Database : MEDLINE
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[PMID]: 29524917
[Au] Autor:Cardona M; Lewis ET; Turner RM; Alkhouri H; Asha S; Mackenzie J; Perkins M; Suri S; Holdgate A; Winoto L; Chang CW; Gallego-Luxan B; McCarthy S; Kristensen MR; O'Sullivan M; Skjøt-Arkil H; Ekmann AA; Nygaard HH; Jensen JJ; Jensen RO; Pedersen JL; Breen D; Petersen JA; Jensen BN; Mogensen CB; Hillman K; Brabrand M
[Ad] Address:The Simpson Centre for Health Services Research, South Western Sydney Clinical School, The University of New South Wales, PO Box 6087, UNSW, NSW, 1466 Australia. Electronic address: magnolia.cardona@unsw.edu.au.
[Ti] Title:Efficacy of a tool to predict short-term mortality in older people presenting at emergency departments: Protocol for a multi-centre cohort study.
[So] Source:Arch Gerontol Geriatr;76:169-174, 2018 Mar 06.
[Is] ISSN:1872-6976
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Prognostic uncertainty inhibits clinicians from initiating timely end-of-life discussions and advance care planning. This study evaluates the efficacy of the CriSTAL (Criteria for Screening and Triaging to Appropriate aLternative care) checklist in emergency departments. METHODS: Prospective cohort study of patients aged ≥65 years with any diagnosis admitted via emergency departments in ten hospitals in Australia, Denmark and Ireland. Electronic and paper clinical records will be used to extract risk factors such as nursing home residency, physiological deterioration warranting a rapid response call, personal history of active chronic disease, history of hospitalisations or intensive care unit admission in the past year, evidence of proteinuria or ECG abnormalities, and evidence of frailty to be concurrently measured with Fried Score and Clinical Frailty Scale. Patients or their informal caregivers will be contacted by telephone around three months after initial assessment to ascertain survival, self-reported health, post-discharge frailty and health service utilisation since discharge. Logistic regression and bootstrapping techniques and AUROC curves will be used to test the predictive accuracy of CriSTAL for death within 90 days of admission and in-hospital death. DISCUSSION: The CriSTAL checklist is an objective and practical tool for use in emergency departments among older patients to determine individual probability of death in the short-term. Its validation in this cohort is expected to reduce clinicians' prognostic uncertainty on the time to patients' death and encourage timely end-of-life conversations to support clinical decisions with older frail patients and their families about their imminent or future care choices.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29511687
[Au] Autor:Pozdzik A; Brochériou I; David C; Touzani F; Goujon JM; Wissing KM
[Ad] Address:Nephrology Department, Centre Hospitalier Universitaire de Bruxelles (CHUB), Brugmann Hospital, Brussels, Belgium.
[Ti] Title:Membranous Nephropathy and Anti-Podocytes Antibodies: Implications for the Diagnostic Workup and Disease Management.
[So] Source:Biomed Res Int;2018:6281054, 2018.
[Is] ISSN:2314-6141
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The discovery of circulating antibodies specific for native podocyte antigens has transformed the diagnostic workup and greatly improved management of idiopathic membranous nephropathy (iMN). In addition, their identification has clearly characterized iMN as a largely autoimmune disorder. Anti-PLA2R1 antibodies are detected in approximately 70% to 80% and anti-THSD7A antibodies in only 2% of adult patients with iMN. The presence of anti-THSD7A antibodies is associated with increased risk of malignancy. The assessment of PLA2R1 and THSD7A antigen expression in glomerular immune deposits has a better sensitivity than measurement of the corresponding autoantibodies. Therefore, in the presence of circulating anti-podocytes autoantibodies and/or enhanced expression of PLA2R1 and THSD7A antigens MN should be considered as primary MN (pMN). Anti-PLA2R1 or anti-THSD7A autoantibodies have been proposed as biomarkers of autoimmune disease activity and their blood levels should be regularly monitored in pMN to evaluate disease activity and predict outcomes. We propose a revised clinical workup flow for patients with MN that recommends assessment of kidney biopsy for PLA2R1 and THSD7A antigen expression, screening for circulating anti-podocytes antibodies, and assessment for secondary causes, especially cancer, in patients with THSD7A antibodies. Persistence of anti-podocyte antibodies for 6 months or their increase in association with nephrotic proteinuria should lead to the introduction of immunosuppressive therapies. Recent data have reported the efficacy and safety of new specific therapies targeting B cells (anti-CD20 antibodies, inhibitors of proteasome) in pMN which should lead to an update of currently outdated treatment guidelines.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1155/2018/6281054

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[PMID]: 29510679
[Au] Autor:Su H; Ye C; Wen Q; Zhu HY; Yi LX; Zhang C
[Ad] Address:Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.
