<?xml version="1.0" encoding="UTF-8"?>
<?xml-stylesheet href="/rss.css" type="text/css"?>
<rdf:RDF xmlns="http://purl.org/rss/1.0/"
    xmlns:cc="http://web.resource.org/cc/"
    xmlns:dc="http://purl.org/dc/elements/1.1/"
    xmlns:extra="http://www.w3.org/1999/xhtml"
    xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/"
    xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#">
    <channel rdf:about="http://www.biomedcentral.com/feeds/latestarticles/journal?journal=bmcnephrol&amp;quantity=&amp;format=rss&amp;version=">
        <title>BMC Nephrology - Latest Articles</title>
        <link>http://www.biomedcentral.com/bmcnephrol/</link>
        <description>The latest research articles published by BMC Nephrology</description>
        <dc:date>2012-02-01T00:00:00Z</dc:date>
        <items>
            <rdf:Seq>
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2369/13/7" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2369/13/6" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2369/13/5" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2369/13/4" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2369/13/3" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2369/13/2" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2369/13/1" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2369/12/70" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2369/12/69" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2369/12/68" />
                            </rdf:Seq>
        </items>
                 <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </channel>
        <item rdf:about="http://www.biomedcentral.com/1471-2369/13/7">
        <title>From red to white urine: a patient`s nightmare with a rather benign outcome</title>
        <description>Background:
Chyluria is a medical condition with presence of chyle in the urine. The disease is most prevalent in endemic regions of Africa and the Indian subcontinent where it is mostly caused by parasitic infections, particularly lymphatic filariasis due to wucheria bancrofti. Non-parasitic chyluria, however, is a very rare finding.Case Presentation: We report the case of a 48 year old woman who developed a lymphorenal fistula with chyluria following ureterrenoscopy with biopsies taken for urological work-up of persistent macrohematuria. Renal biopsy confirmed the diagnosis of benign familial hematuria due to thin basement nephropathy, a condition frequently associated with episodes of macrohematuria.
Conclusions:
This case highlights a rare case of non-parasitic chyluria as a complication of urological work-up for macrohematuria of benign nature.</description>
        <link>http://www.biomedcentral.com/1471-2369/13/7</link>
                <dc:creator>Benjamin Knier</dc:creator>
                <dc:creator>Betarix Bueschges-Seraphin</dc:creator>
                <dc:creator>Karl Hilgers</dc:creator>
                <dc:creator>Kerstin Amann</dc:creator>
                <dc:creator>Michael Uder</dc:creator>
                <dc:creator>Kai-Uwe Eckardt</dc:creator>
                <dc:creator>Johannes Jacobi</dc:creator>
                <dc:source>BMC Nephrology 2012, null:7</dc:source>
        <dc:date>2012-02-01T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2369-13-7</dc:identifier>
                                <prism:require>/content/figures/1471-2369-13-7-toc.gif</prism:require>
                <prism:publicationName>BMC Nephrology</prism:publicationName>
        <prism:issn>1471-2369</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>7</prism:startingPage>
        <prism:publicationDate>2012-02-01T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2369/13/6">
        <title>UT-B-deficient mice develop renal dysfunction and structural damage</title>
        <description>Background:
Urea transporter UT-B is the major urea transporter in erythrocytes and the descending vasa recta in the kidney. In this study, we investigated the effects of long-term UT-B deficiency on functional and structural defect in the kidney of 16-and 52-week-old UT-B-null mice.
Methods:
UT-B-knockout mice were generated by targeted gene disruption and lacked UT-B protein expression in all organs. The urinary concentrating ability of mice was studied in terms of daily urine output, urine osmolality, and urine and plasma chemistries. Changes in renal morphology were evaluated by hematoxylin and eosin staining.
Results:
The UT-B-null mice showed defective urine concentrating ability. The daily urine output in UT-B-null mice (2.5 +/- 0.1 ml) was 1.6-fold higher and urine osmolality (985 +/- 151 mosm) was 1.5-fold lower than those in wild-type mice. The 52-week-old UT-B-null mice exhibited polyuria after water deprivation, although urine osmolality was increased. At 52 weeks of age, over 30.77% of UT-B-null mice exhibited renal medullary atrophy because of severe polyuria and hydronephrosis.
