Current Issue : October - December Volume : 2013 Issue Number : 4 Articles : 6 Articles
Background: Reasons underlying dialysis decision-making in Octogenarians and Nonagenarians have not been\r\nfurther explored in prospective studies.\r\nMethods: This regional, multicentre, non-interventional and prospective study was aimed to describe characteristics and\r\nquality of life (QoL) of elderly (=80 years of age) with advanced chronic kidney disease (stage 3b-5 CKD) newly referred to\r\nnephrologists. Predictive factors of death and dialysis initiation were also assessed using competing-risk analyses.\r\nResults: All 155 included patients had an estimated glomerular filtration rate (eGFR) below 45 ml/min/1.73m2. Most\r\npatients had a non anaemic haemoglobin level (Hb) with no iron deficiency, and normal calcium and phosphate levels.\r\nThey were well-fed and had a normal cognitive function and a good QoL. The 3-year probabilities of death and dialysis\r\ninitiation reached 27% and 11%, respectively. The leading causes of death were cardiovascular (32%), cachexia (18%),\r\ncancer (9%), infection (3%), trauma (3%), dementia (3%), and unknown (32%). The reasons for dialysis initiation were\r\nbased on uncontrolled biological abnormalities, such as hyperkalemia or acidosis (71%), uncontrolled digestive disorders\r\n(35%), uncontrolled pulmonary or peripheral oedema (29%), and uncontrolled malnutrition (12%). No patients with acute\r\ncongestive heart failure or cancer initiated dialysis. Predictors of death found in both multivariate regression models\r\n(Cox and Fine & Gray) included acute congestive heart failure, age, any walking impairment and Hb <10 g/dL. Regarding\r\ndialysis initiation, eGFR <23 mL/min/1.73m2 was the only predictor found in the Cox multivariate regression model\r\nwhereas eGFR <23 mL/min/1.73m2 and diastolic blood pressure were both independently associated with dialysis\r\ninitiation in the Fine & Gray analysis. Such findings suggested that death and dialysis were independent events.\r\nConclusions: Octogenarians and Nonagenarians newly referred to nephrologists by general practitioners were highly\r\nselected patients, without any symptoms of the common geriatric syndrome. In this population, nephrologists� dialysis\r\ndecision was based exclusively on uremic criteria....
Background: The inhibition of dipeptidyl peptidase (DPP) IV shows protective effects on tissue injury of the heart, lung,\r\nand kidney. Forkhead box O (FoxO) transcriptional factors regulate cellular differentiation, growth, survival, the cell cycle,\r\nmetabolism, and oxidative stress. The aims of this study were to investigate whether the DPP IV inhibitor sitagliptin\r\ncould attenuate kidney injury and to evaluate the status of FoxO3a signaling in the rat remnant kidney model.\r\nMethods: Rats were received two-step surgery of 5/6 renal mass reduction and fed on an oral dose of 200 mg/kg/day\r\nsitagliptin for 8 weeks. Before and after the administration of sitagliptin, physiologic parameters were measured. After\r\n8 weeks of treatment, the kidneys were harvested.\r\nResults: The sitagliptin treatment attenuated renal dysfunction. A histological evaluation revealed that\r\nglomerulosclerosis and tubulointerstitial injury were significantly decreased by sitagliptin. Sitagliptin decreased DPP IV\r\nactivity and increased the renal expression of glucagon-like peptide-1 receptor (GLP-1R). The subtotal nephrectomy led\r\nto the activation of phosphatidylinositol 3-kinase (PI3K)-Akt and FoxO3a phosphorylation, whereas sitagliptin treatment\r\nreversed these changes, resulting in PI3K-Akt pathway inactivation and FoxO3a dephosphorylation. The renal expression\r\nof catalase was increased and the phosphorylation of c-Jun N-terminal kinase (JNK) was decreased by sitagliptin.\r\nSitagliptin treatment reduced apoptosis by decreasing cleaved caspase-3 and -9 and Bax levels and decreased\r\nmacrophage infiltration.\r\nConclusions: In rat remnant kidneys, DPP IV inhibitor attenuated renal dysfunction and structural damage. A reduction\r\nof apoptosis, inflammation and an increase of antioxidant could be suggested as a renoprotective mechanism together\r\nwith the activation of FoxO3a signaling. Therefore, DPP IV inhibitors might provide a promising approach for treating\r\nCKD, but their application in clinical practice remains to be investigated....
