Gene/Protein Disease Symptom Drug Enzyme Compound
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 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The perceived prevalence of Chronic kidney disease (CKD) is on the increase worldwide. This has led to considerable debate and controversy as some believe such an increase reflects a genuine increase in the incidence and prevalence of CKD whilst others perceive it to be the result of the ageing of the population with the inherent decline in kidney function associated with advancing age. This review tries to reconcile both views drawing attention to the fact that the age-related decline in kidney function may not be physiological but instead a manifestation of diffuse vascular ageing and atherosclerosis affecting a number of endorgans including the kidneys. Consequently, the so-call age-related chronic kidney disease (CKD) may be better defined as Cardio-Kidney-Damage (C-K-D).
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PMID:C-K-D: more vascular damage than kidney disease. 2008 46

Chronic kidney disease (CKD) is associated with development of atherosclerosis and premature death from cardiovascular disease. The predisposition of patients with CKD to atherosclerosis is driven by inflammation, oxidative stress and dyslipidemia, all of which are common features of this condition. Markers of dyslipidemia in patients with advanced CKD are impaired clearance and heightened oxidation of apolipoprotein-B-containing lipoproteins and their atherogenic remnants, and a reduction of the plasma concentration, antioxidant, and anti-inflammatory properties of high-density lipoprotein (HDL). Studies in animal models of CKD indicate that the disease promotes lipid accumulation in the artery wall and kidney, leading to atherosclerosis, glomerulosclerosis and tubulointerstitial injury. These effects seem to be mediated by an increased cellular influx of lipids, elevated cellular production and reduced cellular catabolism of fatty acids, and impaired antioxidant, anti-inflammatory and reverse lipid transport properties of HDL. Available pharmacological therapies have been largely ineffective in ameliorating oxidative stress, inflammation, HDL deficiency and/or dysfunction, and the associated atherosclerosis and cardiovascular disease in patients with end-stage renal disease. This Review aims to provide an overview of the mechanisms and consequences of CKD-induced HDL deficiency and dysfunction.
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PMID:HDL metabolism and activity in chronic kidney disease. 2030 98

Chronic kidney disease (CKD) is associated with accelerated atherosclerosis and cardiovascular disease, which is largely mediated by oxidative stress. We investigated the effect of three glutathione (GSH) precursors: N-acetyl-cysteine (NAC), cystine as the physiological carrier of cysteine in GSH with added selenomethionine (F1), and NAC fortified with selenomethionine (F2) on oxidative stress induced by spermine (a uremic toxin) in cultured human aortic vascular smooth muscle cells (VSMC). VSMC were exposed to spermine (15 microM) with or without the given antioxidants (dose 50, 100, 200, and 500 microg/ml) or vehicle (control) and assessed for intracellular GSH levels, 4-hydroxy-trans-2-nonenal (4-HNE), and incorporation of 13C from glucose into alanine and protein. Spermine exposure reduced intracellular GSH levels, increased 4-HNE, and impaired glucose metabolism through reduction in pyruvate generation and/or transamination. Treatment with NAC had no effect on intracellular glutathione level. In contrast, F1 maintained intracellular GSH at control levels at all four doses. Subsequent studies performed with 200 microg/ml of F1, F2, or NAC (optimal dose) revealed normalization of 4-HNE, whereas restoration of 13C from glucose to alanine or protein to control values was only noted in the F1 group. Spermine-induced alterations in VSMC ultrastructure were prevented in approximately 90% of cells treated with F1 but only approximately 50% of cells treated with either NAC or F2. In conclusion, F1 was more effective than NAC or F2 in ameliorating spermine-induced reduction in intracellular GSH levels and cellular alterations in VSMC. The cystine-based GSH precursor (F1) is a promising antioxidant, and further studies are needed to examine the effect of this compound in preventing CKD-associated vascular disease.
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PMID:Effects of a novel cystine-based glutathione precursor on oxidative stress in vascular smooth muscle cells. 2059 43

