Source(google.com.pk)
Kidney Disease Biography
Erythropoiesis-Stimulating Agents
See Skali et al and Kaufman.
Despite the lack of strong evidence that treatment of moderate levels of anemia provided mortality or morbidity benefits, erythropoiesis-stimulating agents (ESAs) were a mainstay of anemia management in nondialysis CKD patients. Critically, sparse data are available about the natural history of anemia in nondialysis CKD patients and the pattern of hemoglobin levels in the absence of ESA administration. This month, Skali and colleagues analyze the placebo arm of the TREAT study to investigate hemoglobin levels over time in patients with diabetic patients with CKD stage 3-5, moderate anemia, and minimal or no ESA exposure, reporting that most patients were able to maintain a stable hemoglobin level without long-term ESA therapy. In an accompanying editorial, Kaufman discusses the study by Skali et al in the context of the US FDA recommendations for ESA use.
Frequent Dialysis and Cognitive Function
See Yaffe et al; Kurella Tamura et al and Seliger & Weiner.
Cognitive impairment is common in individuals with CKD, particularly among those treated with dialysis. Cognitive impairment carries substantial risk, including depression and worse perceived quality of life as well as a marked increase in mortality; therefore, understanding the pathogenesis and exploring possible preventive treatments for cognitive impairment in CKD are critical to improving dialysis patient care. In this issue of AJKD, Kurella Tamura and colleagues report the effects of frequent dialysis on cognitive function in individuals participating in the Frequent Hemodialysis Network Trials and conclude that more frequent hemodialysis did not improve executive function or global cognition. Editorialists Seliger and Weiner argue that a reasonable interpretation of these results is that impaired cognitive function in dialysis patients is determined largely by factors other than uremic solute clearance; therefore, given the robust relationship between microvascular disease and cognitive function in earlier stages of CKD, treatments to address cognitive impairment should target microvascular disease and cardiovascular disease risk.
Validating the New CKD-EPI Cystatin C Equation for Estimating GFR
See Horio et al and Masson et al.
The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) recently developed GFR-estimating equations based on standardized serum cystatin C and standardized serum creatinine plus standardized serum cystatin C. In this issue of AJKD, these new equations are put to the test in 2 different patient populations. Horio et al studied the accuracy of these equations among Japanese individuals and report that the formulas perform well; accordingly, the authors suggest that equations based on serum cystatin C could be used in patients of different races without modification. In the study by Masson et al, the authors compared the performances of serum cystatin C and serum creatinine as endogenous markers of GFR in a large cohort of transplant recipients and report data that validates using serum cystatin C–based equations to estimate GFR in these patients.
Posttransplantation Bone Disease
See Alshayeb et al.
Kidney transplant, the most effective treatment for the metabolic abnormalities of CKD, only partially corrects CKD–mineral and bone disorders. Posttransplantation bone disease is markedly different from the mineral and bone disorders often seen in patients with native CKD and is influenced by factors such as immunosuppressive therapy, kidney graft function, hypophosphatemia, and disturbances in the fibroblastic growth factor 23–parathyroid hormone–vitamin D axis. Alshayeb and colleagues review the pathogenesis, diagnosis, and management of posttransplantation bone disease and conclude that, with the lack of sufficient prospective studies evaluating currently available therapies, clinical judgment must serve as the guiding principle to evaluate the risk-benefit of specific therapies for preventing bone loss and fractures in this setting.
Kidney Disease Biography
Erythropoiesis-Stimulating Agents
See Skali et al and Kaufman.
Despite the lack of strong evidence that treatment of moderate levels of anemia provided mortality or morbidity benefits, erythropoiesis-stimulating agents (ESAs) were a mainstay of anemia management in nondialysis CKD patients. Critically, sparse data are available about the natural history of anemia in nondialysis CKD patients and the pattern of hemoglobin levels in the absence of ESA administration. This month, Skali and colleagues analyze the placebo arm of the TREAT study to investigate hemoglobin levels over time in patients with diabetic patients with CKD stage 3-5, moderate anemia, and minimal or no ESA exposure, reporting that most patients were able to maintain a stable hemoglobin level without long-term ESA therapy. In an accompanying editorial, Kaufman discusses the study by Skali et al in the context of the US FDA recommendations for ESA use.
Frequent Dialysis and Cognitive Function
See Yaffe et al; Kurella Tamura et al and Seliger & Weiner.
Cognitive impairment is common in individuals with CKD, particularly among those treated with dialysis. Cognitive impairment carries substantial risk, including depression and worse perceived quality of life as well as a marked increase in mortality; therefore, understanding the pathogenesis and exploring possible preventive treatments for cognitive impairment in CKD are critical to improving dialysis patient care. In this issue of AJKD, Kurella Tamura and colleagues report the effects of frequent dialysis on cognitive function in individuals participating in the Frequent Hemodialysis Network Trials and conclude that more frequent hemodialysis did not improve executive function or global cognition. Editorialists Seliger and Weiner argue that a reasonable interpretation of these results is that impaired cognitive function in dialysis patients is determined largely by factors other than uremic solute clearance; therefore, given the robust relationship between microvascular disease and cognitive function in earlier stages of CKD, treatments to address cognitive impairment should target microvascular disease and cardiovascular disease risk.
Validating the New CKD-EPI Cystatin C Equation for Estimating GFR
See Horio et al and Masson et al.
The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) recently developed GFR-estimating equations based on standardized serum cystatin C and standardized serum creatinine plus standardized serum cystatin C. In this issue of AJKD, these new equations are put to the test in 2 different patient populations. Horio et al studied the accuracy of these equations among Japanese individuals and report that the formulas perform well; accordingly, the authors suggest that equations based on serum cystatin C could be used in patients of different races without modification. In the study by Masson et al, the authors compared the performances of serum cystatin C and serum creatinine as endogenous markers of GFR in a large cohort of transplant recipients and report data that validates using serum cystatin C–based equations to estimate GFR in these patients.
Posttransplantation Bone Disease
See Alshayeb et al.
Kidney transplant, the most effective treatment for the metabolic abnormalities of CKD, only partially corrects CKD–mineral and bone disorders. Posttransplantation bone disease is markedly different from the mineral and bone disorders often seen in patients with native CKD and is influenced by factors such as immunosuppressive therapy, kidney graft function, hypophosphatemia, and disturbances in the fibroblastic growth factor 23–parathyroid hormone–vitamin D axis. Alshayeb and colleagues review the pathogenesis, diagnosis, and management of posttransplantation bone disease and conclude that, with the lack of sufficient prospective studies evaluating currently available therapies, clinical judgment must serve as the guiding principle to evaluate the risk-benefit of specific therapies for preventing bone loss and fractures in this setting.
Kidney Disease
Kidney Disease
Kidney Disease
Kidney Disease
Kidney Disease
Kidney Disease
Kidney Disease
Kidney Disease
Kidney Disease
Kidney Disease
Kidney Disease
Kidney Disease
