Non-dialysis Dependent Chronic Kidney Disease Research Articles

Metabolic syndrome in chronic kidney disease and renal transplant patients in North India

The cluster of biochemical and clinical abnormalities known as metabolic syndrome (MS) has become a public health problem even in developing countries. Previous studies have shown a graded relationship between MS components and worsening renal function in the general population. The prevalence of MS in non-dialysis-dependent CKD (NDD-CKD) and kidney transplant recipients in the North Indian population is unknown. We studied all patients with stable CKD and with renal transplantation attending the nephrology clinic in a large centre in North India over an eight-week period. All transplant patients had stable graft function for 3 months prior to recruitment. MS was defined according to the International Diabetes Federation (IDF) 2007 guidelines. A total of 252 (155 NDD-CKD and 97 renal transplant recipients) patients were studied. MS was present in 86 (34%) patients. The prevalence of MS was similar in NDD-CKD and transplant patients [60 (39%) vs. 26 (27%), P = 0.052]. Patients with MS were older than those without MS (48 ± 12 years-old vs. 40 ± 14 years-old, P < 0.001) and MS was more common in women than in men (59% vs. 26%, P < 0.001). Female gender was an independent risk factor for MS in this population [adjusted OR 5.25 (95% CI: 2.74-10.06)]. With advancing CKD, the prevalence of MS decreased in the NDD-CKD patients. Impaired glucose tolerance and hypertriglyceridemia were independent predictors of MS. Hypertension was not a predictor of MS in NDD-CKD. In transplant recipients, hypertriglyceridemia, hypertension and low HDL cholesterol predicted the risk for MS. MS is common in CKD and renal transplant patients in North India. The risk of MS decreases with declining eGFR in CKD patients. Female gender and hypertriglyceridemia independently predict the risk of MS in both NDD-CKD and transplant recipients.

Association of echocardiographic abnormalities with mortality in men with non-dialysis-dependent chronic kidney disease

The interrelationship of left ventricular hypertrophy (LVH) with ejection fraction (EF) and their impact on mortality in non-dialysis-dependent chronic kidney disease (NDD-CKD) is unclear. We examined the associations of EF and LVH with all-cause mortality in a historic cohort of 650 male US veterans with moderate-to-advanced NDD-CKD. EF and LVH were examined both separately and after categorizing patients according to their concomitant EF and presence/absence of LVH. Associations with mortality were examined in Cox models with adjustments for demographics, blood pressure, comorbidities, smoking status, medication use and biochemical characteristics. EF <30 and 30-50% were associated with higher all-cause mortality compared to EF >50% even after multivariable adjustments [multivariable adjusted hazard ratio, 95% confidence interval (CI): 2.83 (1.86-4.30) and 1.38 (1.06-1.78), P < 0.001 for linear trend]. LVH in itself was not associated with mortality [multivariable adjusted hazard ratio, 95% CI: 0.83 (0.66-1.05), P = 0.12], but the presence of LVH combined with an EF <50% was associated with the highest mortality [multivariable adjusted hazard ratios, 95% CI in patients with EF >50% + LVH, EF ≤ 50%-LVH and EF ≤ 50% + LVH, compared to EF >50%-LVH: 0.84 (0.63-1.13), 1.36 (1.00-1.83) and 1.62 (1.07-2.46)]. Low EF is associated with higher mortality in patients with NDD-CKD. In the presence of a low EF, LVH is also associated with higher mortality. Clinical trials are needed to determine if interventions targeting patients with low EF and LVH can lower mortality in NDD-CKD.

361 Satisfaction With Provider Communication Is Associated With Perceived Disease Knowledge in Patients With Chronic Kidney Disease (CKD)

