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Biomedical subjects

Trond Jenssen

Publications and source records attributed to Trond Jenssen.

At least 19 recordsLinked to original sources
PubMed2006

Albuminuria as risk factor for initiation and progression of carotid atherosclerosis in non-diabetic persons: the Tromsø Study.

AIMS: High levels of microalbuminuria have been associated with severe atherosclerosis. In this prospective, population-based study, we examined whether urinary albumin-to-creatinine-ratios (ACR) in the lower range were associated with the initiation and progression of atherosclerosis. METHODS AND RESULTS: Carotid ultrasonography and measurements of ACR, fibrinogen, monocytes, white cell count, and well-established cardiovascular risk factors were performed in 4037 non-diabetic subjects, 2203 without, and 1834 with pre-existing plaques at baseline. After 7 years new ultrasound measurements were performed. In subjects without pre-existing plaques, 884 had developed at least one plaque during follow-up. Baseline ACR was significantly related to the area of the novel plaques (P for linear trend = 0.009 over the baseline ACR quartiles, after multiple adjustments). The relationship with ACR was clearly modified by fibrinogen (P = 0.001, for the interaction ACR x fibrinogen). Subjects with high levels of both ACR and fibrinogen developed plaques with the largest area. In subjects with pre-existing plaques, ACR was related to plaque-progression (P for linear trend = 0.026, after multiple adjustments). In these individuals, the interaction between fibrinogen and ACR on plaque-growth appeared only in those with minimal atherosclerosis at baseline. CONCLUSION: ACR is positively related to plaque-initiation and plaque-growth. This relationship is substantially modified by fibrinogen in previously plaque-free subjects.

Adult↗
PubMed2006

Calcineurin inhibitor avoidance with daclizumab, mycophenolate mofetil, and prednisolone in DR-matched de novo kidney transplant recipients.

BACKGROUND: Calcineurin inhibitor (CNI)-free regimens posttransplantation have been claimed to conserve graft function in addition to reduce the risk factors for cardiovascular and malignant disease in renal transplant recipients. METHODS: The primary aim of this prospective, open-label, randomized, parallel-group, single-center study was to compare the effect of complete CNI-avoidance posttransplant (daclizumab + mycophenolate mofetil + prednisolone: Dac-group, n=27) with the standard CNI-based immunosuppressive protocol at our transplant unit (cyclosporine A + mycophenolate mofetil + prednisolone: CsA-group, n=27) on renal function (glomerular filtration rate [GFR] determined as plasma clearance of 51Cr-EDTA) in a selected low immunogenic risk population (DR-matched, PRA-negative de novo cadaveric transplant recipients). RESULTS: There were no significant difference in GFR at week 10 (P=0.61), but GFR was significantly (P=0.029) lower in the Dac-group (52+/-20 ml/min) at month 12 than in the CsA-group (69+/-29 ml/min). One-year patient and graft survival did not differ between the two groups. Overall acute rejection rate was 70.4% (19/27) in the Dac-group and 29.6% (8/27) in the CsA-group (P=0.006). CONCLUSIONS: The strategy to select DR-matched, PRA-negative de novo cadaveric transplant recipients for a CNI-avoidance protocol was not successful. The incidence of acute rejection was unacceptable high even though anti-CD25 antibody induction as well as initial higher mycophenolate mofetil doses (3 g/day) were applied, and renal function was significantly lower in the CNI-avoidance patients at 1 year. Other strategies need to be examined for avoidance of CNI's in the early posttransplant period.

Adult↗
PubMed2006

Early posttransplant serum osteoprotegerin levels predict long-term (8-year) patient survival and cardiovascular death in renal transplant patients.

