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PubMed2006

Level of asymmetric dimethylarginine and carotid atherosclerosis in patients with chronic kidney disease.

OBJECTIVE: To determine the association between asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide (NO) synthase, with atherosclerosis in patients with chronic kidney disease (CKD). METHODS: One hundred thirty-eight CKD patients were enrolled in this study. Serum levels of L-arginine, ADMA, and SDMA were measured by high-performance liquid chromatography (HPLC). Common carotid arteries intimae-medial thickness (CCA-IMT), cross-sectional calculated intimae-medial thickness (cIM area) and atherosclerotic plaque were detected by noninvasive high-resolution B-mode ultrasonography. RESULTS: Serum levels of ADMA and SDMA were significantly increased in CKD patients (n=138) compared with age matched healthy subjects (n=42, P<0.01). ADMA and SDMA levels increased with the progression of renal dysfunction and were negatively related to creatinine clearance (Ccr) in pre-dialysis patients (r=-0.315, P<0.05; r=-0.426, P<0.01). Serum levels of ADMA and SDMA in dialysis patients (n=74) were significantly higher than those in pre-dialysis patients (P<0.05). Patients with carotid artery plaques showed significantly higher levels of ADMA compared with those without plaques. Serum levels of ADMA closely correlated with the mean IMT (r=0.471, P<0.01) and cIM area value (r=0.430, P<0.01). These correlations remained significant even after adjusting GFR, age, gender ,and other risk factors for atherosclerosis in the multiple regression analysis. CONCLUSION: Serum levels of ADMA increased with the progression of CKD and may play a role in the pathogenesis of accelerated atherosclerosis in CKD patients.

Adult↗
PubMed2006

Cardiovascular risk in patients with chronic kidney diseases: a time for new risk markers?

The number of patients with end-stage renal disease who need expensive dialysis treatment or transplantation is increasing all over the world. Therefore, new possibilities of prevention and treatment of chronic kidney diseases (CKD) are being looked for. However, patients with CKD represent a population not only at risk for progression to renal failure, but also at even greater risk for cardiovascular (CV) diseases. Extreme CV morbidity and mortality in dialysed patients is well-known, but recent studies stress a high CV risk even at early stage of CKD. Impaired renal function and/or albuminuria are now considered major CV risk factors. The reasons for this are not only a high prevalence of traditional CV risk factors in CKD patients or their insufficient treatment, but also the presence of non-traditional CV risk factors that could be specific for CKD. Some of these novel risk factors, particularly markers of inflammation, endothelial function, hemocoagulation and fibrinolysis are discussed, and their significance in the prediction of CV and renal outcome examined (Tab. 1, Ref 57).

Biomarkers↗
PubMedDate not supplied

Relationship between arterial hypertension and renal damage in chronic kidney disease: insights from ABPM.

BACKGROUND: To date, few studies have used ambulatory pressure monitoring (ABPM) in patients with chronic kidney disease (CKD) before the start of dialysis treatment. The aim of this study was therefore to ascertain the correlates of arterial hypertension assessed by ABPM in CKD patients at their first referral to a nephrologist. METHODS: We studied 244 (164 men; mean age 63 years) nondiabetic patients with CKD. Each patient had blood pres-sure (BP) measured by 24-hour ABPM, creatinine clearance (CrCl) estimated according to the Cockcroft-Gault formula, and Hgb concentration, serum lipids, iPTH, daily urinary protein (Uprot) and sodium (UNa) excretion assessed using routine methods. RESULTS: According to ABPM data analysis, 81 patients were normotensives, 78 were stable hypertensives, 26 had day-time hypertension and 59 had nocturnal hypertension. ANOVA showed both lower CrCl (p=0.0033), and higher Uprot (p<0.0001) in stable and nighttime hypertensives as compared with normotensives and daytime hypertensives. In the whole group each set of both systolic (SBP) and pulse pressure (PP) readings was directly associated with both age and Uprot (p<0.05), and inversely with both CrCl and Hgb (p<0.05). In multivariate analysis, however, Uprot emerged among modifiable risk factors, as the most significant predictor of both SBP and PP; the strength of this association was in the order nighttime PP > nighttime SBP > 24-hour PP > daytime PP > daytime SBP > 24-hour SBP. CONCLUSION: In CKD patients, proteinuria is the strongest correlate of arterial hypertension and particularly of increased nocturnal PP, possibly as an expression of vascular damage. On the basis of these results, ABPM appears to be the most reliable tool for detecting the associations between raised BP (particularly nighttime hypertension) and renal damage in CKD patients not yet on renal replacement therapy (RRT).

