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Chronic kidney disease (CKD) is a major public health problem in the United States. It is estimated that nearly 20 million Americans have some degree of chronic kidney disease defined as an estimated glomerular filtration rate of less than sixty milliliters per minute or evidence of kidney damage by imaging study, biopsy, biochemical testing or urine tests with an estimated glomerular filtration rate more than sixty milliliters per minute. Hypertension is present in more than 80% of patients with CKD and contributes to progression of kidney disease toward end stage (ESRD) as well as to cardiovascular events such as heart attack and stroke. In fact the risk for cardiovascular death in this patient population is greater than the risk for progression to ESRD. Proteinuria is an important co-morbidity in hypertensives with CKD and increase risk of disease progression and cardiovascular events. Treatment of hypertension is therefore imperative. The National Kidney Foundation clinical practice guidelines recommend a blood pressure goal of <130 mmHg systolic and <80 mmHg diastolic for all CKD patients. Recent post-hoc analyses of the Modification of Diet in Renal Disease study indicate that lower blood pressure may provide long-term kidney protection in patients with nondiabetic kidney disease. Specifically a mean arterial pressure <92 mmHg (e.g. 120/80 mmHg) as compared to 102-107 mmHg (e.g. 140/90 mmHg) is associated with reduced risk for ESRD. In most cases achieving this goal requires both non-pharmacologic and pharmacologic intervention. Dietary sodium restriction to no more than 2 grams daily is important. In addition, moderate alcohol intake, regular exercise, weight loss in those with a body mass index greater than 25 kg/M(2) and reduced amount of saturated fat help to reduce blood pressure. The first line pharmacologic intervention should be an angiotensin converting enzyme inhibitor or angiotensin II type 1 receptor blocker in those with diabetes or non-diabetics with more than 200 mg protein/gram creatinine on a random urine sample. For non-diabetics with less than 200 mg protein/gram creatinine on a random urine sample, no specific first-line drug class is recommended. After initial dosing with an ACEi, ARB or other drug, a diuretic should be added to the regimen. Thereafter, beta-blockers, calcium channel blockers, apha blockers and alpha 2 agonists (e.g. clonidine) and finally vasodilators (e.g. minoxidil) should be added to achieve blood pressure goal. Combinations of ACEi and ARB are helpful in reducing proteinuria and may also lower blood pressure further in some some cases. Blood pressure should be monitored closely in hypertensive patients with CKD and both clinic and home blood pressure measurements may help the clinician adjust treatment.
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PMID:Treatment of hypertension in chronic kidney disease. 1629 69

Vascular calcification is often encountered in advanced atherosclerotic lesions and is a common consequence of aging. Calcification of the coronary arteries has been positively correlated with coronary atherosclerotic plaque burden, increased risk of myocardial infarction, and plaque instability. Chronic kidney disease (CKD) patients have two to five times more coronary artery calcification than healthy age-matched individuals. Vascular calcification is a strong prognostic marker of cardiovascular disease mortality in CKD patients. Vascular calcification has long been considered to be a passive, degenerative, and end-stage process of atherosclerosis and inflammation. However, recent evidence indicates that bone matrix proteins such as osteopontin, matrix Gla protein (MGP), and osteocalcin are expressed in calcified atherosclerotic lesions, and that calcium-regulating hormones such as vitamin D3 and parathyroid hormone-related protein regulate vascular calcification in in vitro vascular calcification models based on cultured aortic smooth muscle cells. These findings suggest that vascular calcification is an actively regulated process similar to osteogenesis, and that bone-associated proteins may be involved in the development of vascular calcification. The pathogenesis of vascular calcification in CKD is not well understood and is almost multifactorial. In CKD patients, several studies have found associations of both traditional risk factors, such as hypertension, hyperlipidemia, and diabetes, and uremic-specific risk factors with vascular calcification. Most patients with progressive CKD develop hyperphosphatemia. An elevated phosphate level is an important risk factor for the development of calcification and cardiovascular mortality in CKD patients. Thus, it is hypothesized that an important regulator of vascular calcification is the level of inorganic phosphate. In order to test this hypothesis, we characterized the response of human smooth muscle cell (HSMC) cultures to inorganic phosphate levels. Our findings indicate that inorganic phosphate directly regulates HSMC calcification through a sodium-dependent phosphate transporter mechanism. After treatment with elevated phosphate, there is a loss of smooth muscle lineage markers, such as alpha-actin and SM-22alpha, and a simultaneous gain of osteogenic markers such as cbfa-1 and osteocalcin. Elevated phosphate may directly stimulate HSMC to undergo phenotypic changes that predispose to calcification, and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions. Furthermore, putative calcification inhibitory molecules have been identified using mouse mutational analyses, including MGP, beta-glucosidase, fetuin-A, and osteoprotegerin. Mutant mice deficient in these molecules present with enhanced cardiovascular calcification, demonstrating that specific molecules are normally important in suppressing vascular calcification. These findings suggest that the balance of inducers, such as phosphate, and inhibitors, such as MGP, fetuin-A, and others, are likely to control whether or not calcification occurs under pathological conditions.
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PMID:Vascular calcification in chronic kidney disease. 1650 29