Conclusions:
Long-term UT-B deficiency causes severe renal dysfunction and structural damage. These results demonstrate the important role of UT-B in countercurrent exchange and urine concentration.</description>
        <link>http://www.biomedcentral.com/1471-2369/13/6</link>
                <dc:creator>Lei Zhou</dc:creator>
                <dc:creator>Yan Meng</dc:creator>
                <dc:creator>Tianluo Lei</dc:creator>
                <dc:creator>Dan Zhao</dc:creator>
                <dc:creator>Jing Su</dc:creator>
                <dc:creator>Xuejian Zhao</dc:creator>
                <dc:creator>Baoxue Yang</dc:creator>
                <dc:source>BMC Nephrology 2012, null:6</dc:source>
        <dc:date>2012-01-30T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2369-13-6</dc:identifier>
                                <prism:require>/content/figures/1471-2369-13-6-toc.gif</prism:require>
                <prism:publicationName>BMC Nephrology</prism:publicationName>
        <prism:issn>1471-2369</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>6</prism:startingPage>
        <prism:publicationDate>2012-01-30T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2369/13/5">
        <title>Transfusion burden in non-dialysis chronic kidney disease patients with persistent anemia treated in routine clinical practice: a retrospective observational study</title>
        <description>Background:
Transfusion patterns are not well characterized in non-dialysis (ND) chronic kidney disease (CKD) patients. This study describes the proportion of patients transfused, units of blood transfused and trigger-hemoglobin (Hb) levels for transfusions in severe anemic, ND-CKD patients in routine practice.
Methods:
A retrospective cohort study of electronic medical record data from the Henry Ford Health System identified 374 adult, ND-CKD patients with severe anemia (Hb &lt;10 g/dL and subsequent use of erythropoiesis-stimulating agents [ESA] therapy, blood transfusions, or a second Hb &lt;10 g/dL) between January 2004 and June 2008. Exclusions included those with prior diagnoses of cancer, renal or liver transplant, end-stage renal disease, acute bleeding, trauma, sickle cell disease, or aplastic anemia. A gap of greater than or equal to 1 day between units of blood transfused was counted as a separate transfusion.
Results:
At least 1 transfusion (mean of 2 units; range, 1-4) was administered to 20% (75/374) of ND-CKD patients with mean (+/-SD) follow-up of 459 (+/-427) days. The mean (+/-SD) Hb level closest and prior to a transfusion was 8.8 (+/-1.5) g/dL. Patients who were hospitalized in the 6 months prior to their first anemia diagnosis were 6.3 times more likely to receive a blood transfusion than patients who were not hospitalized (p &lt;0.0001).  Patients with peripheral vascular disease (PVD) were twice as likely to have a transfusion as patients without PVD (p = 0.04).
Conclusions:
Transfusions were prevalent and the trigger hemoglobin concentration was approximately 9 g/dL among ND-CKD patients with anemia.  To reduce the transfusion burden, clinicians should consider other anemia treatments including ESA therapy.</description>
        <link>http://www.biomedcentral.com/1471-2369/13/5</link>
                <dc:creator>Kathleen Fox</dc:creator>
                <dc:creator>Jerry Yee</dc:creator>
                <dc:creator>Ze Cong</dc:creator>
                <dc:creator>John Brooks</dc:creator>
                <dc:creator>Jeffrey Petersen</dc:creator>
                <dc:creator>Lois Lamerato</dc:creator>
                <dc:creator>Shravanthi Gandra</dc:creator>
                <dc:source>BMC Nephrology 2012, null:5</dc:source>
        <dc:date>2012-01-24T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2369-13-5</dc:identifier>
                                <prism:require>/content/figures/1471-2369-13-5-toc.gif</prism:require>
                <prism:publicationName>BMC Nephrology</prism:publicationName>
        <prism:issn>1471-2369</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2012-01-24T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2369/13/4">
        <title>The MDRD equation underestimates the prevalence of CKD among blacks and overestimates the prevalence of CKD among whites compared to the CKD-EPI equation: A retrospective cohort study.</title>
        <description>Background:
Black individuals are far more likely than white individuals to develop end stage renal disease (ESRD). However, earlier stages of chronic kidney disease (CKD) have been reported to be less prevalent among blacks. This disparity remains poorly understood. The objective of this study was to evaluate whether the lower prevalence of CKD among blacks in early stages of CKD might be due in part to an inability of the MDRD equation to accurately determine early stages of CKD in both the black and white population.
