Clinical Journal of the American Society of Nephrology Moving Points in Nephrology http://cjasn.asnjournals.org Clinical Journal of the American Society of Nephrology RSS feed -- recent Moving Points in Nephrology articles 1555-905X Clinical Journal of the American Society of Nephrology 1555-9041 Clinical Journal of the American Society of Nephrology http://cjasn.asnjournals.org/icons/banner/title.gif http://cjasn.asnjournals.org <![CDATA[Introduction: Academic Nephrology 2008]]> http://cjasn.asnjournals.org/cgi/content/short/3/6/1869?rss=1 2008-11-06 info:doi/10.2215/CJN.03630708 American Society of Nephrology 6 3 1869 2008-11-01 1869 Moving Points in Nephrology <![CDATA[New Challenges and Paradigms for Mid-Career Faculty in Academic Medical Centers: Key Strategies for Success for Mid-Career Medical School Faculty]]> http://cjasn.asnjournals.org/cgi/content/short/3/6/1870?rss=1 2008-11-06 info:doi/10.2215/CJN.03900907 American Society of Nephrology 6 3 1874 2008-11-01 1870 Moving Points in Nephrology <![CDATA[The Afterlife for Retiring Deans and Other Senior Medical Administrators]]> http://cjasn.asnjournals.org/cgi/content/short/3/6/1875?rss=1 Career options for individuals leaving the administrative role as dean of a school of medicine or other senior administrative positions are considered. Options discussed include retirement and a variety of other positions both within schools of medicines and in other venues. Many opportunities exist for a challenging and fulfilling career path after leaving the role as a senior administrator in an academic medical center.

]]> 2008-11-06 info:doi/10.2215/CJN.05791207 American Society of Nephrology 6 3 1877 2008-11-01 1875 Moving Points in Nephrology <![CDATA[Nurturing Passion in a Time of Academic Climate Change: The Modern-Day Challenge of Junior Faculty Development]]> http://cjasn.asnjournals.org/cgi/content/short/3/6/1878?rss=1 2008-11-06 info:doi/10.2215/CJN.04240808 American Society of Nephrology 6 3 1883 2008-11-01 1878 Moving Points in Nephrology <![CDATA[Academic Etiquette for the Nephrologist]]> http://cjasn.asnjournals.org/cgi/content/short/3/6/1884?rss=1 Academic etiquette is an underexplored and underemphasized topic. Yet, a collegial atmosphere is essential to accomplish the missions of an academic medical center. Appropriate social, personal, and cultural behaviors are not only desirable, but they are also necessary to practice and emulate. As faculty in an academic center, one may want to share these thoughts with peers, students, and other healthcare providers. As a trainee, one may want dedicated lectures on this topic and to observe the behaviors modeled by mentors. This article attempts to outline principles of appropriate etiquette in the academic workplace. These include issues of loyalty, collegiality, and collaboration in daily activities from research to clinical care. Approaching personal interactions with grace and integrity can be an essential tool in the pursuit of academic excellence and success.

]]> 2008-11-06 info:doi/10.2215/CJN.01750408 American Society of Nephrology 6 3 1886 2008-11-01 1884 Moving Points in Nephrology <![CDATA[Academic Internal Medicine in the United States: Current Trends, Future Implications for Academic Nephrology]]> http://cjasn.asnjournals.org/cgi/content/short/3/6/1887?rss=1 2008-11-06 info:doi/10.2215/CJN.02110508 American Society of Nephrology 6 3 1894 2008-11-01 1887 Moving Points in Nephrology <![CDATA[Introduction to Vitamin D Symposium, March 14, 2008]]> http://cjasn.asnjournals.org/cgi/content/short/3/5/1534?rss=1 A large body of work in diverse clinical and scientific areas has accumulated that supports a role for vitamin D in multiple organ systems and physiologic and molecular processes. The vitamin D receptor is distributed ubiquitously, and by binding with its receptor, vitamin D initiates a series of events that can affect cellular proliferation and differentiation, inflammation, the immune system, and the endocrine system, including the renin-angiotensin system, insulin resistance, and lipid metabolism.

