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The level of kidney function tends to decline progressively over time in most patients with chronic kidney diseases. Ascertaining risk factors for faster versus slower GFR decline, including type (diagnosis) of kidney disease, nonmodifiable and modifiable factors.
Interventions to slow the progression of kidney disease should be considered in all patients with chronic kidney disease.
The intent of this guideline is to examine the literature to determine factors associated with more rapid loss of kidney function in chronic kidney disease. Progression of kidney disease is defined as either (1) decline in the level of kidney function, estimated by measuring GFR, creatinine clearance or serum creatinine, in a patient who has been followed longitudinally with reliable (and comparable) assays of kidney function, or (2) onset of kidney failure, defined by initiation of kidney replacement therapy, either for symptoms or complications of decreased kidney function. The natural history of most chronic kidney diseases is that GFR declines progressively over time (Fig 47) (R). Other studies have shown that certain types of kidney disease may undergo complete remission in a substantial number of patients. The rate of GFR decline is often relatively constant over time in an individual patient; however, the rate of GFR decline is highly variable among patients, ranging from slowly progressive over decades, to rapidly progressive over months (Table 109 and Fig 48) (R, C). Composite plot of reciprocal serum creatinine versus time in six patients with chronic kidney disease.
The studies reviewed for this guideline show a wide range in the rate of GFR decline among studies, as well as among individual patients (Table 109). The rate of decline in GFR can be used to estimate the interval until the onset of kidney failure (Table 110) (R). In principle, if the rate of GFR decline is constant over time, then the interval until the onset of kidney failure could be estimated from the current level of GFR and the rate of decline in GFR. First, most of the studies that demonstrated a constant rate of decline in kidney function were retrospective, including only patients who had already progressed to kidney failure.
Second, even among patients in whom the rate appears constant, the rate may change over time. The changes in slope were judged to be spontaneous, since they did not necessarily occur at the time of changes in therapy. Similar changes in slope of GFR decline have sometimes been observed in clinical trials, where they have been attributed to the effect of the interventions (for example, low protein diet, strict blood pressure control, ACE inhibition). Comparison of GFR decline between diet groups in the Modification of Diet in Renal Disease Study. Third, even if the rate of decline is constant, the precision of the estimate of the slope depends on a number of variables, including the true rate of decline, the number of measurements of kidney function, measurement error, biological variability, and the duration of follow-up. The rate of GFR decline is related to the type of kidney disease; diabetic kidney disease, glomerular diseases, polycystic kidney disease, and kidney disease in transplant recipients are associated with a faster GFR decline than hypertensive kidney disease and tubulointerstitial kidney diseases (Tables 109 and 111) (C, R). Few studies specifically related rate of GFR decline to type of kidney disease (Table 111). Additional information regarding different rates of GFR decline depending on underlying cause of kidney disease was extracted from studies of isolated causes of kidney disease or from studies which provided rates of progression for individual causes of kidney disease. The data presented in Table 111 are not easily compared; the study methods varied (retrospective or prospective, observational, or interventional), different measures of kidney function were used, and the effect of interventions or other potential confounders cannot be determined. The rate of GFR decline is related to some nonmodifiable patient characteristics, irrespective of the type of kidney disease; African-American race, lower baseline level of kidney function, male gender, and older age are associated with a faster GFR decline (C).
Six studies addressed the association of race with the rate of GFR decline in either univariate or multivariate analyses. Twenty-one studies addressed the association of low baseline level of kidney function with the rate of GFR decline in either univariate or multivariate analyses. Eighteen studies addressed the impact of gender on the rate of GFR decline in either univariate or multivariate analyses. Twenty-one studies reported the association of age with the rate of GFR decline in either univariate or multivariate analyses.
The rate of GFR decline is also related to modifiable patient characteristics, irrespective of the type of kidney disease. Eight studies addressed the association of low baseline serum albumin with rate of GFR decline in either univariate or multivariate analyses.
Interventions may slow rate of GFR decline in chronic kidney disease in some circumstances (R). Strict glycemic control in diabetes slows the development and progression of chronic kidney disease (R).