Methods:
We conducted a retrospective cohort study of 97, 451 patients seen in primary care clinic in Veterans Integrated Service Network 2 (VISN 2) over a 7 year period to determine the prevalence of CKD using both the Modification of Diet in Renal Disease (MDRD) Study equation and the more recently developed CKD Epidemiology Collaboration (CKD-EPI) equation.  Demographic data, comorbid conditions, prescription of medications, and laboratory data were recorded. Logistic regression and quantile regression models were used to compare the prevalence of estimated glomerular filtration rate (eGFR) categories between black and white individuals.
Results:
The overall prevalence of CKD was lower when the CKD-EPI equation was used. Prevalence of CKD in whites was 53.2% by MDRD and 48.4% by CKD-EPI, versus 34.1% by MDRD and 34.5% by CKD-EPI in blacks. The cumulative logistic regression and quantile regression showed that when eGFR was calculated by the EPI method, blacks were as likely to present with an eGFR value less than 60 mL/min/1.73 m2 as whites. Using the CKD-EPI equation, blacks were more likely than white individuals to have stage 3b, 4 and 5 CKD. Using the MDRD method, the prevalence in blacks was only higher than in whites for stage 4 and 5 CKD.  Similar results were obtained when the analysis was confined to patients over 65 years of age.
Conclusions:
The MDRD equation overestimates the prevalence of CKD among whites and underestimates the prevalence of CKD in blacks compared to the CKD-EPI equation.</description>
        <link>http://www.biomedcentral.com/1471-2369/13/4</link>
                <dc:creator>Pradeep Arora</dc:creator>
                <dc:creator>Srini Rajagopalan</dc:creator>
                <dc:creator>Nilang Patel</dc:creator>
                <dc:creator>Neha Nainani</dc:creator>
                <dc:creator>Rocco Venuto</dc:creator>
                <dc:creator>James Lohr</dc:creator>
                <dc:source>BMC Nephrology 2012, null:4</dc:source>
        <dc:date>2012-01-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2369-13-4</dc:identifier>
                                <prism:require>/content/figures/1471-2369-13-4-toc.gif</prism:require>
                <prism:publicationName>BMC Nephrology</prism:publicationName>
        <prism:issn>1471-2369</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>4</prism:startingPage>
        <prism:publicationDate>2012-01-20T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2369/13/3">
        <title>Regression of left ventricular mass following conversion from conventional hemodialysis to thrice weekly in-centre nocturnal hemodialysis</title>
        <description>Background:
Increased left ventricular mass (LVM) is associated with adverse outcomes in patients receiving chronic hemodialysis. Among patients receiving conventional hemodialysis (CHD, 3x/week, 4 hrs/session), we evaluated whether dialysis intensification with in-centre nocturnal hemodialysis (INHD, 3x /week, 7-8 hrs/session in the dialysis unit) was associated with regression of LVM.
Methods:
We conducted a retrospective cohort study of CHD recipients who converted to INHD and received INHD for at least 6 months. LVM on the first echocardiogram performed at least 6 months post-conversion was compared to LVM pre-conversion. In a secondary analysis, we examined echocardiograms performed at least 12 months after starting INHD. The effect of conversion to INHD on LVM over time was also evaluated using a longitudinal analysis that incorporated all LVM data on patients with 2 or more echocardiograms.
Results:
Thirty-seven patients were eligible for the primary analysis. Mean age at conversion was 49 +/-12 yrs and 30% were women. Mean pre-conversion LVM was 219 +/- 66 g and following conversion, LVM declined by 32 +/- 58 g (p=0.002). Among patients whose follow-up echocardiogram occurred at least 12 months following conversion, LVM declined by 40 +/- 56 g (p=0.0004). The rate of change of LVM decreased significantly from 0.4 g/yr before conversion, to -11.7 g/yr following conversion to INHD (p&lt;0.0001).