Chronic kidney disease (CKD) independently increases the rates of cardiovascular disease, whereas the severity of kidney disease correlates with increased cardiovascular morbidity and death. Vitamin D is modified in the liver and the kidney to its active form (1,25-dihydroxyvitamin D) by the 25-hydroxy vitamin D 1-hydroxylase enzyme (CYP27B1). The activated vitamin D brings about its actions through the vitamin D receptor (VDR). The VDRs and CYP27B1 have recently been shown to be expressed in several tissues, not directly involved in mineral homeostasis, including the cardiovascular, immune, and epithelial systems. The action of vitamin D in these tissues is implicated in the regulation of endothelial, vascular smooth muscle, and cardiac cell function, the renin-angiotensin system, inflammatory and fibrotic pathways, and immune response. Impaired VDR activation and signalling results in cellular dysfunction in several organs and biological systems, which leads to reduced bone health, an increased risk for epithelial cancers, metabolic disease, and uncontrolled inflammatory responses. Failure of cardiovascular VDR activation results in hypertension, accelerated atherosclerosis and vascular calcification, cardiac hypertrophy with vascular rarification and fibrosis, and progressive renal dysfunction. An emerging body of evidence has prompted attention to the relationship between CKD, mineral bone disorder (CKD-MBD), and cardiovascular disease in the new guidelines from Kidney Disease: Improving Global Outcomes. Vitamin D receptor activators, commonly used to treat CKD-MBD, and an appropriate treatment of vitamin D hormonal system failure in patients with CKD, may help to reduce cardiovascular morbidity and mortality in these patients.
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PMID:The vitamin D system: a crosstalk between the heart and kidney. 2060 45

Chronic kidney disease (CKD) is associated with a high risk of death from cardiovascular disease. Inflammation, oxidative stress, and dyslipidemia, which are common consequences of CKD, contribute to the pathogenesis of atherosclerosis and cardiovascular disease in this population. Dyslipidemia of CKD is characterized by diminished plasma high density lipoprotein (HDL) concentration, impaired HDL anti-oxidant and anti-inflammatory activities, and elevated plasma triglyceride, very low density lipoprotein (VLDL), intermediate density lipoprotein, chylomicron remnants, and oxidized lipids and lipoproteins. The constellation of inflammation, HDL deficiency, and oxidative modification of lipoproteins can cause atherosclerosis and progression of renal disease. We have recently found lipid accumulation in the remnant kidney and the wall of aorta in rats with CKD induced by 5/6 nephrectomy. This was mediated by up-regulation of scavenger receptors involved in the influx of oxidized lipids or lipoproteins, tubular reabsorption of lipid binding proteins through megalin-cubilin complexes, upregulation of fatty acid synthesis, and downregulation of fatty acid oxidation pathways. The combination of increased lipid influx, elevated production and reduced catabolism of lipids, and impaired HDL-mediated reverse cholesterol transport can promote atherosclerosis, glomerulosclerosis, and tubulointerstitial damage. Although statins can be effective in slowing CKD progression in patients with mild-to-moderate CKD, they have consistently failed to mitigate oxidative stress, inflammation, HDL deficiency, or cardiovascular mortality in the end-stage renal disease populations. Similarly, high doses of antioxidant vitamins have failed to either ameliorate oxidative stress, inflammation, or improve overall mortality in end-stage renal disease. This article is intended to provide a brief review of the effects of CKD on HDL structure and function and pathways of lipid influx, efflux, synthesis, and catabolism in the artery wall and the diseased kidney.
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PMID:Lipotoxicity and impaired high density lipoprotein-mediated reverse cholesterol transport in chronic kidney disease. 2079 69

Increasing evidence points to the fact that plasma HDL cholesterol levels do not always accurately predict HDL function including reverse cholesterol transport and modulation of inflammation. These functions appear to have evolved as part of our innate immune system. HDL is anti inflammatory in healthy individuals in the absence of systemic oxidative stress and inflammation. In those with chronic illnesses such as renal failure however, HDL may become dysfunctional and actually promote inflammation. HDL may be thought of as a shuttle whose size can be estimated by HDL cholesterol levels. The content of the shuttle however, is what determines the anti inflammatory potential of HDL and can change from one, supporting reverse cholesterol transport to one that is less efficient in carrying out this function. Chronic kidney disease (CKD), and inflammatory disorder, is associated with development of accelerated atherosclerosis and premature death from coronary artery disease (CAD). Patients with CKD present with dyslipidemia, oxidative stress and systemic inflammation. Among the abnormalities in lipid metabolism in these patients is reduced levels and protective capacity of HDL. Recent studies have shown that HDL from patients with end stage renal disease is not capable of preventing LDL oxidation and that it induces monocyte migration in artery wall model systems. Treatment of plasma from these patients, with an HDL mimetic peptide improved the anti inflammatory properties of patient's HDL and made LDL more resistant to oxidative modification. Animal models of kidney disease also had proinflammatory HDL and treatment with the peptide mimetic improved markers of inflammation and anti inflammatory capacity of HDL. Whether HDL mimetic peptides will have therapeutic benefit in patients with renal failure will have to be determined in clinical studies.
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PMID:Chronic inflammatory disorders and accelerated atherosclerosis: chronic kidney disease. 2122 43

