CKD MNT Module 2: Slow Progression of Chronic Kidney Disease
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CKD MNT Module 2: Slow Progression of Chronic Kidney Disease

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This module reviews how intake of certain nutrients is reflected in urinary excretion; which antihypertensive medications increase the risk for hyperkalemia in CKD; and how diabetes control impacts ...

This module reviews how intake of certain nutrients is reflected in urinary excretion; which antihypertensive medications increase the risk for hyperkalemia in CKD; and how diabetes control impacts CKD and how CKD progression may impact diabetes control. Interventions to lower albuminuria and control lipids in CKD are discussed. Using a case study format, follow Frank's journey as he rapidly approaches kidney failure to see how the diet and medications may interact in hypertension and diabetes in CKD.
At the end, you will be introduced to two other educational resources from NKDEP, Eating Right for Kidney Health and Your Kidney Test Results, and see how to use them when counseling patients.

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  • In this module we will discuss the role of hypertension, diabetes, albuminuria and cardiovascular disease (CVD) in CKD progression. Our case study will follow a patient, Frank, as he approaches kidney failure. You will see how certain anti-hypertensive medications impact Frank's serum potassium and urine albumin levels. Diabetes control and appropriate treatment of hypoglycemia, risk factors and interventions for lowering urine albumin levels, and traditional and non-traditional risk factors for CVD will be discussed. Module_2_4-26 POST EDITING
  • Participants will be able to: 1. Use and interpret biochemical and patient data for assessment of hypertension and CKD 2. Identify commonly prescribed classes of anti-hypertensive medications that may affect serum potassium levels in CKD 3. Associate spontaneous improvement in diabetes mellitus (DM) control with possible CKD progression 4. Modify recommendations for appropriate treatment of hypoglycemia in DM and CKD5. Identify at least two nontraditional risk factors for cardiovascular disease in CKD 5. Identify at least two nontraditional risk factors for cardiovascular disease in CKD Module_2_4-26 POST EDITING
  • Let’s briefly review three important points from the first module. First, diabetes and hypertension are the leading causes of chronic kidney disease in the United States. Much of the increase in the burden in kidney failure is due to type 2 diabetes. Second, urine albumin is a marker for kidney damage and cardiovascular disease. It may also reflect the severity of kidney damage and serve as a prognostic indicator. Finally, people with chronic kidney disease are more likely to die from cardiovascular disease than to progress to end-stage kidney disease. Module_2_4-26 POST EDITING
  • We also want to remind you that the definition of chronic kidney disease is based on either reduced kidney function or evidence of kidney damage or both. Reduced kidney function means a GFR of less than 60 milliliters per minute per 1.73 meters squared present for at least three months. Evidence of kidney damage may include pathologic abnormalities or other markers of kidney damage, such as hematuria. However, in most cases, evidence of kidney damage is albuminuria. Module_2_4-26 POST EDITING
  • This module is focused on the comorbidities associated with chronic kidney disease. These comorbidities, including hypertension, diabetes, and cardiovascular disease, all increase as GFR declines. This figure shows that, as GFR declines as you move right on the horizontal axis, the prevalence of these comorbidities increases on a vertical scale. There is a significant bump in all these comorbidities when the GFR drops below 30. Module_2_4-26 POST EDITING
  • Comorbidities are also associated with rising levels of urine albumin. There’s an increased risk of cardiovascular disease even at very low levels of urine albumin, below the levels that we consider the cutoff for defining CKD, which is 30 milligrams per gram. Module_2_4-26 POST EDITING
  • This module is focused on slowing the progression of kidney disease, and it’s fitting that we will begin with controlling hypertension. Reducing blood pressure is probably the most effective intervention to slow the progression of chronic kidney disease. Module_2_4-26 POST EDITING
  • We will discuss hypertension, sodium intake, and the DASH diet which lowers blood pressure and has been a very effective public health intervention. We’ll also discuss antihypertensive medications used in chronic kidney disease, including medication-induced hyperkalemia. Module_2_4-26 POST EDITING
  • Despite the availability of many different anti-hypertensive drugs, blood pressure is poorly controlled in patients with chronic kidney disease. This figure shows that as GFR declines, rates of uncontrolled hypertension increase. Module_2_4-26 POST EDITING
  • High blood pressure and chronic kidney disease are inextricably linked. High blood pressure causes chronic kidney disease. Kidney disease causes high blood pressure. This results in a self-reinforcing cycle. It’s key, in order to slow progression, to interrupt this cycle. Module_2_4-26 POST EDITING
  • Blood pressure goals are unclear in CKD. There has been a recommendation that all people with chronic kidney disease should have a target blood pressure less than 130/80, and there’s observational data to support this. However, there’s also evidence that controlling all people to this level may be associated with increased morbidity, especially among the elderly. There is not a strong evidence base to justify blood pressure targets below 140/90. Regardless, the major challenge that we face as clinicians is the large number of patients who have uncontrolled hypertension. Module_2_4-26 POST EDITING
  • There is a strong correlation between blood pressure and sodium intake. This has been supported by numerous international observational studies. Module_2_4-26 POST EDITING
  • In general, sodium excretion matches intake. About 90 percent of sodium intake is from salt. Most is absorbed in the small intestine. Sodium is freely filtered by the glomerulus, and, depending on volume status, most is reabsorbed in the tubule. Module_2_4-26 POST EDITING
  • Sodium reabsorption in the tubule is complex. About 60 percent occurs in the proximal tubule. Twenty-five percent is reabsorbed in the loop of Henle, which is where the tubules take a hairpin turn. Five percent is absorbed in the distal convoluted tubule, and a small amount in the collecting duct.
  • Sodium reabsorption is complex, as I mentioned, and there are numerous mechanisms and numerous tubular pumps that are linked in complex ways to acid/base exchange and to chloride reabsorption. There are aldosterone sensitive channels, as well. Module_2_4-26 POST EDITING
  • Kidneys play a very important role in salt and water conservation. Kidneys produce renin, which functions to increase sodium reabsorption. Renin is an enzyme which is produced by the juxtaglomerular epitheloid cells in response to low renal profusion, as occurs in shock. Renin is a key element in maintaining volume status in the face of hypovolemia as part of the Renin-Angiotensin-Aldosterone system. Module_2_4-26 POST EDITING
  • The renin-angiotensin-aldosterone system is important to understand not only because of its physiologic role in maintaining blood pressure, but because several of our most important therapeutic interventions act by blocking this system. Angiotensinogen is converted to angiotensin I by renin, which is then converted to angiotensin II by the angiotensin converting enzyme. Angiotensin II then acts on the adrenal gland to increase secretion of aldosterone, which results in sodium reabsorption and volume expansion, thereby increasing blood pressure. Angiotensin converting enzyme inhibitors block the Renin-Angiotensin system by blocking conversion of angiotensin I to angiotensin II. Angiotensin converting enzyme inhibitors include Lisinopril, Captopril, and a number of other drugs that end with –pril. Angiotensin II receptor blockers such as losartan interrupt the action of angiotensin II and have a similar effect as ACE inhibitors on blood pressure. As we’ll discuss later, both ACE inhibitors and ARBs also have a special protective effect on the kidneys. Module_2_4-26 POST EDITING
  • Initial interventions to reduce blood pressure include lifestyle modifications although most patients do require some anti-hypertensive medications. Weight reduction can result in a modest improvement in blood pressure. The DASH diet has been shown to improve blood pressure. Physical activity further reduces blood pressure. Moderating alcohol consumption will reduce blood pressure as will sodium restriction. Module_2_4-26 POST EDITING
  • We assume these lifestyle modifications are effective in patients with chronic kidney disease, although they have not been extensively studied in this population. Module_2_4-26 POST EDITING
  • Now you will hear more about the DASH diet and hypertension, components of the DASH diet, and why it may not be indicated for people with chronic kidney disease. The DASH diet is effective in lowering blood pressure in the general population. This booklet about educating patients about the DASH diet can be found at the National Heart, Lung, and Blood Institute Web site. Module_2_4-26 POST EDITING
  • The original DASH results were published in 1997. The authors concluded, “a diet rich in fruits, vegetables and low-fat dairy foods, and with reduced saturated fat and total fat can substantially lower blood pressure.” The original DASH pattern had about 3,000 milligrams of sodium. Based on the results, DASH-Sodium was implemented to assess the DASH pattern using different levels of sodium. The DASH-Sodium results were published in 2001 and found , “The reduction of sodium intake to levels below the current recommendation of 100 millimoles per day and the DASH diet, both lower blood pressure substantially with greater effects in combination than singly.” One hundred millimoles of sodium equals 2,300 milligrams of sodium. People who followed the DASH pattern and limited sodium intake to 2,300 milligrams or less per day had lower blood pressures. Module_2_4-26 POST EDITING
  • The DASH pattern for 2,000 calories includes six to eight servings of grains, four to five servings of vegetables, four to five servings of fruits, and two to three servings of fat-free or low-fat milk products. Protein intake is limited to less than or equal to six ounces per day. The pattern includes four to five servings of nuts, seeds and legumes per week. Fats and oils are limited to two to three servings per day. Sweets and added sugars should add up to no more than five tablespoons per week. Module_2_4-26 POST EDITING
  • What were the nutrient profiles of the diet patterns? The DASH combination diet pattern, seen in the far right column, is higher in protein and potassium than the control or fruits and vegetables diet. The control diet had about 14 percent of the total calories from protein, the fruits and vegetables diet had 15 percent protein, and the DASH combination diet had about 18 percent calories from protein. Potassium ranged from 1,750 milligrams in the control diet to over 4,000 milligrams in both the fruits and vegetables diet and combination diet. The sodium intake was about 3,000 milligrams per day. Module_2_4-26 POST EDITING
  • This table shows urinary excretion of potassium, nitrogen, phosphorus, and sodium varied with intake in the DASH study. Both the fruits and vegetables diet and the combination diet contained more potassium; this is reflected in the urinary excretion rates. Urinary potassium excretion increased with increased potassium intake. The third row shows urea nitrogen excretion. The DASH combination diet was higher in protein, and higher protein intake produces more nitrogenous waste. Urea nitrogen excretion reflected protein intake. Phosphorus was not listed in the nutrient profiles, however, urinary excretion was reported. Phosphorus is found in protein-rich foods. The combination diet, with its higher protein content, provided more dietary phosphorus. Urinary phosphorous excretion may reflect protein intake. People who eat more protein will have more nitrogenous waste and phosphorus to excrete into the urine. The bottom row shows sodium intake about equaled sodium excretion. Each pattern had about 3,000 milligrams of sodium. Module_2_4-26 POST EDITING
  • The combination DASH pattern was the most effective in lowering blood pressure. Compared to the control diet, the DASH pattern lowered systolic blood pressure by about 5.5 millimeters of mercury, and the diastolic blood pressure by about three millimeters of mercury. Compared to the control diet, the fruits and vegetables diet lowered blood pressure, but not as effectively as the DASH pattern. Module_2_4-26 POST EDITING