SATISFACTION WITH PROVIDER COMMUNICATION IS ASSOCIATED WITH PERCEIVED DISEASE KNOWLEDGE IN PATIENTS WITH CHRONIC KIDNEY DISEASE (CKD) Julie Wright, Kenneth Wallston, Svetlana Eden, Ayumi Shintani, T. Alp Ikizler, Kerri Cavanaugh. Vanderbilt University Medical Center, Nashville, TN USA Effective patient-provider communication is a crucial component of high quality patient care. Data are scarce regarding patient views of physician communication skills in the setting of pre-dialysis CKD care. Adult patients with non-dialysis dependent CKD (Stages 1-5) were enrolled from April-October 2009 during nephrology clinic visits. Patient satisfaction with provider communication was assessed using the Communication Assessment Tool (CAT), a validated scale for measuring patient perception of physician interpersonal and communication skills. Perceived knowledge was assessed by asking patients to rate their CKD knowledge on a scale from 1 (no knowledge) to 4 (a lot of knowledge) in nine areas and averaged to generate an overall perceived knowledge survey (PiKS) score. Associations between CAT and patient characteristics, including PiKS and a validated measure of objective CKD knowledge, were examined. Of 399 patients enrolled, the mean (SD) age was 57 (16) years. 53% were male, 83% Caucasian, and 77% had CKD Stage 3-5. The mean (SD) CAT and PiKS scores were 4.69 (0.51) and 2.56 (0.61), respectively. CAT was associated only with PiKS (Spearman correlation 0.15, p<0.0001) in unadjusted analysis. Patients of older age (OR 1.22 CI [1.11, 1.35]; p<0.0001 per 10 years), higher eGFR (1.03 [1.02, 1.04]; p<0.0001 per 5 ml/min/1.73m), and higher PiKS (2.15 [1.72, 2.68]; p<0.0001 per 1.0 increment increase) were likely to have higher odds of satisfaction with provider communication in adjusted analysis that also included sex, race, health literacy (REALM survey), income, number of provider visits, and objective knowledge. Adjusted analysis presented no evidence that objective knowledge was associated with CAT score. In addition to advancing age and higher eGFR, patients' perception of their disease specific knowledge may be an important component of their satisfaction with CKD care.

244 Cost-Effective Management of Iron Deficiency Among Patients with Anemia and Non-Dialysis Dependent Chronic Kidney Disease

244 Cost-Effective Management of Iron Deficiency Among Patients with Anemia and Non-Dialysis Dependent Chronic Kidney Disease

258 Risk Factors for 30-Day Hospital Readmission Among Patients with Non-Dialysis Dependent CKD

258 Risk Factors for 30-Day Hospital Readmission Among Patients with Non-Dialysis Dependent CKD

Role of statins in preventing adverse cardiovascular outcomes in patients with chronic kidney disease.

Cardiovascular disease accounts for the majority of deaths in chronic kidney disease (CKD). Dyslipidemia is a well established cardiovascular risk factor. We summarize key aspects of available evidence relating to beneficial effects of statins in nondialysis-dependent CKD, dialysis-dependent CKD and renal transplant recipients. Previous trials and their meta-analyses suggested that statins reduce lipid levels, the risk of cardiovascular disease and all-cause mortality in nondialysis-dependent CKD. The Study of Heart and Renal Protection (SHARP) study that enrolled both dialysis-dependent and nondialysis-dependent CKD patients showed a 17% decrease in major atherosclerotic events with statins or ezetimibe. Similar cardiovascular benefits are observed in renal transplant recipients. However, such positive effects were not found in two recent clinical trials that enrolled hemodialysis patients alone. This lack of benefit might be attributed to differences in the cause of cardiovascular death seen in dialysis patients and smaller sample size. The overall benefits-harms tradeoff may benefit from meta-analysis and individual patient data meta-analysis in hemodialysis patients including the SHARP data. Nondialysis-dependent CKD patients and renal transplant recipients benefit from statins. Statins have also been found to be beneficial in one of the three large trials in hemodialysis patients, a matter which may be further explored.