[Ti] Title:Case report: lipid inclusion in glomerular endothelial and mesangial cells in a patient after contrast medium injection.
[So] Source:BMC Nephrol;19(1):53, 2018 Mar 06.
[Is] ISSN:1471-2369
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: It is well-recognized that injection of iodinated radiographic contrast media (CM) sometimes causes acute renal injury via multiple mechanisms, such as vasoconstriction, toxicity on glomerular endothelium and tubular epithelium and so forth. CASE PRESENTATION: A 51-year-old man developed acute renal injury with proteinuria after CM administration. To our surprise, in his renal biopsy sample the myelin figure like structure was observed in glomerular endothelium and mesangial cells by transmission electron microscopy. However the patient didn't has any clinic clues of Fabry disease and other lysosomal storage disorders. Moreover in vitro cultured glomerular endothelial and mesangial cells we found CM triggers lipid aggregation along with the increased CD36 and decreased ABCA1 abundance. Thus this patient was administrated statin to correct the aberrant lipid trafficking, 2 months later at his next visit we found his renal function partially recovered with reduced proteinuria. CONCLUSIONS: Besides the well-known underlying mechanisms, CM may cause renal impairment by triggering the dysregulated transportation of lipid. Furthermore statin is suggested to be a very promising medicine to decrease side effects of CM.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12882-018-0844-2

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[PMID]: 29506491
[Au] Autor:Shima H; Tashiro M; Yamada S; Matsuura M; Okada K; Doi T; Minakuchi J; Kawashima S
[Ad] Address:Department of Kidney Disease, Kawashima Hospital, 1-39 Kitasakoichiban-cho, Tokushima, 770-0011, Japan. h.shima@khg.or.jp.
[Ti] Title:Cilostazol-induced acute tubulointerstitial nephritis accompanied by IgA nephropathy: a case report.
[So] Source:BMC Nephrol;19(1):52, 2018 Mar 05.
[Is] ISSN:1471-2369
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Cilostazol is an antiplatelet drug that is widely prescribed for the prevention of secondary stroke. Adverse reactions to cilostazol include headaches, palpitations, and diarrhea. Little is known about the nephrotoxicity of cilostazol, such as acute kidney injury. We report a biopsy-proven case of diffuse tubulointerstitial nephritis induced by cilostazol. CASE PRESENTATION: A 69-year-old woman prescribed cilostazol was hospitalized for acute kidney injury. On admission, her renal function deteriorated, with an increased serum creatinine level. Urinalysis showed hematuria, proteinuria, and hyper-beta2-microglobulinuria. A renal biopsy revealed diffuse tubulointerstitial nephritis associated with IgA nephropathy, and gallium-67 scintigraphy showed uptake in the bilateral kidneys. A drug lymphocyte stimulation test for cilostazol was positive, and the patient was diagnosed with cilostazol-induced acute tubulointerstitial nephritis. Despite discontinuation of cilostazol, her renal function rapidly worsened and steroid pulse therapy was initiated, followed by oral high-dose glucocorticoid therapy. After steroid treatment, her serum creatinine level normalized in parallel with urine beta2-microglobulin. CONCLUSION: Cilostazol can induce acute tubulointerstitial nephritis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1186/s12882-018-0854-0

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[PMID]: 29462715
[Au] Autor:Bai X; Li X; Tian J; Xu L; Wan J; Liu Y
[Ad] Address:Division of Nephrology, Nanfang Hospital, Southern Medical University, National Clinical Research Center for Kidney Disease, State Key Laboratory of Organ Failure Research, Guangdong Provincial Institute of Nephrology, Guangzhou, Guangdong, PR China. Electronic address: xiaoyanbai@smu.edu.cn.
