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At least 595 records · Page 33Linked to original sources
PubMed2005

Detection of occult renovascular disease in unexplained chronic kidney disease.

Atherosclerotic renal artery stenosis (RAS) is a recognized cause of renal impairment. RAS is often overlooked in unexplained chronic kidney disease (CKD). A retrospective analysis of renal angiograms was performed to determine the prevalence of occult renovascular disease in 64 (M:F, 46:18; ages 21-81 years [median 60 years]) patients with unexplained CKD. Twelve patients had diabetes mellitus (type II: 11) and 43 were smokers. Median serum creatinine was 5.2 mg/dl (range 1.5-10.6 mg/dl). Group A included patients with unexplained CKD and with no risk factors for RAS and Group B had patients with increased risk for RAS. A narrowing of the renal vessel, main artery or branch, by >50% on renal arteriography was used as diagnostic criteria for RAS. 31/64 patients had positive angiographic findings. Thirteen patients had unilateral RAS, 9 had bilateral RAS, 5 had unilateral stenosis with occlusion on the opposite side, 3 had unilateral occlusion and 1 had a solitary kidney with RAS. 19/34 (54%) in Group A and 12/30 (40%) in Group B had a positive renal angiogram. In 10 patients with a rise in serum creatinine on recent introduction of ACE inhibition, 2 had evidence of RAS on renal arteriography. Eleven patients underwent angioplasty and 2 reconstructive surgeries. In 4 patients, blood pressure control improved and anti-hypertensive drug requirements were reduced, whilst renal replacement therapy was postponed in 4, by 2-24 months. In 18 patients, the lesions were not amenable to angioplasty or reconstructive surgery. Four patients did not benefit in any form with intervention. Occult atheromatous renal vascular disease is a common, not readily predictable and potentially correctable etiology of unexplained CKD.

Adult↗
PubMed2006

Anemia, chronic renal disease and congestive heart failure--the cardio renal anemia syndrome: the need for cooperation between cardiologists and nephrologists.

Many patients with congestive heart failure (CHF) fail to respond to maximal CHF therapy and progress to end stage CHF with many hospitalizations, poor quality of life (QoL), progressive chronic kidney disease (CKD) which can lead to end stage kidney disease (ESKD), or die of cardiovascular complications within a short time. One factor that has generally been ignored in many of these people is the fact that they are often anemic. The anemia in CHF is due mainly to the frequently-associated CKD but also to the inhibitory effects of cytokines on erythropoietin production and on bone marrow activity, as well as to their interference with iron absorption from the gut and their inhibiting effect on the release of iron from iron stores. Anemia itself may further worsen cardiac and renal function and make the patients resistant to standard CHF therapy. Indeed anemia in CHF has been associated with increased severity of CHF, increased hospitalization, worse cardiac function and functional class, the need for higher doses of diuretics, progressive worsening of renal function and reduced QoL. In both controlled and uncontrolled studies of CHF, the correction of the anemia with erythropoietin (EPO) and oral or intravenous (IV) iron has been associated with improvement in many cardiac and renal parameters and an increased QoL. EPO itself may also play a direct role in improving the heart unrelated to the improvement of the anemia--by reducing apoptosis of cardiac and endothelial cells, increasing the number of endothelial progenitor cells, and improving endothelial cell function and neovascularization of the heart. Anemia may also play a role in the worsening of acute myocardial infarction and chronic coronary heart disease (CHD) and in the cardiovascular complications of renal transplantation. Anemia, CHF and CKD interact as a vicious circle so as to cause or worsen each other- the so-called cardio renal anemia syndrome. Only adequate treatment of all three conditions can prevent the CHF and CKD from progressing.

Anemia↗
PubMed2006

Hypertension and kidney disease: a deadly connection.