Quality of care and mortality are worse in chronic kidney disease patients living in remote areas

Many patients with non-dialysis dependent chronic kidney disease (CKD) live far from the closest nephrologist; although reversible, this might constitute a barrier to optimal care. In order to evaluate outcomes, we selected 31,452 outpatients older than 18 years with an estimated glomerular filtration rate (eGFR) less than 45 ml/min per 1.73 m² who had serum creatinine measured at least once during 2005 in Alberta, Canada. We then used logistic regression to examine the association between outcomes of 6545 patients who lived more than 50 km from the nearest nephrologist. Over a median follow-up of 27 months, 7684 participants died and 15,075 were hospitalized at least once. Compared with those living within 50 km, those further away were significantly less likely to visit a nephrologist or a multidisciplinary CKD clinic within 18 months of the index measurement of the eGFR. Similarly, remote dwellers with diabetes were significantly less likely to have hemoglobin A1c evaluated within 1 year of the index eGFR measurement, to have urinary albumin assessed biannually, or to receive an angiotensin converting enzyme inhibitor or receptor blocker in the setting of diabetes or proteinuria. Remote-dwelling participants were also significantly more likely to die or be hospitalized during follow-up than those living closer. Thus, among people with CKD, remote dwellers were less likely to receive specialist care, recommended laboratory testing, and appropriate medications, and were more likely to die or be hospitalized compared with those living closer to a nephrologist.

When is high-dose intravenous iron repletion needed? Assessing new treatment options

High doses of intravenous iron have a role in the treatment of a number of clinical situations associated with iron deficiency, iron deficiency anemia, and blood loss. In the presence of functioning erythropoiesis, iron supplementation alone may be adequate to replenish iron stores and restore blood loss. Where hormone replacement with an erythropoiesis-stimulating agent is required, iron adequacy will optimize treatment. Intravenous iron offers a rapid means of iron repletion and is superior to oral iron in many circumstances, especially in the presence of anemia of chronic disease, where it appears to overcome the block to absorption of iron from the gastrointestinal tract and immobilization of stored iron. The clinical situations where high doses of iron are commonly required are reviewed. These include nondialysis-dependent chronic kidney disease, inflammatory bowel disease, obstetrics, menorrhagia, and anemia associated with cancer and its treatment. The literature indicates that high doses of iron are required, with levels of 1500 mg in nondialysis-dependent chronic kidney disease and up to 3600 mg in inflammatory bowel disease. New formulations of intravenous iron have recently been introduced that allow clinicians to administer high doses of iron in a single administration. Ferumoxytol is available in the US, has a maximum dose of 510 mg iron in a single administration, but is limited to use in chronic kidney disease. Ferric carboxymaltose can be rapidly administered in doses of 15 mg/kg body weight, up to a ceiling dose of 1000 mg. A test dose is not required, and it can be used more widely across a spectrum of iron deficiency and iron deficiency anemia indications. The latest introduction is iron isomaltoside 1000. Again, a test dose is not required, and it can be delivered rapidly as an infusion (in an hour), allowing even higher doses of iron to be administered in a single infusion, ie, 20 mg/kg body weight with no ceiling. This will allow clinicians to achieve high-dose repletion more frequently as a single administration. Treatment options for iron repletion have taken a major leap forward in the past two years, especially to meet the demand for high doses given as a single administration.