  • The DASH pattern lowers blood pressure. The DASH-Sodium study showed lower sodium intake decreased blood pressures further. The typical diet and the DASH pattern were each studied with different levels of sodium intake: 3,450 milligrams, 2,300 milligrams, or 1,150 milligrams. As was seen in the original DASH study, sodium intake was about equal to sodium excretion. People who ate more potassium excreted more potassium, and people who ate more protein excreted more nitrogenous waste and phosphorus. Module_2_4-26 POST EDITING
  • The results of the DASH-Sodium study show sodium restriction provides additional blood pressure benefit to the original DASH diet. The DASH pattern lowered blood pressure at all levels of sodium. In the control diet, blood pressure was lowered with the lowest sodium intake. For people who cannot tolerate the DASH pattern, lowering dietary sodium may help lower blood pressure. Combining the DASH pattern and the lowest sodium intake provided the greatest reduction in blood pressure than either intervention alone. Module_2_4-26 POST EDITING
  • Why shouldn’t the DASH pattern work for CKD? The DASH pattern may not be appropriate for CKD due to protein, phosphorus, or potassium contents. Whole grains are a source of phosphorus and potassium. Vegetables and fruits vary in potassium content. Milk products are a source of protein, sodium, phosphorus, and potassium. Meats, poultry, and fish have protein, phosphorus and potassium, and meat products that are enhanced or processed may have added sodium and phosphorus. Unsalted nuts, seeds and legumes contain protein, phosphorus and potassium. Oils and some fats are virtually sodium free. Salted butter and salted margarine contain sodium. Sweets and added sugars may have added phosphorus. Module_2_4-26 POST EDITING
  • To summarize, the DASH pattern diet may help prevent chronic kidney disease by lowering blood pressure. People who cannot follow the DASH pattern may benefit from lower sodium intake. The DASH pattern’s nutrient profile may not be appropriate for CKD due to the protein, phosphorus and potassium contents. Some people trying to limit sodium intake may use a salt substitute. Please keep in mind salt substitutes are a source of potassium. Module_2_4-26 POST EDITING
  • Controlling blood pressure usually requires a combination of lifestyle changes as well as medication. Many patients will require two or three or more medications. Most patients with chronic kidney disease are volume expanded and control of their blood pressure will usually require a diuretic. Regardless of the drug regimen, sodium restriction is quite important. A sodium restriction of 1,500 mg per day is essential to controlling blood pressure and to getting the maximum renoprotective benefit from drugs which antagonize the renin-angiotensin-aldosterone system. Module_2_4-26 POST EDITING
  • Although the antihypertensive medications that block the renin-angiotensin system are very effective and renoprotective, they do carry a risk of hyperkalemia. Primarily we’re referring to angiotensin converting enzyme inhibitors and angiotensin receptor blockers. The inhibitors include Lisinopril, Captopril and other –pril drugs. Angiotensin receptor blockers include Losartan. Because these drugs decrease aldosterone production, they may result in a reduction in potassium excretion. The risk for hyperkalemia increases with dose. Module_2_4-26 POST EDITING
  • Again, these drugs interfere with the renin-angiotensin system. The converting enzyme inhibitors block the conversion of angiotensin I to angiotensin II. The receptor blockers block the angiotensin II receptor. Module_2_4-26 POST EDITING
  • Because these drugs block the renal-angiotensin system, they increase the risk of hyperkalemia by decreasing secretion of aldosterone. Module_2_4-26 POST EDITING
  • To reiterate, medications which increase the risk for hyperkalemia in CKD include the angiotensin converting enzyme inhibitors and the receptor blockers. In addition, aldosterone antagonists such as spironolactone, renin inhibitors, and potassium sparing diuretics, like triamterene, may increase potassium and should be used cautiously in patients with chronic kidney disease. Module_2_4-26 POST EDITING
  • Many patients diagnosed with chronic kidney disease are automatically instructed on a potassium restriction. Potassium restriction is an individualized recommendation and is not indicated in the absence of hyperkalemia. It is not indicated by any specific level of estimated GFR. Restriction is indicated when potassium is elevated in order to achieve and maintain a safe level. To repeat, potassium restriction is something that should be individualized and not automatically implemented simply because someone carries a diagnosis of chronic kidney disease. Module_2_4-26 POST EDITING
  • However, it is certainly true that potassium levels tend to rise as GFR declines. This figure shows the proportion of patients with potassium over 4.5 increases as you move from left to right, in the direction of decreasing eGFR. Module_2_4-26 POST EDITING
  • ACE inhibitors and angiotensin receptor blockers, by blocking the renin-angiotensin system, may be renoprotective. There is an additional benefit beyond blood pressure control. Possible evidence of this renoprotective benefit is reduction in urine protein excretion. Evidence supports the effectiveness of these medications in chronic kidney disease patients who are normotensive but have elevated levels of urine albumin. MODULE 2 original 3-13 Module_2_4-26 POST EDITING
  • Many patients with chronic kidney disease will require more potent diuretics, usually described as loop diuretics. These diuretics act on the thick ascending loop of the renal tubule and may cause hypokalemia. They decrease sodium reabsorption and lower blood pressure. Less potassium is also reabsorbed and the serum level may decrease. Many people with CKD on loop diuretics do not become hypokalemic due to the concurrent use of ACE inhibitors or angiotensin receptor blockers or because they have fewer functioning nephrons. MODULE 2 original 3-13 Module_2_4-26 POST EDITING
  • The next section briefly covers the nutrition care process for chronic kidney disease and hypertension. Assessment includes a review of the anti-hypertensive medications and monitoring of serum potassium when indicated. The key intervention is reducing sodium intake. The 2010 dietary guidelines recommend limiting sodium to 1,500 milligrams per day for people with diabetes, hypertension, chronic kidney disease, for African Americans and those over age 50. Caution people with CKD that salt substitutes are a source of potassium and should be avoided. We have discussed concerns with the DASH pattern and chronic kidney disease. MODULE 2 original 3-13 Module_2_4-26 POST EDITING
  • We are going to apply this information to a case study. Our case study, Frank, shows how food and medication interaction may result in hyperkalemia. Frank is a 55-year-old man with type 2 diabetes since 2002. He has not taken any medications for the past five years. He has a history of a toe amputation on his left foot. He came to the clinic in January because his right foot was swelling. At that time, blood pressure was 168/98 and he was started on lisinopril, an ACE inhibitor. Frank was told to decrease salt. In order to reduce salt intake he purchased a salt substitute. His eGFR was 34, and his urine albumin-to-creatinine ratio was 6,437 milligrams per gram. He is 66 and one half inches tall and he weighs 205 pounds. MODULE 2 original 3-13 Module_2_4-26 POST EDITING
  • This table shows Frank’s blood pressures and weights and selected lab results. On January 19, his blood pressure was 168/98, eGFR was 34 and potassium was 4.9. Lisinopril 40 milligrams and furosemide 20 milligrams daily were prescribed. On January 29, blood pressure was down to 138/82 and eGFR was stable at 34. Serum potassium was 4.6. He told the nurse he was using salt substitute in place of salt. In April, his blood pressure was 136/78, eGFR was 29, and potassium was 5.5. He missed an appointment with the dietitian in February. In April, the physician increased furosemide to 40 milligrams to lower serum potassium. The physician wanted Frank to continue lisinopril to lower urine albumin. Module_2_4-26 POST EDITING
  • In the far right column, you see data from May. The upper blue text box shows blood pressures. The second blue text box shows UACR decreased from 6,437 to 4,483. The ACE inhibitor reduced the loss of urine albumin. Unfortunately, his serum potassium level is still elevated at 5.5, as shown in the red text box. The physician discontinued lisinopril and started losartan, an angiotensin receptor blocker. For some people, this change may lower potassium. MODULE 2 original 3-13 Module_2_4-26 POST EDITING
  • For Frank, the change from an ACE inhibitor to an angiotensin receptor blocker did not lower serum potassium level. In July, serum potassium is 5.5. He was referred to the dietitian at that time. MODULE 2 original 3-13 Module_2_4-26 POST EDITING
  • Frank’s usual intake is as shown. Breakfast includes two fried eggs, three or four slices of bacon, three slices of wheat toast and at least three cups of coffee with an artificial sweetener. He adds salt substitute to the eggs. His diet is different on weekends. They eat a large brunch, and his wife makes fried potatoes. During the work week, lunch is generally fast foods such as a double meat burger and medium fries. He does not add salt. He drinks diet pop. He may skip lunch on weekends. He usually eats a large piece of meat, two to three slices of bread, with a cup of canned corn or peas. He reported drinking orange juice more frequently, to treat low glucose levels. His serum potassium is high. Foods rich in potassium include salt substitute, coffee, potatoes, large portions of meat, and orange juice. MODULE 2 original 3-13 Module_2_4-26 POST EDITING
  • For educational purposes, the assessment data listed here follows the order found in the International Dietetics and Nutrition Terminology Reference Manual. His intake was described previously. In addition, he will not use glucose tablets to treat low glucose levels. His diet order is 2,200 calories, 1,500 milligrams sodium, with a potassium restriction. He needs to decrease potassium intake from current intake. He received a diabetic diet instruction when first diagnosed with type 2 diabetes. His antihypertensive medications are listed. He weighs 189 pounds. His serum potassium level has been 5.5 for the past three months. His eGFR is down to 22 from 34. The UACR is lower but still very elevated. English is his second language. He is seeing a nephrologist. Social history includes sedentary lifestyle and he lives with his wife and two sons. MODULE 2 original 3-13 Module_2_4-26 POST EDITING
  • Any number of nutrition diagnoses could be considered. The food and medication interaction is a high priority. He was referred due to hyperkalemia. His serum potassium is 5.5, and he takes a medication that reduces potassium excretion. Considering his low eGFR, Frank eats excessive amount of foods rich in potassium. He has a food-related knowledge deficit, as evidenced by use of salt substitute and other foods rich in potassium. Module_2_4-26 POST EDITING
  • As Frank’s eGFR declined, his potassium level increased. He takes a medication that decreases potassium excretion, uses salt substitute, and eats potassium-rich foods. Module_2_4-26 POST EDITING
  • Frank needs to lower his dietary potassium intake at this time. One priority is to eliminate salt substitute. He could use cranberry juice cocktail instead of orange juice to treat low glucose levels. He could eat less meat or fewer potatoes. The goal is based on what he is willing to do. Module_2_4-26 POST EDITING
  • To summarize this section of the module, we discussed hypertension and blood pressure control. Multiple medications are the norm not the exception in kidney disease. Review medication lists as you assess patient needs. Sodium restriction is key to lower blood pressure. Caution people to avoid salt substitutes, particularly if they are taking an ACE inhibitor or an ARB. Restrict dietary potassium when the serum level is high. Module_2_4-26 POST EDITING
  • Diabetes control in chronic kidney disease is a complex topic. There is evidence that good diabetes control prior to the development of kidney disease can prevent the development of kidney disease. Once clinical kidney disease is present, there is not a great deal of evidence that tight control of diabetes has an effect on the progression of kidney disease when compared to less tight control. Other issues that occur in diabetes relate to changes in glucose control as kidney disease progresses. Module_2_4-26 POST EDITING
  • We’re going to discuss glucose and how it affects the nephron. Other topics include insulin and other diabetes medications, advanced glycation end products, diabetes control, treatment of hypoglycemia, and the risk for hyperkalemia in diabetics who are treated with ACE inhibitors and ARBs. Module_2_4-26 POST EDITING
  • As we mentioned in module 1, diabetes is the leading cause of end-stage renal disease in the United States. The blue line here shows the contribution that diabetes makes to the rising burden of kidney disease. Most of this is type 2 diabetes Module_2_4-26 POST EDITING
