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    <recommendedItem id="20100101_19_325"
                     title="MRI Reveals Risk for Kidney Failure in Diabetic Patients (CME/CE)"
                     score="0.008"
                     href="http://www.medpagetoday.com/Nephrology/Diabetes/tb/18195?impressionId=1265777934283"
                     
      So-called silent strokes, visible on cerebral MRI scans, predict kidney failure in patients with type 2 diabetes, Japanese researchers said.&lt;br&gt;
&lt;br&gt;After an average follow-up of 7.5 years, diabetic patients with evidence of small cerebral infarctions at baseline later suffered death or kidney failure at more than twice the rate seen in patients who had not had silent strokes, reported Takashi Uzu, MD, of Shiga University of Medical Sciences in Shiga, Japan, and colleagues.&lt;br&gt;
&lt;br&gt;Silent strokes are a consequence of cerebral microvascular disease and thus may logically accompany the development of similar abnormalities in renal blood vessels, ultimately leading to kidney failure, the researchers explained online in the &lt;em&gt;Journal of the American Society of Nephrology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;It is important to identify individuals who are at risk of progression of diabetic renal disease,&quot; Uzu and colleagues wrote.&lt;/p&gt;
&lt;p&gt;The current standard prognostic test is the albumin-creatinine ratio, but it is not entirely adequate for the purpose, they suggested: &quot;Recent clinical studies have shown that renal insufficiency can occur in the absence of microalbuminuria in patients with type 2 diabetes.&quot;&lt;/p&gt;
&lt;p&gt;But they acknowledged that brain MRI scans would be too expensive and inconvenient for routine prognostic testing.&lt;/p&gt;
&lt;p&gt;&quot;New strategies are needed to determine the presence of renal and/or extrarenal microvascular diseases,&quot; Uzu and colleagues wrote.&lt;/p&gt;
&lt;p&gt;Their study involved 608 patients with type 2 diabetes who had no clinical signs of cerebrovascular or cardiovascular disease or overt nephropathy. Their mean age at baseline was about 60 and the average glycated hemoglobin level was about 8.6%.&lt;/p&gt;
&lt;p&gt;Participants underwent cerebral MRI scans at baseline, with 177 showing evidence of silent cerebral infarctions, defined as focal lesions of at least 3 mm in diameter with low signal intensity on T1-weighted images and high intensity with T2 weighting. Dilated perivascular spaces were distinguished from infarcts with proton density scans. Patients with positive findings who had a history of stroke or transient ischemic attack were excluded.&lt;/p&gt;
&lt;p&gt;Those with silent infarctions at baseline differed significantly from other participants according to several parameters. Not surprisingly, patients with cerebral infarcts on average were somewhat older (63 versus 57), had had diabetes for a longer period of time (9.8 years versus 7.6), had higher blood pressure (146.8 mm Hg systolic versus 136.5 ), and were more likely to have a history of smoking (58% versus 46%). All differences were significant at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.01.&lt;/p&gt;
&lt;p&gt;On the other hand, baseline fasting plasma glucose and glycated hemoglobin levels were both significantly lower in the patients who&apos;d had silent infarctions: mean 163 mg/dL versus 176 for glucose and 8.3% versus 8.7% for HbA1c (&lt;em&gt;P&lt;/em&gt;&amp;#8804;0.01 for both).&lt;/p&gt;
&lt;p&gt;Patients were followed for up to 10 years, with a mean of 7.5. The primary outcome was end-stage renal disease or death, and Uzu and colleagues chose a secondary outcome combining dialysis with doubling of serum creatinine.&lt;/p&gt;
&lt;p&gt;Kaplan-Meier curves for the patients with and without silent infarctions at baseline indicated that the primary outcome occurred at equal rates through the first four years of follow-up, but then the curves diverged abruptly.&lt;/p&gt;
&lt;p&gt;At year eight, approximately 6% of the noninfarcted group had experienced the primary outcome, compared with 21% of those who&apos;d had silent strokes (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.0001), according to Uzu and colleagues.&lt;/p&gt;
&lt;p&gt;Curves for the secondary outcome began diverging by year three. At year eight, about 6% of the noninfarct participants had gone to dialysis or had serum creatinine levels double, whereas these endpoints occurred in nearly 30% of the infarct group (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.0001).&lt;/p&gt;
&lt;p&gt;Overall, the hazard ratio associated with baseline silent cerebral infarctions for the primary outcome during follow-up was 2.44 (95% CI 1.36 to 4.38).&lt;/p&gt;
&lt;p&gt;The hazard ratio for death alone was somewhat smaller (1.61, 95% CI 0.71 to 3.62), indicating that most of the risk measured by the primary outcome was actually in end-stage renal disease.&lt;/p&gt;
&lt;p&gt;For the secondary outcome, the hazard ratio was 4.79 (95% CI 2.72 to 8.46).&lt;/p&gt;
&lt;p&gt;All the hazard ratios reflected adjustments for age, sex, duration of diabetes, body mass index, smoking status, HbA1c, blood pressure, serum lipids, and standard lab indices of kidney function at baseline.&lt;/p&gt;
&lt;p&gt;Estimated glomerular filtration rate (eGFR) during follow-up also decreased faster in patients with silent strokes. After five years, mean eGFR had fallen by 8 ml/min/m&lt;sup&gt;2&lt;/sup&gt; in the patients without silent infarcts at baseline compared with 10.5 ml/min/m&lt;sup&gt;2&lt;/sup&gt; in those with cerebral microvascular disease.&lt;/p&gt;