HIGHLIGHTS FROM THE LITERATURE

HIGHLIGHTS FROM THE LITERATURE

Fibroblast Growth Factor, A Review

The recent identification of fibroblast growth factor (FGF)23 has filled in the gaps of our understanding of calcium– phosphate regulation. Together with its cofactor Klotho, FGF-23 is a phosphaturic factor that influences vitamin D metabolism and renal re-absorption of phosphorus in order to maintain serum phosphate levels within the normal range. In chronic kidney disease (CKD), FGF-23 levels rise in parallel with declining kidney function before any significant rise is perceived in serum phosphate concentration. Increased serum FGF-23 levels in CKD patients were found to be independently associated with ventricular hypertrophy and endothelial dysfunction after correcting for traditional markers of calcium–phosphate metabolism. FGF-23 has been implicated in various human diseases including autosomal dominant hypophosphatemic rickets (ADHR), X-linked hypophosphatemia (XLH), tumor induced osteomalacia and familial tumoral calcinosis. Lastly, in prospective studies, elevated serum FGF-23 levels predicted rapid disease progression in non-dialysis dependent CKD patients and increased mortality in chronic hemodialysis patients. The growing knowledge and understanding of FGF-23 may provide potential answers with regards to prevention and management of CKD [1]. The FGF family is comprised of polypeptides that share a common region of amino peptide residues. Seven human FGF subfamilies have been identified; FGF-23 belongs to the FGF19 subgroup including FGF 19, 21 and 23 having very different physiological functions despite sharing a similar disulphide bond which is absent in most other families. FGF23 is a central regulator of phosphate homeostasis, enhancing phosphorus excretion and suppressing1-alpha hydroxylase activity in the kidney [2, 3], whereas FGF-19 is involved in bile acid synthesis and FGF-21 stimulates insulinindependent glucose uptake in adipocytes and reduces triglyceride levels. The active form of FGF-23 is an approximately 32-kD (251 amino acids) protein with its gene located on chromosome 12 [4, 5]. It is mainly expressed in osteocytes [6, 7], and also expressed in pericyte-like cells around the venous sinuses, the ventrolateral thalamic nucleus, and in the thymus. The contribution of sites other than bone to circulating FGF-23 levels is still unclear. It is clear, however that there are high levels of expression in the osteocytes and that because osteocytes are the most abundant cell in bone, this suggests that the serum levels of FGF-23 are derived mainly from bone [8]. FGF-23 exerts its biological effects through activation of FGF receptors in a Klotho dependent manner, as a Klotho/ FGF-Receptor complex binds to FGF-23. Klotho is a transmembrane protein, the gene expression of which was detected in distal renal tubular cells, parathyroid gland, the pituitary gland, ovary, testis, skeletal muscle, duodenum, pancreas and choroid plexus. It is unclear why Klotho is G. C. Chibesakunda (*) :C. S. Brecklin Department of Medicine/Section of Nephrology, University of Illinois Medical Center at Chicago, 820 S Wood Street (MC 793), Chicago, IL 60612, USA e-mail: gracecc@uic.edu

A randomized controlled trial comparing intravenous ferric carboxymaltose with oral iron for treatment of iron deficiency anaemia of non-dialysis-dependent chronic kidney disease patients

Background. Iron deficiency is a common cause of anaemia and hyporesponsiveness to erythropoiesis-stimulating agents (ESAs) in non-dialysis-dependent chronic kidney disease (ND-CKD) patients. Current intravenous iron agents cannot be administered in a single high dose because of adverse effects. Ferric carboxymaltose, a non-dextran parenteral iron preparation, can be rapidly administered in high doses.Methods. This open-label trial randomized 255 subjects with glomerular filtration rates ≤ 45 mL/min/1.73 m2, haemoglobin ≤ 11 g/dL, transferrin saturation ≤ 25%, ferritin ≤ 300 ng/mL, and stable ESA dose to either intravenous ferric carboxymaltose 1000 mg over 15 min (with up to two additional doses of 500 mg at 2-week intervals) or oral ferrous sulphate 325 mg thrice daily for a total of 195 mg elemental iron daily for 56 days.Results. In the modified intent-to-treat population, the proportion of subjects achieving a haemoglobin increase ≥ 1 g/dL at any time was 60.4% with ferric carboxymaltose and 34.7% with oral iron (P < 0.001). At Day 42, mean increase in haemoglobin was 0.95 ± 1.12 vs 0.50 ± 1.23 g/dL (P = 0.005), mean increase in ferritin was 432 ± 189 ng/mL vs 18 ± 45 ng/mL (P < 0.001) and mean increase in transferrin saturation was 13.6 ± 11.9% vs 6.1 ± 8.1% (P < 0.001). Treatment-related adverse events were significantly fewer with ferric carboxymaltose than with oral iron (2.7% and 26.2%, respectively; P < 0.0001).Conclusions. We conclude that 1000 mg ferric carboxymaltose can be rapidly administered, is more effective and is better tolerated than oral iron for treatment of iron deficiency in ND-CKD patients.

Vitamin D supplementation in chronic kidney disease: a systematic review and meta-analysis of observational studies and randomized controlled trials.

