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Interventions to reduce clinical inertia in cardiac risk factor management in renal transplant recipients.

ABSTRACT: Cardiovascular disease (CVD) is the leading cause of death in renal transplant recipients (RTRs). Clinical inertia (CI) is defined as "recognition of the problem, but failure to act." The effect of educational interventions in minimizing CI in CVD risk factor management was assessed. Educational sessions were conducted among 201 RTRs to inform them about their goals for blood pressure (BP), low-density lipoprotein cholesterol (LDL-C) and glycated hemoglobin (HbA1c). Physicians were reminded about treatment goals using checklists. Pre-intervention and post-intervention CI was measured as "no action" or "appropriate action" by the physicians. Post-intervention percentage of RTRs with "no clinical action" for BP, LDL-C, and HbA1c control decreased from 10.8% to 3.8% (P=.02), 28.2% to 11.1% (P=.008), and 10.3% to 4.5% (P=.05), respectively, while those with "appropriate action" increased from 66.2% to 83.3% (P<.001), 68.7% to 79.4% (P=.008), and 85.1% to 93.2% (P=.03), respectively. Educational interventions and patient participation were shown to reduce CI.

SUBMITTER: Kohok DD

PROVIDER: S-EPMC8031565 | biostudies-literature | 2014 Feb

REPOSITORIES: biostudies-literature

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Interventions to reduce clinical inertia in cardiac risk factor management in renal transplant recipients.

Kohok Dhanashri D DD Shah Silvi S Kumar Rakesh R Venuto Lisa L Gudleski Gregory G Venuto Rocco R

Journal of clinical hypertension (Greenwich, Conn.) 20140117 2

Cardiovascular disease (CVD) is the leading cause of death in renal transplant recipients (RTRs). Clinical inertia (CI) is defined as "recognition of the problem, but failure to act." The effect of educational interventions in minimizing CI in CVD risk factor management was assessed. Educational sessions were conducted among 201 RTRs to inform them about their goals for blood pressure (BP), low-density lipoprotein cholesterol (LDL-C) and glycated hemoglobin (HbA1c). Physicians were reminded abou ...[more]

PMID: 24433451

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Project description:Mycophenolic acid (MPA), an immunosuppressive drug widely used in kidney transplantation, has been suggested to have anti-fibrotic effects. To analyze at a genomic level these effects, we prospectively studied a group of stable kidney transplant recipients (n=35) on cyclosporine (CyA) and azathioprine treatment. Twenty patients were converted from azathioprine to MPA (MPA group) and 15 patients continued on azathioprine (AZA group). RNA was extracted by peripheral blood mononuclear cells at baseline and 3 months thereafter. Genomic analysis, performed on 5 randomly-selected MPA patients, revealed that 17 genes discriminated the transcriptomic profile after conversion. Neutral endopeptidase (NEP), an enzyme degrading angiotensin-II, was the most significant up-regulated gene. NEP expression level was inversely correlated to proteinuria at baseline and after conversion. Immunohistochemistry on graft biopsy of 33 independent patients demonstrated higher glomerular and tubular NEP protein expression in CyA+MPA (n=13) compared to CyA+AZA (n=12) and CyA alone (n=8). Glomerular NEP levels were inversely correlated to proteinuria and glomerulosclerosis. Tubular NEP expression was inversely correlated to interstitial fibrosis. Incubation of proximal tubular cells with MPA led to a dose- and time-dependent increase of NEP gene expression. The direct influence of MPA on NEP expression may suggest a novel therapeutic effect of this drug. For microarray analysis, we studied 5 randomly selected patients included in the training group. Patients included in this group were, at the time of enrollment (T0), on standard maintenance immunosuppression with Cyclosporine (Neoral, Novartis, Basel, mean±SD of daily dose: 160.1±37.1mg), prednisone (5 mg daily) and Azathioprine (50 mg daily). Twenty patients, at T0, were switched from Azathioprine to EC-MPS (Myfortic, Novartis, Basel, 720 mg bid) for their need of allopurinol therapy (EC-MPS group). However, to avoid confounding factors, allopurinol treatment did not start until the end of our study (3 months). For the microarray analysis, we randomly selected 5 patients from the EC-MPS group. PBMC both at T0 and at T1 (3 months after the switching of the therapy) were immediately isolated from 20 ml of whole blood by Ficoll–Hypaque (Flow Laboratories, Irvine, UK) density gradient centrifugation. Total RNA was extracted by RNeasy mini kit (QIAGEN Inc., Valencia, CA) according the manufacturer’s instructions. Total RNA was processed and hybridized to the Affymetrix GeneChips Human Genome U133 Array Set HG-U133A (Affymetrix)(Affymetrix, Santa Clara, CA)

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Interventions to reduce clinical inertia in cardiac risk factor management in renal transplant recipients.

Publications

Interventions to reduce clinical inertia in cardiac risk factor management in renal transplant recipients.

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