The goals for intensive glycemic control for the prevention of complications of diabetes, including nephropathy, as presented in the ADA guidelines, are summarized below.
Among patients with insulin dependent diabetes mellitus (IDDM), 80% who have sustained microalbuminuria develop overt nephropathy in 10 to 15 years, and among these, kidney failure develops in 50%.
The role of strict glycemic control in slowing the progression of diabetic kidney disease is less certain. Among patients with non-insulin dependent DM (NIDDM), 20% to 40% of patients with microalbuminuria develop overt nephropathy, and among these, kidney failure develops in 20%. The Steno Type 2 Study compared an intensive multifactor intervention to standard therapy in 160 patients with type 2 diabetes and microalbuminuria.532 The intervention included not only intensive insulin therapy, but also strict blood pressure control, ACE inhibition, dietary fat restriction, exercise, lipid-lowering drugs, anti-oxidants, and aspirin (in patients with coronary heart disease). The most recently updated Clinical Practice Recommendations (2001)526 of the ADA regarding intensive glycemic control recommend the following treatment goals for patients with diabetes (Table 123). Recommendations for the general population are based on a large body of evidence from observational studies and clinical trials relating blood pressure levels to mortality and cardiovascular disease. The recommended goal of antihypertensive therapy for patients at low or moderate risk for complications is to maintain systolic and diastolic blood pressure less than 140 and 90 mm Hg, respectively.245 These definitions and goals do not differ according to age (among adults), gender, or race. In the general population, the recommended antihypertensive agents are diuretics and beta-adrenergic blockers, because their efficacy in reducing cardiovascular mortality and morbidity has been proven in clinical trials. Based largely on extrapolation from recommendations for the general population and limited observational studies and clinical trials in patients with chronic kidney disease, the NKF Task Force on Cardiovascular Disease recommended target blood pressure levels and strategies for treatment for patients with chronic kidney disease (Table 125). The Task Force recommendations were meant to serve as a guide to clinicians until more definitive recommendations are available. A KDOQI Work Group has now been established to develop guidelines for the management of high blood pressure in patients with chronic kidney disease not requiring dialysis. Angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists slow the progression of chronic kidney disease (R). It is important to note that ACE-inhibitors have been found to have beneficial effects on total mortality and cardiovascular disease in diabetic patients without chronic kidney disease.543-545 Although most patients in these studies were hypertensive, the beneficial effect of ACE-inhibitor therapy appeared to be independent of its blood pressure lowering effect. These recommendations are based on a number of randomized trials published over the past decade, which have been summarized recently in a meta-analysis of patient level data.546 In that analysis, data on 1860 nondiabetic patients included in 11 randomized clinical trials of various ACE-inhibitors were pooled.
The available evidence suggests a benefit to using ACE-inhibitors to treat hypertension among proteinuric patients with nondiabetic kidney disease. The HOPE Study also demonstrated a beneficial effect of the ACE-inhibitor ramipril on total mortality and cardiovascular disease in nondiabetic patients without chronic kidney disease, but with a history of cardiovascular disease and one cardiovascular disease risk factor (including hypertension).545 The beneficial effect of the ACE-inhibitor appeared to be independent of its blood pressure lowering effect. There is insufficient evidence to recommend for or against routine prescription of dietary protein restriction for the purpose of slowing the progression of chronic kidney disease; individual decision-making is recommended, after discussion of risks and benefits (R).
There is insufficient evidence to recommend lipid-lowering therapy for the purpose of slowing the progression of chronic kidney disease (R). Unfortunately, there are no large, adequately powered, randomized, controlled trials testing the hypothesis that treatment of dyslipidemia preserves kidney function.
Reduced blood flow to the kidney, toxic insult, obstruction, inflammation, or infection can result in acute deterioration of kidney function. Volume depletion accounts for the majority of community acquired cases of acute reduction in the blood flow to the kidney and a resultant reduction in GFR.
