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	<title>Virtual Journal Club &#187; Am J Kidney Dis</title>
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	<description>Division of Hospital Medicine Virtual Journal Club</description>
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		<title>Urgent-Start Peritoneal Dialysis: A Quality Improvement Report.</title>
		<link>http://beckerinfo.net/JClub/2011/10/25/urgent-start-peritoneal-dialysis-a-quality-improvement-report/</link>
		<comments>http://beckerinfo.net/JClub/2011/10/25/urgent-start-peritoneal-dialysis-a-quality-improvement-report/#comments</comments>
		<pubDate>Tue, 25 Oct 2011 11:53:32 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

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		<description><![CDATA[
        Urgent-Start Peritoneal Dialysis: A Quality Improvement Report.
        Am J Kidney Dis. 2011 Oct 21;
        Authors:  Ghaffari A
        Abstract
        BACKGROUND: Compared with hemodialysis, peritoneal dialysis (PD) is a cost-effective an...]]></description>
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        <p><b>Urgent-Start Peritoneal Dialysis: A Quality Improvement Report.</b></p>
        <p>Am J Kidney Dis. 2011 Oct 21;</p>
        <p>Authors:  Ghaffari A</p>
        <p>Abstract<br>
        BACKGROUND: Compared with hemodialysis, peritoneal dialysis (PD) is a cost-effective and patient-centered option with an early survival advantage, yet only 7% of patients with end-stage renal disease in the United States receive PD. PD underutilization is due in part to nephrologists&#39; unfamiliarity with directly starting PD in patients who present with kidney failure requiring urgent initiation of dialysis. DESIGN: Quality improvement report. SETTING &amp; PARTICIPANTS: Single-center study whereby 18 patients who presented urgently with chronic kidney disease stage 5 without a plan for dialysis modality were offered PD as the initial modality of dialysis. Concurrently, 9 patients started on PD therapy nonurgently were included as the comparative group. QUALITY IMPROVEMENT PLAN: An urgent-start PD program was developed to support and standardize the process by which patients without a plan for dialysis modality were started on PD. This included rapid PD access placement, PD nursing education, and administrative support. Standardized protocols were created for modality selection, initial prescription, and prevention and management of complications. MEASURES: Short-term (90-day) clinical outcomes (Kt/V, hemoglobin, iron saturation, parathyroid hormone, phosphorus, calcium, and albumin) and complications (peritonitis, exit-site infections, leaks, and catheter malfunction) were compared between the urgent-start and non-urgent-start PD groups. RESULTS: Short-term clinical outcomes were similar between the 2 groups for all parameters except uncorrected serum calcium level, which was lower in the urgent-start group (P = 0.02). Peritonitis, exit-site infection, catheter-related complications, and other complications were similar between the 2 groups, although the number of minor leaks was higher in the urgent-start group. LIMITATIONS: This is a single-center nonrandomized study with a small sample size. CONCLUSIONS: Our structured program shows safety and feasibility in starting PD in patients with kidney failure who present without a plan for dialysis modality. The steps laid out in this report can provide the framework for creating local urgent-start PD programs.<br>
        </p><p>PMID: 22019332 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<title>Decongestive Treatment of Acute Decompensated Heart Failure: Cardiorenal Implications of Ultrafiltration and Diuretics.</title>
		<link>http://beckerinfo.net/JClub/2011/10/23/decongestive-treatment-of-acute-decompensated-heart-failure-cardiorenal-implications-of-ultrafiltration-and-diuretics/</link>
		<comments>http://beckerinfo.net/JClub/2011/10/23/decongestive-treatment-of-acute-decompensated-heart-failure-cardiorenal-implications-of-ultrafiltration-and-diuretics/#comments</comments>
		<pubDate>Sun, 23 Oct 2011 19:13:45 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

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		<description><![CDATA[
        Decongestive Treatment of Acute Decompensated Heart Failure: Cardiorenal Implications of Ultrafiltration and Diuretics.
        Am J Kidney Dis. 2011 Oct 17;
        Authors:  Freda BJ, Slawsky M, Mallidi J, Braden GL
        Abstract
        ...]]></description>
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        <p><b>Decongestive Treatment of Acute Decompensated Heart Failure: Cardiorenal Implications of Ultrafiltration and Diuretics.</b></p>
        <p>Am J Kidney Dis. 2011 Oct 17;</p>
        <p>Authors:  Freda BJ, Slawsky M, Mallidi J, Braden GL</p>
        <p>Abstract<br>
        In patients with acute decompensated heart failure (ADHF), treatment aimed at adequate decongestion of the volume overloaded state is essential. Despite diuretic therapy, many patients remain volume overloaded and symptomatic. In addition, adverse effects related to diuretic treatment are common, including worsening kidney function and electrolyte disturbances. The development of decreased kidney function during treatment affects the response to diuretic therapy and is associated with important clinical outcomes, including mortality. The occurrence of diuretic resistance and the morbidity and mortality associated with diuretic therapy has stimulated interest to develop effective and safe treatment strategies that maximize decongestion and minimize decreased kidney function. During the last few decades, extracorporeal ultrafiltration has been used to remove fluid from diuretic-refractory hypervolemic patients. Recent clinical studies using user-friendly machines have suggested that ultrafiltration may be highly effective for decongesting patients with ADHF. Many questions remain regarding the comparative impact of diuretics and ultrafiltration on important clinical outcomes and adverse effects, including decreased kidney function. This article serves as a summary of key clinical studies addressing these points. The overall goal is to assist practicing clinicians who are contemplating the use of ultrafiltration for a patient with ADHF.<br>
        </p><p>PMID: 22014726 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<title>Hyponatremia in Hospitalized Cancer Patients and Its Impact on Clinical Outcomes.</title>
		<link>http://beckerinfo.net/JClub/2011/10/19/hyponatremia-in-hospitalized-cancer-patients-and-its-impact-on-clinical-outcomes/</link>
		<comments>http://beckerinfo.net/JClub/2011/10/19/hyponatremia-in-hospitalized-cancer-patients-and-its-impact-on-clinical-outcomes/#comments</comments>
		<pubDate>Wed, 19 Oct 2011 21:03:51 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

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		<description><![CDATA[
        Hyponatremia in Hospitalized Cancer Patients and Its Impact on Clinical Outcomes.
