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PubMed2005

N-terminal pro-B-type natriuretic peptide for predicting coronary disease and left ventricular hypertrophy in asymptomatic CKD not requiring dialysis.

BACKGROUND: N-Terminal pro-B-type natriuretic peptide (NT-proBNP) level predicts underlying heart disease in the general population. However, because NT-proBNP clearance may depend on renal function, the significance of an elevated level in patients with chronic kidney disease (CKD) without cardiac symptoms is uncertain. We sought to determine whether there is an association between NT-proBNP level and coronary artery disease (CAD) and left ventricular hypertrophy (LVH) in this population. METHODS: We enrolled 207 ambulatory patients with CKD not on dialysis therapy. Medical records were reviewed for cardiac history and risk factors. NT-proBNP and troponin T (cTnT) levels were measured. Echocardiograms were analyzed from 99 patients. RESULTS: NT-proBNP levels were elevated in 116 patients (56%), and 67 patients (33%) had experienced prior CAD events (myocardial infarction or revascularization). The prevalence of advanced age, diabetes, prior CAD events, myocardial injury (cTnT > 0.03 ng/mL [>0.03 microg/L]), and LVH increased, whereas glomerular filtration rate decreased, across quartiles of NT-proBNP levels. After adjustment for glomerular filtration rate, cTnT level, age, and diabetes, NT-proBNP remained an independent indicator of prior CAD events compared with quartile 1 (cTnT range, 4 to 116 pg/mL) for quartile 2 (range, 122 to 490 pg/mL): odds ratio, 1.6; 95% confidence interval, 0.5 to 5.0; for quartile 3 (range, 490 to 1,819 pg/mL): odds ratio, 5.3; 95% confidence interval, 1.7 to 16.2; and for quartile 4 (>1,975 pg/mL): odds ratio, 4.1; 95% confidence interval, 1.3 to 13.5. For patients with echocardiograms, NT-proBNP level predicted prior CAD events independent of LVH. CONCLUSION: NT-proBNP level elevation in asymptomatic patients with CKD reflects underlying ischemic heart disease and hypertrophy independent of renal function in a population with anticipated high cardiac morbidity.

Adult↗

PubMed2006

A randomized crossover trial comparing sevelamer with calcium acetate in children with CKD.

BACKGROUND: A multicenter, randomized, open-label, crossover study was performed to compare the efficacy and safety of sevelamer, a calcium-free phosphate binder, with calcium acetate in pediatric patients with chronic kidney disease (CKD). METHODS: Children (age, 0.9 to 18 years) with CKD undergoing hemodialysis or peritoneal dialysis or with a glomerular filtration rate of 20 or greater and less than 60 mL/min/1.73 m2 (> or = 0.33 and < 1.00 mL/s/1.73 m2) were randomly assigned to the following treatment scheme: 2 weeks of washout followed by 8 weeks of treatment with either sevelamer or calcium acetate in a crossover fashion. Phosphorus, calcium, and intact parathyroid hormone in serum were measured every 2 weeks, and phosphate binder dosages were adjusted, if needed. Serum lipid and vitamin concentrations were measured at the beginning and end of each treatment period. The primary end point was the decrease in serum phosphorus levels after 8 weeks of treatment. RESULTS: Forty-four patients were screened. Altogether, data for 18 patients (5 girls) aged 12.4 +/- 4.1 years were used for the crossover analysis. There was no significant difference in serum phosphorus levels at 8 weeks after the start of treatment in both groups. Total cholesterol (-27%) and low-density lipoprotein cholesterol (-34%) levels decreased significantly with sevelamer treatment (P < 0.02 and P < 0.005). An increased incidence of hypercalcemia (P < 0.0005) was observed with calcium acetate treatment, whereas metabolic acidosis was more frequent with sevelamer treatment (P < 0.005). CONCLUSION: Treatment of children with CKD with sevelamer and calcium acetate provides similar phosphorus level control. The marked decrease in lipid levels and lower rate of hypercalcemia may augment the long-term benefit of sevelamer.

