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Diabetic patients are at increased risk for adverse outcomes of surgery. These adverse outcomes are related to pre-existing complications of diabetes, especially atherosclerotic disease, nephropathy (and perhaps increased susceptibility to other renal toxins), and peripheral and autonomic neuropathy. Hyperglycemia is associated with likely risks for poorer wound healing, increased susceptibility to infection, and probable loss of administered nutrients through glycosuria. Insulin use has the flexibility of timing and dose in the postoperative management of most diabetic patients. The combinations of intermediate-acting and long-acting insulins and short-acting insulins usually are related to the experience and preferences of the treating physicians and allied health professionals. Intravenous insulin (always R) may be limited to administration in the ICU because of the need for frequent blood glucose monitoring and rapidity of glucose response to intravenous insulin. The use of short-acting insulin analogues has been shown to work well as premeal insulin or for rapidly treating marked hyperglycemia in the outpatient setting. Meal delivery in the hospitalized patient may not be timed as precisely as in the home situation. Nurses may be responsible for many patients. The rapid-acting analogues may be associated with increased risk for hypoglycemia in the hospitalized patient if insulin cannot be given immediately before a meal. These rapid-acting insulin analogues usually are limited to circumstances in which the patient can determine the dose and self-administer just before ingestion of the meal. The long-acting insulin analogues may not afford enough flexibility in many situations in which daily dosages changes are occurring in intermediate-acting and long-acting insulins. Oral glucose-lowering agent use in the postoperative state usually is limited to selected patients, including patients who have been on such agents before surgery, who have only mild elevations of blood glucose, who are able to ingest oral medications, and who do not have significant comorbid conditions (or significant risk for such conditions) that may be contraindications to use of such agents (see Table 3). Sulfonylureas and other insulin secretagogues (e.g., meglitinide, nateglinide) lower glucoses acutely. The risk for hypoglycemia is slightly less with the nonsulfonylurea agents. Efficacy and side effects limit the use of carbohydrase inhibitors for hospitalized patients. The glucose-lowering effects of biguanides and thiazolidinediones usually are not rapid enough for hospitalized patients who have never taken these medications. For patients who have been on a biguanide or thiazolidinedione before admission, these agents often are restarted in the postoperative period when oral intake of medications is possible and hepatic and renal function are stable. The hospital period affords an opportunity to review long-term management issues related to diabetes and its complications. Instruction on the importance of medical nutrition therapy, glycemic control, management of hypertension, dyslipidemia, and aspirin use as well as basic guidelines for foot care should be carried out during the hospitalization and at the time of discharge. Similarly, appropriate arrangements for medical nutrition therapy, general diabetes education (especially for newly diagnosed diabetic patients), and regular medical follow-up are important to ensure long-term, excellent surgical and medical outcomes.
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PMID:Postoperative management of the diabetic patient. 1156 95

Obesity has been shown to be an independent risk factor for coronary heart disease. The insulin resistance associated with obesity contributes to the development of other cardiovascular risk factors, including dyslipidemia, hypertension, and type 2 diabetes. The coexistence of hypertension and diabetes increases the risk for macrovascular and microvascular complications, thus predisposing patients to cardiac death, congestive heart failure, coronary heart disease, cerebral and peripheral vascular diseases, nephropathy, and retinopathy. Body weight reduction increases insulin sensitivity and improves both blood glucose and blood pressure control. Metformin therapy also improves insulin sensitivity and has been associated with decreases in cardiovascular events in obese diabetic patients. Antihypertensive treatment in diabetics decreases cardiovascular mortality and slows the decline in glomerular function. However, pharmacological treatment should take into account the effects of the antihypertensive agents on insulin sensitivity and lipid profile. Diuretics and beta-blockers are reported to reduce insulin sensitivity and increase triglyceride levels, whereas calcium channel blockers are metabolically neutral and ACE inhibitors increase insulin sensitivity. For the high-risk hypertensive diabetic patients, ACE inhibition has proven to confer additional renal and vascular protection. Because hypertension and glycemic control are very important determinants of cardiovascular outcome in obese diabetic hypertensive patients, weight reduction, physical exercise, and a combination of antihypertensive and insulin sensitizers agents are strongly recommended to achieve target blood pressure and glucose levels.
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PMID:Treatment of obesity hypertension and diabetes syndrome. 1156 61