Kidney disease may be the cause or a consequence of hypertension. Hypertension affects 25% of the adult population in the United States. Similarly, chronic kidney disease (CKD) and end-stage renal disease (ESRD) have been steadily increasing in incidence because of the increasing age of the US population and rise in the incidence of risk factors, including hypertension. Substantial evidence supports the notion that elevated blood pressure is the most significant risk factor for the development of CKD. Microalbuminuria has been shown to be the early marker of hypertensive renal disease. Furthermore, therapy to reduce microalbuminuria was associated with delay in the progression of renal disease. Black Americans are at higher risk for developing hypertensive nephrosclerosis than whites. Hypertension is a major risk factor for cardiovascular events in patients with CKD and ESRD and those who have undergone renal transplantation. Studies have documented that elevated serum creatinine and CKD are risk factors for a cardiovascular event. Tight blood pressure control has been shown to reduce microalbuminuria and proteinuria and to delay progression of renal disease. Tailoring the choice of antihypertensive medication to the clinical setting to achieve a blood pressure goal is critical in reducing complications from this deadly connection.

Black or African American↗
PubMed2006

Cardiometabolic syndrome and chronic kidney disease.

Chronic kidney disease (CKD) is increasingly recognized as a major risk factor for end-stage renal disease (ESRD), cardiovascular (CV) disease, and CV-related premature death. More than 8 million people in the United States have CKD; therefore, preventive stratiegies should be directed at identifying risk factors for this condition. There is growing evidence implicating the cardiometabolic syndrome, a clustering of CV risk factors that include obesity, insulin resistance, compensatory hyperinsulinemia, dysglycemia, atherogenic dyslipidemia, and hypertension. Factors mediating this relationship include increased glomerular filtration, increased vascular permeability, oxidative and endoplasmic reticulum stress, activation of the renin-angiotensin system, and inappropriate secretion of growth factors. The consequences are microalbuminuria, a marker of inflammation and endothelial dysfunction, renal vascular proliferation, extracellular matrix expansion, and CKD. Prevention of CKD should be directed at controlling all components of the cardiometabolic syndrome, with the ultimate goal of reducing the burden imposed by ESRD.

Albuminuria↗
PubMed2006

Anemia and cardiovascular disease in diabetic nephropathy.

Cardiovascular disease (CVD) is the major cause of morbidity and mortality in people with diabetes and in those with chronic kidney disease (CKD). Diabetes, occurring in epidemic proportions in the United States and worldwide, is also the leading cause of CKD and kidney failure. Identification of modifiable risk factors for CVD in patients with diabetes and CKD is thus of paramount importance. Anemia is increasingly recognized as a potential CVD risk factor in patients with diabetic nephropathy, in whom it is generally more severe and occurs at an earlier stage of CKD. In this review, we discuss the epidemiologic evidence, pathophysiologic mechanisms, and the current research findings, highlighting the role of anemia as a potential modifiable risk factor for CVD in patients with diabetic nephropathy, a particularly vulnerable population for CVD.

Anemia↗
PubMed2005

The African American Study of Kidney Disease: do these results indicate that 140/90 mm hg is good enough?

Current national guidelines recommend aggressive lowering of blood pressure (< 130/80 mm Hg) in patients with chronic kidney disease (CKD). In this paper, we summarize recent clinical trial data evaluating the effect of lower blood pressure goals on renal outcomes. The epidemiologic data relating blood pressure to progression of kidney disease, the Modification of Diet in Renal Disease (MDRD) study (in patients with > 1 g proteinuria/d), and meta-analyses of angiotensin-converting enzyme (ACE) inhibitor clinical trials all support lower blood pressure goals in CKD patients, particularly those with proteinuria. The African American Study of Kidney Disease and Hypertension (AASK) supports lower blood pressure goals in terms of reduction of proteinuria, but demonstrates no additional benefit for clinical renal outcomes. Similarly, the second Ramipril Efficacy in Nephropathy study (REIN-2) shows that in patients with proteinuric nondiabetic renal disease who are receiving ACE inhibitors, a lower than usual blood pressure goal does not improve renal outcomes. However, there are limited clinical trial data evaluating the effects of low blood pressure on the increased cardiovascular risk seen in patients with CKD. Pending further clinical studies, current recommendations to target tight blood pressure control (< 130/80 mm Hg) in patients with CKD appear reasonable.