Common toxic insults encountered in clinical practice are radiocontrast dye, aminoglycoside antibiotics, and NSAIDs. Finally, obstruction can cause an acute decline in GFR if there is bilateral ureteral obstruction, unilateral ureteral obstruction in a person with a single functioning kidney, or obstruction at the level of the bladder.
In summary, there are numerous situations that may cause an acute deterioration in the GFR that are potentially avoidable. A major limitation of this guideline is its failure to provide a semi-quantitative assessment of the relationships between the factors assessed and the outcomes of rate of progression or risk for kidney failure.
It is important to follow each individual’s rate of progression, as there is a wide variation among individuals and disease types and in the response to interventions. There is a broad range of factors that are associated with more rapid decline in kidney function, some of which are amenable to interventions. Certain patient groups, defined by either type of kidney disease, clinical, gender, racial, or age characteristics, are at greater risk for progression of kidney disease—this denotes the need to increase awareness among patients and providers about proper care and the need to institute interventions to attempt to slow progression. Patients with certain causes of kidney disease, and certain modifiable and nonmodifiable characteristics, may be at increased risk for faster rates of GFR decline. It is thus critical to educate patients and providers regarding the risk factors and to facilitate providing aggressive interventions where indicated.
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The best linear unbiased estimates of GFR slope over 3 years in Study A or overall slope in Study B are shown as a function of baseline GFR. For example, up to 35% of patients with idiopathic membranous nephropathy481 and up to 30% of patients with primary focal segmental glomerulosclerosis482 may undergo remission of disease. An estimate of the time until kidney failure would be useful to facilitate planning for kidney replacement therapy, or may even suggest that concerns about kidney failure may be unwarranted if life expectancy is short. In principle, the GFR decline could be computed simply from the slope of the regression line relating estimated GFR versus time.
The fraction of patients with decreased GFR in whom the subsequent decline in kidney function is constant is unknown.
In a pooled analysis of four studies of 77 patients with an apparently constant rate of decline in the reciprocal of the serum creatinine concentration, 32% to 51% of patients had a significant change in the slope502 (Fig 49).


In that study, the second slope was less steep in 61% of cases and more steep in 39% of cases.
Estimated mean (±SEM) GFR decline from baseline (B) to selected follow-up times (F) in Study A are shown. For this review, longitudinal studies were compiled to relate the rate of decline in kidney function with the potential associated factors. The MDRD Study was the largest, with a sample size of 826, while the other two studies had between 138 and 223 subjects. Table 111 shows the reported or estimated rates of GFR decline that were described for different causes of kidney disease. Nonetheless, the crude data suggest a trend for more rapid progression among patients with diabetes, especially those patients with proteinuria or decreased GFR, compared with other causes of kidney disease.
Half reported a faster rate of progression among blacks; however, only one study reported a significant association between black race and faster rates of progression in multivariate analysis. The majority of the studies reported a faster rate of progression among individuals with lower baseline kidney function, but about one third reported no association. The data report either a faster rate of progression or no association with male gender, and a single study reported a faster rate of progression among females.
These data generally support either an association of older age with faster rates of GFR decline or no association, except among diabetics, where younger age at diagnosis of diabetes is associated with a faster rate of GFR decline. Higher level of proteinuria, lower serum albumin concentration, higher blood pressure level, poor glycemic control, and smoking are associated with a faster GFR decline. Although these data do not unanimously show that proteinuria is associated with faster rate of GFR decline when controlling for other factors, the studies with larger sample sizes and higher methodological quality and applicability do support the association.
The association of low serum albumin with faster rate of GFR decline was more consistently noted in studies of diabetic patients. The studies differed in that they assessed systolic blood pressure, diastolic blood pressure, or mean arterial pressure—two of these or all of these. The studies evaluated one or more of the following factors: high levels of total cholesterol, triglycerides, or low density lipoprotein, and low levels of high density lipoprotein. It was beyond the scope of this Work Group to perform a systematic review of the literature on interventions to lower the rate of GFR decline. The American Diabetes Association (ADA) has set forth a Position Statement with guidelines for the care of patients with diabetes mellitus (DM),526 with specific attention to the complication of kidney disease,527 based on the results of the Diabetes Control and Complications Trial (DCCT)528 and extensive review of other published research.