]]> 2008-08-26 info:doi/10.2215/CJN.01130308 American Society of Nephrology 5 3 1534 2008-09-01 1534 Moving Points in Nephrology <![CDATA[Vitamin D in Health and Disease]]> http://cjasn.asnjournals.org/cgi/content/short/3/5/1535?rss=1 Vitamin D functions in the body through both an endocrine mechanism (regulation of calcium absorption) and an autocrine mechanism (facilitation of gene expression). The former acts through circulating calcitriol, whereas the latter, which accounts for more than 80% of the metabolic utilization of the vitamin each day, produces, uses, and degrades calcitriol exclusively intracellularly. In patients with end-stage kidney disease, the endocrine mechanism is effectively disabled; however, the autocrine mechanism is able to function normally so long as the patient has adequate serum levels of 25(OH)D, on which its function is absolutely dependent. For this reason, calcitriol and its analogs do not constitute adequate replacement in managing vitamin D needs of such patients. Optimal serum 25(OH)D levels are greater than 32 ng/mL (80 nmol/L). The consequences of low 25(OH)D status include increased risk of various chronic diseases, ranging from hypertension to diabetes to cancer. The safest and most economical way to ensure adequate vitamin D status is to use oral dosing of native vitamin D. (Both daily and intermittent regimens work well.) Serum 25(OH)D can be expected to rise by about 1 ng/mL (2.5 nmol/L) for every 100 IU of additional vitamin D each day. Recent data indicate that cholecalciferol (vitamin D3) is substantially more potent than ergocalciferol (vitamin D2) and that the safe upper intake level for vitamin D3 is 10,000 IU/d.

]]> 2008-08-26 info:doi/10.2215/CJN.01160308 American Society of Nephrology 5 3 1541 2008-09-01 1535 Moving Points in Nephrology <![CDATA[Vitamin D and Osteogenic Differentiation in the Artery Wall]]> http://cjasn.asnjournals.org/cgi/content/short/3/5/1542?rss=1 Vascular calcification is widespread, particularly in patients with chronic kidney disease, who receive, among other treatments, active vitamin D supplements. Emerging evidence indicates that vascular calcification is a regulated process that resembles embryonic endochondral osteogenesis, involving osteoblastic differentiation of vascular smooth muscle cells. In experimental animal models, high dosages of vitamin D consistently promote vascular calcification. In particular, the vitamin D–fed rat is frequently used as a model to assess putative regulators of calcific vasculopathy. The artery wall calcification in these animals most likely results from multiple mechanisms involving systems physiology of the complex, bone-vascular-renal-endocrine axis. Genetically engineered mice with upregulated vitamin D signaling pathways have also shed light on the molecular intermediaries, including fibroblast growth factor-23 and transcriptional intermediary factor 1-. In contrast to the studies of animals, studies of humans show that vitamin D has an inverse relationship or little effect. This difference between in vitro and in vivo findings is most likely, again, due to the complex, systemic feedback regulatory mechanisms that control calcium-phosphate metabolism. Recent epidemiologic evidence suggests that there is a narrow range of vitamin D levels in which vascular function is optimized. Levels above or below this range seem to confer a significant increase in risk for cardiovascular disease. There is some evidence to suggest that dietary vitamin D may be carried by lipoprotein particles into cells of the artery wall and atherosclerotic plaque, where it may be converted to active form by monocyte-macrophages. These findings raise interesting questions regarding the effects of vitamin D intake on atherosclerotic calcification and cardiovascular risk.

]]> 2008-08-26 info:doi/10.2215/CJN.01220308 American Society of Nephrology 5 3 1547 2008-09-01 1542 Moving Points in Nephrology <![CDATA[Vitamin D and Sunlight: Strategies for Cancer Prevention and Other Health Benefits]]> http://cjasn.asnjournals.org/cgi/content/short/3/5/1548?rss=1 Vitamin D deficiency is a worldwide health problem. The major source of vitamin D for most humans is sensible sun exposure. Factors that influence cutaneous vitamin D production include sunscreen use, skin pigmentation, time of day, season of the year, latitude, and aging. Serum 25-hydroxyvitamin D [25(OH)D] is the measure for vitamin D status. A total of 100 IU of vitamin D raises blood level of 25(OH)D by 1 ng/ml. Thus, children and adults who do not receive adequate vitamin D from sun exposure need at least 1000 IU/d vitamin D. Lack of sun exposure and vitamin D deficiency have been linked to many serious chronic diseases, including autoimmune diseases, infectious diseases, cardiovascular disease, and deadly cancers. It is estimated that there is a 30 to 50% reduction in risk for developing colorectal, breast, and prostate cancer by either increasing vitamin D intake to least 1000 IU/d vitamin D or increasing sun exposure to raise blood levels of 25(OH)D >30 ng/ml. Most tissues in the body have a vitamin D receptor. The active form of vitamin D, 1,25-dihydroxyvitamin D, is made in many different tissues, including colon, prostate, and breast. It is believed that the local production of 1,25(OH)2D may be responsible for the anticancer benefit of vitamin D. Recent studies suggested that women who are vitamin D deficient have a 253% increased risk for developing colorectal cancer, and women who ingested 1500 mg/d calcium and 1100 IU/d vitamin D3 for 4 yr reduced risk for developing cancer by >60%.

