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PubMed2005

Low rates of testing and diagnostic codes usage in a commercial clinical laboratory: evidence for lack of physician awareness of chronic kidney disease.

Improving outcomes for chronic kidney disease (CKD) requires early identification and recognition by physicians. There are few data on rates of testing or use of diagnostic codes for CKD. A cross-sectional analysis was performed of patients who were older than 40 yr and had one or more laboratory tests between April 1, 2002, and March 31, 2003, at a Laboratory Corporation of America regional laboratory. Objectives were to determine the frequency of testing for serum creatinine; prevalence of CKD, defined as estimated GFR <60 ml/min per 1.73 m2; and sensitivity of diagnostic codes for CKD for patients with and without risk factors for CKD and with or without cardiovascular disease (CVD). Of the 277,111 patients, 19% had serum creatinine measured, compared with 33 and 71% who had measurements of serum glucose and lipids, respectively. Patients with hypertension, diabetes, and age >60 yr were more likely to be tested for serum creatinine with odds ratio (OR; 95% confidence interval) of 2.09 (2.05 to 2.14), 1.22 (1.19 to 1.25), and 1.24 (1.22 to 1.27) respectively. Among patients tested, 30% had CKD. Sensitivity and specificity of kidney disease diagnostic codes compared with CKD defined by estimated GFR <60 ml/min per 1.73 m2 were 11 and 96%, respectively. In patients with hypertension, diabetes, age >60 years, and CVD, rates of testing and sensitivity of diagnostic codes were 53 and 14%, respectively. Low rates of testing for serum creatinine and insensitivity of diagnostic codes for CKD, even in high-risk patients, suggests inadequate physician awareness of CKD and limited utility of administrative databases for identification of patients with CKD.

Adult↗

PubMed2003

Outcomes of anaemia management in renal insufficiency and cardiac disease.

Cardiac disease represents a major cause of morbidity and mortality in dialysis patients, and is also a well-established feature of chronic kidney disease (CKD). Anaemia has also been shown to be a key component not only of dialysis and CKD but also of cardiac disease, including congestive heart failure (CHF). Furthermore, published clinical and laboratory data suggest that anaemia, CHF and CKD are interrelated, each causing the other to worsen and thus resulting in a 'vicious cycle' of disease progression which we have called the Cardio-Renal Anaemia syndrome. In this syndrome anaemia may cause CKD or be caused by CKD, anaemia may cause CHF or be caused by CHF and CHF may cause CKD or be caused by CKD. Numerous publications have borne out the fact that anaemia correction through epoetin treatment provides great benefit to CKD patients. Additionally, there is evidence to suggest that these benefits may be extended to patients with cardiac disease. Uncontrolled and controlled studies of the effect of subcutaneous epoetin treatment in anaemic patients with both CHF and CKD show significant improvements in both cardiac and renal function. Despite these findings, however, it is apparent that anaemia correction is not implemented rigorously within both CHF and CKD populations. Greater awareness of the need for early anaemia correction therapy is therefore required. Cooperation between nephrologists and others who are caring for CHF patients, especially cardiologists, is crucial.

Anemia↗

PubMed2004

Lipids enhance alpha1-adrenoceptor pressor sensitivity in patients with chronic kidney disease.