Chronic kidney disease (CKD) is a growing epidemic in the United States and worldwide, with nearly two thirds of CKD patients also having diabetes, hypertension, or both. Morbidity and mortality among patients with CKD are high, as are the costs associated with care, which is highly fragmented. Disease management (DM) programs are designed to coordinate the delivery of care to patients, improve clinical outcomes, and reduce costs along the continuum of care. The goals of DM programs in CKD patients are to fill the gaps in current care by focusing on four key areas: (1) slowing the progression of CKD, (2) identifying and managing the complications of CKD, (3) identifying and managing associated comorbid conditions, and (4) smoothing the transition to renal replacement therapy (RRT). To be successful, this approach requires multidisciplinary collaboration among physicians (eg, primary care physicians, endocrinologists, cardiologists, nephrologists, surgeons) and participating caregivers including nurses, dieticians, social workers, and pharmacists. Patient identification, limited reimbursement, late patient referral, and lack of primary care physician and nephrologist knowledge about the importance and details of CKD management are all barriers that must be overcome for such programs to be successfully implemented. Considering the magnitude of the opportunity, DM applied to CKD is a promising approach to the care of this vulnerable population.
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PMID:The case for disease management in chronic kidney disease. 1662 Jan 94

The incidence of end stage renal disease in patients who have not experienced a classic primary renal disease is dramatically increasing. Chronic kidney disease (CKD) in these patients is due to diabetes, mostly type 2, hypertension and generalised atherosclerosis. As these patients are frequently diagnosed as having renal function impairment only in the late phase, more effort should be undertaken to diagnose them earlier, that is, at a time when renoprotective measures can still be undertaken. For that purpose, measurement of the estimated glomerular filtration rate (GFR) might be helpful. To properly interpret those measurements, however, we need to be aware of the pros and cons of the use of formulas to estimate the GFR. Most likely, a better way to detect subjects at risk of CKD in the early phase is screening by dipstick proteinuria or preferably by testing for (micro-) albuminuria. Because microalbuminuria not only indicates increased renal but also enhanced cardiovascular risk, the benefits of such screening programmes may have a much greater affect than only preventing renal disease.
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PMID:Prevention of chronic kidney disease: the next step forward! 1675 39

Chronic kidney disease (CKD) often accompanies cardiovascular disease (CVD). Trends foretelling a greater burden of CKD and CVD are largely a result of increasing frequencies of obesity, hypertension, and diabetes. Nutritional therapy occupies a critical role in reducing risk factors and preventing progressive damage to the kidneys and heart. Nutritional assessment and treatment should take into account both health concerns. This review examines several diet components and eating styles for efficacy in the treatment of these conditions. A variety of dietary regimens claim to provide health benefits, but rigorous scientific validation of long-term efficacy is frequently lacking. An urgent need exists for eating styles that reduce risk of chronic diseases and that are acceptable and achievable in free-living populations. We describe our ongoing study, a randomized controlled trial comparing the American Heart Association Step II diet and a Mediterranean diet, in survivors of a first myocardial infarction. The primary end point is a composite of mortality and major CVD events. Because many in this population have CKD, indicators of kidney damage and function are prespecified secondary end points. Results of this trial should provide insight into optimal dietary interventions for persons with both CVD and CKD.
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PMID:Implications of chronic kidney disease for dietary treatment in cardiovascular disease. 1682 32

Obesity is one of the most preventable causes of morbidity and mortality of the 21st century. Chronic kidney disease (CKD) has been a largely overlooked consequence of obesity; however, accumulating evidence elucidates the association. Obesity is at the core, promoting a cascade of secondary pathologies including diabetes, dyslipidemia, inflammation, hypertension, and the metabolic syndrome; these comorbidities constitute great risk for CKD. With the diagnosis of CKD, there is an increased threat of cardiovascular disease and the attendant increase in morbidity and mortality rates. Substantial weight loss in the obese population can be effectively achieved and maintained through bariatric surgery, which confers major health benefits by producing resolution or improvement of obesity-related comorbidities. This surgical procedure presents an early hazard of acute on chronic kidney failure, which is offset by a potential improvement in the risk of CKD progression with anticipated improvement in hypertension, diabetes, and CKD risk factors. Future research is needed to describe the clinical course and risks and benefits of bariatric surgery in the CKD population.
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PMID:Bariatric surgery for morbid obesity: risks and benefits in chronic kidney disease patients. 1704 26