  • Glucose affects the kidneys in complicated ways. Glucose is filtered by the glomerulus and almost completely reabsorbed in the proximal tubule. When the amount of glucose filtered exceeds the tubules’ ability to reabsorb it, glucose appears in the urine. The threshold for this phenomenon is approximately 180 to 200 milligrams per deciliter. So, when the blood glucose exceeds 200 milligrams per deciliter, glucose is likely to appear in the urine. Glucose is often co-absorbed with sodium, resulting in volume expansion. The nephrons are also involved in gluconeogenesis, and contribute about 20 percent of the overall endogenous release of glucose. Module_2_4-26 POST EDITING
  • It’s important to realize that hyperglycemia is associated with hyperfiltration, and, as you’ll see shortly, early in the course of diabetes, hyperglycemia results initially in an increase in estimated GFR. There is hypertrophy of the glomerulus and tubule and increased pressure and flow through the kidney, resulting in nephron damage. Diabetic kidney disease is generally, not always, associated with progressive increase in urine albumin. Module_2_4-26 POST EDITING
  • The natural history of diabetic nephropathy is diagrammed here. Along the horizontal axis is duration of hyperglycemia. The vertical axes show GFR on the left and albuminuria on the right. The red line, which tracks GFR, initially increases after the onset of hyperglycemia. Then, after a period of time, it gradually decreases. Around the time that GFR passes back through the normal range, increases in urine albumin, represented by the grey line, become apparent. As a result, the first clinical sign of diabetic kidney disease is usually an increase in urine albumin. Although the estimated GFR may be normal at that point, it may actually be on a downward slope, decreased from the supernormal levels that it reached earlier. As time progresses, there’s continual loss of GFR and an increase in urine albumin until the GFR declines to such a degree that urine albumin decreases. Module_2_4-26 POST EDITING
  • Advanced glycation end-products are formed by non-enzymatic sequential glycation and oxidation reaction of sugars with free amino groups on proteins, lipids and nucleic acids. The reaction is reversible depending on the sugar levels in the blood. Increased levels of AGEs are found in diabetes and chronic kidney disease. The kidneys excrete AGEs and AGEs may accumulate with aging. Module_2_4-26 POST EDITING
  • The structure and function of proteins may be altered as glycation increases. Slow turnover proteins, such as the glomerular basement membrane, are particularly prone to modification. Other proteins that may be glycosylated include collagen and elastin in blood vessel walls, and LDL. Module_2_4-26 POST EDITING
  • Inflammation may increase as AGE levels increase. You will hear more about AGEs and food preparation techniques in module 4. Module_2_4-26 POST EDITING
  • You may be familiar with a common AGE. The hemoglobin A1C is an AGE. A1C results are used to monitor diabetes control and estimates the average blood glucose for the past 2 –3 months. A1C levels correlate with diabetes complications. Module_2_4-26 POST EDITING
  • The estimated average glucose or eAG level, can be estimated from the A1C result. An A1C of 14 percent means the estimated average glucose is 355. Both eAG and eGFR are estimates. A1C is now used to diagnose diabetes. A normal A1C is between 4.0 and 5.6 percent. Prediabetes is diagnosed when the A1C is between 5.7 to 6.4 percent. An A1C greater than or equal to 6.5 percent is one of the parameters used to diagnose diabetes. Module_2_4-26 POST EDITING
  • The kidneys play an active role in insulin metabolism. Less than one percent of filtered insulin is excreted in the urine. Insulin, proinsulin, and C-peptide are catabolized by the kidneys. This reflects about one third of total endogenous insulin metabolism. The kidneys are the primary site for metabolism of exogenous or injected insulin, as well. Circulating insulin levels are higher as CKD advances, often because of decreased metabolism. As a result, the risk for hypoglycemia increases with decreasing GFR. Module_2_4-26 POST EDITING
  • Not only are there changes in insulin sensitivity and catabolism, but the kidney is the site of metabolism of many oral agents as well. As a result, medications may need to be discontinued or adjusted as CKD progresses. Module_2_4-26 POST EDITING
  • In kidney disease, as in all patients with diabetes, there’s a delicate balance between maintaining the best possible glycemic control while avoiding hypoglycemia. The risk of tighter glucose control may increase as kidney disease progresses and as patients become more frail and less tolerant of hypoglycemic episodes. Module_2_4-26 POST EDITING
  • Because of these concerns, the hemoglobin A1C goal should be individualized in chronic kidney disease. The goal for the general population, as you’re aware, is a hemoglobin A1C of less than seven. You should bear in mind that less stringent control may be indicated in people with CKD, with frequent, severe hypoglycemic episodes, limited life expectancy, and advanced micro and macrovascular complications. Module_2_4-26 POST EDITING
  • As we mentioned earlier, once patients have established diabetic nephropathy tight glucose control has not been shown to slow progression of kidney disease. However, there is evidence that control of newly diagnosed diabetes may help prevent chronic kidney disease in both type 1 and type 2 diabetics. Module_2_4-26 POST EDITING
  • The UKPDS study showed that glycemic control of newly diagnosed type 2 diabetes lowers the risk of albuminuria. The study looked at newly diagnosed patients in the first 10 years following diagnosis. Intensive control was defined as a hemoglobin A1C less than seven, compared to 7.9 percent in the control group. In the group with tighter control, there was a 34 percent reduction in albuminuria. However, the long term benefit was not as clear. Module_2_4-26 POST EDITING
  • As we mentioned previously, there is not strong evidence to support tight glucose control to slow kidney disease progression in diabetes of long duration. Advanced glycated end products may alter or destroy slow turnover proteins, such as the glomerular barrier, and this may explain why tight control does not have a protective benefit. However, there is no reason not to expect that better control will protect other organs, including the eyes, the nervous system, and the cardiovascular system. Module_2_4-26 POST EDITING
  • Carbohydrates still count in diabetic kidney disease. In general, women with diabetes may see improved glucose levels when carbohydrates are limited to 45 to 60 grams per meal. For men, limiting carbohydrates to 60 to 75 grams per meal may help control glucose levels. Fifteen to 30 grams of carbohydrate may be tolerated for snacks. Adjustments are made, based on the weight, glycemic targets, and acceptance by the individual. Module_2_4-26 POST EDITING
  • The type of carbohydrate matters in chronic kidney disease. Milk is a source of protein, sodium, phosphorus and potassium. Processed grains may have added sodium. Whole grains have more phosphorus and potassium. Legumes are rich in protein, phosphorus, and potassium and may have added sodium. Starchy vegetables, such as potatoes, are a source of potassium. Fruit has potassium. Sweets and added sugars may have added phosphorus. Module_2_4-26 POST EDITING
  • High protein diets are not recommended for people with diabetic kidney disease. Dietary protein may transiently increase the glomerular filtration rate and renal blood flow rates. High intakes of animal protein may be associated with elevated urine albumin excretion in people with both hypertension and diabetes. Module_2_4-26 POST EDITING
  • The protein requirement for CKD is still under debate. On average, the western diet contains 1.2 to 1.4 grams of protein per kilogram of body weight. The recommended dietary allowance for protein is 0.8 grams of protein per kilogram body weight. Different groups have different recommendations for protein. In general, the RDA is considered adequate. Helping people achieve that level may seem like a protein restriction. Module_2_4-26 POST EDITING
  • The total amount of protein may be more important than the type of protein. Long-term consumption of high protein diets, either type, animal or vegetable protein, may cause renal injury or accelerate chronic kidney disease. Module_2_4-26 POST EDITING
  • Heart-healthy foods are recommended. The National Cholesterol Education Program recommends limiting total fat to 25 to 35 percent of calories. Cholesterol should be limited to 200 milligrams per day or less. Adding two grams of plant stanols or sterols per day and increasing soluble fiber may be beneficial. Module_2_4-26 POST EDITING
  • All of the guidelines provide direction. Recommendations are individualized. Module_2_4-26 POST EDITING
  • If someone with diabetes and kidney disease has a decrease in A1C or an increased frequency of hypoglycemia without any change in medication, diet or exercise, consider the possibility that kidney disease is progressing. Module_2_4-26 POST EDITING
  • People with diabetic kidney disease may think they do not have diabetes anymore when diabetes medications are discontinued. The risk for hypoglycemia increases as CKD progresses and medications change. Module_2_4-26 POST EDITING
  • Glucose tablets are effective in treating hypoglycemia without adding potassium. Frank, our case study, was experiencing more frequent hypoglycemia. He drank orange juice to treat low glucose levels. His serum potassium level increased due to medication and potassium intake. Colas are a source of phosphorus. Light colored soda pop is a better choice to treat hypoglycemia in CKD. Module_2_4-26 POST EDITING
  • The potassium content of juice varies. Any kind of juice can treat hypoglycemia. Cranberry juice cocktail would be a better choice for Frank. Four ounces contains 18 milligrams of potassium. Four ounces of orange juice contains 229 milligrams of potassium. Module_2_4-26 POST EDITING
  • Frank is the man who came in with a swollen right foot. His potassium levels increased due to reduced renal function, medication and dietary intake. Additional information about diabetes is found in the lower third of this table. His random glucose level was 211 in January and 63 in April. When he first presented, A1C was 9.4 percent. Within two or three months, the A1C was down to 7.9 percent on five milligrams of glyburide. Frank is experiencing frequent hypoglycemic reactions. The physician initially reduced the dose of glyburide to 2.5 milligrams. This was discontinued due to continued hypoglycemia. Glipizide was prescribed. Module_2_4-26 POST EDITING
  • This is the same assessment information presented previously with updates shown in italics. Frank experiences low glucose levels when he skips meals. Diabetes medications have been added. His A1C is down to 6.1 percent from 7.9 percent in April. Module_2_4-26 POST EDITING
  • Frank’s eGFR and A1C declined. His diabetes medication was changed. Module_2_4-26 POST EDITING
  • The nutrition diagnoses could be inconsistent carbohydrate intake and excessive potassium intake. Frank skips meals and uses orange juice to treat hypoglycemia. Module_2_4-26 POST EDITING
  • Initially Frank needed to learn about dietary sources of potassium including salt substitute and orange juice. As far as diabetes is concerned, he could eat a small snack between brunch and supper on weekends. He could take glucose tablets, or drink four ounces of a lower potassium juice to treat hypoglycemia. Module_2_4-26 POST EDITING
  • To summarize this section, the renal threshold for glucose is 180 to 200 milligrams per deciliter. Advanced glycation end-products are a concern. Glycosylation may change the shape and function of proteins. The A1C goal is individualized. An improvement in glycemic control without a change in therapy may indicate CKD is progressing. Hyperkalemia is a concern. ACE inhibitors and ARBs increase the risk for hyperkalemia. Treat low blood glucose appropriately. Use a juice low in potassium or light-colored soda pop if potassium levels are high. Module_2_4-26 POST EDITING
  • We’re now going to talk about the importance of urine albumin and the basis of therapy to reduce urine albumin excretion. Baseline urine albumin level may predict the risk of CKD progression. Higher levels of urine albumin are associated with a worse prognosis. Module_2_4-26 POST EDITING
  • Module_2_4-26 POST EDITING To review what we discussed in the first module, the urine albumin test measures albumin in the urine, or albuminuria. An increase in urine albumin may be the earliest sign of chronic kidney disease. Urine albumin that’s filtered into the tubule may exacerbate kidney damage. The level of urine albumin may reflect the severity of kidney damage and reducing urine albumin may be associated with slower progression. Finally, urine albumin is a risk factor for cardiovascular disease, a marker for cardiovascular risk.