[Ti] Title:A new model of diabetic nephropathy in C57BL/6 mice challenged with advanced oxidation protein products.
[So] Source:Free Radic Biol Med;118:71-84, 2018 Feb 17.
[Is] ISSN:1873-4596
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:There remains a lack of robust mouse models with key features of advanced human diabetic nephropathy (DN). Few options of murine models of DN require mutations to be superimposed to obtain desired phenotypic characteristics. Most genetically modified mice are on the C57BL/6 background; however, they are notorious for resistance to develop DN. To overcome these conundrums, this study reports a novel DN model by challenging with advanced oxidation protein products (AOPPs) in streptozotocin-induced diabetic C57BL/6 mice. AOPPs-challenged diabetic C57BL/6 mice were more sensitive to develop progressive proteinuria, causing a 5.59-fold increase in urine albumin to creatinine ratio as compared to diabetic controls by 24 weeks. Typical lesions were present as demonstrated by significant diffuse mesangial expansion, diffuse podocyte foot process effacement, increased glomerular basement membrane thickness, focal arteriolar hyalinosis, mesangiolysis, and mild interstitial fibrosis. These changes were alleviated by losartan treatment. Collectively, these results suggest that AOPPs can accelerate the progression of DN in the resistant C57BL/6 mouse strain. Our studies offer a novel model for studying the pathogenesis of DN that resembles human diabetic kidney disease. It also makes it possible to interrogate the role of specific genetic modifications and to evaluate novel therapeutics to treat DN in preclinical setting.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29270765
[Au] Autor:Hamano T
[Ad] Address:Department of Comprehensive Kidney Disease Research (CKDR), Osaka University Graduate School of Medicine, D11, 2-2 Yamadaoka, Suita, Osaka, Japan. hamatea@kid.med.osaka-u.ac.jp.
[Ti] Title:Vitamin D and renal outcome: the fourth outcome of CKD-MBD? Oshima Award Address 2015.
[So] Source:Clin Exp Nephrol;22(2):249-256, 2018 Apr.
[Is] ISSN:1437-7799
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:Bone fracture, cardiovascular events, and mortality are three outcomes of chronic kidney disease-mineral and bone disorder (CKD-MBD), and the umbrella concept originally described for dialysis patients. The reported association of serum phosphorus or fibroblast growth factor 23 (FGF23) levels with renal outcome suggests that the fourth relevant outcome of CKD-MBD in predialysis patients is renal outcome. We found that proteinuria of 2+ or greater with a dipstick test was associated with low vitamin D status due to urinary loss of 25-hydroxyvitamin D (25D). Moreover, active vitamin D or its analogues decrease proteinuria. Given our finding that maxacalcitol does not repress renin, the reduction of proteinuria by this agent is likely due to direct upregulation of the nephrin and podocin in podocytes. Moreover, this agent downregulates the mesenchymal marker desmin in podocytes and blocks transforming growth factor-beta autoinduction, leading to attenuation of renal fibrosis in a unilateral ureteral obstructive (UUO) model. These facts are reminiscent of the suppression of epithelial-mesenchymal transition (EMT) by vitamin D. EMT blockage may explain our finding that vitamin D prescription in renal transplant recipients is associated with a lower incidence of cancer. We also reported that low vitamin D status and high FGF23 levels predict a worse renal outcome. However, administration of massive doses of 25D exacerbates renal fibrosis in UUO kidneys in 1alpha-hydroxylase knockout mice. Moreover, FGF23 inhibits 1alpha-hydroxylase in proximal tubules and monocytes. Taken together, local 1,25(OH) D in the kidney tissue but not 25D seems to protect the kidney.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Process
[do] DOI:10.1007/s10157-017-1517-3

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[PMID]: 29523959
[Au] Autor:Steinberg M; Gaut JP; Hmiel SP; Kakajiwala A
[Ad] Address:Department of Pediatrics, Washington University in St. Louis School of Medicine, St. Louis, USA.
[Ti] Title:The light at the end of the tunnel: an unusual case of acute kidney injury in a pediatric patient: Answers.
[So] Source:Pediatr Nephrol;, 2018 Mar 09.