Conclusion:
Conversion to INHD is associated with a significant regression in LVM, which may portend a more favourable cardiovascular outcome. Our preliminary findings support the need for randomized controlled trials to definitively evaluate the cardiovascular effects of INHD.</description>
        <link>http://www.biomedcentral.com/1471-2369/13/3</link>
                <dc:creator>Ron Wald</dc:creator>
                <dc:creator>Andrew Yan</dc:creator>
                <dc:creator>Jeffrey Perl</dc:creator>
                <dc:creator>Depeng Jiang</dc:creator>
                <dc:creator>M Donnelly</dc:creator>
                <dc:creator>Howard Leong-Poi</dc:creator>
                <dc:creator>Philip McFarlane</dc:creator>
                <dc:creator>Jordan Weinstein</dc:creator>
                <dc:creator>Marc Goldstein</dc:creator>
                <dc:source>BMC Nephrology 2012, null:3</dc:source>
        <dc:date>2012-01-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2369-13-3</dc:identifier>
                                <prism:require>/content/figures/1471-2369-13-3-toc.gif</prism:require>
                <prism:publicationName>BMC Nephrology</prism:publicationName>
        <prism:issn>1471-2369</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2012-01-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2369/13/2">
        <title>Pro/anti-inflammatory cytokine gene polymorphisms and chronic kidney disease: a cross-sectional study</title>
        <description>Background:
The aim of this study was to explore the associations between common potential functional promoter polymorphisms in pro-/anti-inflammatory cytokine genes and kidney function/chronic kidney disease (CKD) prevalence in a large Japanese population.
Methods:
A total of 3,323 subjects aged 35-69 were genotyped for all 10 single nucleotide polymorphisms (SNPs) in the promoter regions of candidate genes with minor allele frequencies of &gt;0.100 in Japanese populations. The estimated glomerular filtration rate (eGFR) and CKD prevalence (eGFR &lt;60 ml/min/1.73m2) of the subjects were compared among the genotypes.
Results:
A higher eGFR and lower prevalence of CKD were observed for the homozygous variants of IL4 -33CC (high IL-4 [anti-inflammatory cytokine]-producing genotype) and IL6 -572GG (low IL-6 [pro-inflammatory cytokine]-producing genotype). Subjects with IL4 CC + IL6 GG showed the highest mean eGFR (79.1 ml/min/1.73m2) and lowest CKD prevalence (0.0%), while subjects carrying IL4 TT + IL6 CC showed the lowest mean eGFR (73.4 ml/min/1.73 m2) and highest CKD prevalence (17.9%).
Conclusions:
The functional promoter polymorphisms IL4 T-33C (rs2070874) and IL6 C-572G (rs1800796), which are the only SNPs that affect the IL-4 and IL-6 levels in Japanese subjects, were associated with kidney function and CKD prevalence in a large Japanese population.</description>
        <link>http://www.biomedcentral.com/1471-2369/13/2</link>
                <dc:creator>Rieko Okada</dc:creator>
                <dc:creator>Kenji Wakai</dc:creator>
                <dc:creator>Mariko Naito</dc:creator>
                <dc:creator>Emi Morita</dc:creator>
                <dc:creator>Sayo Kawai</dc:creator>
                <dc:creator>Nobuyuki Hamajima</dc:creator>
                <dc:creator>Megumi Hara</dc:creator>
                <dc:creator>Naoyuki Takashima</dc:creator>
                <dc:creator>Sadao Suzuki</dc:creator>
                <dc:creator>Toshiro Takezaki</dc:creator>
                <dc:creator>Keizo Ohnaka</dc:creator>
                <dc:creator>Kokichi Arisawa</dc:creator>
                <dc:creator>Hiroshi Hirohata</dc:creator>
                <dc:creator>Keitaro Matsuo</dc:creator>
                <dc:creator>Haruo Mikami</dc:creator>
                <dc:creator>Michiaki Kubo</dc:creator>
                <dc:creator>Hideo Tanaka</dc:creator>
                <dc:source>BMC Nephrology 2012, null:2</dc:source>
        <dc:date>2012-01-09T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2369-13-2</dc:identifier>
                                <prism:require>/content/figures/1471-2369-13-2-toc.gif</prism:require>
                <prism:publicationName>BMC Nephrology</prism:publicationName>
        <prism:issn>1471-2369</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2012-01-09T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2369/13/1">
        <title>The impact of different GFR estimating equations on the prevalence of CKD and risk groups in a Southeast Asian cohort using the new KDIGO guidelines </title>
        <description>Background:
Recently, the Kidney Disease: Improving Global Outcomes (KDIGO) group recommended that patients with CKD should be assigned to stages and composite relative risk groups according to GFR (G) and proteinuria (A) criteria. Asians have among the highest rates of ESRD in the world, but establishing the prevalence and prognosis CKD is a problem for Asian populations since there is no consensus on the best GFR estimating (eGFR) equation. We studied the effects of the choice of new Asian and Caucasian eGFR equations on CKD prevalence, stage distribution, and risk categorization using the new KDIGO classification.