  • We use the urine albumin-to-creatinine ratio to assess and monitor kidney damage. As we mentioned earlier, the cutoff for normal is less than 30 milligrams per gram. Persistent urine albumin greater than 30 milligrams per gram on a spot urine specimen is considered evidence of kidney damage. Finally, it’s important to monitor albumin excretion over time. Module_2_4-26 POST EDITING
  • Increased urine albumin occurs as a result of damage to the filtration barrier in the kidney. There’s increased glomerular permeability, which allows albumin to cross the glomerular capillary basement membrane. Higher levels of protein in the urine are not only a sign of kidney damage, but their presence in the tubules may exacerbate kidney damage. Module_2_4-26 POST EDITING
  • There are several known risk factors for albuminuria. We know that hypertension, diabetes, smoking and obesity are associated with increased urine albumin. Possible risk factors include high sodium intake, excessive protein intake, hyperlipidemia, and inflammation. Module_2_4-26 POST EDITING
  • Elevated urine albumin is associated with increased risk of adverse renal events, and lowering urine albumin may decrease the risk of progression. Here are the results of two important studies, represented schematically. The figure on the left shows that the risk of adverse renal events, including loss of half of kidney function, dialysis, or death, increases with the level of urine albumin at the time of diagnosis of CKD. The right hand figure shows the risk of an adverse renal event in relation to the response in the reduction of urine albumin following initiation of an angiotensin receptor blocker. As you move to the right, there is a greater reduction in urine albumin in response to treatment, and that’s associated with a decreased risk of renal events. So, high levels of urine albumin predict a bad outcome. Response to therapy as evidenced by decrease in urine albumin is associated with decreased risk for a bad outcome. Module_2_4-26 POST EDITING
  • ACE inhibitors and angiotensin receptor blockers, two families of drugs that we use to interrupt the renal-angiotensin system, lower urine albumin and may be renoprotective. They have a benefit that goes beyond what we find from the improved blood pressure. In controlled studies they have been shown to improve outcomes when compared to other antihypertensive agents which produce the same level of blood pressure control. In general, the renoprotective benefit is associated with a reduction in urine albumin. Based on these findings, you will see patients who are prescribed these drugs for elevated levels of urine albumin, even though their blood pressure is not elevated. MODULE 2 original 3-13 Module_2_4-26 POST EDITING
  • Smoking is associated with increased urine albumin excretion. There appears to be a dose-dependent increase in urine albumin among smokers in the general population. Smoking appears to be an independent predictor for elevated urine albumin in patients with hypertension and is an independent risk factor for the onset and progression of albuminuria in type 1 and type 2 diabetes. Finally, smoking may increase the risk for progression of renal failure for patients with primary kidney disease as well. Module_2_4-26 POST EDITING
  • Obesity may be a risk factor for abnormal urine albumin levels. Intentional weight loss may help decrease proteinuria. Weight loss due to diet restrictions, exercise, anti-obesity medications or bariatric surgery may lower protein in the urine. However, we do not know if weight loss slows progression of CKD. Intentional or planned weight loss may be beneficial in CKD. However, unintentional weight loss is not a good sign. Intake may decline spontaneously as eGFR declines. Module_2_4-26 POST EDITING
  • Observational data show lowering sodium intake may lower urine albumin levels. Module_2_4-26 POST EDITING
  • The relationship between urine albumin and dietary protein remains unclear. Animal protein intake may be associated with higher urine albumin excretion rates. This relationship may depend on the baseline urine albumin level. Module_2_4-26 POST EDITING
  • Observational data show animal protein intake may have an effect on urine albumin. The Nurses' Health Study found two or more servings of red meat per week may increase the risk of microalbuminuria. The Multi-Ethnic Study of Atherosclerosis, which includes Caucasians, African Americans, Hispanic and Chinese participants found an association between meat and poultry intake and higher urine albumin levels. Data from NHANES III show high protein intake may be associated with higher urine albumin if the person has both hypertension and diabetes. Module_2_4-26 POST EDITING
  • We discussed the DASH diet previously. The DASH pattern is higher in protein. A follow-up study found no difference in albumin excretion rates when the AER was less than 7 milligrams per 24 hours. However, there was a difference for those who had a higher baseline AER. The fruits and vegetables diet contained about 10 grams less of animal protein than the other patterns. Module_2_4-26 POST EDITING
  • This figure shows the differences in urine albumin excretion after 8 weeks of the diets. The control diet is shown in maroon, the gold bar is the fruits and vegetables diet, and the DASH diet is represented in green. The left set of bars shows people with an AER less than 7. The mean albumin excretion is about the same after 8 weeks. The right set of bars shows those with AERs above 7 and the difference between the diets after 8 weeks. The mean albumin excretion is higher in the control and the DASH pattern compared to the fruits and vegetables diet. Module_2_4-26 POST EDITING
  • A meta-analysis published in 1996 found low-protein diets may slow the increase in albuminuria in people with type 1 diabetes. A supplemented very low-protein diet is associated with decreased proteinuria. This type of diet is used more commonly in Europe. The diet contains 0.3 grams of predominantly vegetable protein per kilogram body weight and includes supplementation with essential amino acids and keto acids. Keto acids are the nitrogen-free analogues of amino acids. This nutrition therapy is associated with a decrease in proteinuria. Module_2_4-26 POST EDITING
  • Interventions to reduce urine albumin levels include blood pressure control and reduced sodium intake. For people with diabetes, good control early may help prevent albuminuria later. Planned weight loss, reducing excessive protein intake, and tobacco cessation may help lower urine albumin levels. Module_2_4-26 POST EDITING
  • Elevated urine albumin may be associated with more rapid progression of kidney disease. Frank’s UACR was very high and decreased with treatment. However, his eGFR declined from 34 to 22 in about six months. The interventions that may have helped lower the UACR included lisinopril, which was discontinued due to hyperkalemia. He reported using less salt and he lost weight. Some of the weight change may be attributed to the diuretic. Module_2_4-26 POST EDITING
  • Cardiovascular disease is the leading cause of morbidity and mortality in people with chronic kidney disease. People with kidney disease don’t usually die from kidney disease. Most commonly they die from cardiovascular disease. Module_2_4-26 POST EDITING
  • We’re going to talk about cardiovascular risk and chronic kidney disease, both traditional risk factors and non-traditional risk factors. We’re going to talk about dyslipidemia in chronic kidney disease, use of statins, non-traditional risk factors, and nutritional interventions to address both traditional and non-traditional risk factors. Module_2_4-26 POST EDITING
  • NHANES data demonstrate that lipid abnormalities are associated with declining GFR. In this figure, GFR decreases as we move from left to right. As eGFR diminishes, LDL and triglycerides increase. Module_2_4-26 POST EDITING
  • As we’ve noted, patients with CKD have high prevalence of traditional risk factors for cardiovascular disease, including hypertension, diabetes, hyperlipidemia, smoking, increased age and inflammation. In addition, some of the comorbidities of chronic kidney disease are also associated with increased risk of cardiovascular disease. These include albuminuria, anemia, and abnormal calcium and phosphorus metabolism. Module_2_4-26 POST EDITING
  • The pattern of dyslipidemia in chronic kidney disease may increase the risk of cardiovascular disease. Triglycerides are increased and may be very elevated in patients who have high levels of proteinuria. Patients with CKD may have decreased high density lipoprotein levels and low or normal low density lipoprotein levels. The smaller, denser, LDL particles are more prone to oxidation and accumulation in vessel walls. Module_2_4-26 POST EDITING
  • Specific targets for lipid lowering therapy for people with chronic kidney disease have not been established and may be similar to those for the general population. Certainly, persons with chronic kidney disease should be considered at high risk for cardiovascular disease. The lack of data reflects, in part, the exclusion of CKD patients from many cardiovascular disease clinical trials. Module_2_4-26 POST EDITING
  • Statins are quite effective in reducing hepatic cholesterol synthesis and have been shown to significantly reduce all cause cardiovascular mortality in persons with chronic kidney disease. Although statins do not appear to slow chronic kidney disease progression, they may reduce proteinuria. Statins should be used with caution in patients with chronic kidney disease. There may be an increased prevalence of side effects, particularly muscle inflammation and elevated liver function tests. Careful monitoring is indicated. Module_2_4-26 POST EDITING
  • Inflammation appears to play an important role in patients with cardiovascular disease. This may be particularly important in patients with chronic kidney disease. Inflammation may modify the risk relationship between cholesterol and cardiovascular disease in the CKD population. In patients with normal C-reactive protein, elevated cholesterol levels may be associated with an increased risk of cardiovascular disease. In patients with elevated CRP levels and elevated cholesterol, increased risk appears to be associated predominantly with inflammation. Thus, it may be the chronic inflammatory state associated with chronic kidney disease that may be the key factor raising cardiovascular risk. Module_2_4-26 POST EDITING
  • As we mentioned earlier, some of the comorbidities of chronic kidney disease may also be risk factors for cardiovascular disease. These include albuminuria, anemia, and disturbances of mineral metabolism. Module_2_4-26 POST EDITING
  • The nutrition recommendations may be similar to those in the general population. The evidence is scarce, as most studies about CVD exclude people with kidney disease. The 2010 dietary guidelines recommend keeping trans fats as low as possible. Limit synthetic sources of trans fats, including partially hydrogenated oils and other solid fats. People with CKD need to read the ingredient list for partially hydrogenated oils, and limit use of those products. Products with less than 0.5 grams trans fats per serving may show zero grams of trans fats on the Nutrition Facts label, per labeling guidelines. Module_2_4-26 POST EDITING
  • Plant stanols and sterols may help lower LDL in the general population and for those with diabetes. Certain spreads may be enriched with plant stanols or sterols. They may reduce LDL cholesterol by 15 percent. Their effectiveness in CKD is unknown. The spreads vary in sodium content as well as calories. Per tablespoon, these products have 80 to 110 milligrams of sodium, and 45 to 70 calories. They should be substituted isocalorically. These products may contain potassium sorbate. Read the ingredient list. Module_2_4-26 POST EDITING
  • Soluble fiber has been found to reduce heart disease in the general population. Recommendations may vary. Twenty five to 30 grams of total fiber per day, including 7 to 13 grams of soluble fiber may help reduce LDL. Food rich in total fiber or soluble fiber may also be a source of potassium and phosphorus. Bran is higher in potassium and phosphorus. Bran cereals may have added sodium. Module_2_4-26 POST EDITING
  • Legumes are a source of soluble fiber, potassium, and phosphorus. Grains prepared without salt, shown at the top of this table, vary in fiber, potassium, and phosphorus. Beans and peas are very rich in potassium and contain phosphorus. Canned products may have added sodium. Monitor potassium levels and counsel appropriately. Module_2_4-26 POST EDITING
  • A few fruits and two vegetables are shown here, each with different levels of soluble fiber, potassium, phosphorus and sodium. The skin or peel of an apple has potassium. Berries tend to be lower in potassium. The items shown are low in phosphorus and protein. Module_2_4-26 POST EDITING
  • The absorption of dietary phosphorus depends on the source. More than ninety percent of phosphorus in food additives is absorbed. The phosphorus in animal foods such as meat or milk is not absorbed as readily. Phytates in plant foods inhibit phosphorus absorption. People can identify added phosphorus by reading the ingredient list for PHOS. Module_2_4-26 POST EDITING