Chronic kidney disease (CKD) is associated with a high risk of death from coronary artery disease and may modify the response to standard cardiovascular therapies. Treatment of subjects with CKD should ideally be based on evidence from randomized, clinical trials, but how often subjects with CKD have been excluded from these trials is uncertain. We undertook this study in order to quantify how often subjects with moderate to advanced CKD were excluded from large cardiovascular trials. MEDLINE and the reference list of selected articles were searched in order to identify large, randomized, controlled trials of five different coronary artery disease therapies published between 1998 and 2005. Exclusion criteria and reported clinical characteristics of subjects were abstracted. Rates of exclusion and reporting of baseline characteristics of study participants were compared for CKD, diabetes, history of smoking, and hypertension. Eighty-six trials randomizing 411 653 patients were identified. More than 80% of trials excluded subjects with end-stage renal disease and 75.0% excluded patients with CKD. Subjects with diabetes, hypertension, or a history of smoking were excluded less than 4% of the time. Baseline renal function of study participant was reported in only 7% of trials. Patients with CKD are frequently excluded from coronary artery disease trials and renal function of randomized subjects is rarely reported. These findings reinforce the notion that available data on the treatment of coronary artery disease in subjects with CKD have significant limitations and should be generalized to the treatment of subjects with CKD cautiously.
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PMID:The exclusion of patients with chronic kidney disease from clinical trials in coronary artery disease. 1705 Nov 42

Chronic kidney disease (CKD) represents a major global public health concern. Efforts to prevent and/or slow progression of CKD are essential. Lead nephropathy, characterized by chronic tubulointerstitial nephritis, is a well-known risk of chronic, high-level lead exposure. However, in recent years, lead exposure has declined sharply, particularly in developed countries. We reviewed epidemiologic research in general, occupational, and patient populations to assess whether lead, at current exposure levels, still contributes to nephrotoxicity. Other pertinent topics, such as risk in children, genetic susceptibility, and co-exposure to cadmium, are also considered. The data reviewed indicate that lead contributes to nephrotoxicity, even at blood lead levels below 5 microg/dl. This is particularly true in susceptible populations, such as those with hypertension (HTN), diabetes, and/or CKD. Low socioeconomic status is a risk factor for both lead exposure and diseases that increase susceptibility. Future public health risk for lead-related nephrotoxicity may be most significant in those rapidly developing countries where risk factors for CKD, including obesity and secondary HTN and diabetes mellitus, are increasing more rapidly than lead exposure is declining. Global efforts to reduce lead exposure remain important. Research is also needed to determine whether specific therapies, such as chelation, are beneficial in susceptible populations.
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PMID:Lead-related nephrotoxicity: a review of the epidemiologic evidence. 1706 79

Chronic kidney disease (CKD) is a major problem worldwide. It threatens the lives and health of many people and places severe financial burdens on health economies of even the wealthiest countries. It is clear that the approach to prevention is multifaceted including prevention of cardiovascular disease. Inhibitors of the RAS are the drugs of initial choice in preventing progressive CKD, and may be used cautiously in advanced renal insufficiency. In addition blood pressure must be optimally controlled to < 130/80 mm Hg. Treatment of late CKD results only in a risk reduction and not a prevention of end stage renal disease. It is vital that patients at risk for CKD should be identified early before overt renal damage. Screening for microalbuminuria in patients with hypertension, metabolic syndrome and diabetes is particularly important.
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PMID:Importance of modulating the renin-angiotensin system in preventing renal complications of hypertension. 1718 80

Chronic kidney disease (CKD) is a serious condition associated with premature mortality, decreased quality of life, and increased health-care expenditures. Untreated CKD can result in end-stage renal disease and necessitate dialysis or kidney transplantation. Risk factors for CKD include cardiovascular disease, diabetes, hypertension, and obesity. To estimate the prevalence of CKD in the United States (overall and by health risk factors and other characteristics), CDC analyzed the most recent data from the National Health and Nutrition Examination Survey (NHANES). This report summarizes the results of that analysis, which determined that 16.8% of the U.S. population aged >/=20 years had CKD, according to 1999-2004 NHANES data, compared with 14.5% from the 1988-1994 NHANES (i.e., NHANES III), an increase of 15.9% based on crude estimates of prevalence. Persons with diabetes or cardiovascular disease had a greater prevalence of CKD than persons without those conditions. The results underscore the need to continue surveillance for CKD and its risk factors in the United States and to implement new strategies to reduce the number of persons with this condition.
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PMID:Prevalence of chronic kidney disease and associated risk factors--United States, 1999-2004. 1733 26


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