patients had antibody against ReLPS but that cross-reacts with chlamydial LPS. Immunoblot analysis of sera using purified C. pneumoniae elementary bodies showed that recognition of the 40 kDa C. pneumoniae major outer membrane protein was rare (20%). Reactivities with proteins with Mw of 42 K (70%), 60 K (65%), 98 K (55%) and 52 K (50%) were often noted. To study reactivity of chlamydial HSP 60 in sarcoidosis sera, sarkosyl-soluble (contains the 60 kDa HSP) and sarkosyl-insoluble (contains the 60 kDa structural protein) fractions of C. pneumoniae elementary bodies were prepared. The 60 kDa structural protein was recognized with equal frequency by sera from patients with sarcoidosis and acute respiratory infection, while the HSP 60 was more frequently recognized by sera with acute respiratory infection than sarcoidosis. Recombinant fusion proteins expressed from pGEX-2T containing overlapping DNA fragments of the C. pneumoniae 60 kDa HSP gene were purified. Different recognition patterns were identified for sera from sarcoidosis patients and from patients with acute C. pneumoniae respiratory infection.

Adult↗

Identification of 17 mutations in ten exons in the COL4A5 collagen gene, but no mutations found in four exons in COL4A6: a study of 250 patients with hematuria and suspected of having Alport syndrome.

Conditions for polymerase chain-reaction amplification of ten exon regions (Exons 3, 7, 11 through 13, and 15 through 19) of the collagen COL4A5 gene and four exon regions (Exons 2, and 12 through 14) of the COL4A6 gene were sequenced and established in this study. These Type IV collagen genes contain 51 and 48 exons, respectively. The sequences of these exons were determined in the two genes in 250 male patients with hematuria and suspected Alport syndrome. Seventeen mutations were found in nine of the ten exons studied in the COL4A5 gene in 17 patients, whereas no mutations were identified in COL4A6. One mutation was identical in two patients known to be unrelated. The results indicate that mutations in COL4A5 that leading to renal failure are more frequent than those involved in classic Alport syndrome, and also that mutations in COL4A6 are not likely to cause this disease. Furthermore, mutations in COL4A5 are distributed quite randomly and no "hot spots" were found.

Adolescent↗

Iron availability is transiently improved by intravenous iron medication in patients on chronic hemodialysis.

Iron deficiency is common in hemodialysis patients, particularly if they are on recombinant human erythropoietin (rHuEPO) therapy. Ten anemic patients (hemoglobin concentration 89 +/- 2.2 g/l, mean +/- SEM) on hemodialysis with either storage (serum-ferritin < 60 mg/l) and/or functional (S-transferrin saturation < or = 17%) iron deficiency were followed for 5 weeks. During the first 3 weeks they were given 100 mg of iron dextran on 10 consecutive dialysis sessions. Half of the patients were concomitantly treated with rHuEPO. Iron therapy resulted in a rapid elevation in serum transferrin iron saturation from 11 +/- 1.5% to 80 +/- 7.2% (p < 0.0001), but it decreased to pre-treatment levels within 2 weeks after discontinuation of iron therapy. Serum ferritin concentration increased from 157 +/- 73 mg/l to 434 +/- 105 mg/l during iron therapy (p < 0.0001). In spite of this only 4 patients (2 rHuEPO treated) responded and had a hemoglobin increment > 10 g/l. In the whole group serum transferrin receptor (TfR) levels remained stable, but increased after the cessation of iron dextran only in the rHuEPO treated patients (p < 0.01). In the responders the TfR levels were higher during iron therapy than in the nonresponders (p < 0.02). In an attempt to explain the resistance to iron therapy, serum concentrations of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1b (IL-1b) were also analyzed.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Urinary excretion of cytokines and complement SC5b-9 in idiopathic membranous glomerulonephritis.