Aged↗
PubMed2006

Correlation of anemia, secondary hyperparathyroidism with left ventricular hypertrophy in Chronic Kidney Disease patients.

AIMS: To demonstrate the correlation of anemia and intact parathormone with left ventricular hypertrophy in a cohort of Chronic Kidney Disease (CKD) patients in a tertiary care centre. METHODS: A cross-sectional study was done over 2 years on 230 renal failure patients (160 males, 70 females), aged 15-75 years, who had elevated serum creatinine and reduced GFR. The patients were assessed based on clinical history and a number of laboratory parameters including serum creatinine, calcium, iPTH level, Hb, Hct, GFR and LVMI. Settings : Patients were seen as inpatients and outpatients in a tertiary care centre. RESULTS: In CKD stages I, II and III, 51% of the patients had anemia Hb<11gm/dl), 16%of the patients had elevated iPTH, 79% of male patients and 71% of female patients had LVH. In Stage IV CKD, 55% of the patients had anemia, 25% of the patients had elevated iPTH, 74% of male patients and 100% of female patients had LVH. In stage V CKD, 76% of the patients had anemia, 31% of the patients had elevated iPTH, 77% of male patients and 96% of female patients had LVH. In all five stages, 78% of male patients and 71% of female patients with elevated iPTH had LVH, 81% of male patients and 90% of female patients with anemia had LVH. Systemic hypertension was present in 69% of the patients. CONCLUSION: Anemia is widely prevalent in our cohort of CKD patients. Severity of anemia is correlated to LVH and secondary hyperparathyroidism in these patients.

Adolescent↗
PubMed2025

Deciphering Clonal Hematopoiesis of Indeterminate Potential: Methods, Mechanisms, and Implications for Kidney Diseases.

CKD afflicts over 10% of US adults, with its prevalence increasing sharply with age. Clonal hematopoiesis of indeterminate potential (CHIP) is a common, genetically heterogeneous blood cell disorder characterized by the age-related clonal expansion of hematopoietic cells driven by leukemogenic somatic mutations yet without hematologic malignancy or dysplasia. While CHIP is a strong risk factor of future hematologic malignancy (estimated at approximately 0.5% per year, compared with <0.1% for those without CHIP), it is also linked to two-fold higher cardiovascular disease in epidemiologic, cell-based, and murine studies. However, more recent work has implicated CHIP with kidney outcomes, such as CKD as well as AKI, independent of traditional risk factors. This review covers the observations and proposed hypotheses linking CHIP and kidney disease. The review also underscores the need for further research to elucidate the distinct pathways through which CHIP may contribute to CKD and its comorbidities, considering the heterogeneity within CKD stages and etiologies, as well as whether CHIP is a causal driver of kidney disease or a marker of aging and comorbidity. Finally, we discuss the potential of anti-inflammatory treatments to mitigate CHIP's adverse effects on kidney health, aiming to improve management strategies for patients with CHIP-associated kidney diseases.

Humans↗
PubMed2006

A comparison of pathomolecular markers of fibrosis and morphology in kidney from autopsies of African Americans and whites.

African Americans have an increased incidence of chronic kidney disease (CKD) due to hypertension and arteriosclerosis and increased death due to coronary artery disease, compared with whites. The pathogenesis of CKD involves the increased presence and activation of myofibroblasts and macrophages, promotion of tubulointerstitial fibrosis, and effects of tubulointerstitial cell mitosis and apoptosis. We hypothesized that increased risk of hypertensive vascular disease may be identified by renal pathomolecular markers that are associated with progressive CKD. Renal sections were available from 50 autopsies of 33 African Americans (55% males) and 17 whites (76% males) undergoing forensic autopsy for unexpected death. Sclerotic glomeruli, severity of cortical fibrosis, and renal arteriolosclerosis, total glomerular number (N (glom)), average glomerular volume (V (glom)), birth weights, and blood pressure were known. Presence and locality of markers for myofibroblasts (alpha-SMA), macrophages (CD68), collagen, pro-fibrotic transforming growth factor-beta1 were scored in renal autopsies, and tubulointerstitial apoptosis was recorded. The results demonstrated a strong positive correlation between age, cortical fibrosis and alpha-SMA (p<0.05), and between CD68 and hypertension and coronary artery disease (p<0.05). The findings confirm the role of myofibroblasts and macrophages in pathogenesis of human CKD. However, the markers showed no significant relationships to V (glom), N (glom), birth weight, or race.

