- Decrease ESRD incidence rates
- Decrease cardiovascular mortality in ESRD patients
- Increase pre-ESRD preparations to decrease ESRD-related morbidity
- Decrease racial and gender disparities in kidney transplantation rates
- Increase periodic microalbuminuria screening in persons with diabetes
- Increase treatment to preserve renal function in persons with diabetes and proteinuria
- Increase screening for renal disease in persons with hypertension
- Optimize blood pressure control in persons with renal disease
- Increase counseling about renal risk factors
- Increase intensive management of CVD risk in persons with renal disease
Reduce the incidence, morbidity, mortality and health care costs of chronic kidney disease.
Renal disease: A synonym for kidney disease. The two terms are used interchangeably in this chapter.
Glomerular filtration: The process by which the kidneys filter the blood, clearing it of toxins.
Glomerular filtration rate (GFR): An important measure of kidney function, the rate at which the blood is cleared by glomerular filtration. Normal GFR values in adults are between 100 and 150 ml/min. One of the most important hallmarks of chronic renal disease is a progressive decline in the rate of glomerular filtration. Generally a GFR below 75 ml/min represents clinically significant renal insufficiency. A GFR of less than 10 ml/min represents renal failure of a severity usually requiring renal replacement therapy to maintain life.
Chronic renal insufficiency, chronic renal failure and end-stage renal disease are the terms used in this chapter to describe the continuum of increasing renal dysfunction and decreasing GFR. Because of the progressive nature of kidney disease, for most patients they represent successive stages in disease.
Chronic renal insufficiency: The stage in chronic renal disease in which damage to the kidney has already resulted in significant impairment of renal function but systemic manifestations are minimal. In this stage, in fact, most patients are asymptomatic. Chronic renal insufficiency is usually identified because the serum creatinine is slightly elevated (greater than 1.5 mg/dl in men or 1.2 mg/dl in women, and greater than age-specific normative values in children.) The serum creatinine test is insensitive, however, and as noted below, does not identify all people who have chronic renal insufficiency. Although precise GFR limits cannot be assigned to this stage of disease, typically patients with chronic renal insufficiency have a GFR between 30 ml/min and 75 ml/min.
Chronic renal failure: The stage in chronic renal disease in which renal dysfunction has progressed to a level to result in systemic manifestations. These include a rise in the blood concentration of urea, creatinine, and phosphate, which are removed by the kidneys, and other manifestations such as anemia, bone disease, acidosis, and salt and fluid retention. Growth failure may be seen in children. Most patients with chronic renal failure progress to end-stage renal disease.
End-stage renal disease (ESRD): The stage in chronic renal disease in which renal replacement therapy, dialysis or kidney transplantation, is needed to sustain life. ESRD is generally an irreversible state. Glomerular filtration rate is usually less than 10 ml/min.
Proteinuria: Abnormal levels of protein in the urine. Proteinuria is a marker for structural kidney damage or inflammation, and may also be involved in the pathogenesis of progressive renal injury. Increased risks of developing progressive renal disease1, 2 , of death 3, 4, and of death due to cardiovascular diseases5 have been documented in persons with persistent proteinuria. Urine protein can be estimated by a dipstick method, which provides a semi-quantitative estimate of concentration. More accurate measures include determining the ratio of urine protein to urine creatinine or the amount of protein excreted by a person in a 24-hour period.
Microalbuminuria: Abnormally elevated levels of albumin in the urine, (but at levels too low to be detectable by the dipstick method used to test for protein in the urine). Increased urinary excretion of albumin, even if the concentration is too low to be detectable as dipstick proteinuria, has been associated with increased risk of progressive kidney disease in diabetics6, 7 and increased risk of subsequent mortality in persons with8 and without diabetes9, 10 and in elderly individuals11. Microalbuminuria can be measured in several ways. If a random urine sample is used, the albumin concentration in the first-voided morning urine or the ratio of urine albumin to urine creatinine can be used. If a timed urine collection is available, an albumin excretion rate can be determined. Urine albumin concentrations of 30-300 (ug/ml, urinary albumin to creatinine ratios of >3.5 mg/mmol, and urine albumin excretion rates of >15 (ug/min have all been used as cutoff values for detection of microalbuminuria.
Serum or plasma creatinine: A blood chemistry measurement that is used to estimate the level of kidney function. Serum creatinine is an important index for monitoring progression of disease in persons with chronic renal disease. Elevations in serum creatinine are an insensitive marker of early chronic renal insufficiency. However, in advanced renal failure, a change in serum creatinine is a more reliable indicator. This test remains the most widely available method used to estimate the glomerular filtration rate, or to monitor changes in level of renal function12.
Diabetes mellitus: A chronic disease due to insulin deficiency and/or resistance to the action of insulin and associated with hyperglycemia. Diabetes is the leading cause of end-stage renal disease.
Type 1: Type I diabetes (previously called insulin dependent diabetes mellitus, IDDM) is an autoimmune destructive disease of the insulin-producing cells of the pancreas, typically with onset under age 30. Insulin therapy is required.
Type 2: Type 2 diabetes (previously called non-insulin-dependent diabetes mellitus, NIDDM, or adult-onset diabetes) is the most common form of diabetes. Its hallmark is insulin resistance. Therapy can include insulin, but in many persons diet and/or oral agents are used to control hyperglycemia.
United States Renal Data System: (USRDS) A national database of information on ESRD patient incidence, mortality and morbidity outcomes. The USRDS is based primarily on data collected by the Health Care Financing Administration's Medicare ESRD Program, and is funded by a contract from the National Institutes of Health13. This database contains information on approximately 93 percent of all patients treated for ESRD in the United States. Most of the data cited in this HP 2010 chapter derive from USRDS reports. As noted, these numbers reflect reported cases of treated end-stage renal disease, and therefore do not include patients who die without treatment, or patients whose care is not reported to the USRDS.