Background: We describe a case of a fever of unknown etiology that was caused by a caseating tubercle\r\ngranuloma which produced erythropoietin. To our knowledge, this is the first report of an erythropoietinproducing\r\ngranuloma.\r\nCase presentation: A 48-year-old Japanese man with a 5-year history of maintenance hemodialysis for diabetic\r\nnephropathy presented with an intermittent fever over a few months. During febrile periods he developed erythema\r\nnodosum on his legs. Computed tomography showed axillary lymph node enlargement and this was further\r\ncorroborated by a gallium scan that revealed high gallium uptake in these nodes. A Mantoux test was positive and an\r\ninterferongamma release assay for tuberculosis diagnosis was also positive. Lymph node tuberculosis was suspected and\r\nthe patient underwent lymphadenectomy. Histological analysis of the lymph nodes revealed a caseating granuloma that\r\nshowed positive results on an acid-fast bacteria stain and a Mycobacterium tuberculosis polymerase chain reaction test.\r\nAfter lymphadenectomy, however, the patient�s hemoglobin levels rapidly decreased from 144 to 105 g/L, and this was\r\nfurther compounded by a decrease in serum erythropoietin from 223 mIU/mL to 10.7 mIU/mL by postoperative day 21.\r\nWe suspected the tubercle to be a source of the erythropoietin and this was further confirmed by in situ hybridization.\r\nConclusions: We report for the first time ectopic erythropoietin production by a tuberculous lymph node. Our\r\nobservations are substantiated by a postoperative decline in his erythropoietin level and a clinical requirement for\r\nerythropoietin treatment....
Background: Nasal colonization with methicillin-resistant Staphylococcus aureus (MRSA) is a well defined risk factor\r\nfor subsequent bacteremia and death in various groups of patients, but its impact on outcome in patients receiving\r\nlong-term hemodialysis (HD) is under debate.\r\nMethods: This prospective interventional cohort study (performed 2004 to 2010) enrolled 289 HD outpatients of an\r\nurban dialysis-unit. Nasal swab cultures for MRSA were performed in all patients upon first admission, at transfer\r\nfrom another dialysis facility or readmission after hospitalisation. Nasal MRSA carriers were treated in a separate\r\nward and received mupirocin nasal ointment. Concomitant extra-nasal MRSA colonization was treated with 0.2%\r\nchlorhexidine mouth rinse (throat) or octenidine dihydrochloride containing antiseptic soaps and 2% chlorhexidine\r\nbody washes (skin). Clinical data and outcome of carriers and noncarriers were systematically analyzed.\r\nResults: The screening approach identified 34 nasal MRSA carriers (11.7%). Extra-nasal MRSA colonization was\r\nobserved in 11/34 (32%) nasal MRSA carriers. History of malignancy and an increased Charlson Comorbidity Index\r\nwere significant predictors for nasal MRSA carriers, whereas traditional risk factors for MRSA colonization or markers\r\nof inflammation or malnutrition were not able to discriminate. Kaplan-Meier analysis demonstrated significant\r\nsurvival differences between MRSA carriers and noncarriers. Mupirocin ointment persistently eliminated nasal MRSA\r\ncolonization in 26/34 (73.5%) patients. Persistent nasal MRSA carriers with failure of this eradication approach had\r\nan extremely poor prognosis with an all-cause mortality rate >85%.\r\nConclusions: Nasal MRSA carriage with failure of mupirocin decolonization was associated with increased mortality\r\ndespite a lack of overt clinical signs of infection. Further studies are needed to demonstrate whether nasal MRSA\r\ncolonization represents a novel predictor of worse outcome or just another surrogate marker of the burden of\r\ncomorbid diseases leading to fatal outcome in HD patients....