]]> 2008-08-26 info:doi/10.2215/CJN.01350308 American Society of Nephrology 5 3 1554 2008-09-01 1548 Moving Points in Nephrology <![CDATA[Vitamin D and Kidney Disease]]> http://cjasn.asnjournals.org/cgi/content/short/3/5/1555?rss=1 Abnormalities in vitamin D metabolism play a major role in the pathogenesis of secondary hyperparathyroidism in chronic kidney disease. The gradual and progressive decline in 1,25-dihydroxyvitamin D in the course of chronic kidney disease is the result of several mechanisms that limit the ability of the failing kidney to maintain the levels of 1,25-dihydroxyvitamin D despite increasing levels of parathyroid hormone. Recent observations have indicated that chronic kidney disease seems to be associated with a high incidence of nutritional vitamin D insufficiency or deficiency as manifested by decreased levels of 25-hydroxyvitamin D. This contributes to the inability to maintain the levels of 1,25-dihydroxyvitamin D; therefore, current practice guidelines suggest repleting vitamin D status by the administration of native vitamin D as a first step in the therapy of the abnormalities of bone and mineral metabolism in chronic kidney disease. The efficacy of this therapy is extremely variable, and active vitamin D sterols may be required, especially as kidney disease progresses. The importance of the abnormal vitamin D metabolism is being investigated vigorously in view of the observations that vitamin D may have important biologic actions in many tissues in addition to bone and parathyroid. Thus, observational data have suggested potential survival benefits of vitamin D sterol administration in this clinical setting, and experimental data have suggested a potential beneficial effect of vitamin D sterols on the progression of kidney disease. Further work is required to define the mechanisms involved and to examine the effects of vitamin D therapy on outcomes in randomized, controlled trials.

]]> 2008-08-26 info:doi/10.2215/CJN.01150308 American Society of Nephrology 5 3 1560 2008-09-01 1555 Moving Points in Nephrology <![CDATA[Introduction: New Insights, Treatments, and Management Strategies for ADPKD]]> http://cjasn.asnjournals.org/cgi/content/short/3/4/1195?rss=1 2008-06-27 info:doi/10.2215/CJN.00460108 American Society of Nephrology 4 3 1196 2008-07-01 1195 Moving Points in Nephrology <![CDATA[Approaches to Testing New Treatments in Autosomal Dominant Polycystic Kidney Disease: Insights from the CRISP and HALT-PKD Studies]]> http://cjasn.asnjournals.org/cgi/content/short/3/4/1197?rss=1 Autosomal dominant polycystic kidney disease (ADPKD) is an inherited systemic disease characterized by a prolonged subclinical course of gradual renal cyst expansion, resulting in massively enlarged kidneys and renal failure by the fifth to sixth decade. Renal cyst expansion results in intrarenal ischemia and activation of the renin-angiotensin-aldosterone system (RAAS) and relates to the development and maintenance of hypertension in ADPKD. Hypertension relates to disease progression in ADPKD with regard to renal volume, proteinuria, cardiovascular complications, and progression to end-stage renal disease. Novel magnetic resonance imaging methods developed in the Consortium for Radiologic Imaging for the Study of Polycystic Kidney Disease (CRISP) provide accurate estimates of change in renal volume over a short period of time in ADPKD patients with intact renal function. In CRISP an increase in renal volume of 63.4 ml/yr was found. PKD1 status, male gender, hypertension, reduced renal blood flow, and proteinuria are associated with increased renal volume and change in renal volume over time. HALT-Polycystic Kidney Disease (HALT-PKD) is designed to test whether blockade of RAAS and/or rigorous blood pressure control play a role in slowing renal progression during early (using magnetic resonance imaging methods developed in CRISP) and during late (using measures, including composite of time to doubling of serum creatinine, onset of end-stage renal disease, or death) phases in ADPKD. Findings from CRISP and the rationale for interventions in ADPKD are described, and the design of the HALT-PKD clinical trial is outlined.

