Current Issue : January - March Volume : 2012 Issue Number : 1 Articles : 7 Articles
The incidence of BK virus infection in kidney transplant recipients has increased over recent decades, coincident with the use of\r\nmore potent immunosuppression. More importantly, posttransplant BK virus replication has emerged as an important cause of\r\ngraft damage and subsequent graft loss. Immunosuppression has been accepted as a major risk for BK virus replication. However,\r\nthe specific contribution of individual immunosuppressive medications to this risk has not been well established. The purpose of\r\nthis paper is to provide an overview of the recent literature on the influence of the various immunosuppressant drugs and drug\r\ncombinations on posttransplant BK virus replication. Evidence supporting the various immunosuppression reduction strategies\r\nutilised in the management of BK virus will also be briefly discussed....
Background: MELAS syndrome (MIM ID#540000), an acronym for Mitochondrial Encephalopathy, Lactic Acidosis\r\nand Stroke-like episodes, is a genetically heterogeneous mitochondrial disorder with protean manifestations and\r\noccasional kidney involvement. Interest in the latter is rising due to the identification of cases with predominant\r\nkidney involvement and to the hypothesis of a link between mitochondrial DNA and kidney neoplasia.\r\nCase presentation: We report the case of a 41-year-old male with full blown MELAS syndrome, with lactic acidosis\r\nand neurological impairment, affected by the ââ?¬Å?classicââ?¬Â 3243A > G mutation of mitochondrial DNA, with kidney\r\ncancer. After unilateral nephrectomy, he rapidly developed severe kidney functional impairment, with nephrotic\r\nproteinuria. Analysis of the kidney tissue at a distance from the two tumor lesions, sampled at the time of\r\nnephrectomy was performed in the context of normal blood pressure, recent onset of diabetes and before the\r\nappearance of proteinuria. The morphological examination revealed a widespread interstitial fibrosis with dense\r\ninflammatory infiltrate and tubular atrophy, mostly with thyroidization pattern. Vascular lesions were prominent:\r\nlarge vessels displayed marked intimal fibrosis and arterioles had hyaline deposits typical of hyaline\r\narteriolosclerosis. These severe vascular lesions explained the different glomerular alterations including ischemic\r\nand obsolescent glomeruli, as is commonly observed in the so-called ââ?¬Å?benignââ?¬Â arteriolonephrosclerosis. Some rare\r\nglomeruli showed focal segmental glomerulosclerosis; as the patient subsequently developed nephrotic syndrome,\r\nthese lesions suggest that silent ischemic changes may result in the development of focal segmental\r\nglomerulosclerosis secondary to nephron loss.\r\nConclusions: Nephron loss may trigger glomerular sclerosis, at least in some cases of MELAS-related nephropathy.\r\nThus the incidence of kidney disease in the ââ?¬Å?survivorsââ?¬Â of MELAS syndrome may increase as the support therapy of\r\nthese patients improves....
Background: Although recent studies indicate that renal ischemic preconditioning (IPC) protects the kidney from\r\nischemia-reperfusion (I/R) injury, the precise protective mechanism remains unclear. In the current study, we\r\ninvestigated whether early IPC could upregulate hypoxia inducible transcription factor-1a (HIF-1a) expression and\r\ncould reduce endoplasmic reticulum (ER) stress after renal I/R and whether pharmacological inhibition of nitric\r\noxide (NO) production would abolish these protective effects.\r\nMethods: Kidneys of Wistar rats were subjected to 60 min of warm ischemia followed by 120 min of reperfusion\r\n(I/R group), or to 2 preceding cycles of 5 min ischemia and 5 min reperfusion (IPC group), or to intravenously\r\ninjection of NG-nitro-L-arginine methylester (L-NAME, 5 mg/kg) 5 min before IPC (L-NAME+IPC group). The results\r\nof these experimental groups were compared to those of a sham-operated group. Sodium reabsorption rate,\r\ncreatinine clearance, plasma lactate dehydrogenase (LDH) activity, tissues concentrations of malonedialdehyde\r\n(MDA), HIF-1a and nitrite/nitrate were determined. In addition, Western blot analyses were performed to identify\r\nthe amounts of Akt, endothelial nitric oxide synthase (eNOS) and ER stress parameters.\r\nResults: IPC decreased cytolysis, lipid peroxidation and improved renal function. Parallely, IPC enhanced Akt\r\nphosphorylation, eNOS, nitrite/nitrate and HIF-1a levels as compared to I/R group. Moreover, our results showed\r\nthat IPC increased the relative amounts of glucose-regulated protein 78 (GRP78) and decreased those of RNA\r\nactivated protein kinase (PKR)-like ER kinase (PERK), activating transcription factor 4 (ATF4) and TNF-receptorassociated\r\nfactor 2 (TRAF2) as judged to I/R group. However, pre treatment with L-NAME abolished these beneficial\r\neffects of IPC against renal I/R insults.\r\nConclusion: These findings suggest that early IPC protects kidney against renal I/R injury via reducing oxidative\r\nand ER stresses. These effects are associated with phosphorylation of Akt, eNOS activation and NO production\r\ncontributing thus to HIF-1a stabilization. The beneficial impact of IPC was abolished when NO production is\r\ninhibited before IPC application....
