Chronic Kidney Disease

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The population of patients with CKD worldwide is growing at a tremendous rate. Consequently, these high-risk patents are now encountered much more frequently in the cardiac catheterization laboratory. In one recent registry, for example, 25% of patients undergoing PCI had at least mild CKD.14 For the interventional cardiologist, identifying these patients is important for two reasons. First, this group

Risk factors Integer score

Risk factors Integer score

Figure 5-2. Risk score for determining risk of contrast-induced nephropathy and dialysis after percutaneous coronary intervention. CHF, congestive heart failure; CIN, contrast-induced nephropathy; eGFR, estimated glomerular filtration rate; IABP, intra-aortic balloon pump; SCr, serum creatinine. (From Mehran R, Aymong ED, Nikolsky E, et al: A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: Development and initial validation. J Am Coll Cardiol 2004;44:1393.)

Mehran Score

Figure 5-2. Risk score for determining risk of contrast-induced nephropathy and dialysis after percutaneous coronary intervention. CHF, congestive heart failure; CIN, contrast-induced nephropathy; eGFR, estimated glomerular filtration rate; IABP, intra-aortic balloon pump; SCr, serum creatinine. (From Mehran R, Aymong ED, Nikolsky E, et al: A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: Development and initial validation. J Am Coll Cardiol 2004;44:1393.)

Figure 5-3. Relationship of measured serum creatinine levels to measured glomerular filtration rates in the Modification of Diet in Renal Disease Study in men (A) and in women (B). Confidence intervals for serum creatinine levels were wider at lower levels of GFR. (From Levey AS, Bosch JP, Lewis JB, et al: A more accurate method to estimate glomerular filtration rate from serum creatinine: A new prediction equation. Modification of Diet in Renal Disease Study Group [comment]. Ann Intern Med 1999;130:464.)

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represents those patients who are at the highest-risk for developing renal dysfunction after PCI and who require specific preventive therapies before their procedure. Second, patients with CKD at baseline are also more likely to have worse cardiovascular outcomes after their procedure. This latter finding results, in part, from the well-established relationship between CKD and cardiovascular disease.

Several clinical factors are useful in identifying individuals at increased risk for CKD. Estimates of the incidence and prevalence of CKD indicate that 20 million people are currently affected in the United States,21 with diabetes mellitus and hypertension accounting for as much as 70% of the disease burden in this country. Additional clinical factors associated with CKD include autoimmune diseases, systemic infections, urinary stones, lower urinary tract obstruction, reduction in kidney mass, exposure to certain drugs such as NSAIDs, recovery from acute kidney failure, and a family history of kidney disease. Several sociodemographic factors are also useful in identifying individuals at increased risk for CKD. Ethnic minority populations, including African Americans, Native Americans, and Hispanic Americans, bear a disproportionate burden of advanced CKD22 and are more likely to develop ESRD than are whites.23 Such disparities also may result, in part, from differences in education, household income, and insurance status.24,25 Different rates of access to care and to delivery of higher-quality care are also likely to be important factors.26

Until recently, defining patients with CKD was problematic because of the multitude of nonstan-dardized definitions and inaccurate assessments of glomerular filtration rate (GFR). In the cardiovascular literature, for example, a serum creatinine level of greater than 1.5 mg/dL was commonly used to identify CKD at baseline,27 whereas levels greater than 2.0 to 2.5 mg/dL have been used to exclude patients from several large cardiovascular randomized clinical trials. Despite its frequent use, the serum creatinine level alone also has several limitations. Most importantly, a normal serum creatinine value does not necessarily reflect normal kidney function, and standard reference ranges for normal often mis-classify patients with early disease (Fig. 5-3).28 Such errors result from the fact that serum creatinine alone does not accurately reflect the level of GFR because of nonlinear relationships that vary according to age, gender, race, and lean body mass. A number of factors other than changes in true GFR account for this relationship (especially in the presence of CKD), including tubular secretion or reabsorption, generation, and extrarenal elimination of the endogenous filtration marker, creatinine. Furthermore, some drugs, such as trimethoprim in Bactrim, can inhibit tubular secretion of creatinine, whereas others, such as non-creatinine chromogens, can interact with common assays used for measurement.