[Is] ISSN:1432-198X
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Monoclonal gammopathies are a rare diagnosis in pediatric patients. A 19-year-old female patient with past medical history of hypogammaglobulinemia and natural killer cell deficiency and stage III follicular lymphoma, in remission, presented with a right-sided pneumonia, noted to have acute kidney injury and proteinuria. Complement C3 and C4 levels were normal. Anti-double-stranded DNA antibodies, antinuclear antibodies, anti-extractable nuclear antigen antibodies, and antineutrophil cytoplasmic antibodies were negative. A renal biopsy showed numerous fractured tubular casts that were periodic acid-Schiff and silver-stain negative and fuchsinophilic on trichrome stain, with associated giant cells, tubulitis, acute tubular injury, and tubular rupture. The tubular casts had 3+ staining for lambda light chains and 0-1+ staining for kappa light chains. These findings were consistent with light chain cast nephropathy (LCCN). Serum free light chains, serum immunofixation, urine protein electrophoresis, and urine immunofixation studies supported the renal biopsy diagnosis of LCCN. A bone marrow biopsy showed normal trilineage hematopoiesis and also revealed an atypical B cell population detected by flow cytometry. Pathology specimens from lesions in the distal small bowel were characteristic of diffuse large B cell lymphoma (DLBCL). Chemoreduction therapy followed by chemotherapy was initiated for the DLBCL. Three months after initiation of chemotherapy, the patient's creatinine has improved by > 50%. The likely cause of her LCCN was the new diagnosis of a DLBCL. Other risk factors include her history of hypogammaglobulinemia, natural killer (NK) cell deficiency, community-acquired pneumonia, and prior follicular lymphoma. Our patient may be the youngest reported case of LCCN. Treatment of LCCN is based on treating the underlying clonal plasma cell or B cell proliferation, typically with chemotherapy.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s00467-018-3930-6

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[PMID]: 29523957
[Au] Autor:Steinberg M; Gaut JP; Hmiel SP; Kakajiwala A
[Ad] Address:Department of Pediatrics, Washington University in St. Louis School of Medicine, St. Louis, USA.
[Ti] Title:The light at the end of the tunnel: an unusual case of acute kidney injury in a pediatric patient: Questions.
[So] Source:Pediatr Nephrol;, 2018 Mar 09.
[Is] ISSN:1432-198X
[Cp] Country of publication:Germany
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1007/s00467-018-3918-2

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[PMID]: 29523497
[Au] Autor:Okokhere P; Colubri A; Azubike C; Iruolagbe C; Osazuwa O; Tabrizi S; Chin E; Asad S; Ediale E; Rafiu M; Adomeh D; Odia I; Atafo R; Aire C; Okogbenin S; Pahlman M; Becker-Ziaja B; Asogun D; Fradet T; Fry B; Schaffner SF; Happi C; Akpede G; Günther S; Sabeti PC
[Ad] Address:Department of Medicine, Irrua Specialist Teaching Hospital, Irrua, Nigeria; Institute of Lassa fever Research and Control, Irrua Specialist Teaching Hospital, Irrua, Nigeria; Department of Medicine, Faculty of Clinical Sciences, Ambrose Alli University, Ekpoma, Edo, Nigeria. Electronic address: okok
[Ti] Title:Clinical and laboratory predictors of Lassa fever outcome in a dedicated treatment facility in Nigeria: a retrospective, observational cohort study.
[So] Source:Lancet Infect Dis;, 2018 Mar 06.