Black or African American↗
PubMed2006

Management of hypertension in chronic kidney disease.

Optimal blood pressure control (<130/80 mm Hg) in patients with chronic kidney disease (CKD), despite being the main objective of conservative therapy, is rarely achieved in clinical practice. A major area of improvement is the correction of the extracellular volume expansion. This goal can be reached by means of dietary salt restriction (100 mEq/d of NaCl). If this intervention fails, hypertension can be treated by thiazide diuretics in patients with mild CKD, whereas loop diuretics at adequate doses are indicated in patients with more advanced CKD. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are more effective than other drugs in slowing progression of proteinuric diabetic and nondiabetic CKD. However, the control rates of blood pressure are usually inadequate with antihypertensive therapy including only these drugs; therefore, addition of other classes of antihypertensive drugs is often required.

Algorithms↗
PubMed2005

Treatment of osteoporosis in chronic kidney disease and end-stage renal disease.

As glomerular filtration rate (GFR) declines from age-related bone loss or disease that specifically induces a decline in GFR, there are a number of metabolic bone conditions that may accompany the decline in GFR. These metabolic bone conditions span a spectrum from mild-to-severe secondary hyperparathyroidism in early stages of chronic kidney disease (CKD) to the development of additional heterogeneous forms of bone diseases each with its distinctly quantitative bone histomorphometric characteristics. Osteoporosis can also develop in patients with CKD and ESRD for many reasons beyond age-related bone loss and postmenopausal bone loss. The diagnosis of osteoporosis in patients with severe CKD or end-stage renal disease (ESRD) is not as easy to do as it is in patients with postmenopausal osteoporosis (PMO)--neither fragility fractures nor The World Health Organization bone mineral density criteria can be used to diagnose osteoporosis in this population since all forms of renal bone disease may fracture or have low "T scores". The diagnosis of osteoporosis in patients with CKD/ESRD must be done by first the exclusion of the other forms of renal osteodystrophy, by biochemical profiling or by double tetracycline-labeled bone biopsy; and the finding of low trabecular bone volume. In such patients, preliminary data would suggest that oral bisphosphonates seem to be safe and effective down to GFR levels of 15 mL/min. In patients with stage 5 CKD who are fracturing because of osteoporosis or who are on chronic glucocorticoids, reducing the oral bisphosphonate dosage to half of its usual prescribed dosing for PMO seems reasonable from known bisphosphonate pharmacokinetics, though we do need better scientific data to fully understand bisphosphonate usage in this population.

Bone Density↗
PubMed2005

Rationale--Trial to Reduce Cardiovascular Events with Aranesp Therapy (TREAT): evolving the management of cardiovascular risk in patients with chronic kidney disease.

BACKGROUND: Patients with chronic kidney disease (CKD) have a high burden of mortality and cardiovascular morbidity. Additional strategies to modulate cardiovascular risk in this population are needed. Data suggest that anemia is a potent and potentially modifiable risk factor for cardiovascular disease in patients with CKD, but these data remain unsubstantiated by any randomized controlled trial (RCT). Furthermore, the clinical practice guidelines for anemia management in patients with CKD are based on limited data. The need for new RCTs to address critical knowledge deficits, particularly with regard to the impact of anemia therapy on cardiovascular disease and survival, is recognized within the guidelines and independent comprehensive reviews of the existing published trial data. STUDY DESIGN: The Trial to Reduce Cardiovascular Events with Aranesp (Amgen Inc, Thousand Oaks, Calif) (darbepoetin alfa) Therapy (TREAT) is a 4000-patient, multicenter, double-blind RCT, designed to determine the impact of anemia therapy with darbepoetin alfa on mortality and nonfatal cardiovascular events in patients with CKD and type 2 diabetes mellitus. Subjects will be randomized in a 1:1 manner to either darbepoetin alfa therapy to a target hemoglobin (Hb) of 13 g/dL or control, consisting of placebo for Hb > or =9 g/dL or darbepoetin alfa for Hb <9 g/dL until Hb is again Hb > or =9 g/dL. TREAT is event-driven and has a composite primary end point comprising time to mortality and nonfatal cardiovascular events, including myocardial infarction, myocardial ischemia, stroke, and heart failure. TREAT will provide data that are critical to evolution of the management of cardiovascular risk in this high-risk population.

