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At least 775 records · Page 43Linked to original sources
PubMed2006

Renal dysfunction increases the risk of saphenous vein graft occlusion: results from the Post-CABG trial.

OBJECTIVES: Saphenous vein grafts are common among patients with a history of coronary artery bypass graft (CABG) surgery. Chronic kidney disease (CKD) is an established cardiovascular risk factor, but its role in graft disease has not been evaluated. METHODS AND RESULTS: The Post-CABG Trial randomized 1351 patients who had undergone CABG surgery 1-11 years earlier to high- or low-dose lovastatin and to low-dose warfarin or placebo. Coronary angiography was conducted at baseline and after a median follow-up time of 4.2 years. Subjects were grouped according to their baseline estimated glomerular filtration rate (eGFR). The primary trial endpoint was significant graft disease progression assessed angiographically. Additional pre-defined endpoints included occlusion of grafts patent at baseline, change in minimum lumen diameter, and a composite endpoint of recurrent clinical events. Decreasing eGFR was associated with an increased risk of graft occlusion (P(trend)=0.040), but not substantial atherosclerotic progression (P(trend)=0.30), per-graft change in minimum lumen diameter (P(trend)=0.067), or recurrent clinical events (P(trend)=0.86). We did not observe significant effect modification of treatment effects by the presence of CKD. CONCLUSIONS: CKD may be associated with increased risk of atherosclerotic plaque disruption rather than atherosclerotic progression in saphenous vein grafts.

Aged↗
PubMed2006

Prevalence of decreased glomerular filtration rate in patients seeking non-nephrological medical care--an evaluation using IDMS-traceable creatinine based MDRD as well as Mayo Clinic quadratic equation estimates.

BACKGROUND: Data on the prevalence of decreased glomerular filtration rate in Europe are limited. Most of the available studies did not employ laboratory methods providing creatinine concentrations traceable to the reference method, i.e. isotope dilution mass spectrometry (IDMS). METHODS: We therefore conducted a cross-sectional study in the principality of Liechtenstein consecutively enrolling adult patients seeking non-nephrological medical care from whom serum samples were referred for renal function assessment. All measurements were done in one central laboratory. The estimated glomerular filtration rate (eGFR) was calculated based on the determination of IDMS-traceable creatinine by a kinetic Jaffe method (Roche Diagnostics, Switzerland) by means of the MDRD and Mayo Clinic quadratic equations. We further estimated the incidence of end stage renal disease during the next 5 years. RESULTS: For 43% (n=9378) of the entire population>or=25 years renal function assessment was available. An eGFR indicating chronic kidney disease (CKD) stages 3-5 was found in 4.93% when using the MDRD equation and in 3.98 % when using the Mayo Clinic quadratic equation. The two equations had a very good agreement in classifying patients to have an eGFR consistent with CKD stages 3-5 (Cohen's kappa 0.887). Further calculations suggested that among patients aged 80 or younger, annually 42 per 100,000 are going to develop an eGFR<15 ml/min/1.73 m2 over the next 5 years. CONCLUSIONS: 4-5% of patients seeking non-nephrological medical advice have an eGFR consistent with CKD stages 3-5, and a considerable number of subjects is expected to develop end stage renal disease over a 5 year period. In order to obtain comparable kidney function estimates among different institutions it is not only important to use standardized methods to measure creatinine but rather to employ standardized methods to calculate a GFR estimate.

Adult↗
PubMed2005

Hypertension in chronic kidney disease and dialysis: pathophysiology and management.

Hypertension affects 24% of the adult US population. In the United States, 3% of the adult population has an elevated serum creatinine level, and 70% of these patients have hypertension. The prevalence of hypertension in chronic kidney disease (CKD) depends on the patient's age and the severity of renal failure, proteinuria, and underlying renal disease. As patients with CKD progress to end-stage renal disease (ESRD), 86% are diagnosed with hypertension. It has long been recognized that kidney function affects and is affected by hypertension. This article discusses the pathophysiology and management of hypertension in patients with CKD.

Humans↗
PubMed2005

Percutaneous coronary interventions in the high-risk renal patient: strategies for renal protection and vascular protection.