        Am J Kidney Dis. 2011 Oct 14;
        Authors:  Doshi SM, Shah P, Lei X, Lahoti A, Salahudeen AK
        Abstract
        BACKGROUND: Hyponatremia is the...]]></description>
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        <p><b>Hyponatremia in Hospitalized Cancer Patients and Its Impact on Clinical Outcomes.</b></p>
        <p>Am J Kidney Dis. 2011 Oct 14;</p>
        <p>Authors:  Doshi SM, Shah P, Lei X, Lahoti A, Salahudeen AK</p>
        <p>Abstract<br>
        BACKGROUND: Hyponatremia is the most common electrolyte abnormality in clinical practice, yet little is known about its frequency in patients with cancer or its impact on their clinical outcomes. STUDY DESIGN: Retrospective analysis of prospectively collected data. SETTING &amp; PARTICIPANTS: Patients with cancer admitted to the University of Texas M.D. Anderson Cancer Center in 2006 for 3 months. PREDICTOR: Serum sodium levels categorized as eunatremia (serum sodium, 135-147 mEq/L) and mild (134-130 mEq/L), moderate (129-120 mEq/L), and severe (&lt;120 mEq/L) hyponatremia. OUTCOMES: (1) Length of hospital stay and (2) 90-day mortality. RESULTS: In 4,702 admissions in 3,357 patients with cancer, hyponatremia (serum sodium &lt;135 mEq/L) was noted in 47% of admissions. It was mild in 36%, moderate in 10%, and severe in 1%. Hyponatremia was acquired during the hospital stay in 24%. Using the first admission data, mean length of stay was 5.6 ± 5.0 days for patients with eunatremia and 9.9 ± 9.2, 13.0 ± 14.1, and 11.5 ± 12.6 days for those with mild, moderate, and severe hyponatremia, respectively. The respective HRs in the multivariate Cox model for longer hospital stay, using patients with eunatremia as reference, were 1.92 (95% CI, 1.75-2.13; P &lt; 0.01), 2.94 (95% CI, 2.56-3.45; P &lt; 0.01), and 2.32 (95% CI, 1.32-4.00; P = 0.01). 283 (8.4%) deaths occurred during 90 days, and in the multivariate model, the respective HRs for 90-day mortality for mild, moderate, and severe hyponatremia were 2.04 (95% CI, 1.42-2.91; P &lt; 0.01); 4.74 (95% CI, 3.21-7.01; P &lt; 0.01), and 3.46 (95% CI, 1.05-11.44; P = 0.04). These findings were consistent when analyses were repeated with sodium levels in tertiles. LIMITATIONS: Observational study, retrospective, inability to adjust for all comorbid conditions. CONCLUSION: Hyponatremia in patients with cancer is associated with longer hospital stay and higher mortality. Whether long-term correction of hyponatremia would improve these outcomes remains to be determined.<br>
        </p><p>PMID: 22001181 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Therapeutic Response to Vasoconstrictors in Hepatorenal Syndrome Parallels Increase in Mean Arterial Pressure: A Pooled Analysis of Clinical Trials.</title>
		<link>http://beckerinfo.net/JClub/2011/10/05/therapeutic-response-to-vasoconstrictors-in-hepatorenal-syndrome-parallels-increase-in-mean-arterial-pressure-a-pooled-analysis-of-clinical-trials/</link>
		<comments>http://beckerinfo.net/JClub/2011/10/05/therapeutic-response-to-vasoconstrictors-in-hepatorenal-syndrome-parallels-increase-in-mean-arterial-pressure-a-pooled-analysis-of-clinical-trials/#comments</comments>
		<pubDate>Wed, 05 Oct 2011 13:54:11 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

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		<description><![CDATA[
        Therapeutic Response to Vasoconstrictors in Hepatorenal Syndrome Parallels Increase in Mean Arterial Pressure: A Pooled Analysis of Clinical Trials.