Anemia↗
PubMed2006

Risk stratification of patients with chronic kidney disease: results of screening strategies incorporating clinical risk scoring and dobutamine stress echocardiography.

BACKGROUND: Cardiac disease is the principal cause of death in patients with chronic kidney disease (CKD). Ischemia at dobutamine stress echocardiography (DSE) is associated with adverse events in these patients. We sought the efficacy of combining clinical risk evaluation with DSE. METHODS: We allocated 244 patients with CKD (mean age 54 years, 140 men, 169 dialysis-dependent at baseline) into low- and high-risk groups based on two disease-specific scores and the Framingham risk model. All underwent DSE and were further stratified according to DSE results. Patients were followed over 20 +/- 14 months for events (death, myocardial infarction, acute coronary syndrome). RESULTS: There were 49 deaths and 32 cardiac events. Using the different clinical scores, allocation of high risk varied from 34% to 79% of patients, and 39% to 50% of high-risk patients had an abnormal DSE. In the high-risk groups, depending on the clinical score chosen, 25% to 44% with an abnormal DSE had a cardiac event, compared with 8% to 22% with a normal DSE. Cardiac events occurred in 2.0%, 3.1%, and 9.7% of the low-risk patients, using the two disease-specific and Framingham scores, respectively, and DSE results did not add to risk evaluation in this subgroup. Independent DSE predictors of cardiac events were a lower resting diastolic blood pressure, angina during the test, and the combination of ischemia with resting left ventricular dysfunction. CONCLUSION: In CKD patients, high-risk findings by DSE can predict outcome. A stepwise strategy of combining clinical risk scores with DSE for CAD screening in CKD reduces the number of tests required and identifies a high-risk subgroup among whom DSE results more effectively stratify high and low risk.

Adult↗
PubMed2003

Hospitalization during advancing chronic kidney disease.

BACKGROUND: The care of patients with end-stage renal disease (ESRD) is associated with substantial costs to society, much of which is accounted for by a high rate of hospitalization. However, the influence of declining kidney function on hospitalization as ESRD approaches is not well understood. METHODS: We performed a retrospective cohort study of national data to evaluate the frequency of hospitalizations among patients with chronic kidney disease (CKD) who reached ESRD and had at least 2 years of Medicare eligibility before initiation of dialysis therapy. The study period for each patient extended from 2 years before to 6 months after the initiation of dialysis therapy. RESULTS: The study cohort was composed of 109,321 patients with a mean age of 75 years, all of whom initiated long-term dialysis therapy between 1995 and 1998. Mean hospitalization rate was 134 hospitalizations/1,000 patient-months at risk (PMAR). Hospitalization rates gradually increased as ESRD approached, peaking in the 3 months immediately after the initiation of dialysis therapy at 487 hospitalizations/1,000 PMAR. Cause-specific hospitalization rates mirrored this trend and were greatest for placement of vascular access and diagnoses related to cardiovascular (CVD) and infectious disease. CONCLUSION: Hospitalizations during CKD become more frequent with the approach of ESRD. The majority of these hospitalizations, both before and after the initiation of dialysis therapy, are caused by comorbidity related to CKD. These hospitalizations may be favorably impacted on by heightened attention to the prevention and management of CVD and timely placement of vascular access during CKD.

Aged↗
PubMed2006

N-terminal pro-B-type natriuretic peptide and B-type natriuretic peptide for identifying coronary artery disease and left ventricular hypertrophy in ambulatory chronic kidney disease patients.