BACKGROUND: Dyslipidemia in patients with chronic kidney disease (CKD) may contribute to hypertension (HT) by altering neurocirculatory control. To test this notion, we quantified the effects of acutely increasing levels of nonesterified fatty acids (NEFAs) and triglycerides on alpha1-adrenergic pressor sensitivity and baroreflex sensitivity (BRS) in subjects without diabetes with CKD. METHODS: Alpha1 pressor sensitivity was determined before and after increasing NEFA and triglyceride levels with a fat emulsion and heparin infusion in 8 subjects with stage 2 to 3 CKD (glomerular filtration rate, 56 +/- 6 mL/min by 125 I-iothalamate clearance). Seven subjects with HT and 8 normotensive control (CO) subjects with normal renal function and matched to patients with CKD also were studied. RESULTS: Fasting NEFA levels were greater in patients with CKD than in CO subjects (585 +/- 98 versus 321 +/- 32 micromol/L; P < 0.01), but not different from those in subjects with HT (501 +/- 68 micromol/L). Alpha1 pressor sensitivity, defined as the phenylephrine dose that increased mean blood pressure (BP) by 20 mm Hg, was greatest (lowest dose) in subjects with CKD (0.83 +/- 0.11 microg x kg(-1) x min(-1)), followed by those with HT (1.08 +/- 0.19 microg x kg(-1) x min(-1)) and CO subjects (1.34 +/- 0.19 microg x kg(-1) x min(-1); P < 0.05 versus CKD group). BRS, measured as the ratio of change in R-R interval to change in systolic BP during the phenylephrine infusion, was lowest, intermediate, and highest in the CKD, HT, and CO groups, respectively. Increasing NEFA and triglyceride levels significantly enhanced alpha1 pressor sensitivity in all 3 groups and reduced BRS in the CKD and CO groups. CONCLUSION: These observations suggest that the dyslipidemia prevalent in patients with stage 2 to 3 CKD may contribute to HT by enhancing alpha1 pressor sensitivity and impairing baroreflex function.

Adult↗

PubMed2004

A survey of kidney disease and risk-factor information on the World Wide Web.

BACKGROUND: Chronic kidney disease (CKD) is epidemic, and informing those at risk is a national health priority. However, the discrepancy between the readability of health information and the literacy skills of those it targets is a recognized barrier to communicating health information that may promote good health outcomes. Because the World Wide Web has become one of the most important sources of health information, we sought to assess the readability of commonly available CKD information. METHODS: Twelve highly cited English-language, kidney disease Web sites were identified with 4 popular search engines. Each Web site was reviewed for the availability of 6 domains of information germane to CKD and risk-factor information. We estimated readability scores with the Flesch-Kincaid and Flesch Reading Ease Index methods. The deviation of readability scores for CKD information from readability appropriate to average literacy skills and the limited literacy skills of vulnerable populations (low socioeconomic status, health disparities, and elderly) were calculated. RESULTS: Eleven Web sites met the inclusion criteria. Six of 11 sites provided information on all 6 domains of CKD and risk-factor information. Mean readability scores for all 6 domains of CKD information exceeded national average literacy skills and far exceeded the fifth-grade-level readability desired for informing vulnerable populations. Information about CKD and diabetes consistently had higher readability scores. CONCLUSION: Information on the World Wide Web about CKD and its risk factors may not be readable for comprehension by the general public, especially by underserved minority populations with limited literacy skills. Barriers to health communication may be important contributors to the rising CKD epidemic and disparities in CKD health status experienced by minority populations.

Chronic Disease↗

PubMed2006

[Cardiovascular system in patients in different stages of chronic kidney disease].

The term "chronic kidney disease" (CKD) was introduced recently to nephrological literature. CKD is a growing epidemic problem, which affects 11% of adult US population. CKD, particularly with GFR below 60 ml/min/1, 73 m2 is associated with increased risk of cardiovascular morbidity and mortality. It is a result of coexistance of "traditional" cardiovascular risk factors cumulation such as hypertension, lipid and carbohydrate disorders but also "non-traditional" cardiovascular risk factors such as: anemia, calcium-phosphate metabolism disturbances, chronic inflammation and others. The paper discusses changes in left ventricle structure and function, arterial structure and function and cardiovascular calcifications in different stages of chronic kidney disease, and their prognostic significance. Result of the study in 31 CKD patients (GFR 39,4 +/- 14, 1 ml/min/m2) and 18 appearently healthy controls are also presented in the paper. Cardiovascular risk factors assessment, echocardiography, common carotid artery USG with diameter and intima-media thickness (IMT) measurement and aortic pulse wave velocity (PWV) measurement were performed in all participants. We found higher total cholersterol, LDL-cholesterol, triglicerides, CRP, advanced glycation end-products (AGE), and calcium x phosphorus product and lower hemoglobin concentration in CKD patients. Fasting glucose and insulin concentration did not differ between CKD patients and control group but insulin/glucose ratio was higher in CKD group. Abnormal left ventricular heart structure was found in 55% of CKD patients. Carotid artery internal diameter, intima-media thickness and aortic PWV--a marker of increased arterial stiffness - were higher in CKD patients. The study indicates that cardiovascular risk factors and cardiac and arterial abnormalities should be evaluated from the start of CKD.

