Acute myocardial infarction in renal transplant recipients: incidence and prognosis

Gunnarsson, R; Löfmark, Rurik; Nordlander, R; Nyquist, O.; Groth, C. G.

doi:10.1093/oxfordjournals.eurheartj.a061639

Cited by 41 publications

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“…Excessive weight gain, a major problem for many RTx patients, is associated with an increased risk of metabolic and cardiovascular complications, a major cause of morbidity and mortality in renal transplant patients [4,9,11,171. Some weight gain might be favorable in patients who were malnourished at the point of transplantation.…”

Section: Discussionmentioning

confidence: 99%

“…The nutritional status may improve after RTx, as usually an increase in body weight is observed after RTx. However, it has also been shown that a large part of the weight gain after RTx is due to an increase in body fat mass [6,7,12,19,231, which may have untoward metabolic and cardiovascular effects [4,9,171. The steroid immunosuppressive treatment after RTx may play a role in excessive weight gain and increased fat mass in renal transplant patients.…”

Section: Introductionmentioning

confidence: 99%

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Weight changes after renal transplantation: a comparison between patients on 5-mg maintenance steroid therapy and those on steroid-free immunosuppressive therapy

et al. 2003

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Weight changes after renal transplantation: a comparison between patients on 5-mg maintenance steroid therapy and those on steroid-free immunosuppressive therapy Abstract After renal transplantation (RTx), an increase in body weight (BW) is usually observed, in which corticosteroids may play an important role. However, the effects of a low maintenance dosage of corticosteroids on BW have not been studied longitudinally in RTx patients. The aim of this study was to compare changes in BW after RTx in patients on steroid-or steroid-free immunosuppressive therapy and to assess the relationship between posttransplant weight changes and other potentially important factors. The charts of 123 RTx patients (72 male, 5 1 female) were retrospectively examined for BW changes in the first 5 years after RTx. Sixty-six patients were on 5-mg maintenance steroid dose and 57 patients underwent steroid-free immunosuppression. Mean post-transplant BW gain was 3.0 & 5.3 kg after 6 months, 3.9 d= 6.2 kg after 1 year and 6.23~8.6 kg after 5 years. Weight gain in the first year after RTx was related neither to maintenance-nor to cumulative steroid dose, age, gender, occurrence of rejection, or renal function. Weight gain was, however, significantly related to pretransplant BMI and dialysis modality. After the first year, weight gain was significantly and positively related only to the cumulative steroid dose. The course of weight gain in the first year after RTx turned out to be independent from factors such as maintenance-or cumulative steroid dose, age, gender, occurrence of rejection, and renal function; weight gain was, however, dependent on pre-transplant BMI and dialysis modality. After the first year, the weight course was significantly affected by cumulative steroid dose.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Weight changes after renal transplantation: a comparison between patients on 5-mg maintenance steroid therapy and those on steroid-free immunosuppressive therapy

et al. 2003

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“…Earlier clinical studies [1][2][3][4][5] have shown that drug treatment with cyclosporine leads to an elevation of LDL-cholesterol level with a subsequent development of atherosclerosis, which predisposes to premature cardiovascular disease. The exact mechanism whereby cyclosporine augments blood LDL-cholesterol levels is obscure.…”

Section: Discussionmentioning

confidence: 99%

Cyclosporine inhibits catabolism of low-density lipoproteins in HepG2 cells by about 25%

1996

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Cyclosporine is today one of the most widely used immuno-SEE EDITORIAL ON PAGE 735 suppressive drugs and used in most transplantation centers to prevent organ rejection. It is a cyclic polypeptide, consisting of 11 amino acids and has a molecular weight of 1,202 The aim of this study was to elucidate the possible d. It is insoluble in water but soluble in many organic solcauses of elevated low-density lipoprotein (LDL)-choles-vents, and it is thus a lipophilic drug. Cyclosporine selectively terol levels in transplanted patients treated with the im-inhibits the interleukin-2-driven proliferation of activated T munosuppressant drug, cyclosporine. HepG2 cells, from lymphocytes with a subsequent suppression of proliferation a well-differentiated cell-line of hepatoma cells, were and generation of cytotoxic T lymphocytes, while sparing cultured and used as a model for in vitro hepatocytic T-suppressor-cell subpopulations. Patients, who are liver LDL uptake. Different concentrations of cyclosporine, transplant recipients and use this drug to prevent organ rewhich were within the range of concentrations found in jection are, however, prone to be afflicted by cardiovascular humans treated with cyclosporine, were added to tissue disease due to the development of atherosclerosis and atherculture medium together with 125 I-LDL. The results oma formation, a result of cyclosporine-caused elevation of showed that cyclosporine reduced LDL uptake and deg-blood low-density lipoprotein (LDL)-cholesterol levels. 1-5 radation in HepG2 cells by about 25%. The cells wereThe mechanism whereby cyclosporine causes high LDLalso pretreated with cyclosporine for 1 to 24 hours and cholesterol levels to occur has not yet been clarified. Due to then incubated with new medium containing labeled its hydrophobic property, cyclosporine binds to lipoproteins LDL for 2 hours at 4ЊC in an LDL-binding assay. The and in plasma is bound to high-density lipoproteins (33%-data showed that cyclosporine reduced the subsequent 46%), to low-density lipoproteins (28%-35%), and to very-low-LDL binding. Cyclosporine has no toxic effects on HepG2 density lipoproteins (VLDL) (6%-19%) 6,7 ; therefore, lipoprocells, as shown by unchanged growth capacity of the teins act as carriers for cyclosporine. cells. By means of a 50-fold excess of unlabeled LDL,Lipoproteins, according to their densities, are categorized a monoclonal anti-LDL receptor antibody, and dextran into chylomicrons, chylomicron remnants, VLDL, intermedisulfate, we also evaluated if this inhibition of LDL bind-ate-density lipoproteins, LDL, and high-density lipoproteins. ing occurred through the LDL receptor-mediated path-VLDL and LDL are the major cholesterol carriers in the way, through non-LDL receptor-mediated pathways, or blood. VLDL is secreted from the intestine and the liver. 8 through both. The results show that cyclosporine re-Liver-derived VLDL is converted to LDL, and this conversion duces LDL binding and uptake by mainly inhibiting the is primarily mediated by the enzyme lipoprotein li...