Elevated natriuretic peptide levels are common in patients with chronic kidney disease (CKD), as is the presence of coronary artery disease (CAD) and left ventricular hypertrophy (LVH). It was hypothesized that N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) and B-type natriuretic peptide (BNP) levels could identify CAD and LVH in asymptomatic patients with CKD. Clinical, laboratory, and echocardiographic data were collected prospectively in 54 ambulatory patients with CKD not requiring dialysis. CAD was defined by previous myocardial infarction or coronary revascularization. The median age was 70 years (interquartile range [IQR] 57 to 76). Fourteen patients (26%) had CAD, and 30 (56%) had LVH. Median NT-pro-BNP was 724 pg/ml (IQR 168 to 2,950), median BNP was 137 pg/ml (IQR 31 to 391), and the median glomerular filtration rate (GFR) was 31 ml/min/1.73 m2 (IQR 21 to 42). A strong correlation was found between NT-pro-BNP and BNP levels (R = 0.74, p <0.0001), but only moderate correlations were found between NT-pro-BNP and GFR (R = -0.45, p = 0.0006) and between BNP and GFR (R = -0.38, p = 0.005). There was no trend of an increase in the prevalence of LVH or CAD with decreasing GFR. However, across progressive NT-pro-BNP and BNP quartiles, the prevalences of LVH and CAD increased significantly. Receiver-operating characteristic curves showed that these 2 markers are similar and significant predictors for indicating LVH (area under the curve [AUC] 0.72, p = 0.005 for NT-pro-BNP; AUC 0.72, p = 0.007 for BNP) and CAD (AUC 0.80, p = 0.001 for NT-pro-BNP; AUC 0.82, p = 0.0004 for BNP; p = 0.45 for NT-pro-BNP vs BNP). In conclusion, NT-pro-BNP and BNP levels are significant and equivalent indicators of CAD and LVH in asymptomatic patients with CKD.

Aged↗
PubMed2006

Adiponectin and renal function, and implication as a risk of cardiovascular disease.

The relation among adiponectin, renal function, and incident cardiovascular disease (CVD) in patients with different degrees of renal dysfunction was investigated. In total, 150 subjects were included in this study and followed prospectively for a mean of 32 months. At baseline, median adiponectin levels for chronic kidney disease (CKD) stages 1, 2, 3, 4 and 5, as estimated by creatinine clearance (> or =90, 60 to 90, 30 to 60, <30 ml/min), were 3.06, 4.04, 6.43, and 11.9 microg/ml, respectively (p for trend <0.01), and a significant association between adiponectin and CKD stages was also confirmed in multivariate regression analysis (F = 6.2, p <0.001). During follow-up, 31 subjects developed CVD, including myocardial infarction, angina pectoris, stroke, and transient ischemic attack. Gender-specific median values of adiponectin were used to separate the higher group from the lower group, and the Kaplan-Meier curve showed a significantly lower event-free survival rate in the lower adiponectin group (<4.39 microg/ml in men, <6.84 microg/ml in women, chi-square 4.88, p <0.03). The risk factor-adjusted Cox regression showed that an increase in adiponectin per 1 microg/ml was associated with a decrease in the risk of CVD to 0.86 (95% confidence interval 0.75 to 0.96, p = 0.004). In the subgroup with previous ischemic heart disease (IHD; n = 65), a significantly lower event-free survival rate of IHD was also observed in the lower adiponectin group (<4.45 microg/ml in men, <4.49 microg/ml in women, chi-square 3.96, p <0.05). The relative distribution of adiponectin isoforms was examined in patients with severe CKD, and the percentage of the high-molecular-weight form in patients with IHD during follow-up (n = 3) was significantly smaller than that in those without IHD (n = 4, p <0.02). In conclusion, renal function is a significant regulator of adiponectin when categorized by CKD stage, whereas hypoadiponectinemia is a predictor of CVD, including recurrent IHD.

Adiponectin↗
PubMed2005

Protecting renal function in the hypertensive patient: clinical guidelines.