CKD is the most important factor in predict-ing adverse short- and long-term outcomes after PCI. Hence, the rationale for renal end-organ protection is based on chronic renal protection,avoidance of additive renal insults, and a comprehensive CIN prophylaxis. The pathogenesis of CIN goes beyond serum creatinine and involves a unique vascular pathobiology in which interrelates renal and CVD outcomes are interrelated. Attempts at PCI in patients with CKD and ESRD are high-risk procedures, but the risks involved seem to be warranted given comparative outcomes in conservatively treated patients. The benefits of short- and long-term vascular protective therapies in CKD patients have been confirmed, and these therapies are an important component of PCI care.

Angioplasty, Balloon, Coronary↗
PubMed2005

Congestive heart failure in chronic kidney disease: disease-specific mechanisms of systolic and diastolic heart failure and management.

There is a high burden of cardiac disease in the CKD population. Severe LVH, dilated cardiomyopathy, and coronary artery disease occur frequently and result in the manifestations of CHF,which is probably more important with respect to prognosis than symptomatic. Multiple risk factors for CVD include traditional risk factors and those unique to the CKD population. Furthermore, the distinctive aspects of CKD patients sometimes warrant special consideration in making management decisions. Nonetheless, interventions such as controlling hypertension, specific pharmacologic options, lifestyle modification, anemia management, and early nephrology referral are recommended when appropriate.

Cardiomyopathies↗
PubMed2005

Coronary artery disease and peripheral vascular disease in chronic kidney disease: an epidemiological perspective.

The enormous burden of CAD and PVD inpatients who have CKD contributes substantially to increased morbidity and mortality. The increased risk of vascular disease observed in CKD patients is likely to be multifactorial, with contributions from traditional and nontraditional cardiovascular factors. Given the overwhelming evidence on the known benefits of cardioprotective medications, their underuse remains puzzling in a population at enormous risk. During the past 5 years, the research community and national interest groups have made significant progress in organizing a concerted approach to improve the management of patients who have CKD and vascular disease. Much work remains to be done. The development of national guidelines in the management of these patients at high risk for future cardiovascular events will be a welcome step. The evaluation of multitargeted interventions for reduction of cardiovascular risk through randomized clinical trials is desperately needed. Finally, the low use of known cardioprotective strategies in this high-risk group is a serious issue and warrants immediate attention at local and national levels.

Chronic Disease↗
PubMed2004

Secondary hyperparathyroidism: review of the disease and its treatment.

BACKGROUND: Most patients with chronic kidney disease (CKD) stage 5 develop secondary hyperparathyroidism (SHPT). SHPT is an adaptive response to CKD and its associated disruptions in the homeostatic control of serum phosphorus, calcium, and vitamin D. The poor control of mineral and parathyroid hormone (PTH) levels characteristic of SHPT is associated with serious clinical consequences. OBJECTIVE: This review discusses the pathophysiology and consequences of SHPT, as well as the efficacy and limitations of current treatment modalities. METHODS: Literature searches were conducted using the MEDLINE, EMBASE, and BIOSIS databases. Additional information was obtained from Internet web sites, textbooks, and nephrology congress abstracts. RESULTS: Patients with uncontrolled SHPT are at higher risk for cardiovascular morbidity and mortality, hospitalization, bone disease, vascular and soft-tissue calcification, and vascular access failure than patients whose mineral and PTH levels are well managed. New National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI) targets for calcium, phosphorus, calcium-phosphorus product, and PTH control have recently been published with the aim of improving the management of mineral metabolism in CKD patients. Data from observational studies suggest that the majority of patients currently have PTH and mineral levels outside these target ranges. CONCLUSIONS: Given the inadequacies of current therapies, novel agents are being developed that may help improve the management of SHPT.

Calcium↗
PubMed2006

Homocysteine and its determinants in nondialyzed chronic kidney disease patients.