        Am J Kidney Dis. 2011 Sep 28;
        Authors:  Velez JC, Nietert PJ
        Abstract
...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>Therapeutic Response to Vasoconstrictors in Hepatorenal Syndrome Parallels Increase in Mean Arterial Pressure: A Pooled Analysis of Clinical Trials.</b></p>
        <p>Am J Kidney Dis. 2011 Sep 28;</p>
        <p>Authors:  Velez JC, Nietert PJ</p>
        <p>Abstract<br>
        BACKGROUND: Vasoconstrictor therapy has been advocated as treatment for hepatorenal syndrome (HRS). Our aim was to explore across all tested vasoconstrictors whether achievement of a substantial increase in arterial blood pressure is associated with recovery of kidney function in HRS. STUDY DESIGN: Pooled analysis of published studies identified by electronic database search. SETTING &amp; POPULATION: Data pooled across 501 participants in 21 studies. SELECTION CRITERIA FOR STUDIES: Human studies evaluating the efficacy of a vasoconstrictor administered for 72 hours or longer in adults with HRS type 1 or 2. INTERVENTION: Vasoconstrictor therapy. OUTCOMES &amp; MEASUREMENTS: Cohorts&#39; mean arterial pressure (MAP), serum creatinine level, urinary output, and plasma renin activity (PRA) at baseline and subsequent times during treatment. Linear regression models were constructed to estimate mean daily changes in MAP, serum creatinine level, urinary output, and PRA for each study subgroup. Correlations were used to assess for association between variables. RESULTS: An increase in MAP is associated strongly with a decrease in serum creatinine level, but is not associated with an increase in urinary output. Associations were stronger when analyses were restricted to randomized clinical trials and were not limited to cohorts with either lower baseline MAP or lower baseline serum creatinine level. Most studies tested terlipressin as vasoconstrictor, whereas fewer studies tested ornipressin, midodrine, octreotide, or norepinephrine. Excluding cohorts of participants treated with terlipressin or ornipressin did not eliminate the association. Furthermore, a decrease in PRA correlated with improvement in kidney function. LIMITATIONS: Studies were not originally designed to test our question. We lacked access to individual patient data. CONCLUSIONS: An increase in MAP during vasoconstrictor therapy in patients with HRS is associated with improvement in kidney function across the spectrum of drugs tested to date. These results support consideration for a goal-directed approach to the treatment of HRS.<br>
        </p><p>PMID: 21962618 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Comparison of Measured GFR, Serum Creatinine, Cystatin C, and Beta-Trace Protein to Predict ESRD in African Americans With Hypertensive CKD.</title>
		<link>http://beckerinfo.net/JClub/2011/09/29/comparison-of-measured-gfr-serum-creatinine-cystatin-c-and-beta-trace-protein-to-predict-esrd-in-african-americans-with-hypertensive-ckd/</link>
		<comments>http://beckerinfo.net/JClub/2011/09/29/comparison-of-measured-gfr-serum-creatinine-cystatin-c-and-beta-trace-protein-to-predict-esrd-in-african-americans-with-hypertensive-ckd/#comments</comments>
		<pubDate>Fri, 30 Sep 2011 01:38:03 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=f27215f36b490a97418d5c8a87b4b7e6</guid>
		<description><![CDATA[
        Comparison of Measured GFR, Serum Creatinine, Cystatin C, and Beta-Trace Protein to Predict ESRD in African Americans With Hypertensive CKD.
        Am J Kidney Dis. 2011 Sep 21;
        Authors:  Bhavsar NA, Appel LJ, Kusek JW, Contreras G, B...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>Comparison of Measured GFR, Serum Creatinine, Cystatin C, and Beta-Trace Protein to Predict ESRD in African Americans With Hypertensive CKD.</b></p>
        <p>Am J Kidney Dis. 2011 Sep 21;</p>
        <p>Authors:  Bhavsar NA, Appel LJ, Kusek JW, Contreras G, Bakris G, Coresh J, Astor BC,  </p>
        <p>Abstract<br>
        BACKGROUND: Identification of persons with chronic kidney disease (CKD) who are at highest risk to progress to end-stage renal disease (ESRD) is necessary to reduce the burden of kidney failure. The relative utility of traditional markers of kidney function, including estimated glomerular filtration rate (eGFR) and serum creatinine level, and emerging markers of kidney function, including cystatin C and beta-trace protein (BTP) levels, to predict ESRD and mortality has yet to be established. STUDY DESIGN: Randomized clinical trial followed by an observational cohort study. SETTING &amp; PARTICIPANTS: 865 African American individuals with hypertensive CKD enrolled in a clinical trial of 2 levels of blood pressure control and 3 different antihypertensive drugs as initial therapy and subsequently followed by an observational cohort study. PREDICTORS: Quintile of measured GFR (mGFR) by iothalamate clearance, serum creatinine, serum creatinine-based eGFR, cystatin C, and BTP values. OUTCOMES &amp; MEASUREMENTS: Incidence of ESRD and mortality. RESULTS: 246 participants reached ESRD during a median follow-up of 102 months. The incidence rate of ESRD was higher with higher quintiles of each marker. The association between higher BTP level and ESRD was stronger than those for the other markers, including mGFR. All markers remained significantly associated with ESRD after adjustment for mGFR and relevant covariates (all P &lt; 0.05), with BTP level retaining the strongest association (HR for highest vs lowest quintile, 5.7; 95% CI, 2.2-14.9). Associations with the combined end point of ESRD or mortality (n = 390) were weaker, but remained significant for cystatin C (P = 0.05) and BTP levels (P = 0.004). LIMITATIONS: The ability of these markers to predict ESRD and mortality in other racial and ethnic groups and in individuals with CKD due to other causes is unknown. CONCLUSIONS: Plasma BTP and cystatin C levels may be useful adjuncts to serum creatinine level and mGFR in evaluating risk of progression of kidney disease.<br>
        </p><p>PMID: 21944667 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>The Risk of Infection-Related Hospitalization With Decreased Kidney Function.</title>
		<link>http://beckerinfo.net/JClub/2011/09/15/the-risk-of-infection-related-hospitalization-with-decreased-kidney-function/</link>
		<comments>http://beckerinfo.net/JClub/2011/09/15/the-risk-of-infection-related-hospitalization-with-decreased-kidney-function/#comments</comments>
		<pubDate>Thu, 15 Sep 2011 19:16:46 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=0927a35570965ff5240af79702868509</guid>
		<description><![CDATA[
        The Risk of Infection-Related Hospitalization With Decreased Kidney Function.