The primary objectives of this analysis were to examine the effects of early posttransplantation (10 wk) serum levels of osteoprotegerin (OPG), mannose-binding lectin (MBL), and MBL-associated serine proteases (MASP; MASP-2 and MASP-3) on long-term (8-yr) patient survival, graft survival, and cardiovascular (CV) death. During a period of 16 mo (1995 to 1996), a total of 173 consecutive renal transplant recipients without diabetes before transplantation were included in a prospective study that was designed to address the impact of metabolic CV risk factors on survival and CV end points. Baseline sera from 172 patients were available for analysis. Follow-up data until January 1, 2004, were obtained from a national renal registry. Patients with high (fourth quartile) serum levels of OPG had significantly higher all-cause mortality (hazard ratio [HR] 6.3; 95% confidence interval [CI] 3.3 to 11.8; P<0.001) and CV death (HR 10.8; 95% CI 3.8 to 30.4; P<0.001) than patients with lower OPG concentrations. After multiple Cox regression analysis, high serum levels of OPG remained an independent predictor of all-cause mortality (HR 6.0; 95% CI 3.1 to 11.6, P<0.001) and CV death (HR 8.2; 95% CI 2.5 to 26.4; P<0.001). Multiple linear regression analysis revealed that age, creatinine clearance, and high-sensitivity C-reactive protein all were independently associated with OPG (R2=0.42). No significant association between OPG and death-censored graft loss was revealed. Serum levels of MBL, MASP-2, and MASP-3 were not significantly associated with patient survival, CV death, or graft loss. Early measured posttransplantation serum OPG is a highly significant independent predictor of death from any cause or CV death in white renal transplant recipients.

Adult↗
PubMed2004

Short-term treatment with rosiglitazone improves glucose tolerance, insulin sensitivity and endothelial function in renal transplant recipients.

BACKGROUND: Insulin resistance (IR) contributes to the development of glucose intolerance (post-transplant diabetes mellitus or impaired glucose tolerance) following renal transplantation. Furthermore, endothelial dysfunction (ED) is associated with IR. Glucose intolerance, IR and ED are all independent risk factors for cardiovascular disease. Therefore, treatment with insulin sensitizers may benefit glucose-intolerant renal transplant recipients. The main objectives of the present study were to investigate the effect of 4 weeks' treatment with the PPAR-gamma agonist rosiglitazone on insulin sensitivity, plasma glucose and endothelial function in renal transplant recipients with glucose intolerance. Safety parameters were also addressed. METHODS: A total of 10 glucose-intolerant renal transplant recipients were treated with rosiglitazone (initially 4 mg/day increasing to 8 mg/day after 1 week). A hyperinsulinaemic euglycaemic glucose clamp, an oral glucose tolerance test and endothelial function assessment with laser Doppler flowmetry were performed both at baseline and at follow-up. RESULTS: Treatment with rosiglitazone was followed by a significantly improved mean glucose disposal rate (from 6.5 to 9.1 g/kg/min; P = 0.02) and a significant decline in fasting and 2 h plasma glucose (from 6.4 to 5.8 mmol/l, P = 0.01 and from 14.2 to 10.6 mmol/l, P = 0.03, respectively). Furthermore, a significant improvement in endothelial function was demonstrated (AUC(ACh); from 389 to 832 AU x min, P = 0.04). No serious adverse events or hypoglycaemic episodes were observed. CONCLUSIONS: Four weeks' treatment with rosiglitazone was associated with increased insulin sensitivity, lowered fasting and 2 h plasma glucose and improved endothelial function in renal transplant recipients with glucose intolerance. The drug was well tolerated and may be a good alternative for treating these patients.

Blood Glucose↗
PubMed2004

Glycated hemoglobin level is strongly related to the prevalence of carotid artery plaques with high echogenicity in nondiabetic individuals: the Tromsø study.