Acetates↗

PubMed2006

Impact of comorbidities on mortality in managed care patients with CKD.

BACKGROUND: Our previous work showed that patients with chronic kidney disease (CKD) were 10 times more likely to die than progress to end-stage renal disease. This study examines the impact of comorbidities on mortality risk in a cohort with CKD at 3 levels of progression and a sex- and age-matched comparison group. METHODS: In a historical, prospective, cohort study, we selected electronic medical record data for health maintenance organization (HMO) members with an index and repeated glomerular filtration rate (GFR) in the range of 15 to 90 mL/min/1.73 m(2) (0.25 to 1.50 mL/s/1.73 m(2)) in 1996 who were followed up for at least 54 months or died during this period. These were matched for birth year and sex with HMO members not meeting GFR criteria, but with the same follow-up criteria. Major comorbid chronic conditions also were identified based on International Classification of Diseases, Ninth Revision, diagnostic codes in the electronic medical record. Conditional logistic regression was used to estimate the relative risk for mortality versus comparison subjects as a function of GFR, age, and other chronic conditions. RESULTS: In the final sample of 19,945 pairs, we found that risk for mortality increases as GFR decreases, but also that both age and other chronic conditions are significant risk factors for mortality. CONCLUSION: Baseline levels of estimated GFR and other major chronic disorders all contributed negatively to survival. The relative impact of these comorbidities was greatest among younger (<60 years) patients with CKD, and their relative effect diminished with age.

Adolescent↗

PubMedDate not supplied

Improving outcomes in CKD and ESRD patients: carrying the torch from training to practice.

Practicing nephrologists are spending more time caring for end-stage renal disease (ESRD) and chronic kidney disease (CKD) patients. Despite this focus, and considerable advances in the understanding of those aspects of care that impact on clinical outcomes, morbidity, mortality, and quality of life for these patients has not improved substantially over the past decade. One of the possible explanations for this lack of progress is the structure of current nephrology training programs, where ESRD and CKD patient care is not emphasized. To address this issue, we developed a short preceptorship for second-year nephrology fellows, including didactic lectures and workshops. Of 67 participating fellows, 50% were from programs offering 3 or fewer months of exposure to outpatient hemodialysis, and 25% reported no exposure to peritoneal dialysis. Of more concern, 25% reported no "official rounds" with an attending nephrologist on dialysis patients. If nephrologists are to take their appropriate place as leaders of the care delivery team, nephrology fellowships must be restructured with appropriate emphasis placed on the comprehensive care of ESRD and CKD patients.

Attitude of Health Personnel↗

PubMedDate not supplied

Can we delay the progression of chronic kidney disease (CKD) by improving collaboration between renal units and primary care teams?

This paper will discuss why nephrology teams should collaborate with primary care teams in delaying the progression of chronic kidney disease (CKD), and explain how they can collaborate to improve the outcomes for patients who eventually need dialysis. The paper will describe the staging of CKD and will discuss evidence-based guidelines for the management of CKD in the community. Practical examples of how a specialist renal nurse can improve communication with primary care and can improve the outcome of patients with early kidney disease will be described.

Disease Progression↗

PubMedDate not supplied

Managing CKD.

The reality is that the majority of the CKD population have one or more co-morbid conditions with a known higher prevalence in ethnic minorities and lower socio-economic groups; combine this with the increase in childhood obesity and prevalence of diabetes and it is clear why we have an epidemic of CKD. Without effective prevention and early detection programmes, this will continue to escalate. Early detection and referral of CKD patients to nephrology teams is pivotal in slowing the progression to ESRD and reducing the demand for dialysis.

Comorbidity↗

PubMed2006

A comparison of dosing regimens of paricalcitol capsule for the treatment of secondary hyperparathyroidism in CKD stages 3 and 4.