Adult↗

PubMed2004

Impact of chronic kidney disease on prognosis of patients with diabetes mellitus treated with percutaneous coronary intervention.

Chronic kidney disease (CKD) is a frequent complication of diabetes mellitus. However, the role of CKD in outcomes of patients with diabetes who have undergone percutaneous coronary intervention (PCI) has not been studied specifically. Therefore, we investigated the impact of CKD on prognosis of patients with diabetes who underwent PCI. Of 1,575 diabetic patients who underwent PCI, 1,046 (66%) had preserved renal function, 492 (31%) had CKD (baseline serum creatinine >1.5 mg/dl or estimated glomerular filtration rate <60 ml/min/1.73 m(2)) without dialysis, and 37 (2.3%) were dependent on dialysis. Patients with CKD versus those without CKD had more in-hospital complications, including mortality (2.6% vs 0.5%, respectively; p <0.0001), neurologic events (3.1% vs 0.6%, p = 0.0001), and gastrointestinal bleeding (2.9% vs 0.9%, p = 0.01). Contrast-induced nephropathy after PCI (increase > or =25% and/or > or =0.5 mg/dl of serum creatinine before PCI vs 48 hours after PCI) was found in 15% of patients without CKD versus 27% of those with CKD, and de novo dialysis was instituted in 0.1% versus 3.1%, respectively. Contrast-induced nephropathy was independently predicted (all p <0.0001) by peri-PCI hypotension (odds ratio [OR] 2.62), insulin treatment (OR 1.84), and volume of contrast medium (OR 1.30). The 1-year mortality rate was strikingly higher (all p <0.0001) in patients with CKD who did not receive dialysis (16%) and those on dialysis (44%) compared with the group with preserved renal function (5%). Contrast-induced nephropathy was among the independent predictors of a 1-year mortality rate (OR 2.75, p <0.001).

Age Factors↗

PubMed2006

Chronic kidney disease in patients with chronic heart failure--impact on intracardiac conduction, diastolic function and prognosis.

BACKGROUND: In patients with chronic heart failure (CHF), chronic kidney disease (CKD) is associated with increased morbidity and mortality, but contributing mechanisms are not well defined. This study tested the impact of CKD on intracardiac conduction, diastolic function and prognosis in patients with underlying CHF. METHODS: We prospectively enrolled 269 patients with stable CHF, of whom 135 had CKD (estimated glomerular filtration rate (eGFR)<60 ml/min/1.73 m(2)). Echo measurements comprised left ventricular dimensions/volumes, ejection fraction, mitral E/A-ratio, deceleration time and tissue Doppler mitral annular velocities (S', E', A'). PQ and QRS intervals were derived from the 12-lead ECG. A cardiac event (cardiac death or urgent cardiac transplantation) was defined as combined study end point. RESULTS: Patients with CKD had longer PQ and QRS intervals, and were in a poorer NYHA functional class as compared to patients without CKD. In patients with CKD, the mitral annular E' velocity was lower, the mitral E/E'-ratio was higher and a restrictive mitral filling pattern was more frequent. By linear regression analysis, PQ and QRS intervals and the mitral E/E'-ratio were inversely related to the eGFR. During a follow-up of 507+/-375 days, 39 patients suffered a cardiac event. In CKD patients, outcome was markedly poorer as compared to those without CKD (event-free survival rate 51% vs. 87% in those without KD, p=0.001) CONCLUSIONS: In patients with CHF, CKD is associated with impaired intracardiac conduction and progressive diastolic dysfunction. Both mechanisms may contribute to increased morbidity and mortality of such patients.