Patients with chronic uremia have a substantially elevated risk of death from cardiovascular disease than do the general population. Although uremic and nonuremic groups share some of the risk factors for cardiovascular mortality, such as older age, diabetes, and inflammation, other factors appear to affect cardiovascular mortality in the opposite direction. For example, being overweight and having hyperlipidemia are established risk factors in the general population, whereas lower body mass index and lower plasma cholesterol have been shown to be risk factors for cardiovascular mortality in end-stage renal disease (ESRD). This paradoxical phenomenon is explained by two facts: (1) that malnutrition is a strong predictor of cardiovascular mortality in ESRD and (2) that plasma lipid levels are lowered in malnutrition. However, it is not known whether atherosclerosis is promoted by malnutrition or by low cholesterol level. Because the cardiovascular mortality rate is theoretically the product of event rate and fatality rate after an event, risk factors for cardiovascular mortality could fall into two categories: those raising the event rate and those affecting the fatality rate. Some factors could work both ways. Patients with ESRD show a significant increase in both event rate and fatality rate. Dyslipidemia is an independent factor affecting atherosclerotic arterial wall changes and cardiovascular events in ESRD. Other factors affecting the cardiovascular event rate in ESRD include diabetes and an elevated homocysteine level. In contrast, factors associated with poor survival after an event include diabetes and anemia. Malnutrition could be a factor causing the fatality rate to rise, although there is no direct evidence supporting this possibility. Further studies are needed to show the differential effects of a risk factor on event rate and fatality rate. Patients with ESRD would have a better chance of living longer by better management of the two categories of risk factors.
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PMID:Paradox of risk factors for cardiovascular mortality in uremia: is a higher cholesterol level better for atherosclerosis in uremia? 1157 13

In the last few decades, clinical and experimental data have established microalbuminuria/proteinuria as an independent risk factor for renal disease and for progression of renal disease in patients with diabetes and in those with essential hypertension. Reduction of proteinuria with the use of angiotensin-converting enzyme inhibitors has been shown in clinical trials to delay or stabilize the rate of progression of renal disease. This effect appears to be independent of any effect on blood pressure control. In conjunction with other therapeutic interventions such as dietary modification and control of serum lipids, it appears that for at least a subgroup of patients, it is possible to delay or prevent progression of kidney failure. More recently, evidence has accumulated that establishes microalbuminuria/proteinuria as an independent risk factor for cardiovascular morbidity and mortality even in those without other clinical evidence of kidney disease. There is frequently a clustering of risk factors in these individuals that includes insulin resistance, salt-sensitivity, hypertension, and dyslipidemia. The mechanism of this relationship of proteinuria and cardiovascular disease is unclear, but the presence of proteinuria as a marker for cardiovascular disease has important implications for the identification and treatment of individuals at risk.
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PMID:Proteinuria and cardiovascular disease. 1157 14