BACKGROUND: High levels of HbA1c have been associated with increased mortality and an increased risk of atherosclerosis assessed as carotid intima-media thickness or plaque prevalence. In the present population-based study, we examined the association between HbA1c and plaque prevalence with emphasis on plaque echogenicity in subjects not diagnosed with diabetes. METHODS AND RESULTS: HbA1c measurements and ultrasonography of the carotid artery were performed in 5960 subjects (3026 women, 2934 men) 25 to 84 years of age. Plaque morphology was categorized into 4 groups from low echogenicity (soft plaque) to strong echogenicity (hard plaque). HbA1c was categorized into 5 groups: <5.0%, 5.0% to 5.4%, 5.5% to 5.9%, 6.0% to 6.4% and >6.4%. Carotid plaque prevalence increased with increasing HbA1c level (P for linear trend=0.002). The OR for hard plaques versus no plaques was 5.8 in the highest HbA1c group (>6.4%) compared with subjects in the lowest group (<5.0%) after adjustment for several possible confounders. The risk of predominantly hard plaques was also significantly associated with HbA1c levels, although the ORs at each level were somewhat lower than for hard plaques. With respect to the risk of soft plaques versus no plaques, no statistically significant relationship with HbA1c levels was found. CONCLUSIONS: Metabolic changes reflected by HbA1c levels may contribute to the development of hard carotid artery plaques, even at modestly elevated levels.

Adult↗
PubMed2004

Dietary intakes differ between renal transplant recipients living in patient hotels versus home.

OBJECTIVE: To compare dietary intake and health-related quality of life approximately 6 to 10 weeks after renal transplantation in patients living at home and at a patient hotel, and how the patients were following a heart-healthy diet according to the current American Heart Association guidelines. DESIGN: Cross-sectional observational study. SETTING: Outpatient clinic at Rikshospitalet University Hospital, Norway. PATIENTS: Forty renal transplant patients, 20 patients (14 men and 6 women) in both groups. There were 4 diabetic patients in each group. METHODS: Dietary intake was assessed by 4-day dietary records. Health-related quality of life was investigated by the SF-36 questionnaire. The main outcome variables were daily energy intake and intakes of protein, total fat, saturated fat, cholesterol, fiber, and fruit and vegetables. The variables were tested by 2-sample t-tests, and significance was set at.05. RESULTS: There was no statistically significant difference in daily energy intake between the groups (P =.08), but there were significantly higher daily intakes of protein (P =.003), total fat (P =.03), monounsaturated fat (P =.02), cholesterol (P =.04), fiber (P =.02), calcium (P =.03), and fruit and vegetables (P =.03) in the group living at the patient hotel. The mean intake of saturated fat was 14.5% of total energy in the group living at home and 14.6% in the group living at the patient hotel. There were no significant differences in health-related quality of life between the groups. CONCLUSION: The results suggest that there are differences in dietary intake in renal transplant patients living at home compared with those at a patient hotel. It seems that neither of the groups follows current guidelines for reducing the risk of cardiovascular disease.

Cardiovascular Diseases↗
PubMed2004

Insulin resistance after renal transplantation: the effect of steroid dose reduction and withdrawal.

Cardiovascular disease is a prevalent and serious complication after solid organ transplantation. Treatment with glucocorticoids is associated with increased risk for diabetes mellitus, insulin resistance, weight gain, hypercholesterolemia, and hypertension, all shown to be independent risk factors for cardiovascular disease. We sought to test the hypothesis that tapering of prednisolone (TAP) the first year after renal transplantation improves insulin sensitivity (IS), and to assess the effect of complete steroid withdrawal (SW) on IS in patients on a cyclosporine-based immunosuppressive regimen. All patients (n = 57) completed two consecutive hyperinsulinemic euglycemic glucose clamp procedures, a TAP group (n = 34) and a control group (n = 12) at 3 and 12 mo after transplantation, and a SW group (n = 11) before and 5 mo after SW. The IS index (ISI) was calculated as the glucose disposal rate divided by mean serum insulin the last 60 min of the clamp. In the TAP group, the mean (range) daily prednisolone was reduced from 16 (10 to 30) to 9 (5 to 12.5) mg accompanied by an average increased ISI of 24% (P = 0.008). In contrast, no significant change in ISI was observed in the control group (0%, P = 0.988). In the SW group, withdrawal of 5 mg prednisolone did not influence mean ISI significantly (-8%, P = 0.206). Lowering daily prednisolone toward 5 mg/d has beneficial effects on insulin action after renal transplantation, but withdrawal of 5 mg prednisolone may not influence IS significantly.