Certain terms, common with other Healthy People 2010 chapters, are important in discussion of the health impact of chronic kidney disease.
Incidence rate: A measure of the number of newcases of disease occurring in a specific population over a specific period of time, usually 1 year. For end-stage renal disease, the best information is based on the incidence of treated end-stage renal disease, reported through Medicare to the USRDS. The available data does not include those patients who die without receiving treatment.
Prevalence rate: A measure of the total number of cases of disease existing in a specific population at a certain point in time (point prevalence) or over a certain period of time (period prevalence).
Scope of the problem
The most important health consequence of chronic kidney disease is the development of renal failure. When renal function has deteriorated to a point where it is no longer adequate to sustain life and the process is considered irreversible, the patient has end-stage renal disease. In 1996, the last year for which complete data is available, 74,116 new patients developed irreversible kidney failure or ESRD14. For virtually all of these individuals the beginning of ESRD, sometimes called renal death, meant permanent dependence on renal replacement therapy to stay alive.
Two methods of treatment are available for these patients, dialysis and renal transplantation. The development of these two methods has been an important advance of modern medicine, which has had an impact on many people. In 1996, 335,014 patients in the United States depended on either dialysis or a kidney transplant to replace the function of their own failed kidneys15. While these are lifesaving treatments, the methods for renal replacement have substantial limitations. They are expensive16 and while life saving, these treatments do not restore normal health. The morbidity and mortality experienced by the treated ESRD population is substantially higher than for the general population17.
In most instances, ESRD develops as the consequence of progressive damage to the kidney over a decade or more. A number of underlying diseases can cause progressive renal failure, most importantly diabetes mellitus, which, in 1996 accounted for 42 percent of incident cases of ESRD, and hypertension which was responsible for 26 percent of incident cases18. Other conditions that contribute significantly to the incidence of chronic renal failure include glomerulonephritis, vasculitis, interstitial nephritis, and genetic and congenital disorders, most importantly polycystic kidney disease19. End-stage renal disease affects persons of all ages. The peak incidence of reported ESRD is in the sixth decade of life, but of the 335,014 ESRD patients treated in 1996 — 25 percent were under age 45 and 2 percent — 6,000 children — were under the age of 2020. ESRD is particularly devastating in childhood, because it often results in impaired growth and development.
Over the last decade there has been a worrisome growth in the incidence of end-stage renal disease. The most recent data from the USRDS show that the incidence rate of ESRD has increased from 142 per million population in 1987 to 276 per million population in 199621. In absolute terms, this represents an increase in the annual number of new cases of ESRD from 34,797 in 1987 to 74,116 in 199622. This growth has been steady, and has occurred in a time period when death rates from other diseases, especially cardiovascular disease, have declined23. The increased incidence is not confined to a single age group; although incidence rates have grown slightly more rapidly for individuals over age 75, sizable increases have been noted in every age group24. The causes of this increase in the number of persons developing ESRD are not completely understood, but one major factor appears to be a national increase in the incidence of diabetes mellitus, particularly Type 225, 26. In 1987, ESRD incidence rate due to diabetes was 45 per million population. In 1996, that had increased 150 percent to a rate of 113 per million population (adjusted for age, race and sex)27.
Impact of kidney disease
Kidney disease has a disproportionate impact on minority populations, especially African-Americans and Native Americans. In 1996, the point prevalence rates of ESRD per million population, (adjusted for age and sex) were 3,404 in African-Americans and 2,761 in Native Americans/Alaskan Natives, compared to 754 in whites, differences of 4.5 and 3.7 fold respectively28. African-Americans develop end stage renal failure at an earlier age than whites; their mean age at ESRD incidence was 55.8 years compared with 62.2 in whites29. African-Americans constitute almost 30 percent of prevalent ESRD patients, as compared to constituting only 12.6 percent of the U.S. population30. The available data on ESRD does not yet separately assess the disease burden for Hispanic Americans, but there is some evidence that this group may also be more vulnerable to kidney failure, particularly from diabetes mellitus31, 32. Data on persons of Asian or Pacific Island ancestry, indicate ESRD incidence rates which are slightly higher than those for whites.
ESRD has a substantial impact on scarce federal resources for health care. The passage in 1972 of the Social Security Amendment P.L.92-603 instituted federally financed health care coverage for dialysis and renal transplantation, effective July 1, 1993. The cost of this program has far exceeded original expectations. Medicare spending in 1996 was estimated to be $10.96 billion, a 12.5 percent increase from the $9.74 billion spent in 1995; and total ESRD spending by all payers in 1996 was estimated to be $14.55, up from $13.05 billion in 199533. While the ESRD population comprised only 0.6% of the total Medicare population in 1994, it consumed 5.1% of Medicare expenditures34. Although there have been modest increases in the cost per patient, the driving force behind the growth in ESRD expenditures has been the increase in number of patients.
Although end-stage renal disease is the most feared consequence of renal disease, chronic renal insufficiency is several times more prevalent and has potential impact on health and well being. The exact prevalence of chronic renal insufficiency is uncertain; the best available estimates derive from national surveys, particularly NHANES III, which included measurements of serum creatinine. Elevations in serum creatinine are, however, an insensitive marker of early chronic renal insufficiency. For example, in a 50 year old person, a creatinine value of 2 mg/dl corresponds to a GFR of only 26 ml/min in a 50 kg woman, or 44 ml/min in a 70 kg man. The corresponding values for a serum creatinine of 1.7 mg/dl are 31 ml/min in a 50 kg woman, and 51 ml/min in a 70 kg man12. In elderly persons, and in persons with low muscle mass or chronically poor protein intake, quite severe impairment in renal function can be present with only minimal elevation of serum creatinine35, 36. Hence, prevalence estimates based on serum creatinine can provide only a lower limit estimate of the number of individuals with chronic renal insufficiency.
