Chronic Kidney Disease and Coronary Artery Disease
Mark J. SarnakKerstin AmannSripal BangaloreJoão L. CavalcanteDavid M. CharytanJonathan C. CraigJohn S. GillMark A. HlatkyAlan G. JardineUlf LandmesserL. Kristin NewbyCharles A. HerzogMichael CheungDavid C. WheelerWolfgang C. WinkelmayerThomas H. MarwickDebasish BanerjeeCarlo BriguoriTara I. ChangChien‐Liang ChenChristopher R. deFilippiXiaoqiang DingCharles J. FerroJagbir GillMario GösslNicole M. IsbelHideki IshiiMeg JardinePhilip A. KalraGünther LauferKrista L. LentineKevin W. LobdellCharmaine E. LokGérard M. LondonJolanta MałyszkoPatrick B. MarkMohamed MarwanYuxin NiePatrick S. ParfreyRoberto Pecoits‐FilhoHelen PilmoreWajeh Y. QunibiPaolo RaggiMarcello RattazziPatrick RossignolJosiah RuturiCharumathi SabanayagamCatherine M. ShanahanGautam R. ShroffRukshana ShroffAngela C. WebsterDaniel E. WeinerSimon WintherAlexander C. WisemanAnthony YipAlexander Zarbock
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Abstract:
Chronic kidney disease (CKD) is a major risk factor for coronary artery disease (CAD). As well as their high prevalence of traditional CAD risk factors, such as diabetes and hypertension, persons with CKD are also exposed to other nontraditional, uremia-related cardiovascular disease risk factors, including inflammation, oxidative stress, and abnormal calcium-phosphorus metabolism. CKD and end-stage kidney disease not only increase the risk of CAD, but they also modify its clinical presentation and cardinal symptoms. Management of CAD is complicated in CKD patients, due to their likelihood of comorbid conditions and potential for side effects during interventions. This summary of the Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference on CAD and CKD (including end-stage kidney disease and transplant recipients) seeks to improve understanding of the epidemiology, pathophysiology, diagnosis, and treatment of CAD in CKD and to identify knowledge gaps, areas of controversy, and priorities for research.Keywords:
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ATTEMPTS to correlate the clinical course of uremic patients with changes in certain serum constituents have been unsuccessful.1 Similarly, efforts to link the development of uremia to specific "toxins" have been inconclusive.2 , 3 To date, no etiologic factor has been identified for the uremic state4 — irrespective of any possible relation between diverse mechanisms that terminate in uremia — that is, "renal failure with retention of nitrogenous catabolites."5 In a previous study reported from this laboratory, uremia was produced in dogs by bilateral ureteral ligation.6 In these animals it was demonstrated by filter-paper electrophoresis that prolongation of the uremic state effected . . .
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Uremic Toxins
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To verify if uremia per se influences the eventual outcome of bacterial challenge, we have set up an experimental model of infection in rats with surgically induced uremia and controls. Our preliminary results indicate that both uremic and control rats die at the same rate when challenged intraperitoneally with LD50 of a Pseudomonas strain. These observations would suggest that uremia per se is not a major determinant of the increased incidence of infectious complications as has been noted in this condition.
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The amount of urea nitrogen on the skin of patients with pruritic and nonpruritic uremia and of normal subjects was determined. Significantly higher values were observed in patients with pruritic uremia. It is suggested that non-protein nitrogen-containing compounds are associated with the development of pruritus in uremia.
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Blood urea nitrogen
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Summary 1. Investigations of blood coagulation in 52 acute, and 38 chronically uremic patients were performed. Clinical bleeding tendency were noted in 16 (30,8%) patients with acute uremia and in 13 (34,2%) with chronic uremia. In 237 extracorporeal dialysis carried out during the last 4 years, bleeding occurred in 55 (22,3%) during the procedure. 2. Both acute and chronic uremia are associated with numerous coagulation disturbances. Single laboratory alterations are not uniformly present in patients with uremia, changes in the thrombelastographic patterns, of the prothrombin and fibrinogen are most frequently found. 3. There was a striking tendency for the thrombelastogram to assume particular patterns similar in appearance either to the narrowing of a bottle-neck, a gradual joining, or to an onion like pattern. It is suggested that blood platelets take part in the development of these changes. 4. In comparing laboratory changes in acute and chronic uremia there are no significant differences in single laboratory changes. Although factor VII tends to be lower in acute uremia as compared with chronic uremia and the prothrombin consumption test lower in chronic uremia than in acute uremia.