Age Distribution↗

PubMed2006

A meta-analysis of the renal safety of isosmolar iodixanol compared with low-osmolar contrast media.

OBJECTIVES: We sought to compare the nephrotoxicity of isosmolar contrast medium (IOCM) iodixanol with low-osmolar contrast media (LOCM) and to identify predictors of contrast-induced nephropathy (CIN). BACKGROUND: Contrast-induced nephropathy is a serious complication of diagnostic and interventional procedures. METHODS: Pooled individual patient data (n = 2,727) from 16 double-blind, randomized, controlled trials in which patients received either intra-arterial IOCM iodixanol (n = 1,382) or LOCM (n = 1,345) were included. Patients were stratified according to chronic kidney disease (CKD), diabetes mellitus (DM), or both. Outcome measures were the maximum increase in serum creatinine (Cr) over baseline and the incidence of postprocedural CIN. RESULTS: The maximum Cr increase within 3 days after contrast medium (CM) administration was significantly smaller in the iodixanol group compared with the LOCM group (0.06 mg/dl vs. 0.10 mg/dl, p < 0.001), particularly in patients with CKD (0.07 mg/dl vs. 0.16 mg/dl, p = 0.004) and CKD + DM (0.10 mg/dl vs. 0.33 mg/dl, p = 0.003). Contrast-induced nephropathy, defined as an increase in Cr > or =0.50 mg/dl within 3 days after CM administration, occurred less frequently in the iodixanol group than in the LOCM group in all patients (1.4% vs. 3.5%, p < 0.001), in CKD patients (2.8% vs. 8.4%, p = 0.001), and in CKD + DM patients (3.5% vs. 15.5%, p = 0.003). Independent predictors of CIN included CKD, CKD + DM, and use of LOCM. CONCLUSIONS: This meta-analysis of pooled data from 2,727 patients indicates that use of the IOCM iodixanol is associated with smaller rises in Cr and lower rates of CIN than LOCM, especially in patients with CKD or CKD + DM.

Contrast Media↗

PubMed2006

[Chronic kidney disease: do generalists and nephrologists differ in their care?].

INTRODUCTION: Chronic kidney disease (CKD) is a major public health problem. We report an evaluation of the CKD perception from a French family physician's (FP) point of view. METHODS: A questionnaire was sent to a representative and independently selected sample of 497 FP, i.e. 20% of the FP working in the administrative region Lorraine. There were 214 completed surveys, i.e. response rate: 43%. RESULTS: Age of FP was: < 40 years of age: 13%, 40-50: 40%, > 50: 47%. The geographic working place was urban: 41%, rural: 22%, urban and rural: 37%. Ninety-nine per cent of FP has a nephrologist, devoted to CKD referral. Twenty-one per cent of FP has a comprehensive picture of CKD and 75% thinks that CKD diagnostic is difficult Thirty per cent of FP were aware of CKD guidelines. For FP, risk-factors for CKD were: hypertension: 93%, diabetes: 99%, age over 65: 64%, urinary infection: 34%, hematuria/proteinuria: 78%, anaemia: 43%, therapeutics associated with risk of renal injury: 79%, all of these circumstances: 20%. The referral decision to a nephrologist was done at a mean creatinine clearance of 41+/-12 ml/min. Age over 80, dementia, and cancer were considered to be a contra-indication of renal replacement therapy, for respectively 30%, 69%, and 63% of FP. CME was associated with better awareness of guidelines, and use of clearance rather than serum creatinin. CONCLUSION: From FP point of view, overall awareness of CKD guidelines is low. In the context of the current nephrology services, greater sharing of CKD care with FP is needed.

Adult↗

PubMed2006

The exclusion of patients with chronic kidney disease from clinical trials in coronary artery disease.