Body Weight↗
PubMed2003

Diagnosing PTDM.

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Diabetes Mellitus↗
PubMed2003

Quantitative measurement of muscle fiber composition in a normal population.

To obtain normative muscle morphology data on a healthy population recruited from a population survey, we examined vastus lateralis biopsies from 58 men and 33 women, aged 26-67 years. Biopsies were measured with automated, computer-aided techniques. Data were analyzed according to gender and age, and the influence of blood pressure, body mass index (BMI), and smoking habits was also examined. Men had larger muscle fibers (fiber area approximately 5400 microm(2)) than women ( approximately 4000 microm(2), P = 0.003). No gender differences were seen in fiber composition, fiber roundness, percentage of connective tissue, or capillary density. Blood pressure did not influence fiber size or composition, but was correlated with fiber roundness in men. BMI was associated with fiber area in men, but not in women. Variations in age, smoking habits, and physical activity did not influence muscle morphology data substantially. Thus, in a normal population, men have larger muscle fibers than women, but similar fiber composition. Variation in gender, BMI, blood pressure, and physical activity may influence morphological features to a minor degree.

Adult↗
PubMed2003

Determinants of insulin secretion after renal transplantation.

The high prevalence of post-transplant glucose intolerance and insulin resistance (IR) is associated with older age, family history of diabetes, immunosuppressive drugs, and antihypertensive therapy. However, the potential determinants of post-transplant beta-cell dysfunction are largely unknown. The objective of the present study was to address this issue in detail. A total of 167 previously nondiabetic renal transplant recipients underwent a 75-g oral glucose tolerance test (OGTT)10 weeks after transplantation. Serum glucose and insulin were measured at 0, 1, and 2 hours. Three insulin release indices (Secr(AUC), Secr(1.phase), and Secr(2.phase)) were calculated to assess the insulin secretory response as the dependent variable. To account for variations in insulin sensitivity (IS), beta-cell function was also estimated as the disposition index (DI); the product of the IS index (ISI(TX)) and Secr(1.phase). Increasing age was strongly and independently associated with a blunted insulin secretory response even after adjustment for IS (P =.001). An 80-year-old recipient had an approximately 50% lower insulin release than a 20-year-old individual, based on the linear regression model. Cytomegalovirus (CMV) disease and treatment with furosemide were both independently associated with beta-cell dysfunction (DI; P <.001 and P =.008). Patients treated with angiotensin-converting enzyme (ACE)-inhibitors had an enhanced absolute insulin release, but the DI was similar in both treated and untreated recipients. We conclude that older age is an important determinant of beta-cell dysfunction after renal transplantation. CMV disease and treatment with furosemide may also negatively influence pancreatic insulin release in renal transplant recipients.

Adolescent↗
PubMed2003

A 6-year prospective study on new onset diabetes mellitus, insulin release and insulin sensitivity in renal transplant recipients.

BACKGROUND: It is well known that both insulin resistance and insulin deficiency are involved in the pathogenesis of post-transplant diabetes mellitus (PTDM), but the relative importance of the two different mechanisms is still under debate. The present prospective longitudinal study was performed over 6 years to investigate the impact of impaired insulin secretion (ISec) and insulin sensitivity (IS) in the development of PTDM in renal transplant recipients. METHODS: A total of 95 non-diabetic patients underwent a 75 g oral glucose tolerance test (OGTT) 10 weeks post-transplant. Six years later, 63 of these recipients were re-examined, the majority (n = 58) with an OGTT. Fasting, 1- and 2-h insulin and glucose levels were measured and used to estimate the insulin secretory response and IS both at baseline and at follow-up. RESULTS: The proportion of recipients with normal glucose tolerance (NGT) rose from 46% (baseline) to 65% (follow-up) (P = 0.008), and median fasting and 2-h serum glucose were reduced by 0.7 mmol/l (P < 0.001) and 1.3 mmol/l (P = 0.039), respectively. The recipients with PTDM at follow-up had a significant decline in the estimated median first and second phase ISec (-58 and -47%, respectively, P = 0.005 for both). The patients who normalized their glucose tolerance from PTDM or IGT at baseline to NGT at follow-up increased their IS significantly (68%, P = 0.002) without significant alterations in ISec. CONCLUSIONS: Impaired ISec seems to be the dominant mechanism in the development of PTDM after renal transplantation. In contrast, normalization of glucose intolerance is associated with improved IS.