Chronic kidney disease (CKD) comprises a group of pathologies in which the renal excretory function is chronically compromised. Most, but not all, forms of CKD are progressive and irreversible, pathological syndromes that start silently (i.e. no functional alterations are evident), continue through renal dysfunction and ends up in renal failure. At this point, kidney transplant or dialysis (renal replacement therapy, RRT) becomes necessary to prevent death derived from the inability of the kidneys to cleanse the blood and achieve hydroelectrolytic balance. Worldwide, nearly 1.5 million people need RRT, and the incidence of CKD has increased significantly over the last decades. Diabetes and hypertension are among the leading causes of end stage renal disease, although autoimmunity, renal atherosclerosis, certain infections, drugs and toxins, obstruction of the urinary tract, genetic alterations, and other insults may initiate the disease by damaging the glomerular, tubular, vascular or interstitial compartments of the kidneys. In all cases, CKD eventually compromises all these structures and gives rise to a similar phenotype regardless of etiology. This review describes with an integrative approach the pathophysiological process of tubulointerstitial, glomerular and renovascular diseases, and makes emphasis on the key cellular and molecular events involved. It further analyses the key mechanisms leading to a merging phenotype and pathophysiological scenario as etiologically distinct diseases progress. Finally clinical implications and future experimental and therapeutic perspectives are discussed.
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PMID:Etiopathology of chronic tubular, glomerular and renovascular nephropathies: clinical implications. 2125 Dec 96

Chronic kidney disease (CKD) is an independent risk factor for cardiac mortality. Accelerated atherosclerosis is frequently seen in patients with CKD. However, even in drug eluting stent era, higher restenosis rate after percutaneous coronary intervention (PCI) for coronary artery disease remains a clinical limitation in patients with CKD. Similar tendency is also seen when treated with endovascular therapy (EVT) for peripheral artery disease. Thus, management for atherosclerotic disease is very difficult in patients with CKD. Recent reports have shown that improvement of devices and/or intensive medical treatment may contribute better clinical outcomes after PCI or EVT in patients with CKD. In addition, inflammatory markers such as C-reactive protein may predict worse clinical outcomes including restenosis in such population.
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PMID:[Interventional revascularization for cardiovascular disease in patients with chronic kidney disease]. 2138 87

Chronic kidney disease (CKD) is frequently observed in patients with arterial hypertension. The same factors that promote the appearance and progression of atherosclerosis can also promote the development of CKD. Two parameters are usually measured to estimate alterations in renal function, the presence of albuminuria, and the estimation of glomerular filtration rate (GFR). Microalbuminuria and a decreased estimated GFR (<60 mL/min/1.73 m(2)) are both accompanied by a significant increase in cardiovascular (CV) risk. Chronic kidney disease can develop all over the cardiorenal continuum and its presence in hypertensive patients with already developed CV disease contributes to a further increase in the development of events and death. Renal protection will in turn obtain CV protection and the treatment to be used is similar to that employed to prevent or to treat established CV disease.
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PMID:Renal function and target organ damage in hypertension. 2144 66

Chronic kidney disease (CKD) is associated with cardiovascular (CV) events caused by advanced atherosclerosis. Computed tomographic coronary angiography (CTA) can accurately diagnose coronary artery disease (CAD) and predict CV outcomes. The aim of the present study was to evaluate whether moderate CKD provides prognostic information for CV events in patients undergoing CTA. In total 885 patients with suspected CAD underwent CTA and were stratified to moderate CKD (85 patients) or no CKD (770 patients) based on a cut-off estimated glomerular filtration rate of 60 ml/min/1.73 m(2). After 896 days of follow-up, 42 patients developed CV events. Annualized CV event rates were 1.2% in patients with no CKD and no CAD, 2.5% in patients with moderate CKD alone, 2.5% in patients with obstructive CAD alone, and 3.7% in those with moderate CKD and obstructive CAD. Multivariate models demonstrated that moderate CKD (hazard ratio 2.39, confidence interval 1.09 to 5.21, p = 0.03) and obstructive CAD (hazard ratio 2.76, confidence interval 1.40 to 5.44, p <0.01) were independent predictors of CV events. Importantly, moderate CKD provided incremental prognostic information in addition to clinical characteristics and obstructive CAD (chi-square 49.4, p = 0.04). In conclusion, moderate CKD was associated with CV events and provided incremental prognostic information.
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PMID:Prognostic value of renal dysfunction for the prediction of outcome versus results of computed tomographic coronary angiography. 2178 94


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