  • To summarize this section - non-traditional risk factors for cardiovascular disease in CKD include elevated urine albumin levels, anemia and abnormal calcium and phosphorus metabolism. Statins are used cautiously in CKD. Foods rich in soluble fiber may be a source of potassium or phosphorus. Phosphorus found in food additives is a concern. Module_2_4-26 POST EDITING
  • The remaining slides summarize the different sections of the module. Controlling blood pressure is key to slowing progression of chronic kidney disease. Multiple medications may be prescribed. We need to review medication lists as part of the assessment process. ACE inhibitors or angiotensin receptor blockers are the medications that increase the risk for hyperkalemia. The names of the ACE inhibitors end with P-R-I-L and the names of the angiotensin receptor blockers end with S-A-R-T-A-N. Limit sodium to 1,500 milligrams per day. Salt substitutes should be avoided. Limit dietary potassium when the serum level is elevated. Potassium restriction is not indicated in the absence of hyperkalemia. Module_2_4-26 POST EDITING
  • Elevated urine albumin excretion may be associated with diabetic kidney disease, but not all people with diabetes will have high urine albumin levels. People with elevated urine albumin levels are at risk for more rapid progression of chronic kidney disease. Good control of diabetes early may lower the risk of developing albuminuria in the future. Tight versus good control may not slow progression. Module_2_4-26 POST EDITING
  • Frequent urination may be a sign the renal threshold for glucose has been exceeded. AGEs or advanced glycation end-products may accumulate in CKD due to reduced clearance. The A1C is also known as glycosylated hemoglobin and is an AGE. The goal for the A1C is individualized. Improved glycemic control of diabetes without a change in therapy or an increased frequency of hypoglycemia may mean CKD is progressing. Medication will change as CKD progresses. Use low-potassium juice instead of high-potassium juice to treat hypoglycemia, particularly when an ACEi inhibitor or ARB is used. Light-colored soda pop does not contain added phosphorus. Module_2_4-26 POST EDITING
  • Urine albumin is a marker of kidney damage. Controlling blood pressure may help reduce urine albumin level. Medications prescribed to control blood pressure may also be anti-proteinuric. Reduce sodium intake to 1,500 milligrams per day. Weight loss, lowering excessive protein intake and tobacco cessation may help lower urine albumin levels. Module_2_4-26 POST EDITING
  • People with CKD are at risk for cardiovascular disease. Non-traditional risk factors include albuminuria, anemia and abnormal calcium and phosphorous metabolism. Let the provider know if someone on a statin complains about more muscle aches and pains. Statins may cause myopathy. Some foods rich in soluble fiber may be higher in potassium and phosphorus. Phosphorus in food additives is absorbed more readily. Module_2_4-26 POST EDITING
  • This module covered a lot of material. Where do you start with patient counseling? The National Kidney Disease Education Program’s Eating Right for Kidney Health may be a good place to start. The diet changes are in steps. The first step is to choose and prepare foods with less salt and sodium. The second step is to eat the right amount and right types of protein. Step 3 is to choose foods that are heart healthy. Module_2_4-26 POST EDITING
  • The next section of the handout goes into a little detail about the first three steps. On the right-hand page, you see step 4 is to choose foods with less phosphorus. The very first bullet within this section is about phosphorus additives. The last step is to choose the right amount of potassium. Reducing protein intake will decrease potassium intake. Fruits and vegetables may be the last foods we want people to limit. Module_2_4-26 POST EDITING
  • Your Kidney Test Results is another handout to consider using. Your Kidney Tests Results include glomerular filtration rate, urine albumin-to-creatinine ratio and blood pressure. In module 3, you will learn more about serum albumin, bicarbonate, potassium, calcium, phosphorus, parathyroid hormone, and Vitamin D. The back side of the kidney test results has A1C, lipids and hemoglobin. Module_2_4-26 POST EDITING

CKD MNT Module 2: Slow Progression of Chronic Kidney Disease CKD MNT Module 2: Slow Progression of Chronic Kidney Disease Presentation Transcript

  • Module 2: Slow Progression of Chronic Kidney Disease (CKD) Hypertension, Diabetes, Urine Albumin, and Cardiovascular Disease
  • 1. Use and interpret biochemical and patient data for assessment of hypertension and CKD 2. Identify commonly prescribed classes of anti- hypertensive medications that may affect serum potassium levels in CKD 3. Associate spontaneous improvement in diabetes mellitus (DM) control with possible CKD progression 4. Modify recommendations for appropriate treatment of hypoglycemia in DM and CKD 5. Identify at least two nontraditional risk factors for cardiovascular disease in CKD Participants will be able to:
  •  Diabetes and hypertension are leading causes of CKD in the United States.  Urine albumin is a marker for kidney damage and cardiovascular disease (CVD); it also marks severity of kidney damage.  People with CKD are more likely to die due to CVD than progress to end-stage renal disease (ESRD). Brief review
  •  Chronic kidney disease − Kidney function  Glomerular filtration rate (GFR) < 60 mL/min/1.73 m2 for > 3 months with or without kidney damage AND/OR − Kidney damage  > 3 months, with or without decreased GFR, manifested by either: − Pathological abnormalities − Markers of kidney damage, e.g., albuminuria » Urine albumin-to-creatinine ratio (UACR) > 30 mg/g CKD is reduced kidney function and/or kidney damage Reference: National Kidney Foundation, 2002
  • Prevalence of co-morbidities by eGFR Reference: Adapted from USRDS 2010 Annual Data Report
  • Prevalence of comorbidities by urine albumin Reference: Adapted from USRDS 2010 Annual Data Report
  • CONTROL BLOOD PRESSURE Hypertension is the second leading cause of CKD in the United States
  •  Hypertension  Sodium intake and excretion  Dietary Approaches to Stop Hypertension (DASH) diet pattern − Lowers blood pressure − May not be appropriate for CKD  Anti-hypertensive medications used in CKD and the risk for hyperkalemia Topics
  • Blood pressure is poorly controlled in people with CKD Reference: Adapted from USRDS 2009 Annual Data Report
  • Hypertension may cause CKD, and CKD may cause worsening hypertension
  •  Target of < 130/80 mmHg is often recommended but without strong evidence.  Uncontrolled hypertension (systolic blood pressure > 160) is a major challenge. Individualized blood pressure goals in CKD References: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571; Jafar et al. Ann Intern Med 2003; 139(4):244–252.
  • A multinational epidemiological study found a significant positive relationship between 24-hour urinary sodium (Na) excretion and blood pressure. Blood pressure may increase as sodium intake increases Reference: Intersalt Cooperative Research Group. BMJ 1988; 297(6644):319–328
  •  About 90% of total sodium intake is from salt.  Most (∼ 98%) is absorbed in small intestine.  Sodium is freely filtered by glomerulus.  About 99% is reabsorbed within the tubules. Sodium intake ≅ excretion Reference: Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate, 2004. Institute of Medicine of the National Academies. The National Academies Press Washington D.C.
  •  ~ 60% in proximal tubule  ~ 25% in loop of Henle  5–7% in distal convoluted tubule  3–5% in collecting duct Sodium is reabsorbed along the tubules Reference: http://www.kidneyatlas.org/book1/adk1_02.pdf
  •  Acid-base exchange  Chloride dependent co-transporters − Sodium, chloride, and/or potassium  Aldosterone-sensitive channel Sodium is reabsorbed by numerous mechanisms along the tubules
  •  Renin is an enzyme produced by the juxtaglomerular epitheloid cells in response to low renal perfusion.  The renin-angiotensin-aldosterone system (RAAS) controls blood pressure. Kidneys produce renin to increase sodium reabsorption Reference: Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate, 2005. Institute of Medicine of the National Academies. The National Academies Press Washington D.C.
  • RAAS helps control sodium and potassium excretion
  • Lifestyle modifications help lower blood pressure in the general population References: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571; Neter et al. Hypertension 2003; 42(5):878–884; Dietary Guidelines, 2010 Modification Recommendation Lowers Systolic Blood Pressure by (Range) Weight reduction •Maintain normal body weight •Body mass index (BMI) 18.5–24.9 kg/m2 5–20 mm Hg / ↓ 10 kg ∼ 4 mm Hg / ↓ 5 kg DASH •Increase potassium (fruits and vegetables) and calcium (dairy) •DASH may be too high in protein, potassium and phosphorus for CKD 8–14 mm Hg Physical activity •At least 30 minutes most days 4–9 mm Hg Moderate alcohol consumption •Women: ≤ 1 drink per day •Men: ≤ 2 drinks per day 2–4 mm Hg Sodium restriction •2,300 mg per day •1,500 mg per day for hypertension, diabetes, and CKD 2–8 mm Hg Modification Recommendation Lowers Systolic Blood Pressure by (Range) Weight reduction •Maintain normal body weight •Body mass index (BMI) 18.5–24.9 kg/m2 5–20 mm Hg / ↓ 10 kg ∼ 4 mm Hg / ↓ 5 kg DASH •Increase potassium (fruits and vegetables) and calcium (dairy) •DASH may be too high in protein, potassium and phosphorus for CKD 8–14 mm Hg Physical activity •At least 30 minutes most days 4–9 mm Hg Moderate alcohol consumption •Women: ≤ 1 drink per day •Men: ≤ 2 drinks per day 2–4 mm Hg Sodium restriction •2,300 mg per day •1,500 mg per day for hypertension, diabetes, and CKD 2–8 mm Hg
  • Lifestyle modifications for blood pressure (BP) have not been studied extensively in the CKD population
  • The DASH diet lowers blood pressure in the general population Reference: http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf
  •  Original DASH • “A diet rich in fruits, vegetables, and low-fat dairy foods and with reduced saturated and total fat can substantially lower blood pressure.”  DASH-Sodium • “The reduction of sodium intake to levels below the current recommendation of 100 mmol* per day and the DASH diet both lower blood pressure substantially, with greater effects in combination than singly.” *100 mmol Na = 2,300 mg Na Both DASH and DASH-Sodium lower blood pressure References: Appel et al. N Engl J Med 1997; 336(16):1117–1124; Sacks et al. N Engl J Med 2001; 344(1):3–10.
  • DASH diet pattern for 2,000 calories Reference: Your Guide to Lowering Your Blood Pressure with DASH, NIH Publication No.06-4082, April 2006 http://www.nhlbi.nih.gov/health/public/heart/hbp/dash/new_dash.pdf Food Group Servings/day Grains (mostly whole) 6–8 Vegetables 4–5 Fruits 4–5 Fat-free, low-fat milk, and milk products 2–3 Meats, poultry, and fish ≤6 ounces (oz.) Nuts, seeds, and legumes 4–5 per week Fats and oils 2–3 Sweets and added sugars ≤ 5 tablespoons (Tbsp.) per week
  • The DASH combination diet pattern is higher in protein and potassium Reference: Adapted from Appel et al. N Engl J Med 1997; 336(16):1117–1124 Control Diet Fruits & Vegetables Diet Combination Diet Nutrient Level per menu Level per menu Level per menu Protein (% of total kcal) 13.8 15.1 17.9 Potassium (mg/day) 1,752 4,101 4,415 Sodium (mg/day) 3,028 2,816 2,859
  • Urinary K increased with increased K intake Urea nitrogen reflected protein intake Urinary phosphorus (P) may reflect protein intake Urinary Na excretion ≅ intake Urinary excretion depended on intake in DASH Reference: Adapted from Appel et al. N Engl J Med 1997; 336(16):1117–1124 Substance excreted (mg per 24 hours) Control Diet Fruits & Veg Diet Combinati on Diet Potassium Run-in Intervention Change 1,385 1,531 146 1,459 2,757 1,298 1,416 2,916 1,500 Urea Nitrogen Run-in Intervention Change 8,592 9,026 434 8,775 9,456 681 8,729 11,583 2,834 Phosphorus Run-in Intervention Change 699 742 713
  •  Compared to the control diet, the DASH combination diet reduced systolic blood pressure (BP) by 5.5 mm Hg and diastolic BP by 3.0 mm Hg.  Compared to control diet, the fruits and vegetables diet reduced systolic BP by 2.8 mm Hg and diastolic BP by 1.1 mm Hg. The combination diet pattern was most effective in lowering blood pressure Reference: Appel et al. N Engl J Med 1997; 336(16):1117–1124
  •  Typical and DASH pattern at different sodium levels  3,450 mg; 2,300 mg; or 1,150 mg sodium  Similar urinary excretion patterns DASH-Sodium showed lower blood pressures with lower sodium intake Reference: Sacks et al. N Engl J Med 2001; 344(1):3–10
  •  The DASH pattern lowered blood pressure at all levels of sodium intake.  In the control diet, blood pressure was lowered with the lowest sodium intake.  Combining the DASH pattern and low sodium intake provided the greatest reduction in blood pressure than either alone. Sodium restriction lowered blood pressure in DASH-Sodium, even in the control diet Reference: Sacks et al. N Engl J Med 2001; 344(1):3–10.