BACKGROUND: Intermittent dosing of calcitriol for secondary hyperparathyroidism (SHPT) has been associated with greater parathyroid hormone (PTH) reduction with fewer calcemic and phosphatemic effects than daily (QD) dosing. METHODS: Secondary analyses of three randomized, double-blind, placebo-controlled multicenter studies in stage 3 and 4 chronic kidney disease (CKD) patients with SHPT were performed to compare three times per week (TIW) with QD dosing of paricalcitol. The pharmacokinetics of TIW and QD dosing of paricalcitol capsules were assessed in a separate group of healthy subjects. RESULTS: Pharmacokinetics revealed similar steady state paricalcitol exposure between dosing regimens. In CKD patients, baseline data were similar between the TIW studies (n = 72, paricalcitol; n = 73, placebo) and QD studies (n = 35, paricalcitol; n = 40, placebo). Both dosing regimens resulted in similar efficacy (91%) for the primary end point of two consecutive > or = 30% decreases in intact PTH from baseline, but the QD regimen resulted in a greater percent reduction in intact PTH from baseline. The chances for developing increased serum calcium and phosphorus levels or Ca x P product were similar between paricalcitol and placebo groups for both treatment regimens. Furthermore, no difference in the risk for these elevations was detected between the TIW and QD regimens. CONCLUSIONS: QD dosing of paricalcitol capsules is as efficacious as TIW dosing in achieving the primary end point (2 consecutive > or = 30% reductions in PTH) in stage 3 and 4 CKD patients with SHPT. Moreover, the QD regimen had no significant effect on hypercalcemia, hyperphosphatemia or Ca x P product as compared with placebo or intermittent dosing.

Adult↗

PubMed2025

Network Interactions of Circulating FGF23, HRG-HMGB1, and Cardiac Disease in CKD.

KEY POINTS: Multitrait analysis of genome-wide association study boosts the statistical power to identify novel genetic traits for fibroblast growth factor 23. A functional genomics approach aided network discovery to identify histidine-rich glycoprotein (HRG) and high-mobility group protein box 1 (HMGB1) as key regulators of cardiac disease in CKD. Integration of clinical and genetic data enhances the discovery power and is crucial for understanding the genetic underpinnings of mineral bone disorder related to CKD. BACKGROUND: Genome-wide association studies (GWAS) have identified numerous genetic loci associated with mineral metabolism markers but have exclusively focused on single-trait analysis. In this study, we performed a multitrait analysis of GWAS (MTAG) of mineral metabolism, exploring overlapping genetic architecture between traits to identify novel genetic associations for fibroblast growth factor 23 (FGF23). METHODS: We applied MTAG to variants common to GWAS of five genetically correlated mineral metabolism markers in participants of European ancestry. We integrated UK Biobank GWAS for blood levels for phosphate, 25-hydroxyvitamin D, and calcium (n=366,484) and Cohorts for Heart and Aging Research in Genetic Epidemiology GWAS for parathyroid hormone (n=29,155) and FGF23 (n=13,716). We then used supervised and unsupervised deep machine learning to identify novel associations between genetic traits and FGF23. RESULTS: MTAG increased the effective sample size for mineral metabolism markers to n=50,325 for FGF23. After clumping, MTAG identified independent genome-wide significant single-nucleotide polymorphisms for all traits, including 62 loci for FGF23. Many of these loci have not been previously reported in single-trait analyses. Through a functional genomics approach, we identified histidine-rich glycoprotein (HRG) and high-mobility group box 1 (HMGB1) as master regulators of downstream canonical pathways associated with circulating FGF23, and both genes were highly enriched in hypertrophied cardiac tissue of deceased hemodialysis patients. In addition, we found that DNMT3A was associated with uremic toxin, 8-hydroxy-2-deoxyguanosine, a biomarker of DNA damage. In silico gene perturbation analysis revealed that DNMT3A is protective in patients with heart failure caused by hypertrophied or dilated cardiomyopathy. CONCLUSIONS: Our findings highlight the importance of MTAG analysis of mineral metabolism markers to boost the number of genome-wide significant loci for FGF23 to identify novel genetic traits. Functional genomics revealed novel networks that inform unique cellular functions and identified HRG and HMGB1 as key master regulators of FGF23 and cardiovascular disease in CKD.

bones, stones, and mineral metabolism↗

PubMed2026

Association between Kidney Tubular Secretory Clearance with Cognitive Function among Adults with CKD in the Systolic Blood Pressure Intervention Trial.