Chronic kidney disease (CKD) is associated with a high risk of death from coronary artery disease and may modify the response to standard cardiovascular therapies. Treatment of subjects with CKD should ideally be based on evidence from randomized, clinical trials, but how often subjects with CKD have been excluded from these trials is uncertain. We undertook this study in order to quantify how often subjects with moderate to advanced CKD were excluded from large cardiovascular trials. MEDLINE and the reference list of selected articles were searched in order to identify large, randomized, controlled trials of five different coronary artery disease therapies published between 1998 and 2005. Exclusion criteria and reported clinical characteristics of subjects were abstracted. Rates of exclusion and reporting of baseline characteristics of study participants were compared for CKD, diabetes, history of smoking, and hypertension. Eighty-six trials randomizing 411 653 patients were identified. More than 80% of trials excluded subjects with end-stage renal disease and 75.0% excluded patients with CKD. Subjects with diabetes, hypertension, or a history of smoking were excluded less than 4% of the time. Baseline renal function of study participant was reported in only 7% of trials. Patients with CKD are frequently excluded from coronary artery disease trials and renal function of randomized subjects is rarely reported. These findings reinforce the notion that available data on the treatment of coronary artery disease in subjects with CKD have significant limitations and should be generalized to the treatment of subjects with CKD cautiously.

Adrenergic beta-Antagonists↗

PubMed2006

Risk factors for chronic kidney disease in a community-based population: a 10-year follow-up study.

The purpose of this study was to explore risk factors affecting the incidence of chronic kidney disease (CKD) in general population. We conducted a 10-year follow-up study with 123 764 (male: 41 012, female: 82 752) adults aged 40 years and over who received community-based annual examinations. The primary outcome for the analysis was the development of CKD during the follow-up period. Predictors for the development of CKD were obtained by the significant hazard ratios (HR) in Cox regression model by sex. During the follow-up period, 4307 subjects (male: 2048, female: 2259) developed CKD stage I or II, and 19 411 subjects (male: 4257, female: 15 154) developed CKD stage III or higher. The baseline-adjusted predictor of developing CKD included age, glomerular filtration rate, hematuria, hypertension, diabetes, serum lipids, obesity, smoking status, and consumption of alcohol. Treated diabetes in male subjects, and treated hypertension, systolic blood pressure >160 mm Hg and/or diastolic blood pressure >100 mm Hg, diabetes, and treated diabetes in female subjects were associated with more than a doubling of the HR. For the development of CKD stage III or higher, proteinuria of >or= + +, and proteinuria and hematuria were associated with more than a doubling of the HR in male subjects. The prevalence of newly developed CKD over 10 years was 23 718 subjects (19.2%) in adults. This study suggested that not only hypertension and diabetes but also several metabolic abnormalities were independent risk factors for developing CKD.

Adult↗

PubMedDate not supplied

Clinical epidemiology of cardiovascular disease in chronic kidney disease prior to dialysis.

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality in patients with end-stage renal disease (ESRD). Both in dialysis and in transplant patients, CVD remains the leading cause of death. There is accumulating evidence that the increase in CVD burden is present in patients prior to dialysis, due to both conventional risk factors as well as those specific to kidney disease. Of importance is that even in patients with mild kidney disease, the risk of cardiovascular events and death is increased relative to patients without evidence of kidney disease. The new classification system proposed by the National Kidney Foundation as part of the Dialysis Outcomes Quality Initiative (DOQI) process describes the five stages of kidney disease, as well as those complications associated with chronic kidney disease (CKD), in particular cardiovascular risk factors and disease. Patients with kidney disease are deemed to be at highest cardiovascular risk. CVD, defined as the presence of either congestive heart failure (CHF), ischemic heart disease (IHD), or left ventricular hypertrophy (LVH), is prevalent in cohorts with established CKD (8-40%). The prevalence of hypertension, a major risk factor for coronary artery disease (CAD) and LVH is high in patients with CKD (87-90%). At least 35% of patients with CKD have evidence of an ischemic event (myocardial infarction or angina) at the time of presentation to a nephrologist. The prevalence of LVH increases at each stage of CKD, reaching 75% at the time of dialysis initiation, and the modifiable risk factors for LVH include anemia and systolic blood pressure, which are also worse at each stage of kidney disease. Even under the care of nephrologists, a change in cardiac status (worsening of heart failure or anginal symptoms) occurs in 20% of patients. The presence of CVD predicts a faster decline of kidney function and the need for dialysis, after controlling for all other factors including glomerular filtration rate (GFR), age, and the presence of LVH. This article describes the new classification system for staging of CKD, defines and describes CVD in CKD, and reviews the evidence and its limitations with respect to the current understanding of CKD and CVD. Specifically, methodologic issues related to survival and referral bias limit our current understanding of the complex interaction of conventional and nonconventional kidney disease-specific risk factors. We identify the importance of well-conducted studies of patient groups with and without CVD, with and without CKD, in order to better understand the complex physiology so that treatment strategies can be appropriately applied.