Background: Care of children and young people (children) with long-term kidney conditions is usually managed\r\nby multidisciplinary teams. Published guidance recommends that whenever possible children with long-term\r\nconditions remain at home, meaning parents may be responsible for performing the majority of clinical caregiving.\r\nMultidisciplinary team members, therefore, spend considerable time promoting parentsââ?¬â?¢ learning about\r\ncare-delivery and monitoring care-giving. However, this parent-educative aspect of cliniciansââ?¬â?¢ role is rarely\r\narticulated in the literature so little evidence exists to inform professionalsââ?¬â?¢ parent-teaching interventions.\r\nMethods/Design: This ongoing study addresses this issue using a combination of quantitative and qualitative\r\nmethods involving the twelve childrenââ?¬â?¢s kidney units in England, Scotland and Wales. Phase I involves a survey of\r\nmultidisciplinary team membersââ?¬â?¢ parent-teaching interventions using:\r\ni) A telephone-administered questionnaire to determine: the numbers of professionals from different disciplines in\r\neach team, the information/skills individual professionals relay to parents and the teaching strategies/interventions\r\nthey use. Data will be managed using SPSS to produce descriptive statistics\r\nii) Digitally-recorded, qualitative group or individual interviews with multidisciplinary team members to explore\r\ntheir accounts of the parent-teaching component of their role. Interviews will be transcribed anonymously and\r\nanalysed using Framework Technique. Sampling criteria will be derived from analysis to identify one/two unit(s) for\r\nsubsequent in-depth study\r\nPhase II involves six prospective, ethnographic case-studies of professional-parent interactions during parentteaching\r\nencounters. Parents of six children with a long-term kidney condition will be purposively sampled\r\naccording to their childââ?¬â?¢s age, diagnosis, ethnicity and the clinical care-giving required; snowball sampling will\r\nidentify the professionals involved in each case-study. Participants will provide signed consent; data gathering will\r\ninvolve a combination of: minimally-obtrusive observations in the clinical setting and familiesââ?¬â?¢ homes; de-briefing\r\ninterviews with participants to obtain views on selected interactions; focussed ââ?¬Ë?verbatimââ?¬â?¢ field-notes, and case-note\r\nreviews. Data gathering will focus on communication between parents and professionals as parents learn caregiving\r\nskills and knowledge. Interviews will be digitally recorded and transcribed anonymously.\r\nDiscussion: This study involves an iterative-inductive approach and will provide a unique, detailed insight into the\r\nsocial context in which professionals teach and parents learn; it will inform professionalsââ?¬â?¢ parent-educative roles,\r\neducational curricula, and health care policy...