  • Food Group Nutrients of Concern for CKD Grains Whole grains: phosphorus, potassium Vegetables Potassium Fruits Potassium Fat-free, low-fat milk , and milk products Protein, sodium, phosphorus, potassium Meats, poultry, and fish Protein, phosphorus, potassium, sodium (“enhanced” and processed) Nuts, seeds, and legumes Protein, phosphorus, potassium, sodium (if salted) Fats and oils May have sodium Sweets and added sugars May have added phosphorus DASH diet pattern and potential nutrients of concern in CKD
  •  DASH and DASH-Sodium patterns lower blood pressure.  The lowest sodium level is the most effective, even with the usual (control) diet.  The DASH pattern may be too high in protein, potassium, and phosphorus for CKD. Summary: The DASH diet may help prevent CKD, but it is not generally used with CKD
  •  Usually > 3 medications, including a diuretic  1,500 mg sodium restriction − Sodium restriction is key to blood pressure control. May need multiple medications and Na restriction to control blood pressure in CKD Reference: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571
  •  These medications block aldosterone production, and this may result in a reduction in potassium excretion.  The risk for hyperkalemia increases with their use.  These medications include: − Angiotensin-Converting Enzyme Inhibitor (ACEi) − Angiotensin Receptor Blocker (ARB) Anti-hypertensive medications that block RAAS increase the risk for hyperkalemia
  • ACEi medications block the RAAS and increase the risk for hyperkalemia
  • ARBs block the RAAS and increase the risk of hyperkalemia
  • Medications that increase risk for hyperkalemia in CKD Referece: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571 Commonly prescribed  Angiotensin-Converting Enzyme Inhibitor (ACEi) – End with “____pril”  Angiotensin Receptor Blockers (ARB) – End with “___sartan Used cautiously in CKD  Aldosterone antagonists  Renin inhibitors  Potassium-sparing diuretics
  •  Specific level of eGFR does not determine need for dietary potassium restriction.  Restriction is to help achieve and maintain a safe serum potassium level ( < 5 mEq/L).  The level of potassium restriction should be individualized. Potassium restriction is not indicated in the absence of hyperkalemia
  • Serum potassium increases as eGFR decreases Reference: Adapted from USRDS 2009 Annual Data Report
  •  Their effects are beyond blood pressure control.  They also reduce protein in the urine (antiproteinuric).  Sometimes these medications are prescribed to lower urine albumin levels in normotensive people. ACEi and ARBs may be renoprotective References: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571; Strippoli et al. Cochrane Database Syst Rev 2010. Kunz et al. Ann Intern Med 2008; 148(1):30–48.
  •  Loop of Henle diuretics bind to co-transporter in loop of Henle. − Less sodium is reabsorbed, and blood pressure is lowered. − Less potassium is reabsorbed, and serum level may decrease.  Many people with CKD on loop diuretics do not become hypokalemic due to ACEi or ARB use and fewer functioning nephrons. Loop diuretics may cause hypokalemia (low potassium)
  •  Assessment − Potential food and anti-hypertensive medication interactions (potassium)  Intervention − Control sodium intake  < 1,500 mg daily − Reduce potassium intake if hyperkalemic  Avoid salt substitutes − DASH may not be indicated for CKD. Nutrition Care Process for CKD & HTN Reference: ADA Evidence Library. Evidence-Based Practice Guideline for Hypertension
  • Case study: Food-medication interaction, hyperkalemia, salt substitute Reduced kidney function with high level of urine albumin  Height 66.5”, weight 200.5 pounds (lb.)  Frank is a 55-year-old man  Type 2 DM since 2002  Not taking any medications for past 5 years  History: amputation of left fourth toe  Comes to clinic 1/19 for right foot swelling  BP 168/98 – started on ACEi  eGFR 34  UACR 6,437
  • People with CKD and on ACEi need to use less salt and avoid salt substitutes Date 1/19 1/29 4/2 BP (mmHg) 168/98 138/82 136/78 Weight (lb.) 200.5 196 191 eGFR (> 60) 34 34 29 UACR (mg/g) (< 30) 6,437 K mmol/L (3.5–5.0) 4.9 4.6 5.5 *High Medications - - - • Lisinopril 40 mg • Furosemide 20 mg ↑ 40 mg Diet changes Told to use less salt “stopping salt, trying salt substitute” Missed 2/19 RD appt
  • Date 1/19 1/29 4/2 5/7 BP 168/98 138/82 136/78 142/60 Weight 200.5 196 191 189.4 eGFR (> 60) 34 34 29 UACR (< 30) 6,437 4,483 K (3.5-5.0) 4.9 4.6 5.5 H 5.5 H Medications - - - - • Lisinopril (ACEi) 40 mg Stopped • Furosemide 20 mg 40 mg 40 mg • Losartan (ARB) 50 mg Diet changes Told to use less salt “Stopping salt, trying salt substitute” Missed 2/19 RD appt Missed 4/19 RD appt ACEi lowered blood pressure and urine albumin (UACR) and increased K
  • Date 1/29 4/2 5/7 7/1 BP 138/82 136/78 142/60 146/70 Weight 196 191 189.4 189.4 eGFR (> 60) 34 29 22 UACR (< 30) 6,437 4,483 K (3.5–5.0) 4.6 5.5 H 5.5 H 5.5 H Medications - - - - • Lisinopril Stopped • Furosemide ↑ 40 mg 40 mg 40 mg • Losartan 50 mg 50 mg Diet changes “stopping salt, trying salt substitute” Missed 2/19 RD appt Missed 4/19 RD appt Direct referral to RD Change to ARB did not reduce K
  • Breakfast Lunch Supper 2 fried eggs •salt substitute 3–4 slices of bacon 3 slices of wheat toast with soft margarine Coffee: at least 3 cups with artificial sweetener Wife makes fried potatoes on weekends Fast food Double meat burger Medium fries (trying to limit carbs; doesn’t add more salt now) Diet soda pop May skip lunch on weekends (bigger breakfast) 6–8 oz. fried steak •salt substitute 2–3 slices bread 1 c. canned corn or peas Hot tea with artificial sweetener Uses orange juice to treat low sugars (↑ frequency) Frank’s “usual” diet intake
  • Food/beverage intake Recently stopped salt, now using salt substitute. Using orange juice to treat low sugars. Includes other potassium-rich foods, fast foods. Won’t use glucose tablets. Diet order 2,200 calories; 1,500 mg sodium; potassium restriction Diet experience Instructed on diabetic diet when diagnosed, tries to limit carbs. Medications 50 mg Losartan (changed from 40 mg Lisinopril), 40 mg Furosemide Anthropometrics Height 66.5”, weight 189.4# down 11# since Jan., BMI now 30.1. Left foot 4th toe amputation Biochemical data K 5.5 x 3 months; eGFR 22, was 34 (Jan.); UACR 4,483 mg/g (May), was 6,437 mg/g (Jan.) Personal history 55-year-old male, English is his second language Patient history DM 2 for 8 years, no meds x 5 years. BP 146/70. Originally came to clinic due to right foot swelling. Seeing a nephrologist. Social history Sedentary job, sits for long periods of time. No sick leave, couldn’t make dietitian appointment. Lives in apartment with wife, 2 sons. Assessment (7/1)
  •  Food–medication interaction related to renal dysfunction and blood pressure medication, as evidenced by serum potassium level of 5.5.  Excessive potassium intake related to food-related knowledge deficit as evidenced by use of salt substitute and other foods rich in potassium. Nutrition Care Process (NCP) Diagnoses
  • As eGFR declined, medication and nutrient interaction increased serum K
  •  Initial nutrition education  Priority modification: Reduce potassium intake by eliminating salt substitute; use juice low in potassium (cranberry juice) to treat low sugars.  Collaborate with primary care provider in regard to patient’s hyperkalemia, CKD, and diabetes. Intervention
  • Summary: CKD and hypertension  BP ≤ 130/80 may be beneficial for many  Multiple medications Assessment:  Food–medication interaction − Hyperkalemia  ACEi (____pril)  ARBs (___sartan) Intervention:  Limit sodium − Keep to ≤ 1,500 mg/day − Avoid salt substitutes  Limit potassium when serum level is elevated − Individualized
  • CONTROL DIABETES Spontaneous improvement in diabetes control may indicate progression of kidney disease
  •  Glucose and the nephrons  Insulin and other DM medications  Advanced glycation end products (AGEs)  Diabetes control in CKD  Treatment of hypoglycemia  Risk for hyperkalemia with ACEi and ARBs Topics
  • Diabetes is the leading cause of ESRD in the United States Reference: USRDS 2010 Annual Data Report
  •  Glucose is filtered by glomeruli and almost completely reabsorbed by proximal tubules.  Glucosuria occurs when filtered load exceeds tubules ability to reabsorb the glucose.  Renal threshold is 180–200 mg/deciliter(dL).  Glucose is often co-absorbed with sodium.  The nephrons are involved in gluconeogenesis. − ∼ 20% of overall endogenous release Glucose and the nephrons References: Gerich et al. Diabetes Care 2001; 24(2):382–391; Meyer & Gerich. Curr Diab Rep 2002; 2(3):237–241.
  •  Hyperfiltration − The initial response to hyperglycemia is an increase in GFR, followed by slow decline.  Hypertrophy of glomerulus and tubule − Nephrons may be damaged or destroyed.  Diabetic kidney disease generally, but not always, associated with progressive albuminuria. − Monitor eGFR and UACR. Hyperglycemia is associated with hyperfiltration References: Molitch et al. Diabetes Care 2010; 33(7):1536–1543; Retnakaran et al. Diabetes 2006; 55(6):1832–1839.
  • Natural history of diabetic nephropathy: hyperglycemia causes hyperfiltration, may be followed by albuminuria Reference: Adapted from Friedman, 1999
  •  Advanced glycation end products (AGE) form by nonenzymatic, sequential glycation and oxidation reaction of sugars with free amino groups on proteins, lipids, and nucleic acids.  The initial reaction is reversible, depending on concentration.  They may accumulate in plasma and tissues. − Increased levels are found in DM and CKD − May accumulate with aging Advanced glycation end products form spontaneously Reference: Bohlender et al. Am J Physiol Renal Physiol 2005; 289(4):F645–F659.
  •  Virtually any protein can be glycosylated.  Slow turnover proteins are particularly prone to modification. − Glomerular basement membrane thickening − Blood vessel stiffness  Altered collagen and elastin − Altered low-density lipoprotein (LDL) cholesterol  May not be able to attach to receptor on endothelial cells for clearance AGEs alter protein structure and function Reference: Goldin et al. Circulation 2006; 114(6):597–605; Peppa et al. Clinical Diabetes 2003; 21(4):186–187.
  •  Receptors for AGEs upregulate as AGEs accumulate.  Activation (binding) may induce release of pro- inflammatory and pro-fibrogenic cytokines. AGEs binding to receptors may promote inflammatory response Reference: Schmidt et al. J Clin Invest. 2001; 108(7):949–955.
  •  Glycohemoglobin (gHb) or glycosylated hemoglobin  Sugars cross-link to hemoglobin  Rate of formation is proportional to glucose level and duration  Hemoglobin lifespan is about 4 months  A1C is used to assess long-term DM control  A1C levels correlate with DM complications Hemoglobin A1C is an AGE
  •  A1C estimates average glucose (eAG) level for past 2–3 months.  eAG is similar to eGFR. − Both “estimate” levels.  Normal A1C is 4–5.6%  A1C > 6.5% is now used to diagnose DM. Average glucose levels can be estimated from the A1C Reference: http://professional.diabetes.org/GlucoseCalculator.aspx A1C (%) eAG (mg/dL) 14 355 12 298 10 240 9 212 8 183 7 154 6.5 140 6.0 126
  •  < 1% of filtered insulin is excreted into urine.  Insulin, pro-insulin, C-peptide are catabolized. − About 1/3 total endogenous insulin catabolism − Primary site for exogenous insulin catabolism − Major site for pro-insulin catabolism  Circulating insulin levels are higher as CKD advances.  The risk for hypoglycemia increases with CKD. Insulin is catabolized by the kidneys Reference: Himmelfarb J. In: Mitch WE, Ikizler TA, 2010
  • Diabetes medications may be discontinued or adjusted in CKD Reference: Reilly & Berns Seminars in Dialysis 2010; 23(2):163–168.
