Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury

Polyomavirus-associated nephropathy (PVAN) is an emerging cause of kidney transplant failure affecting 1-10% of patients. As uncertainty exists regarding risk factors, diagnosis, and intervention, an independent panel of experts reviewed the currently available evidence and prepared this report. Most cases of PVAN are elicited by BK virus (BKV) in the context of intense immunosuppression. No specific immunosuppressive drug is exclusively associated with PVAN, but most cases reported to date arise while the patient is on triple immunosuppressive combinations, often comprising tacrolimus and/or mycophenolate mofetil plus corticosteroids. Immunologic control of polyomavirus replication can be achieved by reducing, switching, and/or discontinuing components of the immunosuppressive regimen, but the individual's risk of rejection should be considered. The success rate of this intervention is increased with earlier diagnosis. Therefore, it is recommended that all renal transplant recipients should be screened for BKV replication in the urine: 1) every three months during the first two years posttransplant; 2) when allograft dysfunction is noted; and 3) when allograft biopsy is performed. A positive screening result should be confirmed in <4 weeks and assessed by quantitative assays (e.g. BKV DNA or RNA load in plasma or urine). Definitive diagnosis of PVAN requires allograft biopsy. If PVAN and concurrent acute rejection is diagnosed, antirejection treatment should be considered, coupled with subsequently reducing immunosuppression. The antiviral cidofovir is not approved for PVAN, but investigational use at low doses (0.25-0.33 mg/kg intravenously biweekly) without probenicid should be considered for refractory cases. Retransplantation after renal allograft loss to PVAN remains a treatment option for patients clearing polyomavirus replication.

Polyomavirus-Associated Nephropathy in Renal Transplantation: Interdisciplinary Analyses and Recommendations

Hyponatraemia, defined as a serum sodium concentration !135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution- and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association – European Dialysis and Transplant Association (ERA–EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

/pdf/clinical-practice-guideline-on-diagnosis-and-treatment-of-509w3449ob.pdf

Clinical practice guideline on diagnosis and treatment of hyponatraemia

https://www.kidney-international.org/article/S0085-2538(15)52823-8/pdf

Association between obesity and kidney disease: a systematic review and meta-analysis.

This article updates the Heart Failure Association of the European Society of Cardiology (ESC) 2007 classification of advanced heart failure and describes new diagnostic and treatment options for these patients. Recognizing the patient with advanced heart failure is critical to facilitate timely referral to advanced heart failure centres. Unplanned visits for heart failure decompensation, malignant arrhythmias, co-morbidities, and the 2016 ESC guidelines criteria for the diagnosis of heart failure with preserved ejection fraction are included in this updated definition. Standard treatment is, by definition, insufficient in these patients. Inotropic therapy may be used as a bridge strategy, but it is only a palliative measure when used on its own, because of the lack of outcomes data. Major progress has occurred with short-term mechanical circulatory support devices for immediate management of cardiogenic shock and long-term mechanical circulatory support for either a bridge to transplantation or as destination therapy. Heart transplantation remains the treatment of choice for patients without contraindications. Some patients will not be candidates for advanced heart failure therapies. For these patients, who are often elderly with multiple co-morbidities, management of advanced heart failure to reduce symptoms and improve quality of life should be emphasized. Robust evidence from prospective studies is lacking for most therapies for advanced heart failure. There is an urgent need to develop evidence-based treatment algorithms to prolong life when possible and in accordance with patient preferences, increase life quality, and reduce the burden of hospitalization in this vulnerable patient population.

Advanced heart failure : a position statement of the Heart Failure Association of the European Society of Cardiology

Cytomegalovirus (CMV) infection is reported to be capable of modifying endothelial surface with subsequent increased risk of thromboembolic complications. Nevertheless, there are only sparse reports on its role in the development of bleeding diathesis. Here we report two renal transplant recipients who manifested severe coagulation disorders associated with acute CMV infection. Antiviral therapy was followed by consistent correction of coagulation abnormalities.

Cytomegalovirus-associated bleeding diathesis in renal transplant recipients

Signs and symptoms of fluid overload are the primary reason for hospital admission of patients with acute decompensated heart failure. It has been shown that congestion is a dynamic state with mutual links to both heart failure and renal dysfunction, which is capable of modifying the impact of these two elements on the outcomes. In this article, we provide an overview of the emerging concepts related to pathophysiological aspects of fluid overload in heart failure. Then, methods for objective evaluation of congestion are discussed with emphasis on newer techniques Future studies are needed to determine whether more precise evaluation of fluid overload combined with close monitoring of decongestion process would have a salutary impact on the outcomes of patients with heart failure.

/pdf/congestion-and-the-kidney-heart-cross-talk-in-acute-j3a8ckxt68.pdf

Congestion and the Kidney-Heart Cross Talk in Acute Decompensated Heart Failure

118: Homocysteine Lowering Effect of Adsorptive Dialysis Membranes: A Multicenter, Randomized, Open Study

vancomycin and cefepime was started, which was followed by rapid clinical improvement. She was discharged home on oral amoxicillin–clavulanic acid. Interestingly, 10 days later, all cultures obtained from the exit site at different time points revealed acid-fast bacilli later identified as Mycobacterium fortuitum . The decision was made to use oral clarithromycin and ciprofloxacin for 2 months. Of note, the patient reported using well water for bathing which could be the potential source for atypical mycobacteria; the culture of the water was performed and was negative for mycobacteria. The patient has remained asymptomatic with normal exit site on examination. M. fortuitum is the most commonly reported non-tuberculous mycobacterium associated with PD-associated peritonitis. However, exit site infection with this organism is very rare [4] . There are 2 key educational points in this case. First, immunosuppressive agents, even at very low dose, could still increase a patient’s susceptibility to uncommon and atypical infections. Second, clinical improvement after initial empiric antibiotic therapy in these patients could possibly be due to partial To the Editor, Exit site infection is a well-known complication among patients receiving peritoneal dialysis (PD). Common responsible organisms include Staphylococcus aureus and S. epidermidis [1] . Therefore, current guidelines recommend initial empiric antibiotics that are aimed at these organisms. However, infections secondary to uncommon organisms such as atypical mycobacteria and non-diphtheria corynebacteria are being increasingly reported with the widespread use of antimicrobial prophylaxis of the exit site [2, 3] . We recently encountered a 59-year-old woman with a history of diabetes mellitus and end-stage renal disease treated with PD who presented with fever, chills, redness, and swelling at her PD catheter exit site for the previous 2 days. She had a failed renal transplant 4 months before and was receiving azathioprine 75 mg/day and prednisone 10 mg/day. Examination revealed erythema and edema at the exit site with serosanguinous discharge. PD fluid cell count was not suggestive of PD-associated peritonitis and gram stain from the exit site was negative. The PD catheter exit site infection was diagnosed, and intravenous antibiotic therapy with Received: January 13, 2017 Accepted: February 18, 2017 Published online: March 8, 2017

/pdf/exit-site-infection-in-peritoneal-dialysis-need-for-follow-28aofxc2yo.pdf

Amir Kazory

Papers

Cytomegalovirus-associated bleeding diathesis in renal transplant recipients

Congestion and the Kidney-Heart Cross Talk in Acute Decompensated Heart Failure

118: Homocysteine Lowering Effect of Adsorptive Dialysis Membranes: A Multicenter, Randomized, Open Study

Exit Site Infection in Peritoneal Dialysis; Need for Follow-Up on Cultures Despite Clinical Improvement.

Point-of-care Doppler ultrasonography: a new dimension to kidney imaging.