Three randomized trials of strict glycemic control in type 2 diabetes also demonstrate a beneficial effect of strict glycemic control on the development and progression of diabetic kidney disease.
Fasting blood glucose values rose over time in both groups; the mean HgbA1c was 11% lower in the intervention group.
The results showed a lower incidence of the development and progression of microalbuminuria. There was 73% reduction in the incidence of clinical proteinuria in the intervention group.
The optimal frequency of self monitoring of blood glucose for patients with type 2 diabetes is not known, but it should be sufficient to facilitate reaching glucose goals. The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC-VI),245 the most recently updated ADA Clinical Practice Recommendations (2001),526 the NKF Task Force on Cardiovascular Disease in Chronic Renal Disease,9 and a report from the NKF Hypertension and Diabetes Executive Committees Working Group249 were reviewed for this section. There is general agreement that risk stratification should be used in deciding which patients with high blood pressure should be treated and how intensively245 (Table 124). Target blood pressure is lower in younger patients and related to age, weight and height.533 Patients at greatest risk for complications or who already have evidence of cardiovascular disease are considered for the earliest and more aggressive treatment.
Recent studies show equal efficacy of angiotensin converting enzyme inhibitors (ACE-inhibitors) and calcium channel blockers in the general population.534,535 In addition, alternative target blood pressure and medications may be preferred in those subgroups of patients with comorbid conditions. Large-scale epidemiological studies of cardiovascular disease have included few patients with chronic kidney disease, and most clinical trials of antihypertensive agents to prevent cardiovascular disease have excluded patients with decreased kidney function. The MDRD Study is the largest completed randomized trial on strict blood pressure on the rate of GFR decline in nondiabetic kidney disease. The goals of the Work Group are to determine the recommended blood pressure targets, nonpharmacologic therapy, and antihypertensive drug classes for various causes of kidney disease (including diabetes), with additional recommendations for subgroups of patients based on level of kidney function, level of proteinuria, and, if available, age, gender, and race, for prevention of progression of kidney disease, atherosclerotic cardiovascular disease, and heart failure (including LVH). For this Guideline, the Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC-VI),245 the most recently updated ADA Clinical Practice Recommendations (2001),526 and results of a meta-analysis and selected randomized clinical trials were reviewed. Other studies have shown that there is a benefit in reducing the progression of micro albuminuria in normotensive patients with type 1 diabetes and normotensive and hypertensive patients with type 2 diabetes.
In older patients with bilateral renal artery stenosis and in patients with advanced renal disease even without renal artery stenosis, ACE-inhibitors may cause a rapid decline in renal function. Thus, patients with diabetes and hypertension or chronic kidney disease benefit from ACE-inhibitors. All classes of antihypertensive drugs are effective, and, in most cases, multiple antihypertensive drugs may be needed. The results showed better blood pressure control, lower urine protein excretion and an approximately 30% reduction in the risk of development of kidney failure and the combined endpoint of doubling of baseline serum creatinine or kidney failure in the ACE-inhibitor group.
Thus, non-diabetic patients with chronic kidney disease (especially if they have proteinuria) or cardiovascular disease benefit from ACE-inhibitors. The lack of firm evidence regarding its impact, and the logistic and financial difficulties of providing intensive nutritional intervention, preclude recommendation of a low protein diet in all patients with chronic kidney disease.
Some of observational studies have reported that various dyslipidemias are associated with decreased kidney function in the general population and in patients with chronic kidney disease.480,551-554 However, it is impossible to determine from these studies whether dyslipidemias cause reduced kidney function, result from reduced kidney function, or whether other conditions such as proteinuria cause both reduced kidney function and dyslipidemias.
However, there have been several small studies555-566 and a meta-analysis of these studies.567 This meta-analysis included prospective, controlled trials published before July 1, 1999.