Methods:
The prevalence of CKD and composite relative risk groups defined by eGFR from with Chronic Kidney Disease-Epidemiology Collaboration (CKD-EPI); standard (S) or Chinese(C) MDRD; Japanese CKD-EPI (J-EPI), Thai GFR (T-GFR) equations were compared in a Thai cohort (n = 5526)
Results:
There was a 7 fold difference in CKD3-5 prevalence between J-EPI and the other Asian eGFR formulae. CKD3-5 prevalence with S-MDRD and CKD-EPI were 2 - 3 folds higher than T-GFR or C-MDRD. The concordance with CKD-EPI to diagnose CKD3-5 was over 90% for T-GFR or C-MDRD, but they only assigned the same CKD stage in 50% of the time. The choice of equation also caused large variations in each composite risk groups especially those with mildly increased risks. Different equations can lead to a reversal of male: female ratios. The variability of different equations is most apparent in older subjects. Stage G3aA1 increased with age and accounted for a large proportion of the differences in CKD3-5 between CKD-EPI, S-MDRD and C-MDRD.
Conclusions:
CKD prevalence, sex ratios, and KDIGO composite risk groupings varied widely depending on the equation used. More studies are needed to define the best equation for Asian populations.</description>
        <link>http://www.biomedcentral.com/1471-2369/13/1</link>
                <dc:creator>Chagriya Kitiyakara</dc:creator>
                <dc:creator>Sukit Yamwong</dc:creator>
                <dc:creator>Prin Vathesatogkit</dc:creator>
                <dc:creator>Anchalee Chittamma</dc:creator>
                <dc:creator>Sayan Cheepudomwit</dc:creator>
                <dc:creator>Somlak Vanavanan</dc:creator>
                <dc:creator>Bunlue Hengprasith</dc:creator>
                <dc:creator>Piyamitr Sritara</dc:creator>
                <dc:source>BMC Nephrology 2012, null:1</dc:source>
        <dc:date>2012-01-06T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2369-13-1</dc:identifier>
                                <prism:require>/content/figures/1471-2369-13-1-toc.gif</prism:require>
                <prism:publicationName>BMC Nephrology</prism:publicationName>
        <prism:issn>1471-2369</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>1</prism:startingPage>
        <prism:publicationDate>2012-01-06T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2369/12/70">
        <title>Effects of thyroid hormone analogue and a leukotrienes pathway-blocker on renal ischemia/reperfusion injury in mice </title>
        <description>Background:
Acute renal failure (ARF) is an important clinical problem with a high mortality and morbidity. One of the primary causes of ARF is ischemia/reperfusion (I/R). Inflammatory process and oxidative stress are thought to be the major mechanisms causing I/R. MK-886 is a potent inhibitor of leukotrienes biosynthesis which may have anti-inflammatory and antioxidant effects through inhibition of polymorphonuclear leukocytes (PMNs) infiltration into renal tissues. 3, 5-diiodothyropropionic acid (DITPA) have evidences of improving effects on I/R in heart through modulation of cellular signaling in response to ischemic stress. The objective of present study was to assess the effects of MK-886 and DITPA on renal I/R injury.