Actins↗
PubMed2005

Treatment of secondary hyperparathyroidism of dialysis patients with calcimimetics as a valuable addition to established therapeutic means.

Currently available options for the treatment of hyperparathyroidism secondary to chronic renal failure do not allow the achievement of target values for plasma calcium, phosphorus, and parathyroid hormone in the majority of patients with chronic kidney disease (CKD) stage 5. This is particularly true for CKD patients who have been referred to nephrologists late in the course of their disease and in whom prevention has not been possible. The advent of a new class of therapeutic agents, the calcimimetics, will allow an easier control of already established parathyroid overfunction, as has been demonstrated in several phase II studies and one phase III study with cinacalcet. Future studies will show whether an earlier start of treatment in patients with CKD stage 2, 3, and 4 allows the prevention of secondary hyperparathyroidism. Since all available experience has been gathered in adult patients it is also necessary to test the efficacy and safety of the calcimimetics in children with CKD.

Animals↗
PubMed2006

Assessment and treatment of short stature in pediatric patients with chronic kidney disease: a consensus statement.

Growth failure is a clinically important issue in children with chronic kidney disease (CKD) and is associated with significant morbidity and mortality. Many factors contribute to impaired growth in these children, including abnormalities in the growth hormone (GH)-insulin-like growth factor-I (IGF-I) axis, malnutrition, acidosis, and renal bone disease. The management of growth failure in children with CKD is complicated by the presence of other disease-related complications requiring medical intervention. Despite evidence of GH efficacy and safety in this population, some practitioners and families have been reluctant to institute GH therapy, citing an unwillingness to comply with daily injections, reimbursement difficulties, or impending renal transplantation. Suboptimal attention to growth failure management may be further compounded by a lack of clinical guidelines for the appropriate assessment and treatment of growth failure in these children. This review of growth failure in children with CKD concludes with an algorithm developed by members of the consensus committee, outlining their recommendations for appropriate steps to improve growth and overall health outcomes in children with CKD.

Body Height↗
PubMed2006

Stature in children with chronic kidney disease: analysis of NAPRTCS database.

Despite recent advances in the management of children with chronic kidney disease (CKD), growth remains suboptimal. The purpose of this study was to evaluate factors associated with short stature in children with CKD. We evaluated the chronic renal failure registry of the North American Pediatric Renal Transplant Cooperative Studies (NAPRTCS) to determine the relations among primary diagnosis, age, race, residual renal function, acidosis, anemia, serum phosphorous, calcium, parathyroid hormone (PTH), albumin, and height at entry into the registry in children with CKD. A total of 5,615 patients were entered into the registry between January 1994 and January 2004. We found that older patients, those with glomerular filtration rate (GFR) >50 ml min(-1) 1.73 m(-2), black patients and patients with focal segmental glomerulosclerosis (FSGS) were at lower risk of being short at entry. Anemia (hematocrit below 33%) was an independent risk factor for short stature. Acidosis, serum phosphorous, calcium, albumin and PTH at registration were poor predictors of short stature. Age, race, primary diagnosis, and residual renal function were associated with short stature in children with CKD.

Adolescent↗
PubMed2006

Serum cystatin C and left ventricular diastolic dysfunction in children with chronic kidney disease.

Previous studies indicate that serum cystatin C predicts incident heart failure in older adults. Children with chronic kidney disease (CKD) develop left ventricular (LV) diastolic dysfunction, often the initial abnormality of cardiac function. We hypothesized that cystatin C might predict LV diastolic dysfunction in children with CKD. Fifty-seven subjects, aged 6-21 years, with stage 2-4 CKD underwent echocardiography. Diastole was assessed from transmitral Doppler [maximum early (E wave) and late (A wave) diastolic flow velocities (E/A ratio)] and from tissue Doppler [septal mitral annular peak velocities (E')]. LV filling pressures were determined, using a ratio of E/E'. Fourteen (25%) patients had low E' and 15 (26%) had high E/E'. Children with abnormal E' or E/E' had significantly higher cystatin C levels than children with normal indices (P<0.05). Neither serum creatinine nor measured glomerular filtration rate (GFR) significantly correlated with E' or E/E'. Stepwise multiple regression analysis showed that cystatin C (beta=-0.825, P=0.023) and left ventricular mass (LVM) index (beta=0.099, P=0.006) independently predicted E'; LVM index independently predicted E/E' (beta=0.0173, P=0.01). We conclude that, in contrast to measured GFR or serum creatinine level, elevated serum cystatin C might be associated with diastolic dysfunction in children with CKD.