Cardiovascular Diseases↗

PubMed2006

Disordered mineral metabolism and vascular calcification in nondialyzed chronic kidney disease patients.

It is well established that abnormalities in mineral metabolism are apparent early in the course of chronic kidney disease (CKD) and result in clinically relevant consequences such as renal osteodystrophy. Furthermore, there is emerging evidence linking some of these abnormalities (hyperphosphatemia) to the high cardiovascular morbidity and mortality experienced by nondialyzed patients with CKD. Most studies have evaluated vascular calcification in patients with stage 5 CKD. Reports published over the last 2 years show that the process begins rather early in CKD and is particularly severe among elderly and type 2 diabetic patients. Furthermore, "calcium begets calcium", such that the calcification burden in early CKD is an important predictor of subsequent progression, including the rapid increase seen in stage 5 CKD. There is an increasing body of evidence that supports the thesis that elevated serum levels of phosphorus and calcium and deficiency of inhibitors of calcification (for example, fetuin-A) are important in the progression of vascular calcification in patients with end-stage renal disease. However, the concentrations of calcium and phosphorus shown to induce mineralization in cell culture studies are not observed in most patients until late in stage 4 or stage 5 CKD. Cross-sectional and longitudinal studies have also been unable to show a correlation between serum levels of markers of disordered mineral metabolism and severity of vascular calcification. Future studies should evaluate the pathogenetic role of phosphorus retention, which occurs early in the course of CKD, in the induction and/or progression of vascular calcification. Finally, there is a need to identify alternative pathogenetic mechanisms that may be important causes of the high calcification burden observed early in CKD.

Bone Density↗

PubMed2004

Cardiovascular disease in chronic kidney disease from a cardiologist's perspective.

PURPOSE OF REVIEW: Cardiovascular disease accounts for the majority of morbidity and mortality in patients with chronic kidney disease (CKD). This review therefore concentrates on CKD from the viewpoint of the cardiologist. RECENT FINDINGS: Studies have identified several explanations for this observation, including high rates of risk factors for cardiovascular disease, lesser use of cardioprotective strategies, adverse outcomes with cardiovascular drugs and procedures, and accelerated atherosclerosis and myocardial disease in CKD. Because recent studies have rigorously controlled for confounding factors, there is an emerging recognition that CKD is an independent cardiovascular risk state. Conversely, CKD appears to be the result of systemic atherosclerosis. The relative under-utilization of cardioprotective therapies has been an increasingly reported finding in the literature. It appears that conventional cardiovascular risk factor reduction in both the chronic and acute care settings has a greater relative benefit in those patients with CKD than in those with normal renal function. SUMMARY: CKD is an independent cardiovascular risk state. Hence, there is a strong rationale for research in CKD patients into the pathogenesis of CVD. In addition, there are multiple opportunities for improving cardiovascular outcomes in patients with CKD, including both chronic and acute cardiovascular risk reduction.

Cardiovascular Diseases↗

PubMed2004

Cost of medical care for chronic kidney disease and comorbidity among enrollees in a large HMO population.