Methods:
A total of 24 Adult males of Swiss albino mice were randomized to four groups: I/R group (n = 6), mice underwent 30 minute bilateral renal ischemia and 48 hr reperfusion. Sham group (n = 6), mice underwent same anesthetic and surgical procedures except for ischemia induction. MK-886-treated group: (n = 6), I/R + MK-886 (6 mg/kg) by intraperitoneal injection. DITPA-treated group: (n = 6), I/R + DITPA (3.75 mg/kg) by intraperitoneal injection.After the end of reperfusion phase mice were sacrificed, blood samples were collected directly from the heart for determination of serum TNF-a, IL-6, urea and Creatinine. Both kidney were excised, the right one homogenized for oxidative stress parameters (MDA and GSH) measurements and the left kidney fixed in formalin for histological examination.
Results:
Serum TNF-&#945;, IL-6, urea and Creatinine, kidney MDA levels and scores of histopathological changes were significantly (P &lt; 0.05) elevated in I/R group as compared with that of sham group. Kidney GSH level was significantly (P &lt; 0.05) decreased in I/R group as compared with that of sham group. MK-886 treated group has significantly (P &lt; 0.05) lowered levels of all study parameters except for GSH level which was significantly (P &lt; 0.05) higher as compared with that of I/R group. DITPA caused non-significant (P &gt; 0.05) changes in levels of all study parameters as compared with that of I/R group.
Conclusion:
The results of the present study show that MK-886 significantly ameliorated kidney damage that resulted from I/R. For DITPA, as its administration might not be successful, administration using a different protocol may give different effects on I/R.</description>
        <link>http://www.biomedcentral.com/1471-2369/12/70</link>
                <dc:creator>Najah Hadi</dc:creator>
                <dc:creator>Fadhil Al-amran</dc:creator>
                <dc:creator>Ayad Hussein</dc:creator>
                <dc:source>BMC Nephrology 2011, null:70</dc:source>
        <dc:date>2011-12-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2369-12-70</dc:identifier>
                                <prism:require>/content/figures/1471-2369-12-70-toc.gif</prism:require>
                <prism:publicationName>BMC Nephrology</prism:publicationName>
        <prism:issn>1471-2369</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>70</prism:startingPage>
        <prism:publicationDate>2011-12-23T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2369/12/69">
        <title>Survival in dialysis patients is not different between patients with diabetes as primary renal disease and patients with diabetes as a co-morbid condition.</title>
        <description>Background:
On dialysis, survival among patients with diabetes mellitus is inferior to survival of non-diabetic patients. We hypothesized that patients with diabetes as primary renal disease have worse survival compared to patients with diabetes as a co-morbid condition and aimed to compare all-cause mortality between these patient groups.
Methods:
Data were collected from the Netherlands Cooperative Study on the Adequacy of Dialysis (NECOSAD), a multicenter, prospective cohort study in which new patients with end stage renal disease (ESRD) were monitored until transplantation or death. Patients with diabetes as primary cause of ESRD were compared with patients with diabetes as co-morbid condition and both of these patient groups were compared to patients without diabetes. Analysis was performed using Kaplan-Meier and Cox regression.
Results:
Fifteen % of the patients had diabetic nephropathy as primary renal disease (N = 281); 6% had diabetes as co-morbid condition (N = 107) and 79% had no diabetes (N = 1465). During follow-up 42% of patients (N = 787) died. Compared to non-diabetic patients, mortality risk was increased for both patients with diabetes as primary renal disease HR: 1.9 (95% CI 1.6, 2.3) and for patients with diabetes as co-morbid condition HR: 1.7 (95% CI 1.3, 2.2). Mortality was not significantly higher in patients with diabetes as primary renal disease compared to patients with diabetes as co-morbid condition (HR 1.06; 95% CI 0.79, 1.43).