This cross-sectional study aimed to investigate the prevalence of hyperhomocysteinemia, the determinants of plasma total homocysteine concentrations, and the relationship of total homocysteine with nutritional parameters in a sample of patients with chronic kidney disease (CKD) and not yet on dialysis. The study was done with outpatients from the Nephrology Division of the Federal University of São Paulo and Oswaldo Ramos Foundation. Sixty-six patients with CKD (70% male; age 58.6+/-15.6 years [mean+/-standard deviation]) with moderate to severe renal impairment (creatinine clearance=29.8+/-14.3 mL/min [0.5+/-0.24 mL/sec]), clinically stable, and older than 18 years were included. A group of 20 healthy subjects from the clinic staff was also studied for reference values for plasma homocysteine, folate, and vitamin B-12 concentration. Fasting blood samples were collected to determine plasma total homocysteine, folate, vitamin B-12, and creatinine. To calculate creatinine clearance, a 24-hour urine collection sample was obtained. The assessment of nutritional status included anthropometric parameters. Pearson correlation, Mann-Whitney test, and multiple linear regression analysis were used for statistical analyses. The main results showed that the concentration of total homocysteine in the patients was significantly increased compared with the healthy subjects (3.4+/-1.7 vs 1.41+/-0.42 mg/L [25.4+/-12.2 vs 10.4+/-3.1 micromol/L]; P<0.001). Plasma folate and plasma vitamin B-12 were in the normal range and did not differ between patients and healthy individuals. A high prevalence of hyperhomocysteinemia (total homocysteine >1.89 mg/L [14 micromol/L]) was found in the patients (89%). Plasma total homocysteine did not correlate with any of the nutritional parameters studied and did not differ between patients in terms of whether they were using or not using folic acid supplementation (3.07+/-1.09 vs 3.55+/-1.78 mg/L [22.7+/-8.1 vs 26.3+/-13.2 micromol/L]; P=0.47), although plasma folate was significantly higher in the supplemented group (12.6+/-3.0 vs 8.0+/-3.6 ng/mL [28.5+/-6.8 nmol/L vs 18.1+/-8.2 nmol/L]; P<0.001). According to the multiple regression analysis, the determinants of total homocysteine were only plasma folate, plasma vitamin B-12, and creatinine clearance (r2=0.20). In conclusion, a high prevalence of hyperhomocysteinemia was found in our sample of nondialyzed patients with CKD. The determinants of total homocysteine levels were plasma folate, plasma vitamin B-12, and creatinine clearance. No association between nutritional parameters and total homocysteine was observed.

Anthropometry↗
PubMed2006

Urinary tract infections in cats with hyperthyroidism, diabetes mellitus and chronic kidney disease.

The prevalence of urinary tract infections (UTIs) in cats with hyperthyroidism (n=90), diabetes mellitus (DM) (n=57) and chronic kidney disease (CKD) (n=77) was evaluated retrospectively. It was found to be 12% in cats with hyperthyroidism and DM, respectively, and 22% in cats with CKD. Associations between UTIs and clinical signs, biochemical markers in serum and urinalyses were investigated. Many of the cats with UTIs had no clinical signs of lower urinary tract disease or changes in their laboratory values indicative of infection. Therefore, a urinalysis alone should not be used to exclude UTIs in these cats. UTIs are relatively common in cats with hyperthyroidism, DM and CKD, and urine cultures are recommended as part of the basic diagnostic plan for cats suspected of suffering from these conditions.

Animals↗
PubMed2006

Progression of left ventricular hypertrophy in children with early chronic kidney disease: 2-year follow-up study.

OBJECTIVE: To determine the prevalence and incidence of left ventricular hypertrophy (LVH) and LV geometry and identify variables associated with LV mass (LVM) growth and development of LVH in children and adolescents with chronic kidney disease (CKD). STUDY DESIGN: A 2-year longitudinal study of children with CKD (glomerular filtration rate [GFR] 15-89 mL/minute/1.73 m2). Thirty-one subjects had baseline and repeated echocardiography. RESULTS: Six (19%) of 31 children had LVH at baseline; the prevalence of LVH increased to 39% at 2-year follow-up. Eccentric LVH was the most common geometric pattern throughout the study. Among 25 children with initially normal LVM index, 8 (32%) developed new LVH. Children with incident LVH had significantly higher mean parathyroid hormone (iPTH), lower hemoglobin and calcium levels at baseline, and significantly larger increase in iPTH during a follow-up than children with normal LVM index. Stepwise regression analysis showed that lower initial LVM index and hemoglobin level and interval increase in iPTH and nighttime systolic blood pressure (SBP) load during a follow-up independently predicted interval increase in LVM index. CONCLUSIONS: LVH progresses in children during early stages of CKD. More aggressive control of anemia, BP, and hyperparathyroidism might be important in preventing the development of LVH in these patients.