Direct measurements of GFR may be more accurate, but they require either intravenous infusions of exogenous filtration markers such as inulin, iothal-amate, iohexol, and ethylenediaminetetraacetic acid (EDTA) or the careful collection of timed urine specimens. However, these methods also have significant measurement errors and are too expensive and difficult to perform in routine practice. Indirect measurements of GFR are obtained by incorporating serum creatinine values into formulas such as the Cock-croft-Gault equation or the Modification of Diet in Renal Disease (MDRD) study equation.29 Although the MDRD study equation has generally been purported to have less bias, both formulas have limitations in accuracy, especially for patients with normal kidney function.30 In addition, these formulas do not perform well for many other individuals who were not well represented in the cohorts from which these equations were developed, including those who have very high or very low muscle mass, weight, or age; are severely ill or hospitalized; ingest no meat or large amounts of meat; or are from minority racial and ethnic groups such as Asians or Hispanics.30 More recently, serum cystatin C has been suggested as a superior alternative to serum creatinine in quantifying GFR in patients with CKD, because cystatin C has a fairly constant rate of production.30 However, serum levels of cystatin C may also be influenced by age, gender, and muscle mass.31 In addition, many laboratories are not yet equipped to perform this test.

The National Kidney Foundation now specifically defines CKD as the presence of sustained abnormalities of renal function, manifested by either a reduced GFR or presence of kidney damage. Kidney damage is defined as structural or functional abnormalities of the kidney, in the presence or absence of decreased GFR, that is manifested by either pathologic abnormalities (assessed by renal biopsy) or markers of kidney damage including laboratory abnormalities (in the composition of blood or urine) and radiographic abnormalities (on imaging tests).29 Once GFR has been assessed, patients with CKD can be stratified into five stages (Table 5-3) in order of increasing impairment: stage 1, GFR > 90 mL/min per 1.73 m2; stage 2 , 60-89 mL/min; stage 3, 30-59 mL/min; stage 4, 15-29 mL/min; and stage 5, less than 15 mL/min. Patients with GFRs of 60 mL/min or higher are considered to have CKD if they meet additional criteria, demonstrating evidence of kidney damage based on pathologic, laboratory, or imaging tests. Such markers of kidney damage include proteinuria, abnormalities of the urinary sediment, and abnormal radiologic findings. In all cases, CKD requires that kidney disease has persisted for 3 months or longer.

Patients with advanced CKD are at particularly high risk for complications after interventional procedures, because they are close to requiring initiation of renal replacement therapy but have not yet reached

ESRD. They also are far more likely to die or suffer cardiovascular events than to progress to ESRD.32,33 Even patients with milder forms of CKD are at greater risk for cardiovascular events than for adverse renal outcomes.34 The risk of adverse outcomes is progressive, with an independent, graded association between reduced GFR and risk of hospitalizations, cardiovascular events, and death.32,34,35 Consequently, the National Kidney Foundation, the American Heart Association, and the Seventh Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure have classified the presence of CKD as a cardiovascular risk factor.29,33,36

Mechanisms by which renal dysfunction increases cardiovascular risk are unclear and under investigation. The progressive increase in cardiovascular risk associated with declining kidney function is largely explained by a larger burden of traditional risk factors.37 However, CKD is also associated with many nontraditional risk factors associated with renal decline, including albuminuria, proteinuria, homo-cysteinemia, elevated uric acid levels, anemia, dysregulation of mineral metabolism and arterial calcification, oxidative stress, inflammation, malnutrition, endothelial dysfunction, insulin resistance, and conditions promoting coagulation, all of which are associated with accelerated atherosclerosis.27,29,33 Finally, another contributing factor may be the paradox of lower rates of appropriate therapy with risk-factor modification and intervention among CKD patients than in the general population, despite established awareness of their high cardiovascular risk, a concept referred to as "therapeutic nihilism."38

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Diabetes 2

Diabetes 2

Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...

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