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“…Usually glucocorticoids and cyclosporine with addition of azathioprine are used to prevent organ rejection in transplant recipients. However, both glucocorticoids and cyclosporine can cause an elevation of LDL cholesterol levels, [1][2][3][4][5][6][7][8] and we have shown earlier that the cause of elevated LDL-cholesterol levels in cyclosporinetreated patients is a down-regulation of hepatic LDL receptors.…”

Section: Discussionmentioning

confidence: 99%

“…In previous studies, we have shown that the immunosuppressive drug ment of atherosclerosis as a result of increased levels of LDL cholesterol. [1][2][3][4][5][6][7][8] Other clinical studies have also shown that the cyclosporine inhibits catabolism of low-density lipoproteins (LDL) mainly by reducing the expression of LDL-receptor use of glucocorticoids in chronic diseases, such as rheumatoid arthritis and systemic lupus erythematosus, increases messenger RNA (mRNA), thus explaining the increased plasma levels of LDL cholesterol observed in patients treated the liability for development of atherosclerosis due to development of hyperlipidemia. …”

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confidence: 99%

Additive inhibitory effect of hydrocortisone and cyclosporine on low-density lipoprotein receptor activity in cultured HepG2 cells

Rayyes

1997

Hepatology

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Both glucocorticoids and cyclosporine are used to prevent widely used to prevent organ rejection in transplant recipients in combination with cyclosporine and azathioprine. Sevrejection in organ transplant recipients. However, long-term treatment with these drugs is known to induce hyperlipidemia eral clinical studies have shown that glucocorticoids or cyclosporine, or both in combination, increase the developand premature development of atherosclerosis. In previous studies, we have shown that the immunosuppressive drug ment of atherosclerosis as a result of increased levels of LDL cholesterol. [1][2][3][4][5][6][7][8] Other clinical studies have also shown that the cyclosporine inhibits catabolism of low-density lipoproteins (LDL) mainly by reducing the expression of LDL-receptor use of glucocorticoids in chronic diseases, such as rheumatoid arthritis and systemic lupus erythematosus, increases messenger RNA (mRNA), thus explaining the increased plasma levels of LDL cholesterol observed in patients treated the liability for development of atherosclerosis due to development of hyperlipidemia. 9-11with cyclosporine. In the present study, our objective was to investigate the mechanism by which glucocorticoids increase The aim of the present study was to elucidate the mechanism by which glucocorticoids (e.g., hydrocortisone) elevate plasma levels of LDL cholesterol. We studied the catabolism of LDL in the human hepatoma cell line HepG2. Our results blood levels of LDL cholesterol. Because the liver is responsible for about two thirds of the catabolism of LDL (mainly show that hydrocortisone at physiologically relevant concentrations inhibits LDL binding, uptake, and degradation in a by the LDL receptor pathway), we performed the experiments on the hepatoma cell line HepG2, a well-defined, hudose-dependent way. Moreover, hydrocortisone also reduces the expression of LDL-receptor mRNA in a dose-dependent man-derived cell line that has maintained secretory functions, such as lipoprotein secretion, as well as functional LDL way. Cyclosporine also has an additive inhibitory effect on hydrocortisone in the catabolism of LDL. The 3-hydroxy-3-receptors. 12,13 In previous studies, we showed that cyclosporine reduces methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor fluvastatin reverses the inhibitory effect of both hydrocorti-the uptake of LDL by HepG2 cells mainly because of decreased expression of LDL-receptor protein.14 We also found sone and cyclosporine. We conclude that treatment with hydrocortisone and/or cyclosporine induces increased plasma that the cyclosporine-induced reduction of LDL uptake can be reversed by 3-hydroxy-3 methylglutaryl coenzyme A levels of LDL cholesterol because of reduced hepatic LDL receptor activity. HMG-CoA reductase inhibitors reverse this (HMG-CoA) reductase inhibitors, 15 thus verifying earlier clinical observations. 16,17 In the present work, we studied the undesirable effect and thus reduce the risk of the development of atherosclerosis in patients subjected to immunosuppress...

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Acute myocardial infarction in renal transplant recipients: incidence and prognosis

Cited by 41 publications

References 0 publications

Weight changes after renal transplantation: a comparison between patients on 5-mg maintenance steroid therapy and those on steroid-free immunosuppressive therapy

Weight changes after renal transplantation: a comparison between patients on 5-mg maintenance steroid therapy and those on steroid-free immunosuppressive therapy

Cyclosporine inhibits catabolism of low-density lipoproteins in HepG2 cells by about 25%

Additive inhibitory effect of hydrocortisone and cyclosporine on low-density lipoprotein receptor activity in cultured HepG2 cells

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