Chronic kidney disease (CKD) afflicts up to 20 million people in the United States, but little is known about their health care costs. The authors analyzed costs and resource use associated with CKD by using National Kidney Foundation staging definitions. Patients insured through a large health maintenance organization with a laboratory finding of CKD (defined as estimated GFR between 15 and 90 ml/min per 1.73 m(2) in 1996 followed by a second GFR below 90 at the next creatinine measurement occurring at least 90 d later) were followed from 1996 for up to 66 mo. The final cohort included 13,796 persons with CKD and their age- and gender-matched controls; 1741 in stage 2; 11,278 in stage 3; and 777 in stage 4. Depending on stage, cases had 1.9 to 2.5 times more prescriptions, 1.3 to 1.9 times more outpatient visits, were 1.6 to 2.2 times more likely to have had an inpatient stay, and had 1.8 to 3.1 more stays than did controls. Total per patient follow-up costs were [$total, (95% CI) cases and controls, respectively] $38,764 (95% CI, 37,033 to $40,496) and $16,212 (95% CI, $15,644 to $16,780) in stage 2; $33,144 (95% CI, $32,578 to $33,709) and $18,964 (95% CI, $18,730 to $19,197) in stage 3; and $41,928 (95% CI, $39,354 to $44,501) and $19,106 (95% CI, $18,212 to $20,000) in stage 4. Cases with no CKD-related comorbidities had costs double that of controls with no CKD-related comorbidities, and comorbidities related to CKD were more costly to manage than CKD alone. Future research in this area could be usefully directed toward analyzing the clinical and economic consequences of better managing or preventing comorbidities in patients with CKD.

Aged↗

PubMed2004

Enhanced expression of receptor for advanced glycation end products in chronic kidney disease.

Inappropriate chronic inflammation associated with progressive, chronic kidney disease (CKD) reflects sustained activation of immunocompetent cells, like monocytes/macrophages. Advanced glycation end products (AGE) accumulate in CKD, but it is unclear if they stimulate monocytes by binding with the receptor for AGE (RAGE). Posited was the notion that RAGE plays a contributory role to monocyte-mediated systemic inflammation of progressive CKD. Peripheral blood monocytes were isolated from 102 patients without diabetes with varying severity of CKD. RAGE expression on peripheral blood monocytes increased with worsening CKD (r2 = 0.73) and was strongly correlated with plasma levels of pentosidine, a marker for AGE (r = 0.71). Strongly positive statistical correlations were observed in patients with CKD between monocyte RAGE and plasma levels of tumor necrosis factor alpha (TNF-alpha) (r = 0.61), the monocyte activation marker, neopterin (r = 0.65), and the systemic acute phase reactant, C-reactive protein (r = 0.44). Monocytes obtained from patients with CKD showed a monotonic increase in the number and affinity of specific AGE binding sites and increased production of TNF-alpha under stimulation of AGE. All these upregulatory responses in uremic monocytes could be largely blocked by an anti-RAGE antibody. It was concluded that RAGE expression was upregulated on monocytes from patients with CKD. Enhanced RAGE may amplify AGE-induced monocytes perturbation and contribute to monocyte-mediated systemic inflammation in progressive CKD.

Adult↗

PubMed2004

"Renalism": inappropriately low rates of coronary angiography in elderly individuals with renal insufficiency.