        Am J Kidney Dis. 2011 Sep 7;
        Authors:  Dalrymple LS, Katz R, Kestenbaum B, de Boer IH, Fried L, Sarnak MJ, Shlipak MG
        Abstract
        BACKGR...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>The Risk of Infection-Related Hospitalization With Decreased Kidney Function.</b></p>
        <p>Am J Kidney Dis. 2011 Sep 7;</p>
        <p>Authors:  Dalrymple LS, Katz R, Kestenbaum B, de Boer IH, Fried L, Sarnak MJ, Shlipak MG</p>
        <p>Abstract<br>
        BACKGROUND: Moderate kidney disease may predispose to infection. We sought to determine whether decreased kidney function, estimated by serum cystatin C level, was associated with the risk of infection-related hospitalization in older individuals. STUDY DESIGN: Cohort study. SETTING &amp; PARTICIPANTS: 5,142 Cardiovascular Health Study (CHS) participants with measured serum creatinine and cystatin C and without estimated glomerular filtration rate (eGFR) &lt;15 mL/min/1.73 m(2) at enrollment. PREDICTOR: The primary exposure of interest was eGFR using serum cystatin C level (eGFR(SCysC)). OUTCOME: Infection-related hospitalizations during a median follow-up of 11.5 years. RESULTS: In adjusted analyses, eGFR(SCysC) categories of 60-89, 45-59, and 15-44 mL/min/1.73 m(2) were associated with 16%, 37%, and 64% greater risk of all-cause infection-related hospitalization, respectively, compared with eGFR(SCysC) ?90 mL/min/1.73 m(2). When cause-specific infection was examined, eGFR(SCysC) of 15-44 mL/min/1.73 m(2) was associated with an 80% greater risk of pulmonary and 160% greater risk of genitourinary infection compared with eGFR(SCysC) ?90 mL/min/1.73 m(2). LIMITATIONS: No measures of urinary protein, study limited to principal discharge diagnosis. CONCLUSIONS: Lower kidney function, estimated using cystatin C level, was associated with a linear and graded risk of infection-related hospitalization. These findings highlight that even moderate degrees of decreased kidney function are associated with clinically significant higher risks of serious infection in older individuals.<br>
        </p><p>PMID: 21906862 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<item>
		<title>Venous Thromboembolism in Patients With Reduced Estimated GFR: A Population-Based Perspective.</title>
		<link>http://beckerinfo.net/JClub/2011/08/31/venous-thromboembolism-in-patients-with-reduced-estimated-gfr-a-population-based-perspective/</link>
		<comments>http://beckerinfo.net/JClub/2011/08/31/venous-thromboembolism-in-patients-with-reduced-estimated-gfr-a-population-based-perspective/#comments</comments>
		<pubDate>Wed, 31 Aug 2011 21:32:14 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=df41f5848a3defde46ea256cab462e2f</guid>
		<description><![CDATA[
        Venous Thromboembolism in Patients With Reduced Estimated GFR: A Population-Based Perspective.
        Am J Kidney Dis. 2011 Aug 26;
        Authors:  Parikh AM, Spencer FA, Lessard D, Emery C, Baylin A, Linkletter C, Goldberg RJ
        Abstr...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>Venous Thromboembolism in Patients With Reduced Estimated GFR: A Population-Based Perspective.</b></p>
        <p>Am J Kidney Dis. 2011 Aug 26;</p>
        <p>Authors:  Parikh AM, Spencer FA, Lessard D, Emery C, Baylin A, Linkletter C, Goldberg RJ</p>
        <p>Abstract<br>
        BACKGROUND: An increased frequency of venous thromboembolism (VTE) has been shown in patients with decreased kidney function measured by decreased estimated glomerular filtration rate (eGFR). However, present practices with respect to VTE prevention and management in patients with decreased eGFR in general population settings are uncertain. STUDY DESIGN: Observational study. SETTING &amp; PARTICIPANTS: Community investigation of 1,509 metropolitan Worcester, MA, residents with a validated VTE in 1999, 2001, and 2003 with further follow-up for up to 3 years. PREDICTOR: Patients with VTE classified further according to eGFR on presentation: &lt;30, 30-59, 60-89, or ?90 mL/min/1.73 m(2) (reference group). OUTCOMES: Recurrent VTE, major bleeding episodes, and all-cause mortality. MEASUREMENTS: Demographic and clinical characteristics, treatment practices, and study outcomes were extracted from patients&#39; hospital and outpatient medical records; eGFR was estimated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. RESULTS: Patients with VTE with eGFR &lt;30 mL/min/1.73 m(2) were at increased risk of recurrent VTE (HR, 1.83; 95% CI, 1.03-3.25), major bleeding episodes (HR, 2.30; 95% CI, 1.28-4.16), and all-cause mortality (HR, 1.70; 95% CI, 1.12-2.57) during a 3-year follow-up. Patients with decreased eGFR also presented with more comorbid conditions and were less likely to be discharged on any form of anticoagulant therapy (72.6%, 81.0%, 82.1%, and 87.3% for eGFR &lt;30, 30-59, 60-89, and ?90 mL/min/1.73 m(2), respectively; P &lt; 0.001). LIMITATIONS: Decreased eGFR status is presumed based on creatinine values on clinical presentation. The impact of drug dosage, timing, type of anticoagulant therapy, and medication adherence on study outcomes could not be evaluated. CONCLUSIONS: Severe decreases in eGFR are associated with increased risk of long-term recurrent VTE, bleeding, and total mortality in patients with VTE. A greater frequency of serious comorbid conditions, difficulties implementing available management strategies, and suboptimal VTE prophylaxis during hospital admissions likely contributed to our findings.<br>
        </p><p>PMID: 21872977 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<slash:comments>0</slash:comments>
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		<title>?-Blockers for Prevention of Sudden Cardiac Death in Patients on Hemodialysis: A Propensity Score Analysis of the HEMO Study.</title>
		<link>http://beckerinfo.net/JClub/2011/08/31/%ce%b2-blockers-for-prevention-of-sudden-cardiac-death-in-patients-on-hemodialysis-a-propensity-score-analysis-of-the-hemo-study/</link>
		<comments>http://beckerinfo.net/JClub/2011/08/31/%ce%b2-blockers-for-prevention-of-sudden-cardiac-death-in-patients-on-hemodialysis-a-propensity-score-analysis-of-the-hemo-study/#comments</comments>
		<pubDate>Wed, 31 Aug 2011 21:32:06 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=938e429a5c8d7e50a3b9e0fb9f45bd47</guid>
		<description><![CDATA[
        ?-Blockers for Prevention of Sudden Cardiac Death in Patients on Hemodialysis: A Propensity Score Analysis of the HEMO Study.