  • Balancing Act
  •  Goal for the general population − A1C < 7%  Less stringent goal may be appropriate for: − Frequent severe hypoglycemia − Limited life expectancy − Advanced microvascular (CKD) or macrovascular complications A1C goal is individualized in CKD Reference: Diabetes Care, (suppl 1) 2011
  •  There is evidence that control of newly diagnosed diabetes may help prevent CKD. − Type 1 diabetes (DM 1)  Diabetes Control and Complications Trial (DCCT) − Type 2 diabetes (DM 2)  United Kingdom Prospective Diabetes Study (UKPDS) Good glycemic control early may reduce CKD later
  •  Newly diagnosed, first 10 years − Median age: 54 years (48–60 years)  Intensive control defined as A1C < 7.0% (compared to 7.9%)  34% reduction in albuminuria  Long-term data not as clear UKPDS: Control of newly diagnosed type 2 DM may lower risk of albuminuria Reference: UKPDS 33, 1998; UKPDS 64, 2003
  •  The evidence is not strong.  Control still matters for other organs.  AGEs may have altered or destroyed slow turnover proteins (glomerular barrier). Good control of diabetes of long duration may not be as effective in slowing CKD
  •  45–60 grams per meal for most women  60–75 grams per meal for most men  15 grams per snack  Adjust carbohydrates based on weight, glycemic targets, and individual preference Carbohydrates still count in people with diabetic kidney disease (DKD)
  • Carbohydrate choice Nutrients of concern for CKD Milk Protein, sodium, phosphorus, potassium Processed grains Sodium Whole grains Phosphorus, potassium Legumes Protein, phosphorus, potassium Starchy vegetables Potassium Fruit Potassium Sweets and added sugars May have added phosphorus Type of carbohydrate may matter in DKD
  •  Dietary protein may increase GFR and renal blood flow rates. Animal protein may have greater effect than plant protein.  Dietary protein is a source of nitrogen, phosphorus, potassium, and metabolic acids that need to be filtered and excreted by the kidneys.  Animal protein intake may be a risk factor for increased urine albumin excretion in hypertension and diabetes. High protein diets are not recommended for DKD References: Friedman. Am J Kidney Dis 2004; 44(6):950–962; Bernstein et al. J Am Diet Assoc 2007; 107(4):644–650; Wrone et al. Am J Kidney Dis 2003; 41(3):580–587.
  •  RDA = 0.8 g protein/kg body weight (wt)  American Diabetes Association (2008) recommendations: − Normal kidney function: 15–20% protein calories (usual) − Early CKD: “reduction” to 0.8–1.0 g/kg body wt − Advanced CKD: 0.8 g/kg body wt  American Dietetic Association Evidence Library for Chronic Kidney Disease (accessed 2/4/2011) − 0.8–0.9 g/kg body wt − Protein-restriction may improve urine albumin (albuminuria) Level of protein for DM and CKD may mean avoiding excessive intake Reference: Diabetes Care, 2008
  •  Data are inconclusive for replacing animal protein with vegetable protein to help lower urine albumin.  Long-term consumption of high-protein diets (animal or vegetable protein) may cause renal injury and/or accelerate CKD. − Definition of high-protein  > 0.8 g/kg/day (no CKD) or  > 0.6 g/kg/day (CKD) Reducing total amount of protein may be more important than type of protein References: Diabetes Care, 2008; Bernstein et al. J Am Diet Assoc 2007; 107(4):644–650;
  •  National Cholesterol Education Program (2002) recommendations: − 25–35% total calories from fat  Saturated fat < 7% total calories  Polyunsaturated fat < 10%  Monounsaturated fat < 20% − Cholesterol < 200 mg/day − Plant stanols or sterols 2 grams per day − Increase soluble fiber to 10–25 grams per day Diet should be heart-healthy to reduce risk for CVD in DM (and CKD) Reference: http://www.nhlbi.nih.gov/guidelines/cholesterol/atp3full.pdf
  • Guidelines provide guidance, but we still need to individualize
  • Spontaneous improvement and/or increased frequency of hypoglycemia may indicate CKD is progressing
  •  The risk for hypoglycemia may increase as CKD progresses.  Circulating levels of insulin are higher due to reduced catabolism.  Insulin prescription may be reduced.  Oral medications may change. “I don’t have diabetes any more; my doctor stopped my diabetes pills.”
  •  The risk for hyperkalemia is increased in diabetic kidney disease.  Review medication list for ACEi or ARB. − If prescribed, discuss use of glucose tablets or low-potassium juice to treat hypoglycemia.  Use light-colored soda pop, not dark-colored colas, if using to treat hypoglycemia. Colas have phosphoric acid. Treat hypoglycemia without adding potassium or phosphorus
  • Any “juice” can treat hypoglycemia, even those low in potassium mg
  • Date 1/19 1/29 4/2 5/7 7/1 BP (mmHg) 168/98 138/82 136/78 142/60 146/70 Weight (lbs.) 200.5 196 191 189.4 189.4 eGFR (> 60) 34 34 29 27 22 UACR (mg/g) (< 30) - 6,437 - 4,483 - K (mmol/L ) (3.5-5.0) 4.9 4.6 5.5 5.5 5.5 Glucose (70–99) 211 77 63 - 69 A1C (eAG) 9.4 (223) - 7.9 (180) - 6.1 (128) Medications Glyburide 5 mg - Glyburide 2.5 mg Glipizide 5 mg - He reports - A few low sugars More low sugars Still has low sugars - For Frank: Hypoglycemia and improved glycemic control may indicate CKD progression
  • Food/beverage intake Recently stopped salt, using salt substitute. Using orange juice to treat low sugars. Includes other potassium-rich foods, fast foods. Won’t use glucose tablets. Low sugars when he skips meals. Diet order 2,200 calories; 1,500 mg sodium; potassium restriction Diet experience Instructed on diabetic diet when diagnosed, tries to limit carbs. Medications 50 mg Losartan (changed from 40 mg Lisinopril), 40 mg Furosemide; 5 mg Glipizide (2.5 mg Glyburide discontinued due to low sugars) Anthropometrics Height 66.5”, weight 189.4# down 11# since Jan., BMI now 30.1. Left foot, 4th toe amputation Biochemical data K 5.5 x 3 months; eGFR 22, was 34 (Jan.); UACR 4,483 mg/g (May), 6,437 mg/g (Jan.); A1C 6.1, 7.9% (Apr); random blood sugar 69 Personal history 55-year-old male, English is his second language Patient history DM type 2 for 8 years, no meds x 5 yrs. BP 146/70. Originally came to clinic due to right foot swelling. Seeing a nephrologist. Social history Sedentary job, sits for long periods of time. No sick leave, couldn’t make dietitian appointment. Lives in apartment with wife, 2 sons. Reference: American Dietetic Association, 2010 Assessment (7/1)
  • As eGFR declined, Frank’s DM medication was reduced, then changed
  •  Inconsistent carbohydrate intake related to limited adherence to nutrition-related recommendations, as evidenced by skipped meals and low blood glucose levels  Excessive potassium intake related to nutrition- related knowledge deficit, as evidenced by use of orange juice to treat low blood glucose levels NCP diagnoses Reference: American Dietetic Association, 2010
  • Initial nutrition education Priority modifications: − Eat a small snack between brunch and supper on weekends to prevent hypoglycemia. − Use glucose tablets or juice with less potassium to treat hypoglycemia. Intervention Reference: American Dietetic Association, 2010
  •  Renal threshold for glucose is 180–200 mg/dL.  Sugars cross-linking to proteins changes their shapes and functions (AGEs).  A1C goal is individualized.  Spontaneous improvement in glycemic control may indicate CKD progression and medications may change.  Risk for hypoglycemia occurs with CKD; risk for hyperkalemia occurs with ACEi and ARBs. − Use low-potassium juice to treat hypoglycemia. − Light-colored soda pop is lower in phosphorus than cola. Summary: CKD and diabetes
  •  Baseline urine albumin level may predict risk of CKD progression Urine albumin
  •  Urine albumin measures albuminuria.  Urine albumin may be earliest sign of CKD.  Urine albumin may exacerbate kidney damage.  The level reflects severity of kidney damage.  Reducing albuminuria may be associated with slower progression.  Urine albumin is a risk factor for cardiovascular disease (CVD). − Increased inflammation − Oxidative stress − Marker of endothelial dysfunction Brief review: Urine albumin
  •  “Normal” UACR < 30 mg/g − Current cut-off used to define normal levels  Persistent UACR > 30 mg/g means kidney damage  Spot urine sample  Monitor trends over time Use UACR to assess and monitor kidney damage
  •  Increased glomerular permeability allows albumin (and other proteins) to pass into the urine.  Higher levels of protein within the tubule may exacerbate kidney damage. − Protein may exceed tubule’s ability to reabsorb. Damaged kidneys allow albumin to cross the filtration barrier into the urine
  • Risk factors for albuminuria Reference: de Jong & Brenner. Kidney Int 2004; 66(6):2109–2118.
  • Elevated UACR is associated with risk of renal events; lowering UACR may lower risk of progression References: NIH, February 2010; De Zeeuw et al. Kidney Int 2004; 65(6):2309–2320.
  •  Their effects are beyond blood pressure control.  They also reduce protein in the urine.  Sometimes these medications are prescribed to lower urine albumin levels in normotensive people. ACEi and ARBs may be renoprotective References: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571; Strippoli et al. Cochrane Database Syst Rev 2010. Kunz et al. Ann Intern Med 2008; 148(1):30–48.
  •  Dose-dependent increase in urine albumin in the general population  Independent predictor of elevated urine albumin in primary hypertension  Independent risk factor for onset and progression of albuminuria in DM 1 and DM 2  May increase risk for progression of renal failure in patients with primary renal disease Smoking is associated with albuminuria Reference: Orth. J Am Soc Nephrol 2002; 13(6):1663–1672.
  •  Literature review showed weight loss was associated with decreased proteinuria. − Dietary restrictions − Exercise − Anti-obesity medications − Bariatric surgery  No data to evaluate effect on CKD progression. Intentional weight loss is associated with decreased proteinuria Reference: Afshinnia et al. Nephrol Dial Transplant 2010; 25(4):1173–1183.
  •  In the Netherlands, higher sodium intake was associated with increased urine albumin excretion.  In a 2006 literature review, increasing salt consumption was associated with worsening urine albumin. Reducing sodium intake may reduce urine albumin levels References: Verhave et al. J Intern Med 2004; 256(4):324–330; Jones-Burton et al. Am J Nephrol 2006; 26(3):268–275.
  •  The type of protein may make a difference.  Animal protein may be associated with higher urine albumin excretion.  The relationship may depend on baseline urine albumin level. Relationship between urine albumin and dietary protein intake varies
  •  Two or more servings of red meat per week may increase risk of microalbuminuria. − Nurses Health Study (Lin J et al., 2010)  Nondairy animal foods are associated with albuminuria. − Multiethnic Study of Atherosclerosis (Nettleton et al., 2008)  High protein intake is associated with urine albumin with both hypertension and diabetes. − NHANES III (Wrone et al., 2003) Animal protein intake may be associated with higher urine albumin
  •  Baseline AER < 7 mg/24 hr. − No difference found in AER between diet patterns at 8 weeks.  Baseline AER ≥ 7 mg/24 hr. − 8-week AER was similar in control and DASH.  DASH was 3.8% higher in protein than control diet. − 8-week AER was lower in fruits and vegetables diet.  ~ 1% higher protein compared to control diet  ~ 10 g/day reduction in animal protein Although higher in protein, DASH pattern did not increase urine albumin excretion Reference: Jacobs et al. Am J Kidney Dis 2009; 53(4):638–646.
  • DASH: Baseline urine albumin may affect AER response to change in dietary protein Reference: Adapted from Jacobs et al., 2009
  •  A 1996 meta-analysis found low-protein diet may slow increase in urinary albumin level in insulin- dependent diabetes.  The use of a supplemented very-low-protein diet is associated with decrease in proteinuria. Lowering dietary protein may help reduce urine albumin or proteinuria References: Pedrini et al. Ann Intern Med 1996; 124(7):627–632; Chauveau et al. J Renal Nutr 2007; 17(4):250–257.