Higher risk patients (including the elderly) receive more conservative therapy for cardiovascular diseases, even though the relative benefits of therapy tend to be greater. The perceived risk of radiocontrast-associated nephrotoxicity may influence the provision of coronary angiography and subsequent revascularization, especially among individuals with chronic kidney disease (CKD). The aim of this study was to determine whether there is excessive variation in the provision of coronary angiography after acute myocardial infarction on the basis of the presence of CKD and whether there is an association between angiography and mortality. Elderly (age 65 to 89 yr) individuals with acute myocardial infarction from the Cooperative Cardiovascular Project were classified by the presence or absence of CKD (defined as a baseline serum creatinine of 1.5 to 5.0 mg/dl). In CKD patients, the propensity to undergo coronary angiography was determined and the effect of coronary angiography on mortality was estimated using multivariable logistic regression and stratification. Mortality was significantly higher with CKD (52.6 versus 26.4%). Fewer patients with CKD underwent coronary angiography (25.2 versus 46.8%) despite the observation that a similar proportion of patients were deemed appropriate for angiography by standard, published criteria. When limiting the analysis to CKD patients who are considered appropriate, the multivariable estimate of the odds of death associated with coronary angiography was 0.58 (95% confidence interval, 0.50 to 0.67). With adjustment using propensity scores, the odds ratio averaged across propensity score quintiles was 0.62 (95% confidence interval, 0.54 to 0.70). Results were qualitatively similar when patients were stratified by CKD stage IV (estimated GFR <30 ml/min per 1.73 m(2)). There is a large relative decrease in utilization of coronary angiography among patients with CKD. Alteration in practice because of an aversion to the risk of radiocontrast-associated nephrotoxicity ("renalism") is inappropriate, even if the true relative benefit of invasive strategies is a fraction of what is estimated here.

Age Factors↗

PubMed2025

Genetic evidence for repurposing GLP-1 receptor agonists in chronic kidney disease and IgA nephropathy: Metabolic and anti-inflammatory pathways beyond glycaemic control.

AIMS: Despite observational links between glucagon-like peptide-1 receptor agonists (GLP-1RAs) and kidney benefits, causal mechanisms remain unclear. This study aims to dissect genetic causality and mediation pathways underlying the effects of GLP-1RAs on chronic kidney disease (CKD) and related renal outcomes. MATERIALS AND METHODS: Using large-scale Genome - Wide Association Study (GWAS) data, we applied two-sample Mendelian randomisation (MR) to estimate the causal effects of GLP-1RAs on CKD, estimated glomerular filtration rate (eGFR) and subtypes (IgA nephropathy, membranous nephropathy, nephrotic syndrome and chronic glomerulonephritis), with sensitivity analyses. The glycaemic markers (glycated haemoglobin [HbA1c] and blood glucose), type 2 diabetes mellitus (T2DM) and diabetic nephropathy (DN) served as positive controls. Mediation MR assessed body mass index (BMI), lipids, glycaemic markers and inflammatory proteins. Data were sourced from MRC Integrative Epidemiology Unit Open Genome - Wide Association Studies OpenGWAS, FinnGen, GWAS Catalogue and cohort-specific studies. RESULTS: Positive control analyses revealed that genetically predicted GLP-1R activation was associated with reduced levels of HbA1c (p = 4.93E-15) and blood glucose (p = 9.73E-5), as well as a decreased risk of T2DM (p = 2.45E-4) and DN (p = 6.35E-4), fully validating the reliability of the genetic instruments. Genetic proxies for GLP-1R activation lowered risks of CKD (odds ratio [OR] = 0.83, p = 9.22E-9), immunoglobulin A nephropathy (IgAN) (OR = 0.70, p = 2.11E-3) and kidney function preservation (β = 0.01, p = 9.11E-3), but showed null effects on other CKD subtypes. Mediation analyses indicated that fibroblast growth factor 23 (FGF23) suppression mediated 26.57% of the effect on eGFR and 13.50% of CKD protection, whereas metabolic traits (BMI: 2.08% for CKD, 5.51% for eGFR; high-density lipoprotein: 0.79% for CKD, 2.34% for eGFR; HbA1c: 8.25% for eGFR) partially explained the benefits on CKD and eGFR. Only BMI exhibited a mediation effect on IgAN. Sensitivity analyses confirmed minimal pleiotropy. CONCLUSIONS: This study provides robust genetic evidence for repurposing GLP-1RAs in CKD and IgAN through anti-inflammatory (FGF23) and metabolic pathways, extending their utility beyond glucose control. While European ancestry data limit generalisability, our framework prioritises FGF23 and metabolic modulation as key targets for clinical trials in renal protection.

Humans↗