        Am J Kidney Dis. 2011 Aug 26;
        Authors:  Tangri N, Shastri S, Tighiouart H, Beck GJ, Cheung AK, Eknoy...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>?-Blockers for Prevention of Sudden Cardiac Death in Patients on Hemodialysis: A Propensity Score Analysis of the HEMO Study.</b></p>
        <p>Am J Kidney Dis. 2011 Aug 26;</p>
        <p>Authors:  Tangri N, Shastri S, Tighiouart H, Beck GJ, Cheung AK, Eknoyan G, Sarnak MJ</p>
        <p>Abstract<br>
        BACKGROUND: Hemodialysis patients have an elevated risk of sudden cardiac death. Although the efficacy of ?-blockers for the prevention of sudden cardiac death has been proven in the general population, little evidence exists in patients with kidney failure. STUDY DESIGN: Post hoc analysis of the Hemodialysis (HEMO) Study. SETTING &amp; PARTICIPANTS: Participants enrolled in the HEMO Study from May 1995 to February 2001. INTERVENTION: ?-Blocker use ascertained through self-reported questionnaires and dialysis clinic charts. OUTCOMES: Sudden cardiac death adjudicated by a committee as a secondary outcome of interest. MEASUREMENTS: We used Cox proportional hazards regression models, competing risk survival analysis, propensity score matching, and covariate adjustment to study the association of ?-blockers with sudden cardiac death. RESULTS: 1,747 patients were included in this study, and 521 were on ?-blocker therapy at baseline. Mean age was 58 years, 57% were women, and 39% had ischemic heart disease (IHD) at baseline. Baseline ?-blocker use was not associated with lower risk of sudden cardiac death in univariate (cause-specific HR, 0.89; 95% CI, 0.64-1.24), multivariable (cause-specific HR, 0.87; 95% CI, 0.62-1.22), or propensity-matched (cause-specific HR, 0.91; 95% CI, 0.55-1.50) analyses. There was a significant interaction between ?-blocker use and sudden cardiac death (interaction P = 0.03) in patients with (cause-specific HR, 0.65; 95% CI, 0.42-1.01) and without IHD (cause-specific HR, 1.61; 95% CI, 0.92-2.80). LIMITATIONS: Observational nature of the study. CONCLUSIONS: In hemodialysis patients without preexisting IHD, ?-blocker use was not associated with lower risk of sudden cardiac death. However, there was a trend toward benefit in those with IHD.<br>
        </p><p>PMID: 21872979 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<title>The Role of Functional Status in Discharge to Assisted Care Facilities and In-Hospital Death Among Dialysis Patients.</title>
		<link>http://beckerinfo.net/JClub/2011/08/11/the-role-of-functional-status-in-discharge-to-assisted-care-facilities-and-in-hospital-death-among-dialysis-patients/</link>
		<comments>http://beckerinfo.net/JClub/2011/08/11/the-role-of-functional-status-in-discharge-to-assisted-care-facilities-and-in-hospital-death-among-dialysis-patients/#comments</comments>
		<pubDate>Fri, 12 Aug 2011 00:33:57 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

		<guid isPermaLink="false">http://beckerinfo.net/JClub/?guid=db284b199b9101cf0589bfeba6f5479c</guid>
		<description><![CDATA[
        The Role of Functional Status in Discharge to Assisted Care Facilities and In-Hospital Death Among Dialysis Patients.
        Am J Kidney Dis. 2011 Aug 4;
        Authors:  Sood MM, Rigatto C, Bueti J, Jassal V, Miller L, Verrelli M, Bohm C, M...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>The Role of Functional Status in Discharge to Assisted Care Facilities and In-Hospital Death Among Dialysis Patients.</b></p>
        <p>Am J Kidney Dis. 2011 Aug 4;</p>
        <p>Authors:  Sood MM, Rigatto C, Bueti J, Jassal V, Miller L, Verrelli M, Bohm C, Mojica J, Roberts D, Komenda P</p>
        <p>BACKGROUND: Functional status is an important component in the assessment of hospitalized patients. We set out to determine the scope, severity, and prognostic significance of impaired functional status in acutely hospitalized dialysis patients. STUDY DESIGN: Retrospective cohort study. SETTING &amp; PARTICIPANTS: 1,286 hospitalized dialysis patients admitted and discharged from 1 of 11 area hospitals in Manitoba, Canada, from September 2003 to September 2010 with an activity of daily living (ADL) assessment within 24 hours of admission. PREDICTOR: The 12-point ADL score assesses 6 domains (bathing, toileting, dressing, incontinence, feeding, and transferring) and scores them as independent or supervision only (score, 0), partial assistance (1), and full assistance (2). Thus, higher score indicates worse functional status. Parametric and nonparametric tests were used as appropriate to determine differences in baseline characteristics. OUTCOMES: Multivariable logistic regression and Cox proportional hazards assessed the association between functional status, in-hospital death, and discharge to an assisted care facility. RESULTS: During the study period, 250 (19.4%) and 72 (5.6%) patients experienced the outcomes of in-hospital death or discharge to an assisted care facility. Abnormalities in functional status were present in &gt;70% of the cohort. ADL score within 24 hours of admission combined with age differentiated risks of death and discharge to an assisted care facility home, ranging from 4.8%-46.6% and 0.6%-17.8%, respectively. After adjustment, ORs of death and discharge to an assisted care facility were 1.16 (95% CI, 1.11-1.22; P &lt; 0.001; C statistic = 0.79) and 1.25 (95% CI, 1.14-1.36; P &lt; 0.001; C statistic = 0.91) per 1-point increase in ADL score, respectively. Findings were consistent after accounting for the competing outcomes of in-hospital death or discharge to an assisted care facility versus discharge to home. LIMITATIONS: A 1-time measurement of ADLs could not differentiate temporary from long-term deterioration in functional status. CONCLUSIONS: Impaired functional status is common at the time of admission in the dialysis population. A single ADL score measurement at admission combined with age is highly predictive of poor outcomes in the hospitalized dialysis population.</p>
        <p>PMID: 21820221 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<title>Approach to the Evaluation of a Patient With an Increased Serum Osmolal Gap and High-Anion-Gap Metabolic Acidosis.</title>
		<link>http://beckerinfo.net/JClub/2011/07/29/approach-to-the-evaluation-of-a-patient-with-an-increased-serum-osmolal-gap-and-high-anion-gap-metabolic-acidosis/</link>
		<comments>http://beckerinfo.net/JClub/2011/07/29/approach-to-the-evaluation-of-a-patient-with-an-increased-serum-osmolal-gap-and-high-anion-gap-metabolic-acidosis/#comments</comments>
		<pubDate>Sat, 30 Jul 2011 00:33:49 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

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		<description><![CDATA[
        Approach to the Evaluation of a Patient With an Increased Serum Osmolal Gap and High-Anion-Gap Metabolic Acidosis.