Vitamin D deficiency is highly prevalent among patients with chronic kidney disease (CKD). The benefits and harms of vitamin D supplementation (ergocalciferol or cholecalciferol) were assessed in patients with nondialysis-dependent CKD, dialysis-dependent CKD, and renal transplant recipients. MEDLINE (1966 to September 2009), SCOPUS (September 2009), and nephrology conference proceedings were searched for relevant observational and randomized controlled trials (RCTs). Treatment effects were summarized as mean differences (MDs) with 95% confidence intervals (CIs) using a random effects model. Separate analyses were conducted for observational studies and RCTs. Twenty-two studies (17 observational and 5 RCTs) were included. There was a significant improvement in 25-hydroxyvitamin D (MD 24.1 ng/ml, 95% CI 19.6 to 28.6) and an associated decline in parathyroid hormone (PTH) levels (MD -41.7 pg/ml, 95% CI -55.8 to -27.7) among observational studies. PTH reduction was higher in dialysis patients. Among RCTs, there was a significant improvement in 25-hydroxyvitamin D (MD 14 ng/ml, 95% CI 5.6 to 22.4) and an associated decline in PTH levels (MD -31.5 pg/ml, 95% CI -57 to -6.1). A low incidence of hypercalcemia and hyperphosphatemia was reported with vitamin D supplementation. Cardiovascular and skeletal effects of vitamin D supplementation have not been studied. Included studies were mostly of low to moderate quality. Available evidence from low-to-moderate quality observational studies and fewer RCTs suggests that vitamin D supplementation improves biochemical endpoints. However, whether such improvements translate into clinically significant outcomes is yet to be determined.

PA21: a novel phosphate binder for the treatment of hyperphosphatemia in chronic kidney disease

Limitations of conventional phosphate binders have led to the development of novel non-calcium, non-aluminium agents for use in patients with chronic kidney disease (CKD). The iron-based agent PA21 (stabilized polynuclear iron(III)-oxyhydroxide) has high phosphate binding capacity in vitro. This study was undertaken to investigate the uptake of iron after oral administration of PA21 in order to identify any potential risk of iron overload in the clinical setting, and to obtain a preliminary assessment of the effect of PA21 on serum phosphate levels prior to larger trials over a longer treatment period. An open-label, Phase I study was undertaken in which PA21 10 g/day was administered for 7 days to 8 nondialysis-dependent CKD patients (Stages 3 - 4), 8 maintenance hemodialysis patients and 8 healthy subjects. In addition, a single dose of radiolabeled PA21 was administered to determine iron uptake. Median iron uptake (range) was 0.06% (0.008 - 0.44%), 0.02% (0 - 0.04%) and 0.43% (0.16% - 1.25%) in the nondialysis-dependent CKD patients, hemodialysis patients and healthy subjects, respectively. Serum phosphate level decreased over the 7-day treatment period in the nondialysis patients (1.44 + or - 0.29 mmol/l to 1.10 + or - 0.27 mmol/l, p < 0.01) and the hemodialysis patients (2.85 + or - 0.78 mmol/l to 2.25 + or - 0.85 mmol/, p < 0.01). The most common adverse event was diarrhea (n = 9); all cases were mild to moderate. Findings from this short-term study indicate that PA21 may be an efficacious and well-tolerated phosphate binder with low iron uptake that may offer a promising alternative to existing hyperphosphatemia therapies. These results will need to be confirmed with longer-term, controlled studies.

Randomized Evaluation of efficacy and safety of ferric carboxymaltose in Patients with iron deficiency Anaemia and Impaired Renal function (REPAIR-IDA): rationale and study design

Patients with iron deficiency anaemia (IDA) in the setting of non-dialysis-dependent chronic kidney disease (NDD-CKD) may benefit from treatment with intravenous (IV) iron. Ferric carboxymaltose (FCM) is a novel IV iron formulation designed to permit larger infusions compared to currently available IV standards such as Venofer(R) (iron sucrose). The primary objective of REPAIR-IDA is to estimate the cardiovascular safety and efficacy of FCM (two doses at 15 mg/kg to a maximum of 750 mg per dose) compared to Venofer(R) (1000 mg administered as five infusions of 200 mg) in subjects who have IDA and NDD-CKD. REPAIR-IDA is a multi-centre, randomized, active-controlled, open-label study. Eligible patients must have haemoglobin (Hgb) < or = 11.5 g/dL and CKD defined as (1) GFR < 60 mL/min/1.73 m(2) on two occasions or (2) GFR < 90 mL/min/1.73 m(2) and either evidence of renal injury by urinalysis or elevated Framingham cardiovascular risk score. Two thousand and five hundred patients will be randomized to FCM or Venofer(R) in a 1:1 ratio. The primary efficacy endpoint is mean change in Hgb from baseline to the highest observed Hgb between baseline and Day 56. The primary safety endpoint is the proportion of subjects experiencing at least one of the following events: death due to any cause, non-fatal myocardial infarction, non-fatal stroke, unstable angina requiring hospitalization, congestive heart failure requiring hospitalization or medical intervention, arrhythmias, hypertension or hypotension during the 120 days following randomization. REPAIR-IDA will assess the efficacy and safety of two 750-mg infusions of FCM compared to an FDA-approved IV iron regimen in patients with NDD-CKD at increased risk for cardiovascular disease.