Idiopathic membranous glomerulonephritis (iMGN) has previously been shown to be associated with urinary excretion of terminal complement complexes while increased urinary levels of cytokines have been reported in mesangial proliferative glomerulonephritis. In the present cross-sectional study urinary excretion of IL-1 beta, TNF-alpha, IL-6, and soluble C5b-9 (SC5b-9) was examined for 23 patients with iMGN, 16 patients with diabetic nephropathy (DNP), and 17 healthy subjects. IL-1 beta excretion (pg/mg crea) was significantly higher in iMGN patients (375, range 162-11,000) than in DNP patients (39, range 22-59, P < 0.001) or healthy controls (151, range 23-481, P < 0.001). TNF-alpha excretion rate (pg/mg crea) was clearly higher (38, range 21-700) in iMGN patients than in DNP patients (14, range 8-52, P < 0.001) or healthy subjects (11, range 7-26, P < 0.001). Median IL-6 excretion (pg/mg crea) was only marginally higher in iMGN patients (73, range 0-850) than in healthy subjects (64, range 3-158, P = 0.02) but significantly higher than in DNP patients (29, range 17-47, P < 0.001). No significant correlation with corresponding serum values was observed for urinary IL-6 or TNF-alpha excretion. Urinary IL-1 beta and TNF-alpha correlated with decreased renal function. Five of 23 patients showed progression of iMGN over a follow-up of 6 months. The excretion of all cytokines, TNF-alpha in particular, was significantly higher in patients with a progressive disease than in the other patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Long-term survival in idiopathic membranous glomerulonephritis: can the course be clinically predicted?

72 adult patients with idiopathic membranous glomerulonephritis (iMGN), 92% having proteinuria 3 g/24 h or more, were studied for the clinical evolution of the disease and factors which might be involved in the development of chronic renal insufficiency (CRI). At 10 years, 46% were in complete or partial remission, 4% had the nephrotic syndrome (NS), 26% had some degree of CRI, and 24% were dead or started on dialysis. The actuarial patient and kidney survival rates were 80% and 64%, respectively at 10 years. Patient survival rate was not affected by gender, age (after adjustment for age- and sex-matched population) or the severity of NS at diagnosis. 20 patients showed CRI and apart from the more frequent (p < 0.05) presence of CRI at diagnosis, no clinical features discriminated them from those having intact renal function. Furthermore, no clinical factors at diagnosis predicted the final renal function among the 72 patients. However, it appeared that the evolution of clinical status of iMGN was rapid CRI appearing 1.4 (median, range from 0 to 15.1) years after the diagnosis. At one and two years, renal function correlated significantly (r = 0.54, p < 0.0001 at two years) with the final renal function. What is more, the type of the evolution of proteinuria over the first two years gave valuable information on the eventual deterioration of renal function. Patients having stable non-nephrotic grade proteinuria and those in whom NS disappeared, had excellent renal outcome while those in particular showing an increased severity of NS had poor prognosis in terms of renal survival.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Alpha-1-antitrypsin, CRP and interleukin-6 in ANCA-positive vasculitis.

Alfa-1-antitrypsin (a-1-AT), C-reactive protein (CRP) and interleukin-6 (IL-6) serum levels were measured during different phases of anti-neutrophil cytoplasmic antibody (ANCA)-positive vasculitis. Correlation between ANCA and these variables was observed. Both a-1-AT and CRP fluctuations indicated changes in activity that could not always be detected by ANCA. On the other hand, these acute phase proteins were also less specific. IL-6 was not as sensitive as CRP and a-1-AT, a clearly increased mean value was observed only in patients with high ANCA titers.

Antibodies, Antineutrophil Cytoplasmic↗

Impaired renal function after pregnancy in renal transplant recipients.

Twenty-two renal transplant recipients had 29 posttransplant pregnancies and 39 male transplant recipients became fathers to 65 children between 1971 and 1991. Of the deliveries of the female patients, 62% took place between the third and sixth year after transplantation. Seven patients had 2 pregnancies. Mean follow-up time after the first posttransplant pregnancy was 7.5 years. The patients survived the pregnancy well, but the increase in serum creatinine concentration from the prepregnancy level, registered 3 months and 1 year after delivery, was higher than in matched control patients without pregnancy at corresponding times after transplantation (the increase in serum creatinine was 47.7 and 61.2 mumol/L in the pregnant patients versus -2.7 and 5.4 mumol/L in the control patients, P < 0.0001 and P < 0.02, respectively). All pregnant and control patients were alive at the end of follow-up, but the long-term graft survival of those with a pregnancy was significantly (P < 0.005) worse than in the control patients. Ten-year graft survival was 69% in the pregnant versus 100% in the control patients. Although 80% of the neonates born to a mother with a transplanted kidney were below the mean for gestational age, the weight and length at birth were within normal limits and no severe intrauterine growth retardation was documented.