Patients with end-stage renal disease (ESRD) suffer from a secondary form of complex dyslipidemia consisting of both quantitative and qualitative abnormalities in serum lipoproteins resulting from alterations in lipoprotein metabolism and composition. The prominant features of uremic dyslipidemia are an increase in serum triglyceride levels (due to elevated very low density lipoprotein [VLDL]-remnants and intermediate-density lipoprotein [IDL]) and low high-density lipoprotein (HDL) cholesterol. Low-density lipoprotein (LDL) cholesterol often is normal, but the cholesterol may originate from the atherogenic small and dense LDL subclass (sdLDL). The apolipoprotein B (apoB)-containing part of the lipoprotein may undergo modifications (enzymatic- and advanced glycation end-product [AGE]-peptide modification, oxidation, or glycosilation). Modifications contribute to impaired LDL receptor-mediated clearance from plasma and promote prolonged circulation. While LDL particles undergo a vicious cycle of accumulation and modification, reverse cholesterol transport is also impaired due to low lecithin:cholesterol acyltransferase (LCAT) and paraoxonase activity. Therefore, discoid HDL particles are structurally altered and hepatic cholesterol clearance is limited. The composition of HDL may also be altered during states of inflammation. The contribution of this complex and atherogenic form of dyslipidemia to cardiovascular disease in patients with renal disease is unclear at present. Most studies are negative in demonstrating the predictive power of serum lipids for the development of cardiovascular disease. This is most likely due to interference with deteriorating aspects of the activated acute-phase response. Nevertheless, patients with renal disease belong to a very high cardiovascular risk group and dyslipidemia should most likely be subjected to sufficient lipid-lowering therapy in most patients. Because it is also still unclear whether we have available therapies with sufficient impact on LDL size, remnant lipoprotein-lowering, and restoration of HDL function, we urgently need the results from large scale intervention trials such as the 4D-trial and the CHORUS study.
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PMID:Abnormalities in uremic lipoprotein metabolism and its impact on cardiovascular disease. 1157 15

Cardiovascular mortality is substantially higher in patients with end-stage renal disease (ESRD). Lipoprotein abnormality in ESRD is one of the possible risk factors for advanced atherosclerosis. Uremic dyslipidemia is characterized by increased plasma triglycerides due to elevated very low density lipoprotein (VLDL) and decreased high-density lipoprotein (HDL). Plasma total or low-density lipoprotein (LDL) cholesterol is rarely elevated in hemodialysis patients. The "LDL" by standard assay methods consists of intermediate-density lipoprotein (IDL) and LDL devoid of IDL. Although "LDL" is not increased, IDL is markedly elevated in uremic plasma. We previously showed that aortic stiffness of hemodialysis patients was associated positively with VLDL, IDL, and LDL devoid of IDL and that IDL is the best lipoprotein predictor of aortic stiffness. The IDL level is correlated positively with plasma total cholesterol, triglyceride, and "LDL" levels. Importantly, increased IDL is found in ESRD patients with "normal" "LDL"cholesterol levels, indicating that the target "LDL" level should be lower than that for the general population. More than 40% of hemodialysis patients exceeded the upper limit (15 mg/dL, 95th percentile level) of IDL cholesterol in healthy subjects. Based on a linear relationship between IDL and "LDL," the normal range of IDL cholesterol (<15 mg/dL) corresponds to "LDL" cholesterol by the Friedewald equation below 100 mg/dL in hemodialysis patients. Statins effectively and safely reduce "LDL," including IDL in patients treated with hemodialysis or peritoneal dialysis. The effect of lipid-lowering therapy on cardiovascular mortality in ESRD, however, awaits the results of ongoing prospective trials.
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PMID:Atherogenic lipoproteins in end-stage renal disease. 1157 18

Cardiovascular disease is the leading cause of morbidity and mortality in end-stage renal disease. Causes include those usually found in the general population, those related to the uremic status, and those related to dialytic treatment. Hypertension, hypotension, anemia, hypoalbuminemia, malnutrition, dyslipidemia, reactive C protein, calcium-phosphate product, dialysis modalities, and hyperhomocysteinemia are discussed extensively. Special emphasis is put on hyperparathyroidism as a traditional toxin. The emergent role of sleep apnea has been confirmed in animal models as well as in humans studied using polysomnography. There are difficulties in diagnosing coronary disease, because angiography is not risk-free, is expensive, and should be reserved for patients having symptoms of heart failure and/or patients having diabetes mellitus, and/or patients entering a transplantation list. This allows patients with coronary disease to undergo coronary artery bypass (preferably) or percutaneous transluminal angioplasty. Patients for whom surgery is not appropriate should be treated using more traditional medical procedures.
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PMID:The heart in uremia: role of hypertension, hypotension, and sleep apnea. 1157 20