Background: Neutrophil gelatinase associated lipocalin (NGAL) is a biomarker of kidney injury. We examined\r\nplasma levels of NGAL in a cohort of 57 kidney allograft recipients (Tx group, 39 �± 13 years), a uraemic group of\r\n40 patients remaining on the waiting list (47 �± 11 years) and a control group of 14 healthy subjects matched for\r\nage, sex and body mass index (BMI). The kidney graft recipients were studied at baseline before transplantation\r\nand 3 and 12 months after transplantation and the uraemic group at baseline and after 12 months.\r\nMethods: NGAL was measured using a validated in-house Time-Resolved Immuno-flourometric assay (TRIFMA).\r\nRepeated measurements differed by < 10% and mean values were used for statistical analyses. Spearman rank\r\norder correlation analysis and the Kruskal-Wallis non-parametric test were used to evaluate the association of NGAL\r\nconcentrations with clinical parameters.\r\nResults: Plasma NGAL levels before transplantation in the Tx and uraemic groups were significantly higher than in\r\nthe healthy controls (1,251 �µg/L, 1,478 �µg/L vs. 163 �µg/L, p < 0.0001). In the Tx group NGAL concentrations were\r\nassociated with serum creatinine (R = 0.51, p < 0.0001), duration of end-stage renal failure (R = 0.41, p = 0.002) and\r\nleukocyte count (R = 0.29, p < 0.026). At 3 and 12 months plasma NGAL concentrations declined to 223 �µg/L and\r\n243 �µg/L, respectively and were associated with homocysteine (R = 0.39, p = 0.0051 and R = 0.47, p = 0.0007).\r\nConclusions: Plasma NGAL is a novel marker of kidney function, which correlates to duration of end-stage renal\r\nfailure (ESRD) and serum creatinine in uraemic patients awaiting kidney transplantation. Plasma NGAL is associated\r\nwith homocysteine in transplanted patients. The prognostic value of these findings requires further studies....
Background: The aim of this study was to explore the associations between common potential functional\r\npromoter polymorphisms in pro-/anti-inflammatory cytokine genes and kidney function/chronic kidney disease\r\n(CKD) prevalence in a large Japanese population.\r\nMethods: A total of 3,323 subjects aged 35-69 were genotyped for all 10 single nucleotide polymorphisms (SNPs)\r\nin the promoter regions of candidate genes with minor allele frequencies of > 0.100 in Japanese populations. The\r\nestimated glomerular filtration rate (eGFR) and CKD prevalence (eGFR < 60 ml/min/1.73 m2) of the subjects were\r\ncompared among the genotypes.\r\nResults: A higher eGFR and lower prevalence of CKD were observed for the homozygous variants of IL4 -33CC\r\n(high IL-4 [anti-inflammatory cytokine]-producing genotype) and IL6 -572GG (low IL-6 [pro-inflammatory cytokine]-\r\nproducing genotype). Subjects with IL4 CC + IL6 GG showed the highest mean eGFR (79.1 ml/min/1.73 m2) and\r\nlowest CKD prevalence (0.0%), while subjects carrying IL4 TT + IL6 CC showed the lowest mean eGFR (73.4 ml/min/\r\n1.73 m2) and highest CKD prevalence (17.9%).\r\nConclusions: The functional promoter polymorphisms IL4 T-33C (rs2070874) and IL6 C-572G (rs1800796), which are\r\nthe only SNPs that affect the IL-4 and IL-6 levels in Japanese subjects, were associated with kidney function and\r\nCKD prevalence in a large Japanese population....
Background: Transfusion patterns are not well characterized in non-dialysis (ND) chronic kidney disease (CKD)\r\npatients. This study describes the proportion of patients transfused, units of blood transfused and triggerhemoglobin\r\n(Hb) levels for transfusions in severe anemic, ND-CKD patients in routine practice.\r\nMethods: A retrospective cohort study of electronic medical record data from the Henry Ford Health System\r\nidentified 374 adult, ND-CKD patients with severe anemia (Hb < 10 g/dL and subsequent use of erythropoiesisstimulating\r\nagents [ESA] therapy, blood transfusions, or a second Hb < 10 g/dL) between January 2004 and June\r\n2008. Exclusions included those with prior diagnoses of cancer, renal or liver transplant, end-stage renal disease,\r\nacute bleeding, trauma, sickle cell disease, or aplastic anemia. A gap of = 1 days between units of blood transfused\r\nwas counted as a separate transfusion.\r\nResults: At least 1 transfusion (mean of 2 units; range, 1-4) was administered to 20% (75/374) of ND-CKD patients\r\nwith mean (�± SD) follow-up of 459 (�± 427) days. The mean (�± SD) Hb level closest and prior to a transfusion was\r\n8.8 (�± 1.5) g/dL. Patients who were hospitalized in the 6 months prior to their first anemia diagnosis were 6.3 times\r\nmore likely to receive a blood transfusion than patients who were not hospitalized (p < 0.0001). Patients with\r\nperipheral vascular disease (PVD) were twice as likely to have a transfusion as patients without PVD (p = 0.04).\r\nConclusions: Transfusions were prevalent and the trigger hemoglobin concentration was approximately 9 g/dL\r\namong ND-CKD patients with anemia. To reduce the transfusion burden, clinicians should consider other anemia\r\ntreatments including ESA therapy....
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