FDA report: Ferumoxytol for intravenous iron therapy in adult patients with chronic kidney disease

On June 30, 2009, the United States Food and Drug Administration (FDA) approved ferumoxytol (Feraheme injection, AMAG Pharmaceuticals), an iron-containing product for intravenous (IV) administration, for the treatment of iron deficiency anemia in adult patients with chronic kidney disease (CKD). The safety and efficacy of ferumoxytol were assessed in three randomized, open-label, controlled clinical trials. Two trials evaluated patients with nondialysis dependent CKD and a third trial assessed patients undergoing hemodialysis. Randomization was either to ferumoxytol or oral iron. Ferumoxytol was administered as two 510 mg IV injections, separated by 3-8 days. Oral iron, Ferro-Sequels, was administered at a dose of 100 mg twice daily for 21 days. In all three clinical trials, ferumoxytol administration increased the mean blood hemoglobin (Hgb) concentrations by approximately 1.0 g/dL over the 35 day period, a mean increase that was greater than what was observed in patients receiving oral iron. Patients receiving ferumoxytol also had increases in blood transferrin saturation (TSAT) and ferritin values. For the proposed ferumoxytol dosing regimen, 4.9% of patients had serum ferritin >or=800 ng/mL and TSAT >or=50% post-treatment. The most important ferumoxytol safety concerns were hypersensitivity reactions and/or hypotension. Anaphylaxis or anaphylactoid reactions were reported in 0.2% of subjects, and other adverse reactions potentially associated with hypersensitivity (e.g., pruritus, rash, urticaria, or wheezing) were reported in 3.7%. Hypotension was observed in 1.9%, including three patients with serious hypotensive reactions. Ferumoxytol administration may transiently affect the diagnostic ability of magnetic resonance imaging and the drug label provides further information regarding this effect.

Outcomes associated with serum phosphorus level in males with non-dialysis dependent chronic kidney disease

Hyperphosphatemia is associated with higher mortality and increased incidence of end-stage renal disease in patients with non-dialysis dependent CKD (NDD-CKD), but there has not been a concomitant assessment of mortality and progressive kidney disease that would also account for cumulative effects of hyperphosphatemia. In order to account for the cumulative effects of abnormal serum phosphorus we examined associations of not only baseline, but also time-averaged serum phosphorus levels with all-cause mortality, the composite of mortality or ESRD and the slopes of estimated glomerular filtration rate (eGFR), by using Cox models and mixed effects models in a contemporary cohort of 713 males with moderate and advanced NDD-CKD. Higher baseline and time-averaged serum phosphorus were both associated with mortality and with the composite outcome. A 1 mg/dl higher time-averaged serum phosphorus was associated with a multivariable adjusted hazard ratio of all-cause mortality (95% CI) of 1.56 (1.19 - 2.05), p = 0.001. Higher serum phosphorus was associated with a steeper slope of eGFR in unadjusted analyses, but this association became non-significant after multivariable adjustments. The cumulative burden of hyperphosphatemia is associated with increased mortality in patients with moderate and advanced NDD-CKD. Clinical trials are needed to determine if lowering serum phosphorus can result in improved mortality in this population.