Adolescent↗
PubMed2026

Multi-omics reveals that burdock seed aglycone alleviates renal fibrosis by restoring mitochondrial oxidative phosphorylation function.

Renal fibrosis (RF), a common pathological process driving chronic kidney disease (CKD) progression to end-stage renal failure, is closely associated with oxidative phosphorylation (OXPHOS). Arctigenin (ATG), the main active component of burdock seed, exhibits anti-inflammatory and anti-fibrotic activities, but its mechanisms in RF treatment remain unclear. Here, we performed integrated transcriptomic and proteomic analyses to identify key targets and pathways of ATG in a unilateral ureteral obstruction-induced rat RF model. Multi-omics enrichment analysis revealed that NDUFS8 and NDUFS2 were the core targets of ATG, with the OXPHOS pathway as the central intersecting pathway. Our results suggest that ATG exerts anti-renal fibrosis effects by targeting the OXPHOS pathway to inhibit excessive reactive oxygen species production and oxidative stress. SIGNIFICANCE: Chronic kidney disease (CKD) continues to impose an escalating global health and socioeconomic burden, while renal fibrosis (RF), as the convergent pathological endpoint of virtually all progressive nephropathies, remains the principal determinant of irreversible renal failure and adverse clinical outcomes. Despite extensive efforts to develop antifibrotic therapies, effective clinical interventions remain elusive, largely due to the complex and multifactorial nature of RF pathogenesis. In this study, we employed an integrated multi-omics framework encompassing transcriptomics, proteomics, and metabolomics to systematically decipher the antifibrotic mechanism of arctigenin (ATG), a bioactive natural compound derived from traditional Chinese medicine. Our findings identify mitochondrial oxidative phosphorylation as the pivotal regulatory axis underlying the renoprotective effects of ATG and further establish key catalytic subunits of mitochondrial complex I as its direct molecular targets. Mechanistically, ATG not only restores complex I activity and reprograms mitochondrial energy metabolism but also preserves the intracellular stability and localization of these subunits, thereby preventing their aberrant release-mediated inflammatory activation and disrupting the self-perpetuating cycle linking metabolic dysfunction, inflammation, and fibrosis progression. Beyond revealing a previously unrecognized dual mechanism integrating metabolic and inflammatory regulation, this study provides compelling evidence that mitochondrial dysfunction is not merely a secondary consequence of tissue injury but a fundamental driver of fibrotic remodeling. Importantly, our work highlights the translational potential of natural product-based mitochondrial interventions for CKD treatment and supports a broader conceptual shift toward metabolism-centered therapeutic strategies for chronic fibrotic diseases. Given the central role of mitochondrial dysfunction across multiple organs, these findings may also have far-reaching implications for the treatment of systemic fibrosis-related disorders beyond the kidney.

Animals↗
PubMed2006

Herbs or natural substances as complementary therapies for chronic kidney disease: ideas for future studies.

Chronic kidney disease (CKD) is an increasingly common condition with limited treatment options that is placing a major financial and emotional burden on the community. The use of complementary and alternative medicines (CAMS) has increased many-fold over the past decade. Although several compelling studies show renal toxicities and an adverse outcome from use of some CAMS, there is also emerging evidence in the literature that some may be renoprotective. Many nephrologists are unaware of these potential therapeutic benefits in treating CKD, or they are reluctant to consider them in research trials for fear of adverse effects (including nephrotoxicity) or deleterious interaction with co-prescribed, conventional medicines. The increased use of self-prescribed CAMS by their patients suggests that practitioners and researchers should keep abreast of the current information on these agents. A primary goal of this article was to review the available scientific evidence for the use of herbs or natural substances as a complementary treatment for patients with CKD. A further goal was to report the literature on herbs that have been reported to cause kidney failure.