The NHANES III (1988-94) study has documented that the 95th percentile for serum creatinine values in persons above the age of 12 years is 1.5 mg/dl in men, and 1.2 mg/dl in women37. This survey data, together with population counts from the 1990 Census, yield the estimate that 0.4 percent of the total U.S. population aged 12 years or more have a serum creatinine value >2.0 mg/dl and 1.6 percent have a creatinine level >1.7 mg/dl. These correspond to 800,000 and 3 million people with chronic kidney disease respectively.
Prevention and treatment of ESRD
Important risk factors for ESRD include diabetes mellitus, hypertension, proteinuria, a family history of kidney disease, and increasing age. African-American and Native American persons with the above risk factors are at especially high risk for development of ESRD38, 39. Strategies for prevention of ESRD should target these populations.
Under certain circumstances progression of renal disease can be slowed. Three interventions have been shown to have effectiveness in certain defined populations: good glycemic control (for patients with diabetes mellitus), optimum blood pressure control, and use of angiotensin converting enzyme inhibitors. For example, recent studies in patients with type 1 diabetes mellitus have established that tight control of the level of blood sugar can reduce the development of proteinuria40, and the use of angiotensin converting enzyme inhibitors can slow the progression of kidney disease41. Other studies have shown that angiotensin converting enzyme inhibitors can slow progression of non-diabetic kidney disease with patients with heavy proteinuria42. There is substantial evidence that optimum blood pressure control is an important goal to pursue in all patients with proteinuria or chronic renal insufficiency43, 44, and in patients with type 2 diabetes mellitus45, 46.
Interventions to slow the progression of kidney disease and prevent ESRD are likely to have the greatest impact if applied early in the course of the disease. Unfortunately, because kidney disease at early stages is generally asymptomatic, many individuals who would benefit from interventions are not identified, and therapy to slow progression of kidney disease is often begun rather late. Thus, earlier identification of patients at risk for ESRD is essential if the current growth in incidence is to be changed. Microalbuminuria screening and more intensive treatment of patients found to have microalbuminuria, comprise an important part of a strategy to reduce nephropathy in persons with Type 1 diabetes, both in terms of economic indices and clinical outcomes47, 48, 49; and it is reasonable to suspect that this strategy may also be useful in type 2 diabetes.
The care of the patient with chronic renal failure must continue to emphasize interventions to conserve residual renal function, but at a certain stage, it is also important to provide appropriate preparation for initiation of renal replacement therapy. Several studies have provided evidence that many patients with chronic renal failure do not received optimum preparation for ESRD in the year prior to onset of ESRD. This lack of optimal preparation impacts heavily on the cost of ESRD care and on morbidity at the time of onset of ESRD50, 51. The establishment of a vascular access for hemodialysis is an important example. A critical factor in the well-being of patients on hemodialysis is the presence of an functioning vascular access site. Complications and problems related to vascular access sites are a major source of morbidity, and have been estimated to account for as much as 17 percent of ESRD health care costs52. Arterio-venous fistulas, the form of vascular access considered to provide optimum performance for most patients, is ideally placed several months prior to the initiation of dialysis. It is important to note that early placement of arterio-venous fistulas is particularly important for elderly individuals, because arteriosclerotic vessels may take a much longer time to dilate to a usable diameter. However, many patients with chronic renal disease who are placed on dialysis have not had any form of vascular access placed prior to the time of dialysis initiation. There is substantial regional variation in the type of vascular access used, and the timing of vascular access placement53.
Renal transplantation has emerged as the preferred method of therapy for many patients with ESRD, particularly in children. It is well established that renal transplantation confers a survival advantage over dialysis54. Transplantation success rates, especially the 1-year patient and graft survival rates, have steadily improved over the last two decades. For first cadaveric transplants, for example, the annual rate of graft loss for the first year after transplantation has declined from 26.1 percent in 1985 to only 12.4 percent in 199555. For first living related transplant, the graft loss in the first year has decreased from 14% to 7.4%56. For young children, renal transplantation results in better rates of growth57. Given the accumulating evidence for the advantages of transplantation, equal access of all population groups to transplantation is a subject of substantial concern. Minority populations and women have consistently been shown to have longer waiting times and lower rates of kidney transplantation58, 59, 60, 61, 62, 63.
The increasing incidence rates of ESRD, its disproportionate impact on minority populations, the high societal cost of the disease, and the impact on scarce Federal health care resources, all indicate that attention to risk factors for renal impairment and interventions to slow the progression of renal disease are urgently needed.
Progress Toward Year 2000 Objectives
Healthy People 2000 did not include a chapter on chronic kidney disease.
Draft 2010 Objectives
1. Reduce the rate of increase in ESRD incidence rates by one third. (The current average annual increase in ESRD incidence rates is 6%).
||Percent annual increase* |
|Other Latin Americans
|American Indians and Alaskan Nat.
|Alaskan Natives (See American Indians)
|Selected Asian Groups
|Pacific Islanders & Asians
Target Setting Method: Without improved prevention, based on demographics and the increased prevalence of diabetes, incidence rates are predicted to continue to rise 5 to 8% per year.
Data Source: United States Renal Data System (USRDS).
*The current average annual increase in treated ESRD incidence rates of 6% is calculated by comparing the average annual ESRD incidence rates calculated for the time period 1991-1993 to the time period 1994-1996. This goal will be met if the average annual increase in ESRD incidence rates, comparing the time period 1994-1996 to the time period 2008-2010, is 4% or less.
Incidence rates for ESRD, which have been tracked yearly since 1973, have increased steadily every year for the last decade in virtually all population groups. End-stage kidney disease has a disproportionate impact on minority populations. The USRDS statistics document much higher incidence and prevalence rates of ESRD, and also greater average annual increases in incidence rates, among certain ethnic and racial subgroups. The incidence rates of ESRD are also very high among persons aged 65 years and older, and the annualized rate of increase of ESRD in the elderly, particularly due to hypertensive ESRD, is very high. Attention is needed to reduce these disparities64, 65, 66, 67.