Adult↗
PubMed2002

[Protein-creatinine ratio--a simple method for proteinuria assessment in clinical practice].

BACKGROUND: Proteinuria is an indicator of renal disease. Measurement of protein excretion is important for diagnosis and follow-up of renal disease, but measuring 24-hour protein excretion is a cumbersome procedure. MATERIAL AND METHODS: A simplified validated method for measuring excretion is obtained by measuring urine protein/creatinine concentration in a spot urine sample. RESULTS: We have implemented such ratios for clinical routine measurements of proteinuria at Rikshospitalet University Hospital in Oslo. Whenever protein or albumin in urine is requested, the laboratory also measures urine creatinine and reports the ratio in mg protein/mmol creatinine. 24-hour excretion is approximately 10 times the ratio. The rationale for using the ratio is given and proteinuria pathophysiology and potential risks and treatment options are discussed. INTERPRETATION: Our experience is that use of the urine protein/creatinine ratio is a significant improvement. Measurements are now routinely made whereas quantification was rarely performed when 24-hour urine samples were used. We recommend that physicians and laboratories implement the use of this ratio in their daily routines.

Albuminuria↗
PubMed2002

Diagnosing PTDM.

Explore the source record for details and available documents.

Blood Glucose↗
PubMed2002

[Type 2 diabetes and nephropathy--new studies, new treatment strategies?].

BACKGROUND: In industrialised countries the incidence of type 2 diabetes-associated end stage renal disease has doubled over the last ten years. It is important to lower the blood pressure to inhibit progression of renal failure and to prevent micro- and macrovascular disease in these patients. There is an ongoing discussion on what should be the drug of choice. MATERIAL AND METHODS: We discuss the results from three landmark studies, recently published, on the use of angiotensin II antagonists in patients with type 2 diabetics and nephropathy. RESULTS AND INTERPRETATION: All three studies found a renoprotective effect of angiotensin II antagonists that could not be explained by the effect on the blood pressure alone. Blockade of the renin angiotensin system with angiotensin II antagonist should be the basis of treatment in type 2 diabetic nephropathy.

Amlodipine↗
PubMed2002

The impact of impaired insulin release and insulin resistance on glucose intolerance after renal transplantation.

The current knowledge of the pathogenesis of post-transplant glucose intolerance is sparse. This study was undertaken to assess the relative importance of insulin secretion (ISec) and insulin sensitivity (IS) in the pathogenesis of post-transplant diabetes mellitus (PTDM), impaired glucose tolerance (IGT) and impaired fasting glucose (IFG) after renal transplantation. An oral glucose tolerance test (OGTT) was performed in 167 non-diabetic recipients 10 wk after renal transplantation. Fasting, 1-h and 2-h insulin and glucose levels were used to estimate the insulin secretory response and IS. One year after transplantation 89 patients were re-examined with an OGTT including measurements of fasting and 2 h glucose. Ten weeks after transplantation the PTDM-patients had significantly lower ISec and IS than patients with IGT/IFG, who again had lower ISec and IS than those with normal glucose tolerance (NGT). One year later, a similar difference in baseline ISec was observed between the three groups, whereas baseline IS did not differ significantly. Patients who improved their glucose tolerance during the first year, were mainly characterized by a significantly greater baseline ISec, and they received a significantly higher median prednisolone dose at baseline with a subsequent larger dose reduction during the first year, than the patients who had their glucose tolerance unchanged or worsened. In conclusion, both impaired ISec and IS characterize patients with PTDM and IGT/IFG in the early course after renal transplantation. The presence of defects in insulin release, rather than insulin action, indicates a poor prognosis regarding later normalization of glucose tolerance.

Adolescent↗
PubMed2002

Microalbuminuria in hypertension is not a determinant of insulin resistance.