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ObjectiveTo detect concentration variations of Glutamate and γ-aminobutyric acid in brain tissues of acute renal failure rats with uremia encephalopathy and understand the relationship with uremia encephalopathy.MethodsThirty-six male healthy Wister rats were divided into 2 groups by random: 12 in normal control group,24 in model group. In the model group,Cisplatin was administered to induce acute renal failure.The model group was subdivided into uremia group and uremia encephalopathy group. High performance liquid chromatography(HPLC) was used to detect Glutamate γ-aminobutyric acid contents in rat brain tissues of the 3 groups.ResultsConcentrations of glutamate and γ-aminobutyric acid in rat brain tissues of uremia group and uremia encephalopathy group changed.Compared with normal control group,the concentration of Glutamate γ-aminobutyric acid in uremia group showed no significant difference(P0.05).Compared with normal control group and uremia group,uremia encephalopathy group showed significant difference(P0.01).ConclusionThe contents of Glutamate and γ-aminobutyric acid were significantly changed when acute renal failure with uremia encephalopathy occurs.So Glutamate γ and aminobutyric acid may play a great role in the mechanism of uremia encephalopathy.
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Hepatic Encephalopathy
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Hemorrhagic diathesis
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A model is described for the induction in the rat of varying degrees of stable uremia using controlled resection of renal tissue. Three degrees of uremia have been attained: 'mild--blood urea 40--80 mg/100 ml (6.68--13.36 mmol/1); 'moderate'--blood urea 100--200 mg/100 ml (16.7--33.4 mmol/1), and 'severe'--blood urea greater than 200 mg/100 ml (> 33.4 mmol/1). Mild uremia was produced by unilateral nephrectomy; moderate uremia required the resection of 80 +/- 2% of the total renal mass, and severe uremia was produced by 88 +/- 2% nephrectomy. A sham-operative procedure provided an appropriate control for the model. Evaluation of the model has been carried out using analyses of renal function (GFR, concentrating capacity), blood biochemistry, hematological parameters and histological examination. The ability to induce a standardized, stable uremia at predetermined levels, uncomplicated by the administration of nephrotoxic material, represents an advance on existing methods for producing experimental renal failure.
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Bilateral Nephrectomy
Nephrotoxicity
Blood urea nitrogen
Nephrology
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Objective To detect the brain dopamine (DA) and serotonin (5-HT) concentration of acute renal failure rats with nervous system complication and study the mechanism of uremia encephalopathy.Methods 36 female Wister rats were divided into 2 groups by random:12 in control group,24 in model group.In the model group,Cisplatin 10 mg/kg i.p.qd×2 to induce acute renal failure.According to their clinical manifestation,the model group was devided into uremia group and uremia encephalopathy group.Detecting the brain dopamine and serotonin concentration by high performance liquid chromatography (HPLC);and detecting the serum creatinine (SCr).Results The SCr level of uremia group and uremia encephalopathy group (218.83±24.46 μmol/l,404.58±66.99 μmol/l) was higher than that of control group(87.5±17.51 μmol/l),has significant difference(P0.05).The SCr level of uremia encephalopathy group was higher than that of uremia group,has significant difference(P0.05).The brain DA and 5-HT contents of uremia group(0.738±0.104 μg/g,0.358±0.114 μg/g) were lower than those of control group (0.775±0.108 μg/g,0.383±0.106 μg/g),don't have significant difference(P0.05).The brain DA and 5-HT contents of uremia encephalopathy group(0.652±0.091 μg/g,0.242±0.085 μg/g)were lower than those of control group,have significant difference.The brain DA and 5-HT contents of uremia encephalopathy group were lower than those of uremia group,have significant difference(P0.05).The concents of two neurotransmitters don't have linear correlation with SCr(r=,P0.05).Conclusion Cisplatin 10 mg/kg i.p.qd×2 may build acute renal failure succesefully.The brain DA and 5-HT contents have no change when acute renal failure without nervous system complication,but grow lower when with nervous system complication.,so DA and 5-HT may play a role in uremia encephalopathy.More higher the levels of SCr,more chances of nervous system complication.The concents of two neurotransmitters don't have linear correlation with SCr,that is higher level of SCr doesn't mean lower brain DA and 5-HT concent.
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