]]> 2008-06-27 info:doi/10.2215/CJN.00060108 American Society of Nephrology 4 3 1204 2008-07-01 1197 Moving Points in Nephrology <![CDATA[Strategies to Inhibit Cyst Formation in ADPKD]]> http://cjasn.asnjournals.org/cgi/content/short/3/4/1205?rss=1 The many hundreds of cysts that grow and expand and ultimately overwhelm and destroy polycystic kidneys arise from the slow but unrelenting proliferation of tubular epithelial cells, eventually giving rise to very large, thin-walled, fluid-filled structures. The growth of these cystic bodies requires two processes: Cell proliferation and fluid secretion. Cyst epithelial cells seem to have a unique phenotype that could offer opportunities for therapeutic intervention. Current evidence has demonstrated that cAMP drives both abnormal cell proliferation, by stimulating the Ras/mitogen-activated protein kinase (MAPK) pathway, and cyst-filling fluid secretion, by activating the cystic fibrosis transmembrane conductance regulator (CFTR) chloride channel. Both of these cAMP-mediated processes should be considered in the design of strategies targeted to slow cyst growth and enlargement in autosomal dominant polycystic kidney disease.

]]> 2008-06-27 info:doi/10.2215/CJN.05651207 American Society of Nephrology 4 3 1211 2008-07-01 1205 Moving Points in Nephrology <![CDATA[Role of Vasopressin Antagonists]]> http://cjasn.asnjournals.org/cgi/content/short/3/4/1212?rss=1 Alterations in intracellular calcium homeostasis and cyclic adenosine 3',5'-phosphate likely underlie the increased cell proliferation and fluid secretion in polycystic kidney disease. Hormone receptors that affect cyclic adenosine 3',5'-phosphate and are preferentially expressed in affected tissues are logical treatment targets. There is a sound rationale for considering the arginine vasopressin V2 receptor as a target. The arginine vasopressin V2 receptor antagonists OPC-31260 and tolvaptan inhibit the development of polycystic kidney disease in cpk mice and in three animal orthologs to human autosomal recessive polycystic kidney disease (PCK rat), autosomal dominant polycystic kidney disease (Pkd2–/WS25 mice), and nephronophthisis (pcy mouse). PCK rats that are homozygous for an arginine vasopressin mutation and lack circulating vasopressin are markedly protected. Administration of V2 receptor agonist 1-deamino-8-d-arginine vasopressin to these animals completely recovers the cystic phenotype. Administration of 1-deamino-8-d-arginine vasopressin to PCK rats with normal arginine vasopressin aggravates the disease. Suppression of arginine vasopressin release by high water intake is protective. V2 receptor antagonists may have additional beneficial effects on hypertension and chronic kidney disease progression. A number of clinical studies in polycystic kidney disease have been performed or are currently active. The results of phase 2 and 2–3 studies indicate that tolvaptan seems to be safe and well tolerated in autosomal dominant polycystic kidney disease. A phase 3, placebo-controlled, double-blind study in 18- to 50-yr-old patients with autosomal dominant polycystic kidney disease and preserved renal function but relatively rapid progression, as indicated by a total kidney volume >750 ml, has been initiated.

]]> 2008-06-27 info:doi/10.2215/CJN.05281107 American Society of Nephrology 4 3 1218 2008-07-01 1212 Moving Points in Nephrology <![CDATA[Mammalian Target of Rapamycin and Caspase Inhibitors in Polycystic Kidney Disease]]> http://cjasn.asnjournals.org/cgi/content/short/3/4/1219?rss=1 One of the most important abnormalities of the tubular epithelial cells lining the cysts as well as noncystic tubular epithelium is a disturbance in the balance between tubular cell proliferation and apoptosis. Activation of the mammalian target of rapamycin signaling pathway results in increased cell proliferation. Recent studies suggested abnormalities of the mammalian target of rapamycin signaling pathway in polycystic kidney disease. Mammalian target of rapamycin inhibition with sirolimus or everolimus results in attenuation of cyst formation in rat and mouse models of polycystic kidney disease. Apoptosis is a pathologic feature of most models of polycystic kidney disease, including human polycystic kidneys. Caspases, the major mediators of apoptosis, are increased in polycystic kidney disease kidneys. Both in vitro and in vivo studies suggest that caspase or apoptosis inhibition attenuates cyst formation. This review focuses on mammalian target of rapamycin and apoptosis signaling pathways in polycystic kidney disease and the role of mammalian target of rapamycin inhibitors and apoptosis inhibitors as potential therapies to reduce cyst formation.