The available evidence that partial correction of anemia with erythropoietin (and iron) results in improvement in the rate of decline of GFR is therefore inconclusive. Reduced blood flow to the kidney and intrinsic damage to the kidney because of a nephrotoxic or ischemic insult are the most common causes of acute deterioration of GFR.
The most common precipitants of volume depletion are vomiting, diarrhea, poor fluid intake, fever, and diuretic use.
In particular, these are likely to result in acute decline in GFR if there is an additional insult such as sepsis, volume depletion, heart failure, or treatment with ACE inhibitors. The most common causes of obstruction are prostatic hypertrophy, cancer of the prostate or cervix, or retroperitoneal disorders. The clinician should become familiar with the most common causes, in order to prevent avoidable worsening of the course of chronic kidney disease.
Most notably, with many of the studies the results were difficult to compare as they use different measures for kidney function: measured GFR or creatinine clearance, estimation equations for GFR or creatinine clearance, or simply serum creatinine. This review of these studies does not provide a conclusive answer to the causes underlying the more rapid rate of progression or increased risk for kidney failure. There is increasing evidence that certain interventions can slow the decline in GFR and prevent the development of kidney failure in both diabetic and nondiabetic patients. This may require changing the policies of care providers and payers regarding frequency of follow-up and payment for medications. However, there are certain factors whose impact has not been conclusively determined, such as dietary protein intake, hyperlipidemia, and anemia and their treatment. Similarly, in the case of the impact of blood pressure control, conclusions largely come from the observations that patients with lower blood pressures have improved outcomes. 1 (UPI) -- Researchers found combining therapies for ADHD is more effective than individual therapies on their own, according to a series of new studies. 1 (UPI) -- Scientists have developed a smartwatch app to alert nursing home staff to resident needs, with the hope of providing better service and preventing injuries. 1 (UPI) -- The relatively common Epstein-Barr virus may increase breast cancer risk, according to a new study, leading researchers to suggest a vaccine could be useful. 1 (UPI) -- Replacing 3 percent of protein from red meat or eggs with plant proteins, regardless of other lifestyle habits, can reduce the risk of death, researchers say. 1 (UPI) -- Higher BMI was shown in a study of twins to increase risk for diabetes, but did not appear to affect risk for heart attack or death, according to researchers.
1 (UPI) -- The melanoma drug vemurafenib activates proteins in skin, which researchers at the University of California Los Angeles say could help speed wound healing. Our goal is to help patents better manage diabetes (all types) and prevent the associated complications from the disease.
INTRODUCTION: Diabetes-related health improvements achieved from self-management education interventions are not sustained long-term. Now that they have their own studio I’m hoping for a Book of Mormon movie produced by them.
A nurse trained in diabetes education can provide information about managing diet exercising monitoring blood glucose levels and taking drugs.
Treatment involves pharmacologic therapy to reduce insulin resistance along with Antiobesity drugs such as orlistat may reduce insulin resistance and related cardiovascular risk factors Dosing Interactions etc.
The machine is built for heavy use by rowing or health clubs and I believe will last an individual a lifetime. Although some authors have performed a meta-analysis of studies, a quantitative data synthesis was not performed for this Guideline.
For consideration of therapy for diabetic kidney disease, development and worsening of proteinuria was also included in the definition of progression of kidney disease.
The lower, middle and upper lines represent the 10th, 50th (median), and 90th percentiles of the distribution of GFR slopes, respectively. Indeed, studies have shown that the GFR decline does appear relatively constant over time, although other studies have shown that other continuous relationships (such as the logarithm) or non-continuous (spline) relationships may fit the data better in some cases. However, there are a number of limitations to estimation of the slope and extrapolation of the rate of decline to predict the time to development of kidney failure.
The magnitude of the changes in slope was relatively large in comparison to the first slope (mean of 130% of the value of the first slope).
Coupled with the fact that the elderly start from a lower baseline GFR, older individuals with chronic kidney disease deserve special attention and closer follow-up.
Most studies reporting multivariate analyses showed a significant association between elevated blood pressure, based on any measures of blood pressure, and faster rate of GFR decline.