        Am J Kidney Dis. 2011 Jul 26;
        Authors:  Kraut JA, Xing SX
        An increase in serum osmolality and serum osmo...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>Approach to the Evaluation of a Patient With an Increased Serum Osmolal Gap and High-Anion-Gap Metabolic Acidosis.</b></p>
        <p>Am J Kidney Dis. 2011 Jul 26;</p>
        <p>Authors:  Kraut JA, Xing SX</p>
        <p>An increase in serum osmolality and serum osmolal gap with or without high-anion-gap metabolic acidosis is an important clue to exposure to one of the toxic alcohols, which include methanol, ethylene glycol, diethylene glycol, propylene glycol, or isopropanol. However, the increase in serum osmolal gap and metabolic acidosis can occur either together or alone depending on several factors, including baseline serum osmolal gap, molecular weight of the alcohol, and stage of metabolism of the alcohol. In addition, other disorders, including diabetic or alcoholic ketoacidosis, acute kidney injury, chronic kidney disease, and lactic acidosis, can cause high-anion-gap metabolic acidosis associated with an increased serum osmolal gap and therefore should be explored in the differential diagnosis. It is essential for clinicians to understand the value and limitations of osmolal gap to assist in reaching the correct diagnosis and initiating appropriate treatment. In this teaching case, we present a systematic approach to diagnosing high serum osmolality and increased serum osmolal gap with or without high-anion-gap metabolic acidosis.</p>
        <p>PMID: 21794966 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<title>Volume Depletion Versus Dehydration: How Understanding the Difference Can Guide Therapy.</title>
		<link>http://beckerinfo.net/JClub/2011/06/30/volume-depletion-versus-dehydration-how-understanding-the-difference-can-guide-therapy/</link>
		<comments>http://beckerinfo.net/JClub/2011/06/30/volume-depletion-versus-dehydration-how-understanding-the-difference-can-guide-therapy/#comments</comments>
		<pubDate>Thu, 30 Jun 2011 19:19:40 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

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		<description><![CDATA[
        Volume Depletion Versus Dehydration: How Understanding the Difference Can Guide Therapy.
        Am J Kidney Dis. 2011 Jun 24;
        Authors:  Bhave G, Neilson EG
        Although often used interchangeably, dehydration and volume depletion ...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>Volume Depletion Versus Dehydration: How Understanding the Difference Can Guide Therapy.</b></p>
        <p>Am J Kidney Dis. 2011 Jun 24;</p>
        <p>Authors:  Bhave G, Neilson EG</p>
        <p>Although often used interchangeably, dehydration and volume depletion are not synonyms. Dehydration refers to loss of total-body water, producing hypertonicity, which now is the preferred term in lieu of dehydration, whereas volume depletion refers to a deficit in extracellular fluid volume. In particular, hypertonicity implies intracellular volume contraction, whereas volume depletion implies blood volume contraction. Using a case of hyperglycemic hypertonic nonketosis as an example, we examine the changing composition of body fluid spaces to explore the distinction between dehydration and hypertonicity from volume depletion.</p>
        <p>PMID: 21705120 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<title>Cystatin C in Prediction of Acute Kidney Injury: A Systemic Review and Meta-analysis.</title>
		<link>http://beckerinfo.net/JClub/2011/05/24/cystatin-c-in-prediction-of-acute-kidney-injury-a-systemic-review-and-meta-analysis/</link>
		<comments>http://beckerinfo.net/JClub/2011/05/24/cystatin-c-in-prediction-of-acute-kidney-injury-a-systemic-review-and-meta-analysis/#comments</comments>
		<pubDate>Tue, 24 May 2011 13:10:54 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

		<guid isPermaLink="false"></guid>
		<description><![CDATA[
        Cystatin C in Prediction of Acute Kidney Injury: A Systemic Review and Meta-analysis.