Clinical data have established microalbuminuria/proteinuria as an independent risk factor for the development and progression of renal disease in patients with either diabetes or essential hypertension. Decreased kidney function is associated with increased cardiovascular risk, even at modest reductions in estimated creatinine clearance (to approximately 60 mL/min/1.73 m(2)) or modest elevations in serum creatinine (>1.4 mg/dL). Treatment with angiotensin-converting enzyme inhibitors has been shown in clinical trials to delay or stabilize the rate of progression of renal disease. Reduction in cardiovascular events, such as stroke and myocardial infarction, also has been shown in these high-risk individuals. These effects are dependent and independent of blood pressure control, suggesting a nonhemodynamic effect in blockade of the renin-angiotensin system. In conjunction with other therapeutic interventions, such as dietary modification and control of serum lipids, it appears that for at least a subgroup of patients it is possible to delay or prevent progression of kidney failure. There frequently is a clustering of risk factors in these individuals, including insulin resistance, salt sensitivity, hypertension, and dyslipidemia. The mechanism of the relationship between albuminuria and cardiovascular disease is unclear but may be related to endothelial cell dysfunction. Nonetheless, the presence of microalbuminuria/proteinuria as a marker for cardiovascular disease has important implications for the identification and treatment of individuals at risk.
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PMID:Metabolic pathogenesis of cardiorenal disease. 1172 77

Chronic renal failure patients suffer from a secondary form of complex dyslipidemia, similar to the so-called atherogenic dyslipidemia in insulin resistant patients or to diabetic dyslipidemia. The most important abnormalities are an increase in the serum level of triglyceride (elevated VLDL-remnants/IDL), small LDL particles and a low HDL cholesterol. The highly atherogenic LDL subclass, namely LDL-6 or small dense LDL, accumulates in hypertriglyceridemic diabetic hemodialysis patients. All these lipoprotein particles contain apoB, thus much of this complex disorder can be summarized as an elevation of triglyceride-rich apoB containing complex lipoprotein particles. Growing evidence suggests that all of the components of this type of dyslipidemia are independently atherogenic. Further disturbances exist in the dynamics of cholesterol exchange between the various lipoprotein particles and in transport from cells to catabolic sites. The European Joint Task Force and the US National Cholesterol Education Program expert panel have issued guidelines for the general population to lower the cardiovascular risk in hyper- and dyslipidemias. There is preliminary consensus that these guidelines should be applied to dialysis patients. However, the genesis of atherosclerosis in the dialysis population may be different and real benefit from lipid-lowering has not yet been demonstrated in this population. Large-scale, prospective randomized trials (4D-trial, HARP) are underway to determine whether statins reduce cardiovascular complications in diabetic and non-diabetic patients with end-stage renal disease (ESRD) and on hemodialysis treatment.
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PMID:Lipid changes and statins in chronic renal insufficiency and dialysis. 1179 51

During the course of developing clinical practice guidelines to improve outcomes of dialysis patients, it became evident that there existed an even greater opportunity to improve outcomes for all individuals with kidney disease, from the earliest stage of kidney injury through the entire spectrum of its progression to kidney failure, when replacement therapy becomes necessary. The development and adoption of a public health approach to the progressive course of chronic kidney disease could allow for the application of interventional strategies to prevent the loss of kidney function in some cases, to slow the progression of kidney disease in many others, and to ameliorate the complication or comorbidities in those with progressive kidney disease. In order to respond to this need, a new initiative, termed the Kidney Disease Outcomes Quality Initiative (K/DOQI), was launched in January of 2000. This article summarizes the recommendations of the first three set of clinical practice guidelines being developed under this new initiative: Chronic Kidney Disease: Evaluation, Classification and Stratification; Bone Metabolism and Disease in Chronic Kidney Disease, and Dyslipidemias in Kidney Failure.
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PMID:Impact of the new K/DOQI guidelines. 1180 66


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