BACKGROUND: Persons with CKD are disproportionally affected with cognitive impairment, yet the pathophysiology linking the two conditions is unclear. Because kidney tubule secretion is essential for clearance of medications, uremic toxins, and metabolites, we hypothesized that worse tubular secretion would be associated with reduced cognitive function in CKD. METHODS: The Systolic Blood Pressure Intervention Trial tested a systolic blood pressure target <120 mmHg vs. <140 mmHg in hypertensive individuals at high cardiovascular risk. In paired blood and urine specimens from 1,937 participants with eGFR <60 ml/min/1.73m2, we measured 10 endogenous tubule-secreted metabolites and calculated a urine/plasma ratio for each, then averaged these to generate a summary secretion score. We used unadjusted and multivariable-adjusted linear regression and mixed models to evaluate cross-sectional and longitudinal associations of the secretion score with the Montreal Cognitive Assessment, Digit Symbol Coding, and Logical Memory immediate and delayed tests-measured at baseline and months 24 and 48 of follow-up. Multivariable Cox regression evaluated associations with incident probable dementia and mild cognitive impairment, adjudicated by prespecified criteria. RESULTS: Mean age was 73 ± 9 years, 41% were women, mean eGFR was 48.2 ± 11.4 ml/min/1.73m2, median albuminuria was 14.8 [7.1-48.6] mg/g. Lower secretion score was associated with a 0.06 higher adjusted logical memory delayed score (95% CI: 0.02, 0.11) but not with other cognitive tests at baseline or longitudinal cognitive decline. After a median 4.1 years of follow-up, 118 developed probable dementia and 187 developed mild cognitive impairment. Each 1-SD lower secretion score was associated with lower risk of probable dementia (HR 0.78, 95% CI: 0.63, 0.98) but not mild cognitive impairment. CONCLUSIONS: Among Systolic Blood Pressure Intervention Trial participants with CKD, lower estimated tubular secretion was not associated with worse cognition at baseline or during longitudinal follow-up.

Journal Article↗

PubMed2005

The process of implementing a CKD clinic.

Chronic kidney disease patients are complex, and usually have multiple comorbid conditions. It is evident that a CKD clinic can improve clinical outcomes and patient satisfaction. It is widely recognized that education, patient empowerment, early recognition of the disease, and appropriate and timely interventions in patients with CKD can positively influence the clinical outcomes in this population. So why is it so difficult to deliver CKD care?

Ambulatory Care Facilities↗

PubMed2004

Potassium metabolism in patients with chronic kidney disease (CKD), Part I: patients not on dialysis (stages 3-4).

Potassium is the main cation in the intracellular space and its content in healthy adults is around 3700 mmol. Its retention is one of the dangers that accompanies chronic renal failure, especially when glomerular filtration rate (GFR) falls toward 20% of normal. There exist different mechanisms by which hyperkalemia is avoided in patients with renal failure. These include spontaneous restriction of dietary potassium intake to 40-60 mmol/day and aldosterone induced increase in potassium excretion in renal distal tubules and colonic epithelium. Although renal and intestinal adaptation are important in maintaining overall potassium balance during CKD, movement of potassium into the cells is extremely important in the body's acute defense against hyperkalemia, and occurs daily during postprandial potassium overload, through shift of this cation into hepatic cells mediated by insulin and thus avoiding post-prandial hyperkalemia. The above described mechanisms contribute to maintenance of normal serum potassium in patients with CKD.