        Am J Kidney Dis. 2011 May 19;
        Authors:  Zhang Z, Lu B, Sheng X, Jin N
        BACKGROUND: Cystatin C (CysC) has been proposed as a filtration...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>Cystatin C in Prediction of Acute Kidney Injury: A Systemic Review and Meta-analysis.</b></p>
        <p>Am J Kidney Dis. 2011 May 19;</p>
        <p>Authors:  Zhang Z, Lu B, Sheng X, Jin N</p>
        <p>BACKGROUND: Cystatin C (CysC) has been proposed as a filtration marker for the early detection of acute kidney injury (AKI); however, a wide range of its predictive accuracy has been reported. STUDY DESIGN: Meta-analysis of diagnostic test studies. SETTING &amp; POPULATION: Various clinical settings of AKI, including patients after cardiac surgery, pediatric patients, and critically ill patients. SELECTION CRITERIA: Computerized search of PubMed, Current Contents, CINAHL, and EMBASE from inception until November 15, 2010, was performed to identify potentially relevant articles. Inclusion criteria were studies investigating the diagnostic accuracy of CysC level to predict AKI. There were no language restrictions in the search. INDEX TESTS: Increasing or increased serum CysC level or urinary CysC excretion. REFERENCE TESTS: The outcome was the development of AKI, primarily based on serum creatinine level (definition varied across studies). RESULTS: We analyzed data from 19 studies and 11 countries involving 3,336 patients. Of these studies, 13 could be included in the meta-analysis. Across all settings, the diagnostic OR for serum CysC level to predict AKI was 23.5 (95% CI, 14.2-38.9), with sensitivity and specificity of 0.84 and 0.82, respectively. The area under the receiver operating characteristic curve (AUROC) of serum CysC level to predict AKI was 0.96 (95% CI, 0.95-0.97). Subgroup analysis showed that serum CysC was of diagnostic value when measured early (within 24 hours after renal insult or intensive care unit admission). For the diagnostic value of urinary CysC excretion, the diagnostic OR was 2.60 (95% CI, 2.01-3.35), with sensitivity and specificity of 0.52 and 0.70, respectively. The AUROC of urinary CysC excretion to predict AKI was 0.64 (95% CI, 0.62-0.66). LIMITATIONS: Variation in criteria for definitions of index and reference tests, absence of measured glomerular filtration rate in most studies. CONCLUSION: Serum CysC appears to be a good biomarker in the prediction of AKI, whereas urinary CysC excretion has only moderate diagnostic value.</p>
        <p>PMID: 21601330 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<title>Relapsing and Recurrent Peritoneal Dialysis-Associated Peritonitis: A Multicenter Registry Study.</title>
		<link>http://beckerinfo.net/JClub/2011/05/24/relapsing-and-recurrent-peritoneal-dialysis-associated-peritonitis-a-multicenter-registry-study/</link>
		<comments>http://beckerinfo.net/JClub/2011/05/24/relapsing-and-recurrent-peritoneal-dialysis-associated-peritonitis-a-multicenter-registry-study/#comments</comments>
		<pubDate>Tue, 24 May 2011 13:10:33 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

		<guid isPermaLink="false"></guid>
		<description><![CDATA[
        Relapsing and Recurrent Peritoneal Dialysis-Associated Peritonitis: A Multicenter Registry Study.
        Am J Kidney Dis. 2011 May 19;
        Authors:  Burke M, Hawley CM, Badve SV, McDonald SP, Brown FG, Boudville N, Wiggins KJ, Bannister K...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>Relapsing and Recurrent Peritoneal Dialysis-Associated Peritonitis: A Multicenter Registry Study.</b></p>
        <p>Am J Kidney Dis. 2011 May 19;</p>
        <p>Authors:  Burke M, Hawley CM, Badve SV, McDonald SP, Brown FG, Boudville N, Wiggins KJ, Bannister KM, Johnson DW</p>
        <p>BACKGROUND: The causes, predictors, treatment, and outcomes of relapsed and recurrent peritoneal dialysis (PD)-associated peritonitis are poorly understood. STUDY DESIGN: Observational cohort study using Australia and New Zealand Dialysis and Transplant (ANZDATA) Registry data. SETTING &amp; PARTICIPANTS: All Australian PD patients between October 1, 2003, and December 31, 2007, with first episodes of peritonitis. PREDICTORS: Demographic, clinical, and facility variables and type of peritonitis; relapse (same organism or culture-negative episode occurring within 4 weeks of completion of therapy of a prior episode or 5 weeks if vancomycin used); recurrence (different organism occurring within 4 weeks of completion of therapy of a prior episode or 5 weeks if vancomycin used); control (first peritonitis episode without relapse or recurrence). OUTCOMES &amp; MEASUREMENTS: Hospitalization, catheter removal, hemodialysis therapy transfer, death. RESULTS: Of 6,024 PD patients studied, first episodes of relapsed, recurrent, and control peritonitis occurred in 356, 165, and 2,021 patients, respectively. Coagulase-negative staphylococci and Staphylococcus aureus accounted for 48% of relapsing peritonitis (adjusted OR, 1.26 [95% CI, 0.94-1.70] and 1.54 [95% CI, 1.08-2.19], respectively), but were much less likely to be isolated in recurrent peritonitis. Recurrent peritonitis was associated more frequently with fungi (13%; OR, 2.16; 95% CI, 1.12-4.17). The empirical antimicrobial approaches to relapsing and recurrent peritonitis were similar and their subsequent clinical outcomes were comparable. Compared with uncomplicated peritonitis, relapsed and recurrent peritonitis were associated with higher rates of catheter removal (22% vs 30% vs 37%, respectively; P &lt; 0.001) and permanent hemodialysis therapy transfer (20% vs 25% vs 32%; P &lt; 0.001), but similar rates of hospitalization (73% vs 70% vs 70%) and death (2.8% vs 2.0% vs 1.2%). LIMITATIONS: Limited covariate adjustment. Residual confounding and coding bias could not be excluded. CONCLUSIONS: Relapsed and recurrent peritonitis are caused by different spectra of micro-organisms, but are not readily clinically distinguishable at presentation. Empirical treatment with broad-spectrum antibiotics and subsequent adjustment according to antimicrobial susceptibilities results in similar clinical outcomes, albeit with appreciably higher rates of catheter removal and hemodialysis therapy transfer than for uncomplicated peritonitis.</p>
        <p>PMID: 21601333 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<title>Clinical Applications of Biomarkers for Acute Kidney Injury.</title>
		<link>http://beckerinfo.net/JClub/2011/03/20/clinical-applications-of-biomarkers-for-acute-kidney-injury/</link>
		<comments>http://beckerinfo.net/JClub/2011/03/20/clinical-applications-of-biomarkers-for-acute-kidney-injury/#comments</comments>
		<pubDate>Sun, 20 Mar 2011 16:06:29 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

		<guid isPermaLink="false"></guid>
		<description><![CDATA[
        Clinical Applications of Biomarkers for Acute Kidney Injury.