Adolescent↗
PubMed2006

Clinical course of 735 children and adolescents with primary vesicoureteral reflux.

The purpose of this retrospective cohort study was to report the clinical course of children with primary vesicoureteral reflux (VUR). Between 1970 and 2004, 735 patients were diagnosed with VUR and were systematically followed in a single tertiary renal unit. Patients were followed up for a mean time of 76 months (6 months to 411 months). The events of interest were reflux resolution, renal damage, urinary tract infection (UTI), chronic kidney disease (CKD), and hypertension. Survival analysis was performed in order to evaluate reflux resolution and CKD. Renal damage was detected at admission in 319 patients (43.4%). Continuous low-dose antibiotic prophylaxis was administered to 624 patients (91.2%); 499 (73%) patients subsequently had no UTI or fewer than three episodes. The median time of persistence of reflux according to Kaplan-Meier analysis was 38 months for grade I/II [95% confidence interval (95% CI), 33-43], 98 months for grade III (95% CI, 78.5-105), and 156 months for grade IV/V (95% CI, 122-189). Twenty patients (3%) developed hypertension. It was estimated that the probability of CKD was 5% at 10 years after diagnosis of VUR; for children diagnosed after 1990 the probability of CKD was only 2%. Renal function impairment occurred in patients with severe bilateral reflux or in patients with contralateral renal hypoplasia. There has been an improvement of prognosis for patients diagnosed in the past 15 years.

Adolescent↗
PubMed2006

Serum neutrophil gelatinase-associated lipocalin as a marker of renal function in children with chronic kidney disease.

Very few biomarkers exist for monitoring chronic kidney disease (CKD). We have recently shown that serum neutrophil gelatinase-associated lipocalin (NGAL) represents a novel biomarker for early identification of acute kidney injury. In this study, we hypothesized that serum NGAL may also represent a biomarker for the quantitation of CKD. Forty-five children with CKD stages 2-4 were prospectively recruited for measurement of serum NGAL, serum cystatin C, glomerular filtration rate (GFR) by Ioversol clearance, and estimated GFR (eGFR) by Schwartz formula. Serum NGAL significantly correlated with cystatin C (r=0.74, P<0.000). Both NGAL and cystatin C significantly correlated with measured GFR (r=0.62, P<0.000; and r=0.71, P<0.000, respectively) as well as with eGFR (r=0.66, P<0.000 and r=0.59, P<0.000, respectively). At GFR levels of >or=30 ml/min per 1.73 m(2), serum NGAL, cystatin C, and eGFR were all significantly correlated with measured GFR. However, in subjects with lower GFRs (<30 ml/min per 1.73 m(2)), serum NGAL levels correlated best with measured GFR (r=0.62), followed by cystatin C (r=0.41). We conclude that (a) both serum NGAL and cystatin C may prove useful in the quantitation of CKD, and (b) by correlation analysis, NGAL outperforms cystatin C and eGFR at lower levels of measured GFR.

Acute-Phase Proteins↗
PubMed2006

The association of anemia and hypoalbuminemia with accelerated decline in GFR among adolescents with chronic kidney disease.

We sought to describe rates of kidney function decline and to identify modifiable risk factors for CKD progression in a multicenter prospective cohort study of adolescents with CKD aged 11 to 18 years seen semiannually for up to three years. Of the 23 subjects meeting inclusion criteria, the average estimated GFR was 51 +/- 27 ml/min/1.73 m(2) (0.85 +/- 0.45 ml/s/1.73 m(2)) at entry. The overall annualized decline in GFR was 5.6 ml/min/1.73 m(2) (0.093 ml/s/1.73 m(2)) per year (95% confidence interval [95% CI]: 1.9 to 9.3 [0.032 to 0.16]). The adjusted annualized decline in GFR was found to be accelerated in males, as well as among those over 15 years of age. The adjusted annualized decline in GFR was greater among those with either anemia (hematocrit below 36%), or hypoalbuminemia (albumin below 4 g/dl [40 g/L]). After adjustment, anemia was associated with an accelerated decline of 7.8 ml/min/1.73 m(2) (0.13 ml/s/1.73 m(2)) (95% CI: 3.3 to 12 [0.055 to 0.20]) and hypoalbuminemia was associated with an accelerated decline of 17 ml/min/1.73 m(2) (0.28 ml/s/1.73 m(2)) (95% CI: 11 to 22 [0.18 to 0.37]). Further study is needed to evaluate whether treatment of anemia or hypoalbuminemia, as outlined in current clinical care guidelines for CKD, may slow the progression of CKD in adolescents.