[Is] ISSN:1474-4457
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Lassa fever is a viral haemorrhagic disease endemic to west Africa. No large-scale studies exist from Nigeria, where the Lassa virus (LASV) is most diverse. LASV diversity, coupled with host genetic and environmental factors, might cause differences in disease pathophysiology. Small-scale studies in Nigeria suggest that acute kidney injury is an important clinical feature and might be a determinant of survival. We aimed to establish the demographic, clinical, and laboratory factors associated with mortality in Nigerian patients with Lassa fever, and hypothesised that LASV was the direct cause of intrinsic renal damage for a subset of the patients with Lassa fever. METHODS: We did a retrospective, observational cohort study of consecutive patients in Nigeria with Lassa fever, who tested positive for LASV with RT-PCR, and were treated in Irrua Specialist Teaching Hospital. We did univariate and multivariate statistical analyses, including logistic regression, of all demographic, clinical, and laboratory variables available at presentation to identify the factors associated with patient mortality. FINDINGS: Of 291 patients treated in Irrua Specialist Teaching Hospital between Jan 3, 2011, and Dec 11, 2015, 284 (98%) had known outcomes (died or survived) and seven (2%) were discharged against medical advice. Overall case-fatality rate was 24% (68 of 284 patients), with a 1·4 times increase in mortality risk for each 10 years of age (p=0·00017), reaching 39% (22 of 57) for patients older than 50 years. Of 284 patients, 81 (28%) had acute kidney injury and 104 (37%) had CNS manifestations and thus both were considered important complications of acute Lassa fever in Nigeria. Acute kidney injury was strongly associated with poor outcome (case-fatality rate of 60% [49 of 81 patients]; odds ratio [OR] 15, p<0·00001). Compared with patients without acute kidney injury, those with acute kidney injury had higher incidence of proteinuria (32 [82%] of 39 patients) and haematuria (29 [76%] of 38) and higher mean serum potassium (4·63 [SD 1·04] mmol/L) and lower blood urea nitrogen to creatinine ratio (8·6 for patients without clinical history of fluid loss), suggesting intrinsic renal damage. Normalisation of creatinine concentration was associated with recovery. Elevated serum creatinine (OR 1·3; p=0·046), aspartate aminotransferase (OR 1·5; p=0·075), and potassium (OR 3·6; p=0·0024) were independent predictors of death. INTERPRETATION: Our study presents detailed clinical and laboratory data for Nigerian patients with Lassa fever and provides strong evidence for intrinsic renal dysfunction in acute Lassa fever. Early recognition and treatment of acute kidney injury might significantly reduce mortality. FUNDING: German Research Foundation, German Center for Infection Research, Howard Hughes Medical Institute, US National Institutes of Health, and World Bank.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  10 / 65408 MEDLINE  
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[PMID]: 29522949
[Au] Autor:Xu J; Xia Y; Zhang H; Guo H; Feng K; Zhang C
[Ad] Address:Reproductive Medicine Center, Henan Provincial People's Hospital, Zhengzhou University, Zhengzhou 450003, PR China.
[Ti] Title:Overexpression of long non-coding RNA H19 promotes invasion and autophagy via the PI3K/AKT/mTOR pathways in trophoblast cells.
[So] Source:Biomed Pharmacother;101:691-697, 2018 Mar 06.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:BACKGROUND: Preeclampsia (PE), characterized by hypertension and proteinuria, is a leading cause of perinatal and maternal mortality. Considering that mutation of H19 gene is closely associated with PE, we aimed to explore the functional role of long non-coding RNA H19 (lncRNA-H19) in trophoblast cells. METHODS: Expression of lncRNA-H19 in placenta tissues from patients with PE and healthy pregnant women after delivery was determined by quantitative reverse transcription PCR. Then, lncRNA-H19 was abnormally expressed in JEG-3 and HTR-8 cells by stable cell transfection. Cell viability and invasion were assessed by using CCK-8 and Matrigel-coated Millicell system, respectively. Expression of key proteins associated with invasion and autophagy as well as key kinases in the phosphatidylinositol-3-kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR) pathways were measured by Western blot analysis. Number of GFP-labeled autophagosomes was counted under a confocal microscope. RESULTS: Level of lncRNA-H19 in the placenta tissues from PE patients was higher than that from healthy controls. LncRNA-H19 overexpression reduced cell viability but increased invasion of JEG-3 and HTR-8 cells. LncRNA-H19 silence showed the opposite effects. In addition, lncRNA-H19 overexpression promoted autophagy in trophoblast cells. Furthermore, phosphorylated levels of key kinases in the PI3K/AKT/mTOR pathways were enhanced by lncRNA-H19 overexpression while were reduced by lncRNA-H19 silence. CONCLUSION: LncRNA-H19, which was up-regulated in PE, reduced cell viability but promoted invasion and autophagy in trophoblast cells, along with activation of the PI3K/AKT/mTOR pathways. Our study provides a theoretical basis for pathogenesis of PE, aiding to identification of novel therapeutic strategies for PE.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher


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