]]> 2008-06-27 info:doi/10.2215/CJN.05611207 American Society of Nephrology 4 3 1226 2008-07-01 1219 Moving Points in Nephrology <![CDATA[Acute Kidney Injury: Toward an Integrated Understanding through Development of a Research Agenda]]> http://cjasn.asnjournals.org/cgi/content/short/3/3/862?rss=1 2008-04-25 info:doi/10.2215/CJN.04841107 American Society of Nephrology 3 3 863 2008-05-01 862 Moving Points in Nephrology <![CDATA[A Framework and Key Research Questions in AKI Diagnosis and Staging in Different Environments]]> http://cjasn.asnjournals.org/cgi/content/short/3/3/864?rss=1 Background and objectives: Acute Kidney Injury (AKI) is common worldwide, and associated with significant morbidity, mortality, and resource utilization. The RIFLE system of staging AKI correlates with survival in AKI in several settings. A similar AKI definition and staging system that also incorporates lesser degrees of serum creatinine elevation was proposed at the inaugural Acute Kidney Injury Network (AKIN) meeting in 2005. At the Second AKIN meeting in Vancouver, Canada in September 2006, our group developed a research agenda that would test the utility of these diagnostic and staging criteria to predict patient outcomes in a variety of clinical settings and patient groups.

Design, setting, participants & measurements: Three-day, international, consensus conference. A multidisciplinary stakeholder committee was divided into work groups. Recommendations for clinical practice and for future research were developed by the committee as an iterative process. This procedure consisted of a literature review phase and focus group interactions with presentations to the entire committee.

Results: We first proposed a conceptual framework of disease that describes a series of AKI stages, antecedents and outcomes, and allows a description of research recommendations based on transition between AKI stages. We further proposed methods for testing of the definition and development of research questions to establish the utility of new biomarkers for the diagnosis and staging of AKI and associated illnesses.

Conclusions: Retrospective studies should be conducted to initiate the process of validating the AKIN definition of AKI, followed by comprehensive prospective studies that incorporate sampling for emerging AKI biomarkers.

]]> 2008-04-25 info:doi/10.2215/CJN.04851107 American Society of Nephrology 3 3 868 2008-05-01 864 Moving Points in Nephrology <![CDATA[Delivery of Renal Replacement Therapy in Acute Kidney Injury: What Are the Key Issues?]]> http://cjasn.asnjournals.org/cgi/content/short/3/3/869?rss=1 Background and objectives: The prescription and delivery of renal replacement therapy for acute kidney injury is subject to a wide variation and is conditioned by a multiplicity of factors. A variety of renal replacement therapy modalities are now available to treat acute kidney injury; however, there are no standards for the dosage, choice of modality, and intensity and duration of these therapies. Although several observational and interventional studies have addressed these topics, there are no consensus recommendations in this field.

Design, setting, participants, & measurements: The available literature on this topic and draft consensus recommendations for research studies in this area were developed using a modified Delphi approach and an international multidisciplinary network.

Results: The following questions were most important: What is the "dosage" of renal replacement therapy delivered to patients with stage 3 acute kidney injury? What is the optimal "dosage" of renal replacement therapy to maximize patient and renal survival? Is there a minimal "dosage" of renal replacement therapy required in patients with single-organ failure? Does modality of renal replacement therapy selected have an effect on patient and/or renal survival? In cases of continuous renal replacement therapy, does citrate anticoagulation confer a benefit?

Conclusions: This report summarizes the available evidence and elaborates on the key questions and the methods that should be used so that the goal of standardizing the care of patients with acute kidney injury and improving outcomes can be achieved.