Adult↗

Pregnancy in lupus nephropathy.

The purpose of this study was to obtain information about the fetal and maternal outcome of pregnancy in patients with pre-existing lupus nephritis and to evaluate risk factors for poor fetal outcome. Twenty-six pregnancies in 16 patients were retrospectively analyzed. Induced abortions were performed in two patients and one patient had a spontaneous abortion. Of the 23 completed pregnancies, all clinically established on inactive lupus nephritis with normal renal function, seven (30%) were complicated by pre-eclampsia. Two of the three patients with severe pre-eclampsia had increased levels of antiphospholipid antibodies (aPL). Of the 23 newborns, seven (30%) were premature (< 37 weeks) and seven (30%) had neonatal complications. Six of the seven pregnancies associated with neonatal complications were hypertensive. There was one early neonatal death. Four newborns (16%) were severely growth retarded (< -2 SD). The presence of hypertension before pregnancy tended to correlate with low relative birth weight in the newborns (p = 0.079). Flares of systemic lupus erythematosus (SLE) during pregnancy and six months post partum occurred in two (9%) of the 23 completed pregnancies. Renal function was not affected irreversibly in any patient. Thus, the outlook for pregnancy in patients with stable lupus nephritis at conception is good. However, the risk of obstetric complications is greater and fetal morbidity, especially in hypertensive pregnancies, is common.

Abortion, Induced↗

Reversal of steroid-induced insulin resistance by a nicotinic-acid derivative in man.

A recent report suggested that the glucose-free fatty acid (FFA) cycle may contribute to steroid-induced insulin resistance in rats, and that glucose tolerance could be restored to normal when FFA levels were lowered with nicotinic acid. To test this hypothesis in man, we measured insulin sensitivity (by euglycemic insulin clamp in combination with indirect calorimetry and infusion of tritiated glucose) before and after short-term administration of a nicotinic-acid derivative (Acipimox) in 10 steroid-treated, kidney transplant patients with insulin resistance. Thirty-five healthy subjects served as controls. Six of them received Acipimox. Total body glucose metabolism was reduced in steroid-treated patients compared with control subjects (41.7 +/- 3.3 v 50.0 +/- 2.2 mumol/kg lean body mass [LBM].min, P less than .05). The reduction in insulin-stimulated glucose uptake was mainly due to an impairment in nonoxidative glucose metabolism (primarily glucose storage as glycogen) (18.3 +/- 2.8 v 27.2 +/- 2.2 mumol/kg LBM.min, P less than .01). Acipimox lowered basal FFA concentrations (from 672 +/- 63 to 114 +/- 11 mumol/L, P less than .05) and the rate of lipid oxidation measured in the basal state (1.5 +/- 0.2 to 0.6 +/- 0.1 mumol/kg LBM.min, P less than .01) and during the clamp (0.7 +/- 0.2 to 0.03 +/- 0.2 mumol/kg LBM.min, P less than .05). In addition, Acipimox administration normalized total glucose disposal (to 54.4 +/- 4.4 mumol/kg LBM.min), mainly due to enhanced nonoxidative glucose metabolism (to 28.9 +/- 3.9 mumol/kg LBM.min) in steroid-treated patients (both P less than .05 v before Acipimox).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Cortex Hormones↗

Outcome of patients with secondary amyloidosis in dialysis treatment.