African-Americans have the highest overall risk of ESRD, and the excess incidence in African-Americans is not explained by the higher prevalence of diabetes and hypertension in this population68, 69. African-Americans develop end stage renal failure at an earlier age than whites; their mean age at ESRD incidence in 1996 was 55.8 years, compared with 62.2 years in whites70. Native Americans have a much higher risk of diabetic ESRD, compared to whites. Overall, the ESRD incidence rates are 4 fold higher in African-Americans and Native Americans and 1.5 fold higher in Asians and Pacific Islanders than in whites. The annual increase in ESRD incidence rates is also greater in racial and ethnic minorities than in whites. The ESRD incidence rates are increasing at 7% per year for African Americans, 10% per year for Native Americans, and 11% for Asians and Pacific Islanders, compared with 6% per year for whites. Two Native American communities of the Southwest U.S., the Zuni Pueblo, New Mexico and Sacaton, Arizona may have the highest rates of treated ESRD in the world, at 12.6 and 14.0 times the overall US rate, respectively. Projections, based on demographics and the prevalence of diabetes, are for continued increases in incidence rates in Native Americans.
Although complete data are not yet available, there is some evidence that persons of Mexican ancestry may also have a higher risk of developing ESRD, particularly from diabetes mellitus32, 31. The Health Care Financing Administration has recently (1995) changed the way in which data on race/ethnicity are collected on the Medical Evidence Form used to enroll patients into the Medicare ESRD Program, to be able to evaluate a possible association of Hispanic ancestry with risk of ESRD. Information from 1996 suggests that 7 percent of incident ESRD patients are of Mexican ancestry, and another 4 percent are of Hispanic ancestry from other areas.
The disproportionately higher ESRD incidence rates seen among the racial and ethnic minority groups have resulted in a shift in the burden of disease towards these communities. In 1996, nearly 40% of prevalent cases of ESRD were among America's racial minorities. According to the USRDS, in 1996 blacks constituted 29.8% of prevalent ESRD patients as compared to 12.6% of the US population; and Native Americans constituted 1.7% of prevalent ESRD patients as compared to 0.9% of the US population71. In 1996, the point prevalence rate of ESRD per million in the population, (adjusted for age and sex) was 3,404 in African-Americans and 2,761 in Native Americans/Alaskan Natives, compared to 754 in whites, differences of 4.5 and 3.7 fold respectively72.
Most ESRD results from progressive worsening of chronic kidney injury over several years. For example, ESRD from diabetic nephropathy generally occurs 15-20 years after the onset of diabetes. A similar natural history is seen for hypertensive ESRD. Thus, incident cases of ESRD due to diabetes and hypertension in 2010 will mostly occur in persons who have already been diagnosed with these diseases. Implementation of currently available strategies for protection of the kidney, including glycemic control in diabetics, better control of hypertension in high risk populations, and use of converting enzyme inhibitors - offer the best promise for reversing these trends. Secondary prevention efforts may slow the rate of progression of kidney injury in these individuals, delaying the need for renal replacement therapy.
2. Decrease the death rate from cardiovascular diseases in ESRD patients to no more than 50 per 1000 patient years. (Baseline 68 per 1000 patient years)
Target Setting Method: 25% reduction
Data Source: United States Renal Data System (USRDS)
Cardiovascular disease (CVD) is the major cause of death among patients with ESRD73, but the increased risk of CVD in patients with renal insufficiency is evident even before the onset of ESRD. Increased CVD mortality is also seen in individuals with proteinuria or elevated creatinine. In the ESRD population, CVD mortality is estimated to be 30 fold greater than among the general population. The known risk factors for cardiovascular disease in the general population include age, male gender, diabetes, lipid abnormalities, hypertension, and smoking. Elevated homocysteine levels in the blood may also be an important risk indicator in patients in the ESRD population74, 75, 76 and at earlier stages in the progression of renal disease. Strategies to reduce CVD mortality should target risk reduction before the onset of ESRD.
The USRDS provides yearly statistics on mortality in the ESRD population, including the number of ESRD patients who died, and the cause of death as coded by the attending nephrologist, by zip code, state, ESRD Network region, and nation. These data can be used to document progress toward this objective. Some differences in cause of death statistics have been documented between death certificate reports, and registry reports, including the USRDS77. These differences may arise from several causes, including the underreporting of renal disease and ESRD as a cause of death, but the factors associated with these differences are not expected to change over time, and will not reduce the utility of the USRDS registry to monitor progress for this objective.
3. Increase the proportion of ESRD patients who have received adequate care in the period preceding ESRD therapy.
3a. Increase the proportion of incident ESRD patients under care of informed health care providers, 12 months before the start of end-stage therapy to 60 percent. (Baseline: 45 percent)
Target Setting Method: 33 percent improvement
Data Source: United States Renal Data System, DMMS Wave 2
3b. Increase the proportion of incident ESRD hemodialysis patients utilizing arterio-venous fistulas as the primary mode of vascular access to 50 percent. (Baseline: 18 percent)
Target Setting Method: Dialysis Outcomes Quality Initiative (DOQI) guidelines from the National Kidney Foundation Task Force.
Data Source: United States Renal Data System.
Good care of kidney disease patients in the period before renal replacement therapy is implemented is important to reduce the substantial morbidity and mortality associated with ESRD. Appropriate preparation for renal replacement therapy includes attention to reduction of cardiovascular disease risk factors, treatment of anemia, optimum therapy to preserve residual renal function, consultation about nutrition, patient education about methods of renal replacement therapy, and, for patients who elect hemodialysis, access placement planning. In general, these preparations should occur at least 6 months before initiation of renal replacement therapy. Many patients with chronic renal failure are not seen by health care professionals with expertise in renal replacement therapy until they are very close to the time when the renal replacement therapy will be required. In a recent USRDS study, which surveyed 3,468 incident dialysis patients, 55 percent of the patients had not been seen by a nephrologist within 1 year prior to institution of renal replacement therapy, and 33 percent had not been seen even 3 months before the start of renal replacement therapy78. Even though control of diet is a major aspect of pre-ESRD and ESRD management, by the start of renal replacement therapy 46 percent of incident dialysis patients had not seen a dietician. The rate of utilization of arterio-venous fistulas is currently under 20 percent, another index of the need to improve the quality of pre-ESRD care.