Conclusions:
This study in patients with ESRD showed no survival difference between patients with diabetes as primary renal disease and patients with diabetes as a co-morbid condition. Both conditions were associated with increased mortality risk compared to non-diabetic patients.</description>
        <link>http://www.biomedcentral.com/1471-2369/12/69</link>
                <dc:creator>Marielle Schroijen</dc:creator>
                <dc:creator>Olaf Dekkers</dc:creator>
                <dc:creator>Diana Grootendorst</dc:creator>
                <dc:creator>Marlies Noordzij</dc:creator>
                <dc:creator>Johannes Romijn</dc:creator>
                <dc:creator>Raymond Krediet</dc:creator>
                <dc:creator>Elisabeth Boeschoten</dc:creator>
                <dc:creator>Friedo Dekker</dc:creator>
                <dc:creator>Necosad Study Group</dc:creator>
                <dc:source>BMC Nephrology 2011, null:69</dc:source>
        <dc:date>2011-12-19T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2369-12-69</dc:identifier>
                                <prism:require>/content/figures/1471-2369-12-69-toc.gif</prism:require>
                <prism:publicationName>BMC Nephrology</prism:publicationName>
        <prism:issn>1471-2369</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>69</prism:startingPage>
        <prism:publicationDate>2011-12-19T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2369/12/68">
        <title>The clinical and imaging presentation of acute &quot;non complicated&quot; pyelonephritis. A new profile for an ancient disease.</title>
        <description>Background:
Acute pyelonephritis (APN) is differently defined according to imaging or clinical criteria. In adults information on the relationship between imaging and clinical data is lacking.Our study was aimed at analysing the relationship between the clinical and imaging presentation of APN, defined according to imaging criteria (parenchymal involvement at MR or CT scan).
Methods:
All consecutive patients hospitalized for &quot;non-complicated&quot; APN were considered (June 2005-December 2009). Clinical, biochemical and imaging data at hospitalization were analyzed by univariate and logistic regression analysis.
Results:
There were 119 patients, all females, median age 32 years (15-72). At hospitalization, inflammatory markers were elevated (CRP median: 12.1 mg/dL, normal &lt; 0.8). Incomplete presentations were frequent: fever was absent in 6.7%, pain in 17.8%, lower urinary tract symptoms in 52.9%. At CT or MR scan the lesions were bilateral in 12.6%, multiple in 79.8%; abscesses were present in 39.5%. Renal scars were found in 15.1%. Positive cultures were correlated with multiple foci (multivariate OR 4.2; CI 1.139-15.515). No other sign/symptom discriminated between small lesions, abscesses or multifocal involvement.
Conclusions:
APN is a protean disease. In the absence of strict correlation with clinical or biochemical markers, imaging studies are required to assess the severity of kidney involvement.</description>
        <link>http://www.biomedcentral.com/1471-2369/12/68</link>
                <dc:creator>Giorgina Barbara Piccoli</dc:creator>
                <dc:creator>Valentina Consiglio</dc:creator>
                <dc:creator>Maria Chiara Deagostini</dc:creator>
                <dc:creator>Melania Serra</dc:creator>
                <dc:creator>Marilisa Biolcati</dc:creator>
                <dc:creator>Francesca Ragni</dc:creator>
                <dc:creator>Alberto Biglino</dc:creator>
                <dc:creator>Agostino De Pascale</dc:creator>
                <dc:creator>Mauro Felice Frascisco</dc:creator>
                <dc:creator>Andrea Veltri</dc:creator>
                <dc:creator>Francesco Porpiglia</dc:creator>
                <dc:source>BMC Nephrology 2011, null:68</dc:source>
        <dc:date>2011-12-15T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2369-12-68</dc:identifier>
                                <prism:require>/content/figures/1471-2369-12-68-toc.gif</prism:require>
                <prism:publicationName>BMC Nephrology</prism:publicationName>
        <prism:issn>1471-2369</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>68</prism:startingPage>
        <prism:publicationDate>2011-12-15T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <cc:License rdf:about="http://creativecommons.org/licenses/by/2.0/">
        <cc:permits rdf:resource="http://creativecommons.org/ns#Reproduction" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#Distribution" />
        <cc:permits rdf:resource="http://creativecommons.org/ns#DerivativeWorks" />
    </cc:License>
</rdf:RDF>