Both the incidence and prevalence of chronic kidney disease (CKD) are increasing in the United States and worldwide. Patients with both diabetes and hypertension have a dramatically increased risk of cardiovascular and renal events, particularly if both conditions are not effectively controlled. Failure to achieve the goals for blood glucose, blood pressure (BP), and lipids is associated with high morbidity from cardiovascular and renal events as well as the high costs of treating these morbid events. There is increasing evidence that cardiovascular events, renal failure, and premature death can be prevented or delayed by earlier identification and treatment of CKD, as well as by taking measures to prevent its onset. A large subgroup of hypertensive patients may be at increased risk for developing CKD and should be targeted for appropriate monitoring and treatment. Not all antihypertensive regimens are equally effective at preserving renal function. Clinical trials indicate that the primary clinical goal in the treatment of patients with CKD is to lower BP to the recommended goal as well as to reduce albuminuria and proteinuria to the lowest levels possible. This is achieved optimally by using agents that block the renin-angiotensin system in concert with other agents that reduce proteinuria and BP.

Albuminuria↗
PubMed2006

Serum NTX is a practical marker for assessing antiresorptive therapy for glucocorticoid treated patients with chronic kidney disease.

INTRODUCTION: In chronic kidney disease (CKD) patients, serum concentration of type I collagen N-telopeptide (S-NTX) increases as renal function declines because of perturbed bone metabolism by renal dysfunction itself and impaired urinary excretion of NTX. Glucocorticoid (GC), which is often used for the treatment of kidney disease, may enhance bone resorption. We studied the bone resorption state in GC-treated CKD patients and the effects of bisphosphonate on S-NTX. METHODS: We measured S-NTX and creatinine clearance (Ccr) in 48 non-diabetic patients with declining renal function who had never received GC, vitamin D, calcium or bisphosphonate (reference group). Bone markers including S-NTX and BSAP (bone specific alkaline-phosphatase) in 144 patients receiving GC (prednisone equivalent of > or =2.5 mg/day) for more than 6 months (GC-treated group) were measured. We compared the GC-treated group to the reference group in a cross-sectional study. In a longitudinal study, we further followed 55 patients from the GC-treated group, whose Ccr was more than 60 mL/min (CKD stage 1 or 2) for 1 year after 2.5 mg/day of risedronate was commenced. RESULTS: In the reference group, S-NTX was correlated with Ccr (S-NTX = 456.6/Ccr + 4.5, r = 0.797, P < 0.0001). S-NTX values in the GC-treated group were higher than those found in the reference group at any Ccr. We defined the resorption index (RI) as a ratio of measured S-NTX to estimated NTX given by the correlation curve. Whereas BSAP did not change significantly, S-NTX decreased significantly by risedronate treatment. RI decreased from 1.59 (baseline) to 1.54, 1.25 (P < 0.01, versus baseline) and 1.23 (P < 0.01) at 1, 3 and 6 months after the start of therapy, respectively, which means that S-NTX values approached the correlation curve. Percent changes of S-NTX at 3 months were larger in patients with higher pretreatment S-NTX. CONCLUSION: Higher S-NTX in the GC-treated group suggests that bone resorption is enhanced by GC. In CKD patients with mild renal dysfunction, S-NTX is a practical and useful marker for monitoring bone resorption during GC treatment.

Adolescent↗
PubMed2006

Dosing patterns and costs of erythropoietic agents in patients with chronic kidney disease not on dialysis in managed care organizations.