Adolescent↗
PubMed2006

Clinical predictors of neurocognitive deficits in children with chronic kidney disease.

The purpose of the study was to explore associations between neurocognitive function and chronic kidney disease (CKD)-related clinical characteristics. Twenty-nine children, ages 7 to 19 years, with an estimated creatinine clearance (eCrCl) of 4-89 ml/min per 1.73 m2 body surface area were enrolled. Intellectual function (IQ), memory, and attention were measured and expressed as age-based standard scores. Clinical data were obtained by physical examination, laboratory testing, parental questionnaires and medical chart review. Pearson correlations and standard Student's t-tests were used to identify significant (P < 0.05) relationships between targeted clinical variables and neurocognitive scores. Increased CKD severity correlated with lower IQ (P = 0.001) and memory function (P = 0.02). Memory function was lower in children with longer duration of disease (P = 0.03). Similarly, IQ scores were lowest when kidney disease had started at a younger age (P = 0.03) and with a greater percent of life with CKD (P = 0.04). Our findings provide preliminary evidence that increased disease severity, longer duration of disease, and younger age of onset of kidney disease potentially place children with CKD at increased risk of neurocognitive deficits. Additional investigation is required to better quantify these risk factors, particularly regarding how much variability is accounted for by these specific risk factors.

Adolescent↗
PubMed2007

How to define anemia in children with chronic kidney disease?

In a cross-sectional study, we compared the prevalence of anemia based on age- and gender-specific reference intervals for hemoglobin (Hgb) and hematocrit (Hct) with the Kidney Disease Outcomes Quality Initiative (KDOQI) anemia definition (Hgb < 110 g/L) in 351 children with chronic kidney disease (CKD) stages I-V. Cystatin C-based GFRs were 122 +/- 36 mL/min/1.73 m(2) in patients with stage I CKD (n=196), 76 +/- 8 mL/min/1.73 m(2) for stage II (n=104), 45 +/- 9 mL/min/1.73 m(2) for stage III (n=36), and 22 +/- 5 mL/min/1.73 m(2) in patients with stage IV+V CKD (n=15). Fifty-nine patients received iron therapy and 32 patients were treated with Darbepoetin. For Hgb, a total of 90 patients fit the age and gender derived criteria, compared to only 54 patients identified by the KDOQI guidelines (p=0.0010). Similarly, for Hct, a total of 78 patients fit the age and gender derived criteria, which was a significantly higher proportion than the 56 identified by the KDOQI guidelines (r=0.22, p=0.0435). There was a significant correlation between the GFR and both the Hgb Z-score (p=0.0068) and the Hct Z-score (p=0.0128). There was poor agreement between conventional and KDOQI definitions of anemia in children with CKD.

Adolescent↗
PubMed2003

Interim evidence of the renoprotective effect of the angiotensin II receptor antagonist losartan versus the calcium channel blocker amlodipine in patients with chronic kidney disease and hypertension: a report of the Japanese Losartan Therapy Intended for Global Renal Protection in Hypertensive Patients (JLIGHT) Study.

BACKGROUND: Insufficiency of renal function and high blood pressure influence each other and eventually result in life-threatening endstage renal disease. It has been proposed that proteinuria per se is a determinant of the progression of chronic kidney disease (CKD). The therapeutic strategy for patients with proteinuric CKD and hypertension should therefore be targeted with a view not merely toward blood pressure reduction but also toward renoprotection. METHODS: We examined the effect of the angiotensin (AT)1 receptor antagonist losartan and the calcium channel blocker amlodipine, throughout a period of 12 months, on reduction of blood pressure and renoprotection. This was done by assessing amounts of urinary protein excretion, serum creatinine (SCr), and creatinine clearance (CCr) in patients with hypertension (systolic blood pressure [SBP] > or = 140 mmHg or diastolic blood pressure [DBP] > or = 90 mmHg) and CKD (male, body weight [BW] > or = 60 kg: 1.5 < or = SCr < 3.0 mg/dl; female or male BW < 60 kg: 1.3 < or = SCr < 3.0 mg/dl), manifesting proteinuria of 0.5 g or more/day. Losartan was administered once daily at doses of 25 to 100 mg/day, and amlodipine was given once daily at 2.5 to 5 mg/day. No antihypertensive combination therapy was allowed during the first 3-month period. RESULTS: A 3-month interim analysis revealed that, despite there being no difference in blood pressure between the two groups, there was a significant reduction in 24-h urinary protein excretion in the losartan group ( n = 43), but there was no change in the amlodipine group ( n = 43). Analysis of stratified subgroups with proteinuria of 2 g or more/day and less than 2 g/day showed that losartan lowered proteinuria by approximately 24% in both subgroups, while amlodipine lowered proteinuria by 10%, but only in the subgroup of less than 2 g/day (NS). SCr and CCr did not change throughout the period of 3 months in either group. No severe or fatal adverse event was experienced in either group during the study period. CONCLUSIONS: Losartan appeared to be efficacious for renoprotection in patients with proteinuric CKD and hypertension, with the mechanism being independent of its antihypertensive action.