A similar number of studies showed no significant association between poor glycemic control and faster rate of GFR decline in multivariate analyses. However, the large sample sizes and adequate methodological quality and applicability of the studies supporting the association of smoking with faster rate of GFR decline provide reasonable evidence that there may be a deleterious effect of smoking on rate of progression.
The impact of dyslipidemia reported herein is based on whether any one of these factors was associated with a faster rate of progression.
Thus, the goal of this section was to review published guidelines and position statements by reputable national organizations addressing widely accepted interventions. The difference was observed with a mean HgbA1c of 7.2% in the intensively treated versus 9% in the conventionally treated patients. However, the relative importance of strict glycemic control and any of the other factors cannot be determined from this study. The role of self-monitoring of blood glucose in stable diet-treated patients with type 2 diabetes is not known. This section will discuss primarily the target blood pressure level for patients with chronic kidney disease, with only brief reference to the role of specific antihypertensive agents. These subgroups include, among others, patients with chronic kidney disease, diabetes, and cardiovascular disease.
Some of the important randomized trials on the target level of blood pressure in patients with chronic kidney disease due to diabetes and other diseases are summarized below. If blood pressure remains elevated after initiation of an ACE-inhibitor, other antihypertensive agents should be prescribed to achieve target blood pressure.


The beneficial effects of ACE-inhibitors to slow progression appeared to be independent of their effects on blood pressure and proteinuria. The use of ACE-inhibitors must always be done with the consideration that it may have a detrimental effect on GFR in patients with renovascular disease or renal artery stenosis. If blood pressure remains elevated after initiation of an ACE-inhibitor, other antihypertensive agents should be prescribed to achieve the target blood pressure.
As described earlier (Fig 50), there was an initial faster GFR decline in the low-protein diet group, followed by a slower GFR decline thereafter, but no significant benefit over a 3-year interval. Each of these explanations is plausible, and only randomized, controlled trials can adequately test the hypothesis that dyslipidemias cause a decline in kidney function. Three trials published only in abstract form were included,555,556,566 but one of these studies has subsequently been published in a peer-reviewed journal.566 All patients were followed for at least 3 months, but in only 5 studies were patients followed for at least 1 year. Further studies specifically addressing the effects of anemia and its treatment on rate of GFR decline are necessary to clarify this issue. Heart failure can effectively result in a reduction of blood flow to the kidney due to reduced cardiac output, in the face of apparent volume overload. Toxins can cause kidney failure via a number of mechanisms including (not an exhaustive list): (1) alteration of kidney blood flow (NSAIDs, ACE inhibitors, cyclosporine, radiocontrast agents), (2) direct tubular injury (aminoglycosides, radiocontrast, amphotericin B), (3) intratubular obstruction (acyclovir, sulfonamides), (4) allergic interstitial nephritis (NSAIDs, penicillins, cephalosporins, sulfonamides). In addition, kidney stones, blood, fungal infection, and bladder malignancy may result in obstruction.
Further limiting the comparability of the results across the studies is the wide variation in the selection of analytic techniques and presentation of data. In the case of cause of kidney disease, the conclusion that certain causes are associated with faster rates of progression come from the comparison of studies of single causes, using diverse methods to measure or estimate GFR.
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Type 2 diabetes (when not taking insulin) can be adequately managed by using another test called glycosylated hemoglobin or hemoglobin A1c I just hope it goes away. Manly hate having the ball They require more time and Most obese peole or individuals who can’t exercise have multiple co-morbidities such as various heart diseases respiratory disease and metabolic problems.
I also think the rather slim glossary could be expanded somewhat beyond the handful of pages provided to give more novice readers a convenient reference point. Coenzyme Q10 and diabetes – Coenzyme Q10 supplements may improve heart health and blood sugar and help manage high cholesterol and high blood pressure in individuals with diabetes. Control of type II diabetes may include Attention to potential sequelae such as high blood pressure strokesblindness heart complications.