  •  Control blood pressure  Reduce sodium intake  Achieve good control of diabetes early; may help prevent albuminuria  Reduce weight (if obese)  Reduce protein intake, if excessive  Achieve tobacco cessation Interventions for reducing urine albumin
  • For Frank, an elevated urine albumin is a marker of kidney damage and prognosticator for rapid progression of CKD
  • CARDIOVASCULAR DISEASE CVD is the leading cause of morbidity and mortality in people with CKD
  •  CVD risks and CKD − Traditional − Nontraditional  Pattern of dyslipidemia in CKD  Statins  Nontraditional risks  Nutrition interventions Topics
  • Lipid abnormalities may increase as eGFR declines Reference: Astor et al. Am J Epidemiol 2008; 167(10):1226–1234.
  • CKD complications are nontraditional risk factors for CVD Traditional risk factors  Hypertension  Diabetes  Dyslipidemia  Smoking  Age  Inflammation Nontraditional risk factors  Albuminuria  Anemia  Abnormal metabolism of calcium and phosphorus
  •  Increased triglycerides − May be very elevated with massive proteinuria (nephrotic syndrome)  Decreased high-density lipoprotein levels  Low or normal low-density lipoprotein levels − Smaller, denser LDL particles  More prone to oxidation and accumulation in vessel walls Pattern of dyslipidemia in CKD may increase risk of CVD References: Molitch. Clin J Am Soc Nephrol 2006; 1(5):1090–1099; Ruan et al. Nat Rev Nephrol 2009; 5(12):713–721.
  •  Target lipid levels in CKD are unknown and may be similar to those for the general population.  Persons with CKD should be considered at high risk for CVD.  Not many CVD studies include CKD patients. Targets for lipid levels may be similar for CKD
  •  Statins reduce hepatic cholesterol synthesis.  Statins significantly reduce all-cause and CVD mortality in persons with CKD.  Their use does not appear to slow CKD progression but may reduce proteinuria.  Monitor for potential side effects.  Muscle toxicity or elevated liver function tests may be seen with statin use. Statins are used with caution in patients with CKD Reference: Navaneethan et al. Cochrane Database Syst Rev 2009.
  •  Inflammation may modify risk relationship between cholesterol and CVD in this population.  In patients with normal C-reactive protein (CRP), elevating cholesterol levels may be associated with increasing risk of CVD events.  In patients with elevated CRP, elevating cholesterol levels may not be not associated with increased risk of CVD events; inflammation may be associated with increased risk. African-American Study of Kidney Disease and Hypertension (AASK) Inflammation may play a role in CVD in CKD Reference: Contreras et al. J Am Soc Nephrol 2010; 21(12):2131–2142.
  •  Albuminuria  Anemia  Abnormal metabolism of calcium and phosphorus Nontraditional risk factors for CVD
  •  Evidence is scarce for trials with CKD patients  Dietary Guidelines 2010 − Keep trans fats as low as possible  Limit foods with synthetic sources of trans fats − Partially hydrogenated oils − Other solid fats Nutrition recommendations addressing CVD in persons with CKD may be similar to those for the general population Reference: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/PolicyDoc/ExecSumm.pdf
  •  Spreads may reduce LDL cholesterol by 15%.  Effectiveness in CKD patients is unknown.  Spreads vary in sodium and calories: − 80–110 mg sodium/Tbsp. − 45–70 kcal/Tbsp.  Substitute isocalorically.  Some may contain potassium sorbate. Plant stanol and sterol spreads may help lower LDL in general population Reference: Van Horn et al. J Am Diet Assoc 2008; 108(2):287–331.
  •  25–30 grams total fiber suggested per day.  7–13 grams soluble fiber/day may reduce LDL.  Effectiveness in CKD is unknown.  Foods high in soluble fiber may be too rich in potassium and phosphorus for CKD patients.  Foods high in bran may be too rich in potassium, phosphorus, and/or sodium for CKD patients. Soluble fiber may help reduce heart disease in the general population References: Van Horn et al. J Am Diet Assoc 2008; 108(2):287–331; Beto & Bansal. Advances Chronic Kidney Dis 2004; 11(4):391–397.
  • Legumes are rich in potassium and phosphorus; counsel appropriately References: http://www.nhlbi.nih.gov/health/public/heart/chol/chol_tlc.pdf; http://www.nal.usda.gov/fnic/foodcomp/search/ Serving of ½ cup Soluble fiber (grams) K (mg) P (mg) Na (mg) Barley 1 73 42 2 Oatmeal 1 82 90 5 Oat bran 1 101 130 1 Black beans 2 305 120 1 Kidney beans 3 358 122 1 Pinto beans 2 373 126 1 Pinto beans, canned 5.5 (total fiber) 292 110 353 Lentils 1 365 178 2 Chick peas 1 239 138 6 Chick peas, canned 5.3 (total fiber) 206 108 359
  • Some fruits with soluble fiber are rich in potassium; counsel appropriately References: http://www.nal.usda.gov/fnic/foodcomp/search/; http://www.nhlbi.nih.gov/health/public/heart/chol/chol_tlc.pdf Food Soluble fiber (grams) K (mg) P (mg) Na (mg) Apple (3” diameter–medium) 1 195 20 2 Apple, peeled 2.1 (total fiber) 145 18 0 Banana (7”–7 7/8” long) 1 422 26 1 Blackberries (1/2 c.) 1 117 16 1 Orange (3 1/16” diameter – large) 2 333 26 0 Peach (2 2/3” diameter – medium) 1 285 30 0 Peach, canned (2 halves) 1.3 (total fiber) 194 20 3 Pear (1 medium) 2 212 20 2 Broccoli (1/2 c. cooked) 1 229 52 32 Carrots (1/2 c. cooked) 1 183 23 45
  •  More than 90% of phosphorus is absorbed from food additives containing phosphorus. − Read ingredient list for phosphorus.  Phosphorus in animal foods is absorbed more readily than that in plant food.  Phytates in plant foods reduce absorption of phosphorus (e.g., foods rich in soluble fiber). Source of phosphorus affects absorption: additives > animal > plant Reference: Kalantar-Zadeh et al. Clin J Am Soc Nephrol 2010; 5(3):519–530.
  •  Nontraditional risk factors include: − Albuminuria − Anemia − Abnormal calcium and phosphorus metabolism  Statins are used in CKD patients with some caution.  Some foods rich in soluble fiber may be higher in K and P than recommended for CKD patients.  Phosphorus in food additives is absorbed much more readily. Summary: CKD and CVD
  • Summary: CKD and hypertension Assessment:  Food–medication interaction − Hyperkalemia  ACEi (____pril)  ARBs (___sartan) Intervention:  Limit sodium. − 1,500 mg per day − Avoid salt substitutes  Limit potassium when serum level is elevated. − Individualized  Blood pressure control is key to slowing progression.  Multiple medications are used.
  •  Urine albumin excretion is associated with diabetic kidney disease, but not all people will have high urine albumin levels.  High levels of urine albumin may mean more rapid progression of CKD.  Good control of diabetes early may help reduce the risk of albuminuria later.  Tight versus good control may not slow progression. Summary: CKD and diabetes
  •  Renal threshold for glucose is 180–200 mg/dL.  Sugars cross-linking to proteins change their shapes and functions (AGEs).  A1C goal is individualized.  Spontaneous improvement in glycemic control may indicate CKD progression. − Medications may change.  Risk for hypoglycemia with CKD, hyperkalemia with ACEi and ARBs. − Use low-potassium juice to treat hypoglycemia. − Light-colored soda pop is lower in phosphorus than colas. Summary: CKD and diabetes
  •  Urine albumin is a marker of kidney damage.  Control blood pressure. − Particularly with high urine albumin, control is important. − ACEi and ARBs may be antiproteinuric.  Reduce sodium intake to 1,500 mg.  Good control of diabetes early may help prevent albuminuria.  Weight reduction (if obese) may reduce inflammation.  Reduce protein intake, if excessive.  Tobacco cessation is important. Summary: CKD and urine albumin
  •  Nontraditional risk factors include: − Abnormal urine albumin − Anemia − Abnormal calcium and phosphorus metabolism  Statins are used in CKD with some caution.  Some foods rich in soluble fiber may be higher in K and P than recommended for CKD.  Phosphorus in food additives is absorbed more readily. Summary: CKD and CVD
  • An educational handout you can use to get started Reference: http://www.nkdep.nih.gov/resources/nkdep-factsheet-overallpatient-508.pdf
  • Reference: http://www.nkdep.nih.gov/resources/nkdep-factsheet-overallpatient-508.pdf
  • Another educational tool you can start using: Reference: http://www.nkdep.nih.gov/resources/nkdep-ckd-amt-guide-508.pdf
  • This professional development opportunity was created by the National Kidney Disease Education Program (NKDEP), an initiative of the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. With the goal of reducing the burden of chronic kidney disease (CKD), especially among communities most impacted by the disease, NKDEP works in collaboration with a range of government, nonprofit, and health care organizations to: • raise awareness among people at risk for CKD about the need for testing; • educate people with CKD about how to manage their disease; • provide information, training, and tools to help health care providers better detect and treat CKD; and • support changes in the laboratory community that yield more accurate, reliable, and accessible test results. To learn more about NKDEP, please visit: http://www.nkdep.nih.gov. For additional materials from NIDDK, please visit: http://www.niddk.nih.gov.
  • Theresa A. Kuracina, M.S., R.D., C.D.E., L.N. Ms. Kuracina is the lead author of the American Dietetic Association’s CKD Nutrition Management Training Certificate Program and NKDEP’s nutrition resources for managing patients with CKD. Ms. Kuracina has more than 20 years of experience in clinical dietetics with the Indian Health Service (IHS). She is a senior clinical consultant with the National Kidney Disease Education Program (NKDEP) at the National Institutes of Health. She also serves as a diabetes dietitian and coordinator for a diabetes self- management education program at the IHS Albuquerque Indian Health Center in New Mexico, a role in which she routinely counsels patients who have chronic kidney disease (CKD). Meet our Presenters
  • Andrew S. Narva, M.D., F.A.C.P. Dr. Narva is the director of the National Kidney Disease Education Program (NKDEP) at the National Institutes of Health (NIH). Prior to joining NIH in 2006, he served for 15 years as the Chief Clinical Consultant for Nephrology for the Indian Health Service (IHS). Via telemedicine from NIH, he continues to provide care for IHS patients who have chronic kidney disease. A highly recognized nephrologist and public servant, Dr. Narva has served as a member of the Medical Review Board of ESRD Network 15 and as chair of the Minority Outreach Committee of the National Kidney Foundation (NKF). He serves on the NKF Kidney Disease Outcomes Quality Initiative Work Group on Diabetes in Chronic Diabetes and is a member of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure 8 Expert Panel. Meet our Presenters
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  • Quick reference on UACR and GFR in evaluating patients with diabetes and kidney disease. National Kidney Disease Education Program website. http://nkdep.nih.gov/resources/uacr_gfr_quickreference.htm. Reviewed June 30, 2010. Accessed June 13, 2011. Nettleton JA, Steffen LM, Palmas W, Burke, GL, Jacobs DR Jr. Associations between microalbuminuria and animal foods, plant foods, and dietary patterns in the Multiethnic Study of Atherosclerosis. American Journal of Clinical Nutrition. 2008;87(6):1825–1836. Orth SR. Smoking and the kidney. Journal of the American Society of Nephrology. 2002;13(6):1663–1672. Pedrini MT, Levey AS, Lau J, Chalmers TC, Wang PH. The effect of dietary protein restriction on the progression of diabetic and nondiabetic renal diseases: A meta-analysis. Annals of Internal Medicine. 1996;124(7):627–632. References: Albuminuria
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