Adult↗
PubMed2005

Study design and methods for a clinical trial of an oral carbonaceous adsorbent used to prevent the progression of chronic kidney disease (CAP-KD).

BACKGROUND: The number of patients with chronic kidney disease (CKD) in Japan is currently rising. Therefore, measures to control the progression of CKD from a predialysis condition to endstage renal failure are urgently required. We are conducting a clinical trial to investigate the efficacy of an oral carbonaceous adsorbent (Kremezin) in patients at the predialysis stage of progressive chronic kidney disease (the Carbonaceous oral Adsorbent's effectiveness on Progression of chronic Kidney Disease [CAP-KD] trial). METHODS: A multidisciplinary treatment regimen, consisting of antihypertensive therapy (using an angiotensin-converting-enzyme inhibitor and/or an angiotensin II receptor blocker) and a low-protein diet is conventionally used to treat patients with kidney disease. To assess the efficacy of Kremezin in preventing the progression of CKD, we compare two groups of patients, receiving either conventional treatment alone or such treatment paired with Kremezin. The CAP-KD trial is a prospective, multicenter, randomized, open-label, two-arm, parallel-group comparison clinical trial and will be conducted as a researcher-directed study. The primary endpoint of this study is the time to the first event of a composite endpoint, comprising the following: (1) a doubling of serum creatinine (sCr); (2) an increase in sCr level to 6.0 mg/dl or more; (3) endstage renal disease (defined as that requiring dialysis or renal transplantation); and (4) death. Secondary endpoints are as follows: (1) variation in urinary protein; (2) changes in creatinine clearance rate; (3) changes in health-related quality of life; and (4) adverse events. The total number of patients (putative) in this trial will be 450, with 225 patients in each group. Enrollment will take place over 2 years, with a 1-year follow-up period. RESULTS: As this is an ongoing trial, results are not yet available. CONCLUSIONS: We believe that the CAP-KD trial is a well-designed study that will provide internationally relevant evidence concerning the outcomes of treatment in Japanese patients with CKD.

Adult↗
PubMed2005

Anemia and cardiovascular disease, hospitalization, end stage renal disease, and death in older patients with chronic kidney disease.

BACKGROUND: Large observational studies examining the association between anemia and "hard" clinical outcomes are rare in patients with chronic kidney disease (CKD). METHODS: We used the General Medicare 5% Denominator Files to identify patients aged 67 years or more with CKD on December 31, 1999. Outcomes in the ensuing 2 years were compared in patients with and those without anemia (entry period, 1998-1999; follow-up period, 2000-2001). RESULTS: Of 41,522 CKD patients identified, 49.0% had claims of anemia diagnosis. The factors associated (p< 0.0001) with anemia included older age, female gender, black race, and all 10 comorbid conditions studied; adjusted odds ratios (ORs) exceeded 1.5 for age 80 years old or older (OR, 1.54 compared to <70 years), for black race (OR, 1.52), and for co-existing diagnoses of congestive heart failure (OR, 1.64), gastrointestinal bleeding (OR, 3.65), and liver disease (OR, 2.16). During the follow-up period, outcome event rates (expressed per 1000 patient-years) were as follows: renal replacement therapy, 23.5; death, 186.4; congestive heart failure, 390.0; atherosclerotic vascular disease, 410.5; and first hospitalization, 552.6. Using proportional hazards modeling, the presence of anemia was associated (p < 0.0001) with the following adjusted hazards ratios: atherosclerotic vascular disease, 1.09; congestive heart failure, 1.14; renal replacement therapy, 2.61 and death, 1.40. CONCLUSION: A diagnosis of anemia is present in nearly half of all patients with CKD, aged 67 years or more, a group at very high risk of cardiovascular disease, hospitalization, end-stage renal disease, and death. Anemia is associated with each of these events.

Aged↗