Between the years 1974 and 1987, 37 patients with secondary amyloidosis entered dialysis treatment at our department. All had amyloidosis secondary to chronic arthritic disease (35) or to other chronic inflammatory causes (2). Only two patients were maintained on CAPD throughout follow-up; 12 patients (32%) received a kidney transplant. Survival in dialysis at 1 year was 82%, at 2 years 46%, and at 3 years 37%. Survival of amyloidosis patients transplanted at the Finnish transplant centre within the same period was worse at 1 year, but better at 2 and 3 years, 70%, 62%, and 62% respectively, but the difference was not significant. Populations are not compatible, since patients were selected for transplantation. Infection was a common cause of death, 7/18 (39%) deaths; cardiac deaths were less common, only two myocardial infarctions and one cardiac arrhythmia (17%). Symptoms of cardiac amyloid infiltration indicated a poor prognosis, although it did not necessarily predict death of a cardiac cause. Cardiac infiltration of amyloid was more common in autopsy than previously reported (10 of 13 patients), probably indicating longer duration of amyloidosis in patients treated with renal replacement therapy. Patients who died within follow-up had a shorter interval between the start of primary disease and the development of amyloidosis than those who survived, 11.8 versus 17.7 years (P = 0.041), and also a slightly shorter period between diagnosis of amyloidosis and start of dialysis, 3.0 versus 4.4 years (P = 0.129). This indicates that the rate of progression of amyloidosis determines the development of disease-associated complications, and fast progression may predict serious outcome.

Adult↗

Insulin resistance and insulin deficiency in the pathogenesis of posttransplantation diabetes in man.

Although steroids can induce insulin resistance, it is not known whether additional defects in insulin secretion are necessary for the development of diabetes. To address this question, we measured insulin sensitivity (euglycemic insulin clamp in combination with indirect calorimetry and infusion of tritiated glucose) and insulin secretion (hyperglycemic clamp) in three groups of subjects: (1) 10 kidney transplant patients with normal oral glucose tolerance, (2) 14 patients who developed diabetes after kidney transplantation, and (3) 10 healthy controls. Glucose utilization, primarily storage of glucose as glycogen, was reduced by 34% in kidney transplant patients with normal glucose tolerance when compared with healthy control subjects (18.2 +/- 2.9 vs. 27.5 +/- 2.7 microM/L; P less than 0.05). Insulin secretion was normal in relation to the degree of insulin resistance in transplanted non-diabetic patients, thus maintaining a normal oral glucose tolerance. Development of transplantation diabetes was associated with only minor further deterioration of glucose storage (14.7 +/- 2.7 microM/L; P less than 0.001 vs. control subjects), whereas first-phase, second-phase, and glucagon-stimulated insulin secretion measured during hyperglycemic clamping (incremental area under the insulin curve 287 +/- 120, 1275 +/- 419, and 3515 +/- 922 pM) became impaired as compared with nondiabetic kidney transplant patients (769 +/- 216, 3084 +/- 545, and 6293 +/- 533 pM; P less than 0.05). We conclude that both insulin resistance and insulin deficiency are necessary for the development of diabetes in kidney transplant patients.

Adult↗

Metabolic control and progression of complications in insulin-dependent diabetic patients after kidney transplantation.

Patient survival and progression of complications were monitored for 3 years after kidney transplantation in 29 type-1 diabetic patients. Ten age-matched, non-diabetic kidney-transplanted patients served as controls. Five diabetic patients died during follow-up (three cardiovascular events, two infections), three diabetic patients had a non-fatal myocardial infarction and four developed cerebrovascular complications after transplantation. Of the diabetic patients, 69% suffered from proliferative retinopathy before transplantation; 20% of them improved, 65% remained unchanged and 15% deteriorated after transplantation. Motor but not sensory conduction velocity measured from the nervus medianus improved after transplantation. Autonomic neuropathy was observed in 50% of the patients and was unaffected by transplantation. Glycaemic control did not improve significantly during follow-up (HbA1, 10.6 +/- 0.5% before and 9.5 +/- 0.6% 3 years after transplantation). Body weight increased in both diabetic and non-diabetic patients within 3 years after transplantation (from 68 +/- 2 to 77 +/- 6 kg in diabetics, P less than 0.01; from 167 +/- 4 to 77 +/- 6 kg in non-diabetics, P less than 0.01). Subcutaneous fat thickness measured from computer tomography scans of the calf increased in diabetic patients from 5.0 +/- 0.6 to 6.1 +/- 0.9 mm (P less than 0.05). However, the cross-sectional areas of triceps and calf muscles did not increase, suggesting that the increase in body weight was solely due to an increase in fat. It is clear that diabetes-related complications continue to progress and are not influenced by a successful kidney transplant.

Adult↗