4. Improve access to transplantation and reduce racial disparities in renal transplantation rates.
4a. Reduce the median waiting time for renal transplantation for primary transplantation waiting list registrants by one third, to no more than ______ days. (Baseline: Median waiting time for primary registrants: _____ days)
Target Setting Method: 33 % improvement
Data Source: 1997 Report of the OPTN: Waiting List Activity and Donor Procurement, HRSA.
4b. Increase renal transplantation rates at 1 year after registration for the transplantation waiting list by 33%. Increase the cumulative proportion of patients transplanted within 3 years of registration on the transplantation waiting list, by 33%. * (Baseline: Primary registrants transplanted at __ year(s) post-registration: ___%)
||1 year rate
||cumulative 3 year rate |
* Both the 1 year and the 3 year post-registration data points are important and should be tracked.
Target Setting Method: 33% improvement
Data Source: 1997 Report of the OPTN: Waiting List Activity and Donor Procurement, HRSA.
Recent reports have shown that minority transplant registrants, particularly African Americans, wait longer than whites for transplants. Minority populations (again, specifically African Americans) also move up the waiting list at a slower rate than whites 79, 80. The exact causes of this discrepancy are not entirely clear. Racial disparities in waiting times are certainly influenced by genetic and biological factors 81, but they are also affected by the following factors: organ procurement organization request and consent procedures, patient registration practices for a center or region, organ acceptance practices at each transplant center, geographic location, socioeconomic status, cultural attitudes and beliefs about donation, donation rates within each local area, and donor pool 82.
Reports have also documented a lower rate of transplantation for minority populations than for whites83. The Department is working towards the goal of making sure that all Americans have an equal opportunity to receive a transplant, regardless of who they are or where they live. As part of an effort to increase access to transplantation among racial minorities, an attempt should be made to increase organ donation from minority communities. In 1997, the Department of Health and Human Services launched the National Organ and Tissue Donation Initiative in an effort to increase organ and tissue donation. One aspect of the Initiative is to learn more about the factors that improve organ and tissue donation through research and evaluation, with a special emphasis in minority communities.
5. Decrease the incidence rate of end-stage renal disease due to diabetes requiring dialysis or transplantation to no more than 102 per 1,000, 000 population. (Baseline: 113 diabetic ESRD per 1,000,000 persons in 1996)
||1994 - 1996 |
|Native American/Alaskan Native
|Age group 00 - 19
|Age group 20 - 44
|Age group 45 - 64
|Age group 65 - 74
|Age group ≥ 75
Target Setting Method: 10% improvement
Potential Data Sources: United States Renal Data System (USRDS), HCFA.
Convincing, consistent, and continuing scientific evidence exists that with secondary and tertiary prevention, microvascular complications of diabetes, especially diabetic nephropathy, can be substantially reduced. Improved quality of life, diminished mortality, and improved economics all can result from improved clinical and public health diabetes prevention strategies directed to kidney disease, and other microvascular and metabolic complications of diabetes. Monitoring the consequences of these strategies through reduction in chronic renal insufficiency and end-stage renal disease and other microvascular complications should be an important component of the effectiveness of a national public health program.
6. (Developmental) In patients with Type 1 or Type 2 diabetes, and proteinuria, increase the proportion of patients receiving appropriate medical therapy to reduce the incidence and progression of diabetic nephropathy, to more than 50 percent.
Target setting method: Better than the best.
Potential data source: NHANES, Behavioral Risk Factor Surveillance System (BRFSS) diabetes module, National Health Interview Survey.
7. (Developmental) Increase the proportion of hypertensive individuals screened for the presence of renal disease.
7a. Increase the proportion of hypertensive patients tested for kidney function (proteinuria, serum creatinine and BUN) at the time of initial evaluation to more than 95%.
7b. In high risk populations, increase the proportion of hypertensive patients tested annually for proteinuria and increased serum creatinine to more than 75 percent (Baseline less than 50 percent).
Target setting method: Better than the best.
Potential data source: NHANES, Behavioral Risk Factor Surveillance System (BRFSS), National Health Interview Survey (NHIS).
Objective 7a. is consistent with recommendations contained in the Sixth Report of the Joint National Committee on Prevention, Detection and Evaluation of High Blood Pressure84. For the purpose of Objective 7b., high risk populations are considered to include African-Americans, persons aged 65+ years, persons with blood pressure greater than 160/90, and persons with duration of hypertension greater than 10-15 years.
8. (Developmental) In patients with hypertension and proteinuria or chronic renal insufficiency, increase the proportion of patients with optimum blood pressure control to greater than 50 percent.
Target setting method: Better than the best.
Potential data source: NHANES; Behavioral Risk Factor Surveillance System (BRFSS), National Health Interview Survey (NHIS).
The available data would suggest that in patients with chronic renal insufficiency, the blood pressure should be controlled to or less than 130/85 mm Hg. However, in patients with proteinuria in excess of 1.0 gm/24 hours, the blood pressure should be reduced to or below 125/75 mm Hg. These recommendations are contained in the Sixth Report of the Joint National Committee on Prevention, Detection and Evaluation of High Blood Pressure.
9. (Developmental) Increase to more than 75 % the proportion of primary care providers who routinely counsel their patients about the effects of chronic health conditions, such as diabetes (type I and type II), hypertension, family history of genetic kidney diseases, on the development and progression of renal disease.
Target setting method: Better than the best.