BACKGROUND: Epoetin alfa (EPO) and darbepoetin alfa (DARB) are erythropoietic agents indicated in the United States for the treatment of anemia in chronic kidney disease (CKD). OBJECTIVE: This study investigated dosing patterns and costs associated with the use of erythropoietic-stimulating therapy (EST) in patients with CKD not on dialysis who were newly starting EPO or DARB therapy in managed care organizations. METHODS: This was a retrospective analysis of medical claims data from >30 health plans for the period from July 2002 to February 2005. Patients were included if they were aged > or =18 years, had > or =1 claim for CKD within 90 days before the initiation of treatment, had newly started therapy with EPO or DARB, and had received > or =2 doses of treatment. If a patient was undergoing renal dialysis, data were censored 30 days before the first date of dialysis. Patients with a diagnosis of cancer or who had undergone chemotherapy were excluded from the analysis. The mean dosing interval was determined for both groups. Mean weekly doses and costs (using 2005 wholesale acquisition costs), weighted by the treatment duration, were calculated. The frequency of outpatient nephrologist visits was described and included in cost considerations. RESULTS: The study population consisted of 595 patients who received EPO and 260 who received DARB. The EPO group was significantly older than the DARB group (mean age, 63.5 vs 61.2 years, respectively; P = 0.020). The proportion of women was similar between the 2 groups (51.6% and 50.4%). Use of extended dosing (> or =q2wk) was common in both groups (63.2% and 90.8%). The weighted mean weekly dose was 11,536 U for EPO and 42.5 mug for DARB. The mean number of outpatient nephrologist visits during treatment was similar between the 2 groups (3.9 and 3.5). Mean weekly costs (EST drug cost plus cost of nephrologist visits) were significantly lower for EPO compared with DARB (159 dollars vs 205 dollars; P < 0.001). CONCLUSIONS: The majority of these CKD patients newly started on EST in managed care organizations received extended dosing regimens (> or =q2wk) of EPO or DARB. EPO treatment was associated with significantly lower mean weekly costs compared with DARB. The number of outpatient nephrology visits did not differ significantly between groups.

Anemia↗
PubMed2004

Impact of mild or moderate chronic kidney disease on the frequency of restenosis: results from the PRESTO trial.

OBJECTIVES: The goal of this study was to determine if restenosis is increased in mild and moderate chronic kidney disease (CKD) patients after percutaneous coronary intervention (PCI). BACKGROUND: Mortality is increased in CKD after PCI. Restenosis may contribute to increased late mortality. METHODS: We analyzed 11,187 patients with a creatinine <1.8 mg/dl from the Prevention of REStenosis with Tranilast and its Outcomes (PRESTO) trial, grouped by estimated creatinine clearance (CrCl) (<60, 60 to 89, >89 ml/min). The Cox proportional hazards models investigated the association between CrCl group and death, myocardial infarction, and target vessel revascularization (TVR). Generalized estimating equation regression models determined the association between CrCl group and lesion-specific restenosis. RESULTS: At 30 days, there was no difference in myocardial infarction, death, or TVR between the CrCl groups. At nine months, mortality was higher in the lowest CrCl group (2.2%, 1.2%, 0.8%; p < 0.001), which was no longer significant after adjusting for confounding variables. Myocardial infarction and TVR were not different between the groups. In patients undergoing protocol follow-up angiography, restenosis (>/=50%) was not increased with CKD (32%, 32%, 37%; p = 0.02). CONCLUSIONS: Mortality nine months after PCI is mildly increased in mild or moderate CKD patients. However, restenosis is not and does not account for the increased mortality.

Aged↗
PubMed2006

Epidemiology of chronic kidney disease and anemia.

Anemia is a common comorbidity of chronic kidney disease (CKD). As the diseased kidney loses its ability to produce the erythropoietin essential to the production of hemoglobin, anemia ensues. The age-related rise in CKD makes anemia in CKD a problem of increasing prevalence among residents of long-term care facilities. CKD refers to the entire continuum of renal disease that progresses from mildly impaired kidney function (stage 1, glomerular filtration rate [GFR] > or =90 mL/min/1.73 m(2)) to significant deterioration, requiring dialysis or kidney transplant in what is categorized as stage 5 (GFR <15 mL/min/1.73 m(2)). The definition of anemia is controversial. The WHO defines anemia as hemoglobin <13 g/dL for men and <12 g/dL for women. The National Kidney Foundation's Kidney Disease Outcomes Quality Initiative, which is the criteria used for Medicare reimbursement, defines anemia in adult men and postmenopausal women as hemoglobin <12 g/dL, or <11 g/dL in a premenopausal woman.

Age Distribution↗