Background: Current data describing the epidemiology of acute kidney injury (AKI) following repair of ruptured\r\nabdominal aortic aneurysm (rAAA) are limited and long-term outcomes are largely unknown. Our objectives were\r\nto describe the incidence rate, risk factors, clinical course and long-term outcomes of AKI following rAAA repair.\r\nMethods: Retrospective population-based cohort study of all referrals undergoing emergency repair of rAAA in\r\nNorthern Alberta from January 1, 2002 to December 31 2009. Demographic, clinical, physiologic and laboratory data\r\nwere extracted. AKI was defined and classified according to the AKIN criteria.\r\nResults: In total, 140 patients survived to receive emergent rAAA repair. Post-operative AKI occurred in 75.7% of\r\npatients (n = 106), 78.3% (n = 83) of which occurred during the initial 24 hours of ICU admission. AKIN stage 1, 2,\r\nand 3 occurred in 47 (33.6%), 36 (25.7%) and 23 (16.4%), respectively, with 19 patients receiving renal replacement\r\ntherapy (RRT). Several clinical and biochemical patient factors were associated with incident AKI, including baseline\r\nestimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2 (odds ratio [OR] 2.94; 95% CI, 1.15-7.51, p = 0.03),\r\nneed for mechanical ventilation (OR 22.7; 95% CI, 7.0-72.1, p < 0.0001) and vasoactive therapy (OR 9.9; 95% CI,\r\n3.0-32.2, p < 0.0001) and higher mean APACHE II scores (25.7 [8.2] vs. 16.3 [4.9], p < 0.0001). AKI was associated\r\nwith a higher ICU (28.3% vs. 0%; p = 0.0008) and in-hospital case-fatality rate (35.9% vs. 0%, p = 0.0001). Of 102\r\nsurvivors to discharge, 65.7% (n = 67) recovered to baseline kidney function. In multivariable analysis, greater\r\nseverity of AKI (OR 5.01; 95% CI, 2.34-10.7, p < 0.001) and lower baseline eGFR (OR 0.96; 95% CI, 0.93-0.99, p = 0.03)\r\nwere associated with non-recovery. AKI remained independently associated with 1-year mortality after adjusting for\r\nage, sex, comorbidity, and illness severity (OR 5.21; 95% CI, 1.04-26.2, p = 0.045; AUC 0.83; H-L GoF, p = 0.26).\r\nAmong survivors at 1-year, only 63.4% (n = 55) had complete kidney recovery.\r\nConclusions: Following rAAA repair, AKI is a common complication independently associated with long-term postoperative\r\nmortality. A significant proportion of AKI sufferers in this setting fail to recover to baseline kidney function....
Background: Chronic kidney disease (CKD) affects up to 16% of the adult population and is associated with\r\nsignificant morbidity and mortality. People at highest risk from progressive CKD are defined by a sustained decline\r\nin estimated glomerular filtration rate (eGFR) and/or the presence of significant albuminuria/proteinuria and/or\r\nmore advanced CKD. Accurate mapping of the bio-clinical determinants of this group will enable improved risk\r\nstratification and direct the development of better targeted management for people with CKD.\r\nMethods/Design: The Renal Impairment In Secondary Care study is a prospective, observational cohort study,\r\npatients with CKD 4 and 5 or CKD 3 and either accelerated progression and/or proteinuria who are managed in\r\nsecondary care are eligible to participate. Participants undergo a detailed bio-clinical assessment that includes\r\nmeasures of vascular health, periodontal health, quality of life and socio-economic status, clinical assessment and\r\ncollection of samples for biomarker analysis. The assessments take place at baseline, and at six, 18, 36, 60 and 120\r\nmonths; the outcomes of interest include cardiovascular events, progression to end stage kidney disease and death.\r\nDiscussion: The determinants of progression of chronic kidney disease are not fully understood though there are a\r\nnumber of proposed risk factors for progression (both traditional and novel). This study will provide a detailed\r\nbio-clinical phenotype of patients with high-risk chronic kidney disease (high risk of both progression and\r\ncardiovascular events) and will repeatedly assess them over a prolonged follow up period. Recruitment\r\ncommenced in Autumn 2010 and will provide many outputs that will add to the evidence base for progressive\r\nchronic kidney disease....
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