Potential Data Sources: ODPHP Provider Survey, or data may be obtained from private sources, such as managed care organizations and groups providing continuing education to health professionals.
10. (Developmental) Increase to more than 75 % the proportion of primary care providers who provide intensified management of cardiovascular risk factors for all patients with proteinuria or elevated creatinine.
Target setting method: Better than the best.
Potential Data Sources: ODPHP Provider Survey, or data may be obtained from private sources, such as managed care organizations and groups providing continuing education to health professionals.
Related objectives from other HP2010 focus areas
PHYSICAL ACTIVITY AND FITNESS
1., 2., 3., 6., 7., 8. Increase leisure time, sustained, and vigorous physical activity.
13. Increase employer sponsored physical activity and fitness programs.
14. Increase assessment and counseling about physical activity by health care providers.
5. and 6. Saturated fat intake.
3. Smoking cessation.
EDUCATION AND COMMUNITY BASED PROGRAMS:
8. Patient and family education.
9., 10., 11. Community health promotion activities, initiatives and programs. Culturally sensitive programs to increase the awareness of risk factors associated with renal disease in high risk racial/ethnic groups is very important.
27. Burdens caused by environmental hazards.
1. Food borne infections.
2. E Coli G157: H7, and salmonella outbreaks.
OCCUPATIONAL SAFETY AND HEALTH:
9. Decrease the number of adults with blood lead >25 ug/dl to 0%.
10. Decrease the number of adults with occupational exposures leading to blood lead levels >10 ug/dl.
ACCESS TO QUALITY HEALTH SERVICES:
A.1 Increase health care coverage.
A.2 Clinical preventive services.
A.3 Routine lifestyle risk factor evaluation.
A.4 Delivery of clinical preventive services.
A.5 Training of health professionals to address health disparities.
B.2 Lack of access to health care.
B.3 Lack of primary care visits.
B.4 Access to primary care providers in under-served areas.
MEDICAL PRODUCT SAFETY:
4. Linked, automated prescription information.
5. Drug alert systems.
6. Increase health care provider review of the medications being taken by the patient.
7. Increase health care provider interview for alternative/complementary medicine treatments being taken by the patient.
PUBLIC HEALTH INFRASTRUCTURE:
6. Increase access of public health workers to public health information and surveillance data.
7. Increase tracking of achievement of HP2010 objectives to include all objectives, in selected populations.
1. Increase public access to health information.
6. Improve the quality of health information available (ex: on the internet).
1. Decrease incidence of type 2 diabetes mellitus.
2. Decrease prevalence of diabetes mellitus.
3. Increase diagnosis of diabetes in persons with the condition.
6. Decrease cardiovascular disease deaths in persons with diabetes.
13. Evaluate for proteinuria.
14. Decrease diabetic ESRD.
15. Evaluate for blood and serum lipid levels in persons with diabetes.
17. Increase assessment of microalbuminuria in persons with diabetes.
DISABILITY AND SECONDARY CONDITIONS:
1. Develop core data sets on disability.
2. Decrease days of depression in persons with disability.
5. Increase personal and emotional support to persons with disability.
8. Increase employment rates in persons with disability.
HEART DISEASE AND STROKE:
1. Decrease coronary heart disease deaths.
3. Increase knowledge of early warning symptoms of coronary heart disease.
7. Increase the proportion of persons with hypertension whose hypertension is controlled to 50%.
13. Improve treatment of abnormal LDL cholesterol.
14. Decrease the number of stroke deaths.
15. Increase knowledge of early warning symptoms of cerebrovascular disease.
IMMUNIZATION AND INFECTIOUS DISEASES):
1. Decrease the prevalence of vaccine preventable diseases (Hep B).
5. and 22.6 Improve hepatitis B vaccination to decrease the incidence rate of hepatitis B in persons under the age of 25 years, and those above the age of 25 years.
1 Ruggenenti P, Perna A, Mosconi L, Pisoni R, Remuzzi G. Urinary protein excretion rate is the best independent predictor of ESRF in non-diabetic proteinuric chronic nephropathies. Kidney International 53(5): 1209-1216, May 1998.
2 Ruggenenti P; Perna A; Mosconi L; Matalone M; Pisoni R; Gaspari F; Remuzzi G. Proteinuria predicts end-stage renal failure in non-diabetic chronic nephropathies. The "Gruppo Italiano di Studi Epidemiologici in Nefrologia" (GISEN). Kidney Int 63(suppl):S54-7, December 1997.
3 Kannel WB, Stampfer MJ, Castelli WP, Verter J. The prognostic significance of proteinuria: The Framingham Study. American Heart Journal, 108(5): 1347-1352, November 1984.
4 Torffvit O, Agardh C-D. The predictive value of albuminuria for cardiovascular and renal disease. A 5-year follow-up study of 476 patients with Type 1 diabetes mellitus. J Diab Comp 7(1): 49-56, 1993.
5 Wagener DK, Harris T, Madans JH. Proteinuria as a biomarker: Risk of subsequent morbidity and mortality. Environmental Research 66: 160-172, 1994.
6 Alzaid AA. Microalbuminuria in patients with NIDDM: An overview. Diabetes Care 19(1): 79-89, January 1996.
7 American Diabetes Association. Diabetic Nephropathy. Diabetes Care 20 (Supplement 1): S24-S27, January 1997.
8 Schmitz A, Vaeth M. Microalbuminuria: A major risk factor in non-insulin-dependent diabetes. A 10-year follow-up study of 503 patients. Diabetic Medicine 5:126-134, 1988.
9 Haffner SM, Stern MP, Gruber MKK, Hazuda HP, Mitchell BD, Patterson JK. Microalbuminuria. Potential marker for increased cardiovascular risk factors in non-diabetic subjects? Arteriosclerosis 10:727-731, September/October 1990.