Chronic Kidney Disease in the Urban Poor

In the United States, relatively little is known about clinical outcomes of chronic kidney disease (CKD) in vulnerable populations utilizing public health systems. The primary study objectives were to describe patient characteristics, incident ESRD, and mortality in adults with nondialysis-dependent CKD receiving care in the health care safety net. Time to ESRD and time to death were examined among a cohort of 15,353 ambulatory adults with nondialysis-dependent CKD from the Community Health Network of San Francisco. The mean age of the CKD cohort was 59.0 +/- 13.8 years; 50% of the cohort was younger than 60 years and 26% was younger than 50 years. Most (72%) were members of nonwhite racial-ethnic groups, 73% were indigent (annual income <$15,000) and 18% were uninsured. In adjusted analyses, blacks [hazard ratio (95% confidence interval), 4.00 (2.99 to 5.35)], Hispanics [2.20 (1.46 to 3.30)], and Asians/Pacific Islanders [3.84 (2.73 to 5.40)] had higher risks of progression to ESRD than non-Hispanic whites. The higher risk of progression to ESRD among nonwhite compared with white persons with CKD was not explained by lower relative mortality. Adults with CKD stages 3 to 5 cared for within an urban public health system were relatively young and predominantly nonwhite-both factors associated with a higher risk of progression to ESRD. These findings call for targeted efforts to assess the burden and progression of CKD within other public and safety-net health systems in this country.

Outcomes Associated with Serum Calcium Level in Men with Non-Dialysis-Dependent Chronic Kidney Disease

Elevated serum calcium has been associated with increased mortality in dialysis patients, but it is unclear whether the same is true in non-dialysis-dependent (NDD) chronic kidney disease (CKD). Outcomes associated with low serum calcium are also not well-characterized. We examined associations of baseline, time-varying, and time-averaged serum calcium with all-cause mortality in a historic prospective cohort of 1243 men with moderate and advanced NDD CKD by using Cox models. The association of serum calcium with mortality varied according to the applied statistical models. Higher baseline calcium and time-averaged calcium were associated with higher mortality (multivariable adjusted hazard ratio (95% confidence interval): 1.31 (1.13, 1.53); P < 0.001 for a baseline calcium 1 mg/dl higher). However, in time-varying analyses, lower calcium levels were associated with increased mortality. Higher serum calcium is associated with increased long-term mortality (as reflected by the baseline and time-averaged models), and lower serum calcium is associated with increased short-term mortality (as reflected by the time-varying models) in patients with NDD CKD. Clinical trials are warranted to determine whether maintaining normal serum calcium can improve outcomes in these patients.

Prospective Evaluation of Waist Circumference and Visceral Adipose Tissue in Patients with Chronic Kidney Disease

Background: Waist circumference (WC), a simple anthropometric measure, is associated with visceral adipose tissue (VAT) in cross-sectional studies, and thus has been used as a surrogate marker for VAT. However, associations between changes over time in WC and VAT have not been studied in chronic kidney disease (CKD) patients. Methods: This prospective study included 87 nondialysis-dependent CKD patients (54 males, 56.2 ± 10.4 years, BMI 27.3 ± 5.1, GFR 35.9 ± 14.6 ml/min/1.73 m²). VAT area was measured by computed tomography (CT) and WC was measured at the umbilicus level at baseline and after 12 months. Results: Changes in WC correlated significantly but weakly with changes in VAT (r = 0.26, p = 0.016), likely due to a substantially smaller change in WC compared to changes in VAT. This was also reflected by a kappa coefficient of 0.26, i.e. indicative of poor agreement between WC and CT measurements in regards to quantification of changes in VAT. Likewise, the receiver operating characteristic curve analysis identified WC as poor predictor of changes in VAT (area under the curve = 0.62). Conclusion: Anthropometric measurement of WC is poorly correlated with changes in VAT measured by CT in nondialysis-dependent CKD patients. Therefore, caution should be taken when using WC as a surrogate marker of VAT changes in this population.

IS NORMALISING HAEMOGLOBIN IN PATIENTS WITH CKD HARMFUL AND IF SO, WHY?

Symptomatic anaemia is found in patients with chronic kidney disease. Correction of anaemia by erythropoiesis stimulating agents improves quality of life and life expectancy. Data from patients with both dialysis dependent and nondialysis dependent chronic kidney disease now show that the mortality from cardiovascular disease increases if the haemoglobin concentration is corrected above 13.0 g/dl. The mechanism for this increased risk is uncertain.