        Am J Kidney Dis. 2011 Mar 14;
        Authors:  Belcher JM, Edelstein CL, Parikh CR
        Research into novel therapies for acute kidney injury (AKI) has been hampered by r...]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>Clinical Applications of Biomarkers for Acute Kidney Injury.</b></p>
        <p>Am J Kidney Dis. 2011 Mar 14;</p>
        <p>Authors:  Belcher JM, Edelstein CL, Parikh CR</p>
        <p>Research into novel therapies for acute kidney injury (AKI) has been hampered by reliance on a diagnosis predicated on changes in serum creatinine level. As a marker for changing kidney function rather than frank kidney injury, creatinine level lacks sensitivity and specificity for the diagnosis of AKI and shows significant lag time before increasing after injury. It has been unclear whether the failure to translate promising results from animal studies in AKI into successful human trials has been caused by lack of therapeutic efficacy or inappropriately delayed application of the intervention. Multiple novel biomarkers with the potential to revolutionize the timing and accuracy of the diagnosis of AKI currently are under investigation. We have chosen to use one of these biomarkers, interleukin 18 (IL-18), to show the ways in which biomarkers at present can supplement the conventional management of AKI. IL-18 is well suited for this analysis because it is both a mediator of and marker for AKI. We describe 2 cases in which reliance on serum creatinine level for the diagnosis of AKI led to diagnostic and management uncertainty. In the context of these cases, we discuss how IL-18 and other biomarkers can facilitate earlier detection, enhance the differential diagnosis, and allow more prescient prognosis. Additionally, we describe the potential role for biomarkers in prospective trial design and discuss the utility of biomarkers in facilitating adequate powering of trials through more accurate characterization of cases and controls.</p>
        <p>PMID: 21411200 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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		<title>Management of Gram-Positive Coccal Bacteremia and Hemodialysis.</title>
		<link>http://beckerinfo.net/JClub/2011/02/22/management-of-gram-positive-coccal-bacteremia-and-hemodialysis/</link>
		<comments>http://beckerinfo.net/JClub/2011/02/22/management-of-gram-positive-coccal-bacteremia-and-hemodialysis/#comments</comments>
		<pubDate>Tue, 22 Feb 2011 12:11:52 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Am J Kidney Dis]]></category>

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		<description><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>Management of Gram-Positive Coccal Bacteremia and Hemodialysis.</b></p>
        <p>Am J Kidney Dis. 2011 Feb 16;</p>
        <p>Authors:  Fitzgibbons LN, Puls DL, Mackay K, Forrest GN</p>
        <p>Gram-positive cocci are the most common cause of bloodstream infections in hemodialysis patients, with Staphylococcus aureus and coagulase-negative staphylococci causing most infections. Management of these infections often is complicated by limited vascular access options, as well as an increasing prevalence of drug-resistant bacteria in hemodialysis centers, including the emergence of strains of methicillin-resistant S aureus with vancomycin heteroresistance and increasing rates of vancomycin-resistant enterococci, both of which have limited antibiotic treatment options. This article describes the management of these infections based on the organism and its susceptibility profile, including catheter management, antibiotic lock therapies, and systemic antibiotic choices. Although coagulase-negative staphylococci bacteremia often may be managed with preservation of the catheter, antibiotic lock therapy, and intravenous antibiotics, this is rarely the case with S aureus bacteremia because of frequent relapse and the risk of complications, including endocarditis. Enterococcal bacteremia requires more individualization of care, but catheters are less likely to be salvaged, especially when vancomycin-resistant Enterococcus is the causative organism. Finally, strong infection control policies in the hemodialysis unit, conversion from catheter to arteriovenous access when possible, and appropriate use of antibiotics are essential factors in the prevention of these bloodstream infections.</p>
        <p>PMID: 21333430 [PubMed - as supplied by publisher]</p>]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%"><tr><td align="left"></td></tr></table>
        <p><b>Management of Gram-Positive Coccal Bacteremia and Hemodialysis.</b></p>
        <p>Am J Kidney Dis. 2011 Feb 16;</p>
        <p>Authors:  Fitzgibbons LN, Puls DL, Mackay K, Forrest GN</p>
        <p>Gram-positive cocci are the most common cause of bloodstream infections in hemodialysis patients, with Staphylococcus aureus and coagulase-negative staphylococci causing most infections. Management of these infections often is complicated by limited vascular access options, as well as an increasing prevalence of drug-resistant bacteria in hemodialysis centers, including the emergence of strains of methicillin-resistant S aureus with vancomycin heteroresistance and increasing rates of vancomycin-resistant enterococci, both of which have limited antibiotic treatment options. This article describes the management of these infections based on the organism and its susceptibility profile, including catheter management, antibiotic lock therapies, and systemic antibiotic choices. Although coagulase-negative staphylococci bacteremia often may be managed with preservation of the catheter, antibiotic lock therapy, and intravenous antibiotics, this is rarely the case with S aureus bacteremia because of frequent relapse and the risk of complications, including endocarditis. Enterococcal bacteremia requires more individualization of care, but catheters are less likely to be salvaged, especially when vancomycin-resistant Enterococcus is the causative organism. Finally, strong infection control policies in the hemodialysis unit, conversion from catheter to arteriovenous access when possible, and appropriate use of antibiotics are essential factors in the prevention of these bloodstream infections.</p>
        <p>PMID: 21333430 [PubMed - as supplied by publisher]</p>]]></content:encoded>
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