10 Yudkin JS, Forrest RD, Jackson CA. Microalbuminuria as predictor of vascular disease in non-diabetic subjects. Islington Diabetes Survey. The Lancet, pp 530-531, September 3, 1988.
11 Damsgaard EM, Froland A, Jorgensen OD, Mogensen CE. Microalbuminuria as predictor of increased mortality in elderly people. British Medical Journal 300:297-300, 1990.
12 Walser, M. Assessing renal function from creatinine measurements in adults with chronic renal failure. Am J Kidney Disease 32:1-22, 1998.
13 U.S. Renal Data System, USRDS 1998 Annual Data Report, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland, April 1998.
14 USRDS, op cit. Appendix, Table A-1.
15 USRDS, op cit. Appendix, Table B-3.
16 USRDS, op cit. Chapter X, pp. 133-148.
17 USRDS, op cit. Chapter V, pp. 63-78.
18 USRDS, op cit. Appendix, Table A-1.
19 USRDS, op cit. Appendix, Table A-15.
20 USRDS, op cit. Appendix, Table B-3.
21 USRDS, op cit. Appendix, Table A-3.
22 USRDS, op cit. Appendix, Table A-1.
23 National Heart, Lung and Blood Institute. Morbidity and Mortality Chartbook on Cardiovascular Disease, Lung and Blood Disease, Bethesda, MD, Public Health Service.
24 USRDS, op cit. Appendix, Tables A-1, A-2 and A-3.
25 Clark C. How should we respond to the worldwide diabetes epidemic? Diabetes Care 21: 475-476, 1998.
26 Centers for Disease Control and Prevention. National Diabetes Fact Sheet: National Estimates and General Information on Diabetes in the United States. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, 1997.
27 USRDS, op cit. Appendix, Table A-6.
28 USRDS, op cit. Appendix, Table ES-1.
29 USRDS, op cit. Appendix, Table A-14.
30 USRDS, op cit. Appendix, Table B-3.
31 Villalpano CG, Stearn MP et al. Nephropathy in low income diabetics: the Mexico City Diabetes Study. Arch Med Research, 27: 367-372, 1996.
32 Pugh JA, Stern MP, Haffner SM, Eifler CW, Zapata M. Excess incidence of treatment of end-stage renal disease in Mexican Americans. Am J Epidemiol 127: 135-144, 1998.
33 USRDS, op cit. Executive Summary, pp xxiii.
34 Paul W. Eggers, Health Care Financing Administration, personal communication.
35 Perrone RD, Madias NE, Levey AS. Serum creatinine as an index of renal function: New insights into old concepts. Clin Chem 38(10): 1933-1953, 1992.
36 Coresh J, Toto RD, Kirk KA, Whelton PK, Massry S, Jones C, Agodoa LY, Van Lente F, and AASK Pilot Study Investigators: Creatinine Clearance as a measure of GFR in screenees for the African American Study of Kidney Disease and Hypertension (AASK) Pilot Study. Am J Kidney Disease 32: 1-12, 1998.
37 Jones CA, McQuillan GM, Kusek JW, Eberhardt MS, Herman WH, Coresh J, Salive M, Jones CP, and Agodoa LY: Serum Creatinine Levels in the United States Population: The Third National Health and Nutrition Examination Survey (NHANES III). Am J Kidney Disease (in press), 1998.
38 Perneger TV, Klag MJ, Feldman HI, Whelton PK. Projection of hypertension related renal disease in middle-aged residents of the United States. JAMA 269 (10): 1272-1277, 1993.
39 Freedman BI, Tuttle AB, Spray BJ. Familial predisposition to nephropathy in African-Americans with non-insulin-dependent diabetes mellitus. Am J Kidney Disease 25(5):710-713, 1995.
40 The Diabetes Control and Complications (DCCT) Research Group. Effect of intensive therapy on the development and progression of diabetic nephropathy in the Diabetes Control and Complications Trial. Kidney International 47: 1703-1720, 1995.
41 Lewis EJ, Hunsicker LG, Bain RP, et al for the Collaborative Study Group: The effect of angiotensin enzyme inhibition on diabetic nephropathy. N Engl J Med 329: 1456-1462, 1993
42 Ruggenenti P; Remuzzi G. Angiotensin-converting enzyme inhibitor therapy for non-diabetic progressive renal disease. Curr Opin Nephrol Hypertens 6(5):489-95, 1997.
43 Klahr S, Levey AS, Beck GJ, Caggiula AW, Hunsicker LJ, Kusek JW, Striker G, MDRD Study Group: The effects of dietary protein restriction and blood pressure control on progression of chronic renal failure. N Engl J Med 330: 878-884, 1994.
44 Hebert LA, Kusek JW, Greene T, Agodoa LY, Jones CA, Levey AS, Breyer JA, Faubert P, Rolin MT, Wang S and Modification of Diet in Renal Disease Study Group: Effects of blood pressure control on progressive renal disease in Blacks and Whites. Hypertension 30: 428-435, 1997.
45 UK Prospective Diabetes Study Group. Tight blood pressure control reduces the risk of macrovascular and microvascular complications in Type 2 diabetes. British Medical Journal (in press), 1998.
46 Ohkubo Y, Kishikawa H, Araki E, Miyati T, Isami S, Motoyoshi S, Kojima Y, Furuyoshi N, Shichiri M. Intensive insulin therapy prevents the progression of diabetic microvascular complications in Japanese patients with non-insulin dependent diabetes mellitus: a randomized prospective 6-year study. Diabetes Research and Clinical Practice 28: 103-117, 1995.
47 Siegel J, Krolewski A, Warram J, Weinstein M. Cost-effectiveness of screening and early treatment of nephropathy in patients with insulin-dependent diabetes mellitus. J Am Soc Nephrol 3: S111-S119, 1992.
48 Kiberd B, Jindal K. Screening to prevent renal failure in insulin dependent diabetic patients: an economic evaluation. Br Med J 311: 1595-9, 1995.
