http://cjasn.asnjournals.org Clinical Journal of the American Society of Nephrology RSS feed -- recent Mini-Reviews articles 1555-905X Clinical Journal of the American Society of Nephrology 1555-9041 http://cjasn.asnjournals.org/icons/banner/title.gif http://cjasn.asnjournals.org http://cjasn.asnjournals.org/cgi/content/short/3/1/168?rss=1 Renal osteodystrophy is a significant complication in chronic kidney disease. This condition is referred to as mineral and bone disorders in chronic kidney disease, mainly because of its wider ranging impact, including an association with increased mortality and non–bone-related morbidity. Because most of the abnormalities that characterize mineral and bone disorders in chronic kidney disease (e.g., hyperphosphatemia, secondary hyperparathyroidism) are amenable to therapeutic interventions, this field has also been in the cross-hairs of many pharmaceutical companies. The advent of a number of new therapeutic options for mineral and bone disorders in chronic kidney disease has broadened our armamentarium but has also resulted in an intense marketing battle between pharmaceutical companies. The paucity of randomized, controlled trials in this field has allowed the various companies to promote unilaterally data that fit their needs and to attempt to discredit data that support their competitors’ products. Although this attitude is expected and regarded as acceptable in a consumer society, on a scientific level, it has resulted in a polarized and often confused audience: The practicing nephrologists. This article provides a historical overview of how the field of mineral and bone disorders in chronic kidney disease has evolved from a pharmaceutical standpoint, with a critical emphasis of the key moments that resulted in the current acrimonious climate. Also assessed is what the key unanswered questions are in this field, and practical solutions to the discussed issues are provided.

]]> 2008-01-04 info:doi/10.2215/CJN.03850907 American Society of Nephrology 1 3 173 2008-01-01 168 Mini-Reviews http://cjasn.asnjournals.org/cgi/content/short/3/1/174?rss=1 2008-01-04 info:doi/10.2215/CJN.04251007 American Society of Nephrology 1 3 178 2008-01-01 174 Mini-Reviews http://cjasn.asnjournals.org/cgi/content/short/3/1/179?rss=1 Recent clinical studies of mineral metabolism in patients with chronic kidney disease have helped to verify and extend the Kidney Disease Outcomes Quality Initiative practice guidelines for bone metabolism and disease that were published in 2003. In particular, investigations that examined calcium loading, vitamin D therapy, and mortality risk associated with serum calcium and phosphate in dialysis patients have been the most helpful clinically. As a consequence, there is now a growing interest to have the previous guidelines amended accordingly, which will be performed through the Kidney Disease: Improving Global Outcomes working group after a debate within the nephrology community. The new data support this call for revision in an attempt to improve survival of the dialysis patient by emphasizing the importance of intravenous vitamin D therapy and of preventing excess calcium loading. These studies also suggest avenues for future investigation into nontraditional causes and treatments of cardiovascular disease in patients with chronic kidney disease.

]]> 2008-01-04 info:doi/10.2215/CJN.01310307 American Society of Nephrology 1 3 183 2008-01-01 179 Mini-Reviews http://cjasn.asnjournals.org/cgi/content/short/3/1/184?rss=1 Arterial stiffness is recognized increasingly as an important component in the determination of cardiovascular risk, particularly in chronic kidney disease and ESRD populations. Although the technique has been around for nearly 100 yr, in the past 20 to 25 yr, pragmatic noninvasive approaches have allowed the incorporation of arterial stiffness measurements, usually in the form of aortic pulse wave velocity (PWV), into clinical assessment of patients. In populations with high cardiovascular risk, especially those with ESRD, aortic PWV measurements provide predictive utility independent of the standard brachial arterial BP measurements. This review briefly discusses the history of vascular dynamics, the determinants of PWV, and some of the available technologies in current use and concludes with a section on the relevance of arterial stiffness measurements in populations of particular interest to nephrologists.

]]> 2008-01-04 info:doi/10.2215/CJN.03340807 American Society of Nephrology 1 3 192 2008-01-01 184 Mini-Reviews http://cjasn.asnjournals.org/cgi/content/short/3/1/193?rss=1 Pure red cell aplasia in patients who are treated for anemia of chronic kidney disease with erythropoiesis-stimulating agents such as epoetin was first reported in 1998. Although the incidence of pure red cell aplasia peaked in 2002, it remains important for nephrologists to know how to investigate a suspected case of pure red cell aplasia and how to identify other causes of hyporesponsiveness to erythropoiesis-stimulating agents, which account for the vast majority of such cases. The authors reviewed the current status of information in the literature and drew on their personal experiences with patients regarding the diagnosis and management of epoetin-induced pure red cell aplasia. The mechanism for development of epoetin-induced pure red cell aplasia remains unconfirmed. It generally occurs after the production of neutralizing anti-erythropoietin antibodies. Elucidation of a suspected pure red cell aplasia case requires a systematic approach, beginning with simple measurements such as blood cell counts, because most cases of erythropoiesis-stimulating agent hyporesponsiveness are attributable to other causes. If these criteria indicate that the patient's response to erythropoiesis-stimulating agent therapy is very poor, then bone marrow examination and measurement of anti-erythropoietin antibodies is justified. If pure red cell aplasia is confirmed, then cessation of erythropoiesis-stimulating agent therapy and initiation of immunosuppressive therapy are recommended. Continued study of epoetin-induced pure red cell aplasia is needed to help nephrologists prevent or manage future cases and will have implications for the use of other protein-based therapeutic agents.

]]> 2008-01-04 info:doi/10.2215/CJN.02440607 American Society of Nephrology 1 3 199 2008-01-01 193 Mini-Reviews http://cjasn.asnjournals.org/cgi/content/short/3/1/200?rss=1 Nearly two decades ago, recombinant human erythropoietin transformed the management of chronic kidney disease anemia by allowing a more sustained increase in hemoglobin than was possible by intermittent blood transfusion. The treatment was highly effective, but because of the fairly short half-life of the molecule at approximately 6 to 8 h, injections usually had to be administered two to three times weekly. A second-generation erythropoietin analogue, darbepoetin alfa, was then created, with a longer elimination half-life in vivo that translated into less frequent dosing, usually once weekly or once every 2 wk. More recently, another erythropoietin-related molecule has been produced called Continuous Erythropoietin Receptor Activator with an even greater half-life, and other molecules are in development or are being licensed, including biosimilar epoetin products and Hematide. The latter is a synthetic peptide-based erythropoietin receptor agonist that, interestingly, has no structural homology with erythropoietin, and yet is still able to activate the erythropoietin receptor and stimulate erythropoiesis. The search goes on for orally active antianemic therapies, and several strategies are being investigated, although none is imminently available. This article reviews the latest progress with these novel erythropoietic agents in this new era in anemia management.

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