]]> 2008-04-25 info:doi/10.2215/CJN.04821107 American Society of Nephrology 3 3 875 2008-05-01 869 Moving Points in Nephrology <![CDATA[Timing of Initiation and Discontinuation of Renal Replacement Therapy in AKI: Unanswered Key Questions]]> http://cjasn.asnjournals.org/cgi/content/short/3/3/876?rss=1 Patients with acute kidney injury (AKI) often require initiation of renal replacement therapy (RRT). Currently, there is wide variation worldwide on the indications for and timing of initiation and discontinuation of RRT for AKI. Various parameters for metabolic, solute, and fluid control are generally used to guide the initiation and discontinuation of therapy; however, there are currently no standards in this field. Members of the recently established Acute Kidney Injury Network, representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI, participated in a 3-d conference in Vancouver in September 2006 to evaluate the available literature on this topic and draft consensus recommendations for research studies in this area. Key questions included the following: what are the indications for RRT, when should acute RRT support be initiated, and when should RRT be stopped? This report summarizes the available evidence and describes in detail the key questions, and some of the methods of answering them that will need to be addressed with the goal of standardizing the care of patients with AKI and improving outcomes.

]]> 2008-04-25 info:doi/10.2215/CJN.04871107 American Society of Nephrology 3 3 880 2008-05-01 876 Moving Points in Nephrology <![CDATA[Epidemiology of Acute Kidney Injury]]> http://cjasn.asnjournals.org/cgi/content/short/3/3/881?rss=1 Background and objectives: The worldwide incidence of acute kidney injury is poorly known because of underreporting, regional disparities, and differences in definition and case mix. New definitions call for revision of the problem with unified criteria.

Design, setting, participants, & measurements: This article reports on the research recommendations of an international multidisciplinary committee, assembled to define a research agenda on acute kidney injury epidemiology using a modified three-step Delphi process.

Results: Knowledge of incidence and risk factors is crucial because it drives local and international efforts on detection and treatment. Also, notable differences exist between developing and developed countries: Incidence seems higher in the former, but underreporting compounded by age and gender disparities makes available data unreliable. In developing countries, incidence varies seasonally; incidence peaks cause critical shortages in medical and nursing personnel. Finally, in developing countries, lack of systematic evaluation of the role of falciparum malaria, obstetric mechanisms, and hemolytic uremic syndrome on acute kidney injury hampers efforts to prevent acute kidney injury.

Conclusions: The committee concluded that epidemiologic studies should include (1) prospective out- and inpatient studies that measure incidence of community and hospital acute kidney injury and post–acute kidney injury chronic kidney disease; (2) incidence measurements during seasonal peaks in developing and developed countries; and (3) whenever available, use of reliable existing administrative or institutional databases. Epidemiologic studies using standardized definitions in community and institutional settings in developing and underdeveloped countries are essential first steps to achieving early detection and intervention and improved patient outcomes.

]]> 2008-04-25 info:doi/10.2215/CJN.04961107 American Society of Nephrology 3 3 886 2008-05-01 881 Moving Points in Nephrology <![CDATA[Development of a Clinical Research Agenda for Acute Kidney Injury Using an International, Interdisciplinary, Three-Step Modified Delphi Process]]> http://cjasn.asnjournals.org/cgi/content/short/3/3/887?rss=1 Background and objectives: Although acute kidney injury is common and significantly increases the risk for intensive care unit and hospital mortality, little is known about its true incidence or how it can be prevented. Furthermore, key unanswered questions remain about the optimal diagnosis and treatment of patients with acute kidney injury. An international, consensus-based, prioritized research agenda was sought to guide clinical and translational research in acute kidney injury.

Design, setting, participants, & measurements: A three-step modified Delphi process involving 43 participants representing 19 professional societies, organizations, and multiple stakeholder groups ranging from clinical practice to basic science research was conducted.

Results: Twenty research questions were generated across six focus groups. Overall, research priorities generated from nephrologists and intensivists were similar and highly correlated. The stakeholder groups included members from 15 countries. Results from adult and pediatric groups showed important differences, as did results from developing compared with developed countries; however the priority rankings from the developed and developing countries were significantly correlated. Top research priorities in acute kidney injury include determining optimal timing of renal replacement therapy and improving the understanding of the epidemiology of acute kidney injury around the world.

Conclusions: Research recommendations that are highly consistent across various stakeholder groups and between developed and developing countries have been produced. It is hoped that these recommendations will prove valuable in guiding future clinical and translational research in this area.

]]> 2008-04-25 info:doi/10.2215/CJN.04891107 American Society of Nephrology 3 3 894 2008-05-01 887 Moving Points in Nephrology