We bought it for indoor use, so the kids can exert some energy during the months when its too cold or too hot to play outdoors. The GFR slope estimates are not related to baseline GFR, but the variability in slope estimates is higher at higher levels of baseline GFR. These limitations are related principally to whether the rate of decline is truly constant and the precision of the estimate of the rate of decline.
Diagonal dashed lines are extrapolations of the regression lines to earlier and later times. Consequently, the mean error in the interval until reaching the final serum creatinine was also relatively large, 27% of the predicted interval (Fig 49). In the MDRD Study480 and the study by Massy,499 polycystic kidney disease was associated with a faster rate of progression, whereas in the study by Hannedouche,490 polycystic kidney disease was associated with a slower rate of progression. There were only 7 studies that reported no significant association between elevated blood pressure measures and faster rate of GFR decline in multivariate analysis.
Although these data do not unanimously show that poor glycemic control is associated with faster rate of GFR decline when controlling for other factors, the studies with larger sample sizes and higher methodological quality and applicability do support the association.
There were 7 studies that reported in multivariate analyses a significant association between dyslipidemia and faster rate of progression. In keeping with the rest of this section the guideline, only this one study was considered for inclusion in an evidence table (Table 122).
In addition, meta-analyses of randomized trials or data from selected large randomized trials were used to formulate this guideline. The data suggested a lower prevalence of microalbuminuria in the intervention group and a reduced incidence of declining kidney function. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin-2 receptor blockers are discussed in the next section. The Work Group did not find randomized trials on target blood pressure levels in kidney transplant recipients.
In addition, preliminary results of clinical trials with angiotensin receptor antagonists are briefly discussed. This class of agents is contraindicated in pregnancy and therefore should be used with caution in women of childbearing potential. Furthermore, in kidney transplant recipients, ACE-inhibitors may exacerbate hyperkalemia caused by cyclosporine or tacrolimus. These studies have shown either no overall difference in the rate of decline of kidney function in treated compared to untreated groups297,304,306 or compared to pre-treatment rates of decline,568 or a slight benefit in terms of a slower rate of decline of GFR in the treated group294,569 and prolongation of time to ESRD569, or reduced proportion of patients who experienced doubling of baseline serum creatinine in the treated versus untreated groups.305 Each of these studies, as well as a study comparing intravenous with oral iron and erythropoietin for the treatment of anemia in chronic kidney disease,570 also concluded that normalization of hemoglobin or hematocrit had essentially no effect on the rate of decline of kidney function. The risk of developing acute deterioration of kidney function due to volume depletion is highest in the elderly, as they may already have compromised blood flow to the kidneys due to atherosclerotic disease.
The avoidance of potential nephrotoxins, such as intravenous radiographic contrast, certain antibiotics, and NSAIDs must be based on an individualized assessment of the risks of acute decline in GFR versus the therapeutic benefits of treatment.
Unlike with toxic insults, acute decline in GFR due to obstruction is commonly seen in the outpatient setting. Antihypertensive agents, especially ACE-inhibitors and angiotensin-receptor blockers, reduce proteinuria and slow the progression of kidney disease.
A noninterventional prospective cohort study including sufficient numbers of patients with all causes of kidney disease, undergoing similar testing for level of kidney function, would be ideal to evaluate the impact of cause of kidney disease on the rate of decline in GFR.
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Massy and Hannedouche both reported that glomerular disease was associated with a faster rate of progression than tubulointerstitial nephropathy. However, the Work Group concluded that GFR decline is faster than in many other causes of chronic kidney disease given that graft survival rates are approximately 75% at 5 years for living donors and 60% at 5 years for cadaveric donors509 or an approximate half-life until graft failure for kidney transplants of approximately 12 and 7, respectively. These data, though not unanimous, confirm that elevated blood pressure is associated with faster rate of GFR decline when controlling for other factors.
There were 7 studies that reported no significant association between dyslipidemia and faster rate of progression in multivariate analyses. Of the seven studies, three, including Kuriyama, reported an increased rate of progression among patients with lower hematocrit levels; the remaining studies reported no association.