Adaptation, Physiological↗

PubMed2006

Implications of Medicare Part D in CKD anemia treatment.

Treating chronic kidney disease (CKD) anemia successfully requires not only making the correct diagnosis and choosing the appropriate treatment but also taking the steps needed to ensure that residents have access to treatment. This can be challenging with regard to the erythropoiesis-stimulating proteins (ESPs). To ensure access to these products, physicians must be health insurance literate, knowing how different Medicare parts cover the erythropoietin (EPO) products. For example, Medicare Part A places the responsibility for medications on the provider. This means that a long-term care facility is responsible for covering the cost of medications used during the Medicare Part A skilled stay. Medicare Part B covers medications that are provided "incident to" a physician service, including injectables provided by physicians in their offices or during dialysis treatments. Managed care plans, which provide coverage under Medicare Part C, are responsible for all of the benefits available under Medicare Parts A and B. The newest Medicare Part is D, the prescription drug benefit introduced in January 2006. Medicare Part D covers most medications administered to residents in a long-term care facility. For the dually eligible-that is, residents covered by both Medicare and Medicaid-the Medicare Part D program replaces Medicaid drug coverage. Unfortunately, the criteria by which these prescription plans choose to cover products such as ESPs are not based on any specific standard but vary greatly by plan as each has the right to determine coverage criteria. In addition to individualized plan criteria, each plan defines its own process for prior authorization, appeals, and exceptions. Understanding the basic rules of coverage is essential to ensuring access to the ESPs for residents with anemia of CKD.

Anemia↗

PubMed2006

Inter-method variability in PTH measurement: implication for the care of CKD patients.

The National Kidney Foundation/Kidney-Dialysis Outcome Quality Initiative guidelines recommend to maintain the serum intact parathyroid hormone (PTH) concentration between 150 and 300 ng/l in chronic kidney disease (CKD) stage 5 patients. As these limits were derived from studies that used the Allegro intact PTH assay, we aimed to evaluate whether they were applicable to other PTH assays. We compared the PTH concentrations measured with 15 commercial immunoassays in 47 serum pools from dialysis patients, using the Allegro intact PTH assay as the reference. We also evaluated the recovery of graded amounts of synthetic 1-84 and 7-84 PTH added separately to a serum pool. Although the assays were highly correlated, the concentrations differed from one assay to another. The median bias between the tested assays and the Allegro intact PTH assay ranged from -44.9 to 123.0%. When the PTH concentrations were 150 or 300 ng/l with the Allegro intact PTH assay, they ranged with other assays from 83 to 323 ng/l and from 160 to 638 ng/l, respectively. The tested assays recognized 7-84 PTH with various cross-reactivities, whereas a given amount of 1-84 PTH was recovered differently by these assays. We found important inter-method variability in PTH results owing to both antibody specificity and standardization reasons. The unacceptable consequence is that opposite therapeutic attitudes may be reached in a single patient depending on the PTH assay used. We propose to use assay-specific decision limits for CKD patients, or to apply a correcting factor to the PTH results obtained with a given assay.

Adult↗

PubMed2005

Home blood pressure monitoring in CKD.