49 Borch-Johnsen K, Wenzel H, Viberti G, Mogensen C. Is screening and intervention for microalbuminuria worthwhile in patients with insulin dependent diabetes? Br Med J 306: 1722-25, 1993.
50 Ifudu O, Dawood M, Homel P, Friedman EA. Excess morbidity in patients starting uremia therapy without prior care by a nephrologist. Am J Kidney Disease 28: 841-845, 1996.
51 U.S. Renal Data System, USRDS 1997 Annual Data Report, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland, Chapter IV, pp. 49-60, April 1997.
52 USRDS, op. cit., Chapter X, pp. 159
53 USRDS Dialysis Morbidity and Mortality Study, unpublished communication.
54 Port FK, Wolfe RA, Mauger EA, Berling DP, Jiang K: Comparison of survival probabilities for dialysis patients versus cadaveric renal transplant recipients. JAMA; 270:1339-1343, 1993.
55 U.S. Renal Data System, USRDS 1998 Annual Data Report, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland, Appendix Table G.19, April 1998.
56 USRDS, op. cit., Appendix, Table G.43.
57 Turenne MN, Port FK, Strawderman RL, Ettenger RB, Alexander SR, Lewy JE, Jones CA, Agodoa LY, Held PJ. Growth rates in pediatric dialysis patients and renal transplant recipients. Am. J. Kidney Dis.; 30(2): 193-203, 1997.
58 1997 Report of the OPTN: Waiting list activity and donor procurement, Executive Summary, Kidney Volume.
59 Alexander GC, Sehgal AR. Barriers to cadaveric renal transplantation among blacks, women, and the poor. JAMA 280(13):1148-52, 1998.
60 Bloembergen WE, Mauger EA, Wolfe RA. Association of gender and access to cadaveric renal transplantation. Am. J. Kid. Dis. 30(6): 733-738, 1997.
61 Narva, A, Stiles, S, Karp, S, Turak A. Access of native Americans to renal transplantation in Arizona and New Mexico. Blood Purif 14:293-304, 1996.
62 Ozminkowski, RJ, White AJ, Hassol, MSPH, Murphy, M. Minimizing racial disparity regarding receipt of a cadaver kidney transplant. Am J Kidney Disease 30: 749-759, 1997.
63 U.S. Renal Data System, USRDS 1997 Annual Data Report, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland, pp 107-112, April 1997.
64 U.S. Renal Data System, 1998 Annual Data Report (ADR), Table ES-1, pg. xviii, (Summary Table)
65 USRDS, op. cit., Table II-1, pg. 24
66 USRDS, op. cit., Figure II-5, pg. 28
67 USRDS, op. cit., Figure II-8, pg. 30.
68 Whittle JC, Whelton PK, Seidler AJ, Klag MJ. Does racial variation in risk factors explain black-white differences in the incidence of hypertensive end-stage renal disease? Arch Intern Med 151: 1359-64, 1991.
69 Brancati FL, Whittle JC, Whelton PK, Seidler AJ, Klag MJ. The excess incidence of diabetic end-stage renal disease among blacks. A population based study of potential explanatory factors. JAMA 268: 3079-84, 1992.
70 USRDS, op cit. Appendix, Table A-14.
71 USRDS, op cit. Appendix, Table B-3.
72 USRDS, op cit. Appendix, Table ES-1.
73 National Kidney Foundation Task Force on Cardiovascular Disease. Controlling the epidemic of cardiovascular disease in chronic renal disease. Executive Summary, Report from the National Kidney Foundation Task Force on Cardiovascular Disease. October 1998.
74 Bostom AG, Shemin D, Verhoef P, Nadeau MR, Jacques PF, Selhub J, Dworkin L, Rosenberg IH. Elevated fasting total plasma homocysteine levels and cardiovascular disease outcomes in maintenance dialysis patients: A prospective study. Arterioscler Thromb Vasc Biol 17 (11): 2554-8, 1997.
75 Bostom AG, Lathrop L. Hyperhomocysteinemia in end-stage renal disease: prevalence, etiology, and potential relationship to arteriosclerotic outcomes. Kidney Int 52(1): 10-20, 1997.
76 Bostom AG, Shemin D, Lapane KL, Sutherland P, Nadeau MR, Wilson PW, Yoburn D, Bausserman L, Tofler G, Jacques PF, Selhub J, Rosenber IH. Hyperhomocysteinemia, hyperfibrinogenemia, and lipoprotein (a) excess in maintenance dialysis patients: a matched case-control study. Atherosclerosis 125 (1): 91-101, 1996.
77 Perneger TV, Klag MJ, Whelton PK. Cause of death in patients with end-stage renal disease: Death certificates vs registry reports. American Journal of Public Health 83(12): 1735-1738, 1993.
78 U.S. Renal Data System, USRDS 1997 Annual Data Report, National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland, Chapter IV, Figure IV-3, pg 52, April 1997.
79 1997 Report of the OPTN: Waiting List Activity and Donor Procurement, Executive Summary, Kidney Volume. Health Resources and Services Administration
80 Ellison MD, Breen TJ, Guo TG, Cunningham PRG, Daily OP. Blacks and Whites on the UNOS renal waiting list: Waiting Times and Patient Demographics Compared. Transplantation Proceedings 25(4): 2462-2466, 1993.
81 Thompson JS. American society of histocompatibility and immunogenetics crossmatch study. Transplantation 59(11): 1636-1638, 1995.
82 Alexander GC, Sehgal AR. Barriers to cadaveric renal transplantation among blacks, women, and the poor. JAMA 280(13): 1148-1152, 1998.
83 1997 Annual Report of The U.S. Scientific Registry of Transplant Recipients and The Organ Procurement and Transplantation Network, Health Resources and Services Administration.
84 The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. National Institutes of Health, National Heart, Lung, and Blood Institute, Bethesda, Maryland, November 1997.