Patients with higher levels of proteinuria at baseline had a greater beneficial effect of the low blood pressure goal. Full detail of the recommendations of the ADA and JNC-VI is beyond the scope of this work, and the reader is referred to these sources for complete guidelines. Thus, treatment of patients with chronic kidney disease with ACE-inhibitors requires knowledge of the expected benefits and risks of therapy and careful attention to blood pressure, kidney function, serum electrolytes, and possible drug interactions. Whether or not the decision is made to pursue a low protein diet, the Work Group reinforces the importance of maintaining a good nutritional status with advancing chronic kidney disease, which generally would involve evaluation and monitoring by a dietitian, and refers the reader to Guideline 9.
For example, in a patient with debilitating arthritis, avoidance of NSAID use should be considered in light of the benefits of reducing pain and immobility; in a patient with coronary artery disease, the avoidance of intravenous radiocontrast should be weighed against the potential benefits of an angioplasty procedure. Alternatively, a sufficiently large prospective interventional trial could achieve a similar goal. Previously I’ve steered clear of this type of book thinking I can find out just as much with Google. You are asking someone who is pre diabetes signs in mouth diabetes diagnosis diet forced to work a minimum of 12 hours of overtime a week and end up working up 20 to 25 hours a week of overtime. The studies varied in the levels of kidney function assessed, sample sizes, and methodological quality. However, these two studies showed a conflicting result regarding the rate of progression associated with hypertensive kidney disease. Loss of kidney function for transplant recipients is influenced by episodes of rejection, use of immunosuppressive agents, patient gender and size, and quality of the donor kidney, among other factors. The data are not sufficient to conclude that dyslipidemia is associated with a faster rate of progression. The data are not sufficient to conclude that anemia is associated with a faster rate of progression.
There have been several secondary analyses of the data, which provide further information on the effectiveness of these interventions.503 Specifically, comparisons of the distributions of GFR slopes between randomized groups in Study A were consistent with a beneficial effect of the low protein diet group. The results suggested that the rate of decline in GFR was significantly less in patients treated with a lipid-lowering agent compared to placebo.567 No significant heterogeneity in treatment effect was detected between the studies. Anecdotal reports have long suggested the use of chromium supplementation to help control and prevent type 2 diabetes. These studies either excluded diabetics, or had a very small proportion of patients with diabetes in the study sample. At the time of preparation of these guidelines, the African American Study of Kidney Disease and Hypertension (AASK) is nearing completion, and additional information on the benefit of strict blood pressure control in nondiabetic kidney disease is expected in the near future. Consequently, patients with hypertension who have renal insufficiency should receive, unless contraindicated, an ACE-inhibitor (in most cases, along with a diuretic) to control hypertension and to slow progressive renal failure. However, the quality of the studies was generally low, and their small sample sizes and relatively short duration of follow-up make it difficult to conclude that lipid-lowering therapies reduce the rate of decline in GFR in chronic kidney disease. Does uncontrolled child birth at some point become an ethical issue as the population grows larger than the diabetes gene nature genetics earth’s diabetic diet meal plan spanish resources can sustain?
A study by Hyppnen, et al., published in the November 2001 issue of "Lancet," showed that supplementation of vitamin D in infants reduced the incidence of type I diabetes.
The interval predicted from the first regression line was 30 months (left vertical dashed line).
Clearly, adequately powered, randomized controlled trials are needed to determine the role of lipid-lowering therapy in retarding the rate of decline in kidney function in patients with chronic kidney disease. For the record I come from an American evangelical but not fundamentalist background and I see no issue with birth control (condom pill etc.). The evaluation and management of dyslipidemia in patients with chronic kidney disease has been addressed by the NKF Task Force on Cardiovascular Disease in Chronic Renal Disease and is reviewed briefly in Guideline 15.
The prediction error (difference between the actual and predicted intervals) was 10 months (25% of the actual interval).
It is thus unclear whether such severely restricted protein diets can be safely prescribed or even maintained in the absence of frequent dietitian involvement. The management of dyslipidemia in patients with kidney failure is the subject of an ongoing KDOQI Work Group.



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