BACKGROUND: Blood pressure (BP) control is the mainstay of stalling the progression of cardiorenal disease, yet the performance characteristics of BPs obtained in the clinic (CBPs) by routine or standardized methods or at home (HBP) in diagnosing hypertension or assessing its control are unknown. METHODS: Two hundred thirty-two patients (20% black; 4% women; mean age, 67 years; 35% with diabetes) with chronic kidney disease (CKD) underwent a single 24-hour ambulatory BP (ABP) monitoring (ABPM) and concomitant recording of CBP and HBP for 1 week. Hypertension is defined as systolic BP of 130 mm Hg or greater or diastolic BP of 80 mm Hg or greater on average awake 24-hour ABPM. RESULTS: Average ABP was 135.2 +/- 15.9/75.6 +/- 11.0 mm Hg. Thirty-five percent of patients had isolated systolic hypertension; 3%, isolated diastolic hypertension; 27%, combined systolic and diastolic hypertension; and 35%, normotension or well-controlled BP. The prevalence of "white-coat effect" was estimated as 28% to 30% by means of CBPs and 24% by means of HBPs. Well-controlled BP in the clinic, but poorly controlled BP by means of ABPM, masked hypertension, was seen in 26% to 29% by means of CBPs, but only 13% with HBP monitoring. CONCLUSION: In patients with CKD, HBP is superior in reducing the misclassification of hypertension caused by the white-coat effect and masked hypertension commonly seen with CBPs. An average HBP of approximately 140/80 mm Hg appears to be the best correlate of hypertension defined by means of ABPM.

Aged↗

PubMed2005

Metabolic acidosis of CKD: diagnosis, clinical characteristics, and treatment.

Metabolic acidosis is noted in the majority of patients with chronic kidney disease (CKD) when glomerular filtration rate (GFR) decreases to less than 20% to 25% of normal, although as many as 20% of individuals can have acid-base parameters close to or within the normal range. Acidosis generally is mild to moderate in degree, with plasma bicarbonate concentrations ranging from 12 to 22 mEq/L (mmol/L), and it is rare to see values less than 12 mEq/L (mmol/L) in the absence of an increased acid load. Degree of acidosis approximately correlates with severity of renal failure and usually is more severe at a lower GFR. The metabolic acidosis can be of the high-anion-gap variety, although anion gap can be normal or only moderately increased even with stage 4 to 5 CKD. Several adverse consequences have been associated with metabolic acidosis, including muscle wasting, bone disease, impaired growth, abnormalities in growth hormone and thyroid hormone secretion, impaired insulin sensitivity, progression of renal failure, and exacerbation of beta 2 -microglobulin accumulation. Administration of base aimed at normalization of plasma bicarbonate concentration might be associated with certain complications, such as volume overload, exacerbation of hypertension, and facilitation of vascular calcifications. Whether normalization of plasma bicarbonate concentrations in all patients is desirable therefore requires additional study. In the present review, we describe clinical and laboratory characteristics of metabolic acidosis, discuss potential adverse effects, and address benefits and complications of therapy.

Acidosis↗

PubMed2005

Relationship of phosphorus and calcium-phosphorus product with mortality in CKD.

BACKGROUND: Abnormalities of mineral metabolism are prevalent in patients with kidney failure and are associated with increased risk for cardiovascular events. There are limited data investigating relationships of phosphorus and calcium-phosphorus product with outcomes in patients with chronic kidney disease (CKD) stages 3 to 4. METHODS: Serum phosphorus and calcium were measured at baseline in 840 participants from the randomized cohort of the Modification of Diet in Renal Disease Study. Survival status until December 31, 2000, was obtained from the National Death Index. Cox models were performed to assess the relationship of serum phosphorus level and calcium-phosphorus product with all-cause and cardiovascular disease (CVD) mortality. RESULTS: Mean serum phosphorus level was 3.8 +/- 0.7 mg/dL (1.23 +/- 0.23 mmol/L), calcium-phosphorus product was 34.7 +/- 6.3 mg2/dL2, and glomerular filtration rate (GFR) was 33 +/- 12 mL/min/1.73 m2 (0.55 +/- 0.20 mL/s/1.73 m2). All-cause and CVD mortality rates were 25% and 15%. Serum phosphorus level was not related to all-cause mortality in multivariable models (P = 0.46). In unadjusted analysis, serum phosphorus level was associated with (hazard ratio [HR] per 1 mg/dL increase, 1.34; 95% confidence interval [CI], 1.05 to 1.71; P = 0.02) increased risk for CVD mortality, but this association was partly attenuated and not statistically significant after adjustment for GFR and other confounders (HR, 1.27; 95% CI, 0.94 to 1.73; P = 0.12). Calcium-phosphorus product was not associated with all-cause mortality in unadjusted (P = 0.23) or multivariate analysis (P = 0.35). Calcium-phosphorus product was related to CVD mortality in unadjusted (HR per 10 mg2/dL2 increase, 1.30; 95% CI, 1.01 to 1.69; P = 0.04) analysis, but this association was not statistically significant after adjustment for GFR and other confounders (HR, 1.22; 95% CI, 0.89 to 1.66; P = 0.23). CONCLUSION: In the Modification of Diet in Renal Disease Study cohort, serum phosphorus level and calcium-phosphorus product were not statistically associated with all-cause or CVD mortality after adjustment for GFR; however larger studies with additional statistical power are needed to evaluate these relationships, especially in the context of current practice patterns in patients with CKD.