&lt;p&gt;The researchers noted that the study was conducted at two clinical sites, which used somewhat different MRI procedures. But they also indicated that the prevalence of silent infarctions did not differ between the sites.&lt;/p&gt;
&lt;p&gt;Other limitations included use of an older creatinine assay, inclusion of larger silent infarcts which could reflect macrovascular disease, and more patients in the cerebral infarct group who were taking renin-angiotensin system blocking drugs, which have renal impairment as an adverse effect.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;External funding for the study was not reported.&lt;/p&gt;&lt;p&gt;No potential conflicts of interest were reported.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20090101_19_3465"
                     title="Vitamin D Deficiency Tied to ESRD in Blacks (CME/CE)"
                     score="-0.005"
                     href="http://www.medpagetoday.com/Nephrology/ESRD/tb/16693?impressionId=1265777934283"
                     
      &lt;p&gt;Vitamin D deficiency may account for a larger proportion of end-stage renal disease (ESRD) cases among African-Americans than among whites, according to a study adding to a growing body of evidence that the vitamin plays a key role in the progression of kidney disease and need for dialysis.&lt;/p&gt;
&lt;p&gt;Non-Hispanic blacks were nearly three times more likely to eventually require dialysis than non-Hispanic whites (95% CI 1.03 to 7.77), an online article in the October 29 issue of the &lt;em&gt;Journal of the American Society of Nephrology&lt;/em&gt; reported.&lt;/p&gt;
&lt;p&gt;Meanwhile, low levels of 25-hydroxyvitamin D, known as 25(OH)D, accounted for about 58% of cases of ESRD among blacks (95% CI 0.38 to 8.21), the study found.&lt;/p&gt;
&lt;p&gt;&quot;The increased prevalence of 25(OH)D &amp;lt;15 ng/ml among non-Hispanic black individuals seems to explain a substantial proportion of their excess risk for ESRD,&quot; Michal L. Melamed, MD, of Albert Einstein College of Medicine, and colleagues wrote.&lt;/p&gt;
&lt;p&gt;&quot;These results need to be tested in future observational studies, and, if confirmed, then randomized, controlled trials evaluating the renoprotective effects of vitamin D supplementation may be warranted.&quot;&lt;/p&gt;
&lt;p&gt;Most previous studies have shown that non-Hispanic blacks have a similar risk for milder stages of chronic kidney disease, but are at higher risk for ESRD, according to the researchers.&lt;/p&gt;
&lt;p&gt;Earlier studies found an association between low levels of 25(OH)D and higher incidence of hypertension, insulin resistance, peripheral arterial disease, cardiovascular disease and mortality, and suggested it might affect the progression of renal disease.&lt;/p&gt;
&lt;p&gt;Non-Hispanic blacks (and Hispanics) have lower levels of 25(OH)D than non-Hispanic whites, potentially because of darker skin that is less efficient at turning UVB rays from sunshine into vitamin D.&lt;/p&gt;
&lt;p&gt;But no studies have found a link between low 25(OH)D levels and a variety of outcomes in blacks.&lt;/p&gt;
&lt;p&gt;To explore whether low vitamin D could affect ESRD rates in African-Americans, Melamed and colleagues analyzed data from the Third National Health and Nutrition Examination Survey&amp;#8211;linked Medicare claim files on 13,000 Americans.&lt;/p&gt;
&lt;p&gt;The data included measurements of blood levels of 25(OH)D and incidence of ESRD.&lt;/p&gt;
&lt;p&gt;They found that 34% of non-Hispanic black individuals had 25(OH)D levels less than 15 ng/ml compared with 5% of non-Hispanic white individuals (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;The incidence rates of ESRD by race and ethnicity were: &lt;ul&gt; &lt;li&gt;198 (72 to 301) per 1,000,000 person-years for non-Hispanic whites&lt;/li&gt; &lt;li&gt;767 (498 to 1006) per 1,000,000 person-years for non-Hispanic blacks&lt;/li&gt; &lt;li&gt; 387 (200 to 526) per 1,000,000 person-years for Mexican-Americans &lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;After adjusting for demographic, socioeconomic, and clinical and laboratory factors, the researchers found that all participants with 25(OH)D levels less than 15 ng/ml had a 2.6-fold greater incidence of ESRD than those with levels of at least 15 ng/ml (95% 1.00 to 7.05; &lt;em&gt;P&lt;/em&gt;=0.05).&lt;/p&gt;
&lt;p&gt;They noted that the study was observational and could not infer that low vitamin D levels were a direct cause of the higher rates of ESRD.&lt;/p&gt;
&lt;p&gt;They also cautioned that the data may not have reflected a subject&apos;s lifetime vitamin D status, since levels of the vitamin were tested once at the beginning of the study.&lt;/p&gt;
&lt;p&gt;Since the study was based on small sample sizes, the authors considered it &quot;hypothesis generating.&quot;&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was funded by the National Institutes of Health and the American Heart Association.&lt;/p&gt;&lt;p&gt;Co-investigator Thomas H. Hostetter reported receiving consulting fees from Bristol Myers Squibb, Eli Lilly and Wyeth.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20090101_1_218"
                     title="Eating Vegetables May Lower Blood Pressure"
                     score="-0.005"
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