BACKGROUND: Microalbuminuria (MA) clusters with metabolic derangements linked to the insulin resistance syndrome, and is associated with increased risk of cardiovascular disease in both diabetes and hypertension. This study questioned if MA, reflecting endothelial damage, is directly linked to impaired insulin action. METHODS: MA was measured in two 24-hour urine samples in 84 persons with untreated hypertension recruited from a population survey (diastolic blood pressures 90 to 105 mm Hg). Thirty-one percent had MA values>20 microg/min (MA group, N = 26), and these were matched according to age, gender, and body-mass index with hypertensive persons without MA (non-MA group, N = 32) for comparison of the metabolic profile. Insulin sensitivity was measured with clamp techniques. RESULTS: The MA and non-MA groups were similar in their fasting and post-load glucose and insulin levels, in the first (930 +/- 594 vs. 1097 +/- 707 pmol/L) and second (1111 +/- 662 vs. 1163 +/- 702 pmol/L) phases of insulin release during a hyperglycemic clamp, and in their insulin sensitivity indices (0.16 +/- 0.10 vs. 0.17 +/- 0.13, P> 0.3 for all). The MA group had higher systolic blood pressure (157 +/- 13 vs. 150 +/- 12 mm Hg, P = 0.05) and a higher serum level of circulating advanced glycation end products (AGEs; 11.0 +/- 3.0 vs. 7.9 +/- 3.5 U/mL, P = 0.05) than the controls. No associations were found between MA and the insulin sensitivity index, or glucose and insulin levels. Weak associations were found with systolic blood pressure (r = 0.25, P = 0.05), AGEs (r = 0.27, P = 0.05), and smoking habits (r = 0.39, P = 0.01). CONCLUSION: In hypertension, MA is not a determinant of insulin resistance, provided confounding factors such as degree of adiposity are carefully controlled.

Albuminuria↗
PubMed2002

Autoregulation of endogenous glucose production during hyperglucagonemia.

Increased endogenous glucose production (EGP) contributes to fasting hyperglycemia in type II diabetes. In nondiabetic subjects, increased gluconeogenesis from lactate does not increase EGP. Type 2 diabetes is associated with hyperglucagonemia. The present study was undertaken to examine whether physiologic elevation of plasma glucagon overrides autoregulation of EGP. Eight healthy volunteers were studied on 2 occasions, once during a 3-hour infusion of 30 micromol/kg/min Na-lactate and once during a control infusion of Na-bicarbonate. Plasma glucagon, insulin, and growth hormone were clamped at identical levels in both experiments. Rates of appearance of glucose, lactate, and gluconeogenesis from lactate were measured by tracer techniques. Glucagon infusion rate was elevated when the lactate or bicarbonate infusions were started to induce physiologic hyperglucagonemia. Plasma glucagon increased from baseline levels (234 +/- 21 ng/L and 211 +/- 23 ng/L) to 313 +/- 47 ng/L (bicarbonate experiments) and 329 +/- 43 ng/L (lactate experiments, means +/- SE, P >.3). Lactate infusion increased plasma lactate concentrations from 1.1 +/- 0.9 to 4.6 +/- 0.5 mmol/L (P =.0003). Lactate conversion to glucose increased from 1.5+/-0.3 to 2.8+/-0.8 micromol/kg/min (P =.03) and from 1.7 +/- 0.3 to 8.1 +/- 0.8 micromol/kg/min (P =.0003) in the bicarbonate and lactate experiments, respectively. The increments in lactate conversion to glucose differed significantly (P =.0008). Nevertheless, plasma glucose and EGP were not different in the bicarbonate and lactate experiments: 5.4 +/- 0.5 versus 6.6 +/- 0.7 mmol/L (P =.21), and 10.5 +/- 0.6 versus 11.6 +/- 0.6 micromol/kg/min (P =.19). We conclude that in normal volunteers, neither hyperglucagonemia nor the combination of hyperglucagonemia and increased substrate availability alters the autoregulation of EGP.

Adult↗