Adult↗

PubMed2006

Effect of early correction of anemia on the progression of CKD.

BACKGROUND: This study is designed to assess the effect of early and complete correction of anemia by using recombinant human erythropoietin (epoetin) alfa on the progression of chronic kidney disease (CKD). METHODS: Patients were randomly assigned to achieve high (13 to 15 g/dL [130 to 150 g/L]) or low (11 to 12 g/dL [110 to 120 g/L]) hemoglobin-level targets during 4 months of stabilization, followed by 36 months of maintenance. Glomerular filtration rate (GFR) decrease was measured by using iohexol clearance. Quality of life, nutrition, and safety also were monitored. RESULTS: Because of labeling changes for subcutaneous administration of epoetin alfa (Eprex; Johnson and Johnson, Schaffhausen, Switzerland), the study was terminated prematurely. There were 195 patients enrolled in each group; 108 high-hemoglobin and 133 low-hemoglobin patients entered the maintenance phase. Mean maintenance duration was 7.4 months for the high-hemoglobin group and 8.3 months for the low-hemoglobin group. GFR decrease was numerically, but not statistically significantly, lower with the high-hemoglobin group (0.058 versus 0.081 mL/min/1.73 m2/mo [< 0.01 mL/s/1.73 m2/mo]). Physical quality-of-life measures showed trends (Role-Physical, P = 0.055; Physical Function, P = 0.083) or statistically significant improvement (Vitality, P = 0.042) with high hemoglobin levels at the end of the stabilization phase. Adverse events were similar between groups. Cardiovascular adverse events occurred in 25% of the high-hemoglobin and 18% of the low-hemoglobin patients (P = 0.137). Neither epoetin dosage nor hemoglobin level was associated with cardiovascular adverse events or death. CONCLUSION: These data suggest that normalization of hemoglobin levels in patients with CKD is safe. Longer duration studies are needed to clarify efficacy benefits with high hemoglobin levels.

Adolescent↗

PubMed2006

The new KDOQI clinical practice guidelines and clinical practice recommendations for diabetes and CKD.

BACKGROUND/AIMS: The National Kidney Foundation (NKF) recently published new guidelines and clinical practice recommendations for the diagnosis and management of patients with diabetes and chronic kidney disease (CKD). METHODS: Guidelines were developed using an evidence-based approach. When sufficient evidence was lacking, recommendations were developed that reflect expert opinion. RESULTS: Guidelines describe the process for screening and diagnosis of kidney disease in the setting of diabetes and the management of hyperglycemia, hypertension, dyslipidemia, and nutrition. Recommendations describe the management of albuminuria in the normotensive diabetic patient and the potential value of albuminuria as a marker of treatment efficacy; the impact of diabetes and CKD in special populations; the importance of behavioral self-management; and the value of intensive multifaceted intervention in these high risk patients. CONCLUSIONS: The new guidelines and recommendations update and extend the scope of the NKF's Kidney Disease Outcomes Quality Initiative (KDOQI(TM)).

Diabetes Complications↗