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Background Many trials have compared anticoagulation management provided by a pharmacist led anticoagulation clinic versus usual physician care showing the role for clinical pharmacist in the management of anticoagulant therapy, and demonstrating excellent outcomes. In Sudan, there is no published research evaluating the role of pharmacist in providing pharmaceutical care for patients taking warfarin. Objective The objective of the study is to assess the role of clinical pharmacist intervention in warfarin patients compared to usual medical care. Setting This study was conducted in Ahmed Gasim cardiac surgery and renal transplant center warfarin clinic. Methods One hundred thirty-five patients were randomly selected from adult patients on warfarin therapy The history of INR records, and adverse effects for the past year, were recorded. Then patients' warfarin dose adjustments according to INR, was done by the clinical pharmacist for one year. Patients received continuous verbal education and written information about warfarin. Main outcome measure The primary outcome for this study was the INR control, while the secondary outcomes were the bleeding events and hospitalization due to warfarin. Results After the clinical pharmacist intervention there was significant (P < 0.01) improvement in INR control and a significant (P < 0.05) reduction in incidence of bleeding after clinical pharmacist intervention. Hospitalization due to warfarin related complications (bleeding, high INR, low INR) was also significantly (P < 0.001) reduced. Conclusion Clinical pharmacists intervention in warfarin therapy improve INR control, reduce bleeding and hospitalization due to warfarin complications.

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Background There is a paucity of studies in acute kidney injury in the intensive care unit, particularly in Sudan. Objectives The current study has estimated the incidence; risk factors and outcomes of subjects with acute kidney injury developed during admission to the intensive care unit at Fedail Hospital, Khartoum, Sudan. Methodology This was a cross-sectional study conducted in the intensive care unit during the period from July 2018 to June 2019. The data was collected from the clinical profiles of all adult subjects' who have met the published criteria for acute kidney injury. Analysis of association (Chi square test χ 2) and multivariate logistic regression were used to analyze data. Main outcome measure The development of acute kidney injury during the subjects' stay in the intensive care unit, length of hospital stay and death. Results From a total of 187 subjects admitted to the intensive care unit; only (105, 56.2%) have met the inclusion criteria (mean age was 61 ± 3.5 years). The main finding of the study was the high incidence of acute kidney injury 39%. The major significant predictors for the development of acute kidney injury with respective odds ratio (OR) were: sepsis (OR 7.

The mTOR-inhibitor rapamycin is a potent drug used in many immunosuppressive and antiinflammatory therapeutic regimes. In renal transplantation despite its benefical roles rapamycin in some cases can promote renal fibrosis in the kidney but the underlying mechanisms are unknown. In this study, we tested for possible modulatory effects of rapamycin on the cytokine-triggered matrix metalloproteinase 9 (MMP-9)/ tissue inhibitor of metalloproteinase (TIMP)-1 protease-antiprotease system which is critically involved in renal inflammation and fibrosis. Treatment of rat mesangial cells (MC) with rapamycin dosedependently reduced the interleukin 1 (IL-1-triggered increase in gelatinolytic levels as demonstrated by zymography. The reduction in the extracellular MMP-9 content by rapamycin coincided with an attenuation in cytokine-induced steady-state MMP-9 mRNA levels. Conversely, rapamycin caused a dose-dependent increase in cytokine-evoked TIMP-1 expression in a Smad binding element (SBE) -dependent manner. Surprisingly, the attenuation of MMP-9 mRNA levels by rapamycin is accompanied by a potentiation of IL-1-induced MMP-9 promoter activity in which the stimulatory effects by rapamycin are mainly attributed to a proximal AP-1 binding site. Furthermore, the rapamycin-dependent potentiation of MMP-9 expression is accompanied by an amplification of cytokine-triggered activities of nuclear factor B (NF-B) and activator protein 1 (AP-1) transcription factors. Importantly, rapamycin-triggered increase in MMP-9 promoter activity is fully impaired when we used a MMP-9 reporter construct which is under the additional control of the 3´untranslated region (3´-UTR) of MMP-9. Collectively, these data imply that rapamycin inhibits the cytokineinduced MMP-9 mainly through posttranscriptional events and thereby exerts profibrotic activities.