Angelica sinensis↗
PubMed2005

Strategies to retard the progression of chronic kidney disease.

Chronic kidney disease (CKD) is a common and, in advanced cases, highly morbid disorder. The most severe form of CKD is end-stage renal disease (ESRD), in which the patient requires some form of renal replacement therapy to survive. The increasing incidence, prevalence, and costs of ESRD are major national health care concerns; interventions that may prevent or slow the progression of CKD towards ESRD are extremely important and the focus of this article.

Anemia↗
PubMed2005

Traditional and nontraditional cardiovascular risk factors in chronic kidney disease.

Chronic kidney disease (CKD) is public health problem, with as many as 20 million individuals affected in the United States. Patients with CKD should be considered in the highest-risk group for development of cardiovascular disease (CVD), and aggressive treatment of traditional and nontraditional risk factors should be instituted. Additional randomized controlled trials are urgently needed to evaluate potential treatments in this population. This article focuses attention on the major modifiable cardiovascular risk factors in CKD.

Cardiovascular Diseases↗
PubMed2005

Drug dosing in chronic kidney disease.

Patients with chronic kidney disease (CKD) are at high risk for adverse drug reactions and drug-drug interactions. Drug dosing in these patients often proves to be a difficult task. Renal dysfunction-induced changes in human pathophysiology regularly results may alter medication pharmacodynamics and handling. Several pharmacokinetic parameters are adversely affected by CKD, secondary to a reduced oral absorption and glomerular filtration; altered tubular secretion; and reabsorption and changes in intestinal, hepatic, and renal metabolism. In general, drug dosing can be accomplished by multiple methods; however, the most common recommendations are often to reduce the dose or expand the dosing interval, or use both methods simultaneously. Some medications need to be avoided all together in CKD either because of lack of efficacy or increased risk of toxicity. Nevertheless, specific recommendations are available for dosing of certain medications and are an important resource, because most are based on clinical or pharmacokinetic trials.

Biotransformation↗
PubMed2005

Etiology and management of hypertension in chronic kidney disease.

The kidneys are vital in the pathogenesis of hypertension and are also pathologically affected by the presence of hypertension. The prevalence of hypertension in chronic kidney disease (CKD) depends on age, the severity of renal failure, and proteinuria. The intricate and inextricable relationship between CKD and hypertension seems to cause cardiovascular disease that has assumed epidemic proportions. This article discusses the etiology and treatment of hypertension in CKD so that it can be better controlled.

Humans↗
PubMed2005

Calcium and phosphorus metabolism in patients who have chronic kidney disease.

Disturbances in calcium and phosphorus metabolism are almost invariable consequences of chronic kidney disease (CKD). Because the capacity to regulate calcium and phosphorus metabolism becomes compromised progressively as kidney function declines, calcium and phosphorus homeostasis is disrupted and serum calcium or phosphorus levels are perturbed in many patients with CKD. The level of interest in, and concerns about, abnormalities in calcium and phosphorus metabolism among patients with CKD has increased substantially in recent years. Strategies for clinical management are being revised, and recent recommendations differ substantially from those used previously with a renewed emphasis on safety.

Calcium↗
PubMed2006

New insights on inflammation in chronic kidney disease-genetic and non-genetic factors.

Cardiovascular disease (CVD) remains the major cause of morbidity and mortality in chronic kidney disease (CKD). As traditional risk factors cannot alone explain the unacceptable high prevalence and incidence of CVD in this population, inflammation (which is interrelated to insulin resistance, oxidative stress, wasting and endothelial dysfunction) has been suggested to be a significant contributor. Indeed, several different inflammatory biomarkers, such as high sensitivity C-reactive protein (CRP) has been shown to independently predict mortality in CKD patients. The causes of the highly prevalent state of inflammation in CKD are multiple and include factors such as volume overload, co-morbidity, intercurrent clinical events, the dialysis procedure per se as well as genetic factors. Indeed, multiple cytokine DNA polymorphisms may affect the inflammatory state, the clinical phenotype as well as outcome in this patient population.

C-Reactive Protein↗