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CKD MNT Module 3: Complications
 
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Who would have thought that declining kidney function could result in anemia and bone disease? Another case study is used to follow Joseph's journey as he tries to lose weight for placement on the ...

Who would have thought that declining kidney function could result in anemia and bone disease? Another case study is used to follow Joseph's journey as he tries to lose weight for placement on the kidney transplant list. He experiences CKD complications along the way, including anemia, hypoalbuminemia, hyperkalemia, metabolic acidosis, and bone disease. See how NKDEP's Your Kidney Test Results and individual nutrient handouts can be used as part of self-management education.

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  • This module covers certain complications seen in CKD. The risk for anemia, hypoalbuminemia, hyperkalemia, metabolic acidosis, and mineral and bone disorders increase as the estimated glomerular filtration rate (eGFR) decreases. We will follow a patient, Joseph, as his CKD complications impact his life and journey towards kidney failure. You will use the National Kidney Disease Education Program's Your Kidney Test Results as we describe these complications.
  • By the time you finish this module, you should be able to use laboratory parameters to assess anemia, associate the increased risk for hyperkalemia with hyperglycemia and metabolic acidosis, and use and interpret laboratory parameters to assess hypoalbuminemia, metabolic acidosis and mineral and bone disorders of CKD.
  • In the first two modules we discussed kidney anatomy and kidney functions. Nephrons are the working units of the kidneys. As the kidney function declines, people have fewer functioning nephrons. Lab work may show multiple metabolic abnormalities. Fewer functioning nephrons may mean inadequate erythropoietin, which may result in anemia. The kidneys synthesize erythropoietin, the hormone needed for erythropoiesis. Certain substances may accumulate in the blood as kidney function declines. Potassium, hydrogen ion or acid, and phosphorus may accumulate. The kidneys activate vitamin D.
  • Complications may increase as the eGFR decreases. Along the x-axis, you see anemia, potassium, phosphorus, and CO2. The prevalence increases as the eGFR decreases to less than 60, as shown by the gold bars. 4-15 version of Module 3
  • We will discuss what happens to Joseph. Joseph is a 40-year-old man with numerous medical issues, including morbid obesity and type 2 diabetes. When we first meet Joseph, his eGFR is 21 and his urine protein-to-urine creatinine ratio is 6.6 grams per day. The urine protein-to-urine creatinine ratio or Up/Uc is different than the UACR described previously. Up/Uc measures all proteins in the urine. Joseph has significant proteinuria.
  • At the top of are measurements including weight, blood pressure, A1C, and Up/Uc. The second table is supposed to represent a lab report. There are numerous high and low levels in his lab results. 4-15 version of Module 3
  • This table has selected data from a complete blood count. We will start with anemia, at the bottom of this table, specifically hemoglobin. Joseph’s hemoglobin was 10.5 in February. His level improved to 10.9 in July. We will then discuss hyperkalemia. Joseph’s potassium level ranges from 4.7 to 5.5. His serum bicarbonate or CO2 ranges from 16.2 to 23.8. Serum phosphorus ranges from 4.2 to 5.3. His eGFR declines from 21 to 15. Serum albumin increases from 3.0 in April to 3.5 in July. 4-15 version of Module 3
  • The topics covered in this module include anemia, hyperkalemia, and hypoalbuminemia, which is a marker for malnutrition and inflammation. Inflammation plays a significant role in CKD. We will also discuss metabolic acidosis and mineral and bone disorders.
  • Your Kidney Test Results has basic information about the complications of CKD for patients. At this time, you may want to visit the URL http://www.nkdep.nih.gov/resources/nkdep-kidney-test-results-508.pdf to print the PDF Your Kidney Test Results to use with the module. Many patients are interested in their lab results.
  • The first complication of chronic kidney disease we'll discuss is anemia. Anemia may occur early in the course of chronic kidney disease and is generally due to inadequate erythropoietin synthesis by the damaged kidney.
  • The prevalence of anemia increases as GFR declines and affects nearly 50 percent of patients with GFRs less than 30. 4-15 version of Module 3
  • Anemia, complicating chronic kidney disease, generally develops as a result of inadequate erythropoietin synthesis. It may develop early and worsen as kidney function deteriorates. It may develop earlier in people with diabetic kidney disease than people without diabetes. Inadequate iron intake or iron absorption may contribute to anemia as well as decreased erythropoietin.
  • In Joseph's case, his anemia worsened as his GFR declined but treatment resulted in improved hemoglobin levels.
  • There are a number of factors which bear on the development of anemia in chronic kidney disease. Not only is erythropoietin decreased, but there may be decreased responsiveness to erythropoietin. This may result from uremia, chronic inflammation, hyperparathyroidism or folate deficiency.
  • Anemia in chronic kidney disease is associated with increased morbidity and mortality. Observational data show an association with coronary artery disease, hospitalization for cardiac disease, death from congestive heart failure, all cause mortality, and left ventricular hypertrophy.
  • Reviewing some basic physiology, remember that the kidneys act as oxygen sensors in the body. The kidneys are ideally situated for this because of their very high blood flow rate; remember that 20 percent of the cardiac output goes to the kidneys. Tissue hypoxia triggers erythropoietin production. Erythropoietin then stimulates erythrocyte precursors in the bone marrow. Hemoglobin is the primary iron containing protein in erythrocyte transporting oxygen to the tissues. Both erythropoietin and adequate iron are required for increased production of hemoglobin-containing red blood cells for correction of tissue hypoxia.
  • Iron is absorbed, transported, and stored within the body. The iron bound to transferrin reflects the biologically available iron. Ferritin is a reflection of total body iron stores.
  • The absorption of iron is influenced by many different factors. There is increased absorption with iron depletion, with increased red blood cell production, with anemia and hypoxia and when inflammation is not present. There's reduced absorption with inflammation or infection. For example, it's very common to see a decrease in hemoglobin in people with diabetes who develop a lower extremity ulcer.
  • There are a number of additional factors which contribute to inadequate iron stores in chronic kidney disease. A spontaneous decrease in high protein foods such as meat may occur as the eGFR declines. Hepcidin accumulates in chronic kidney disease; hepcidin is a hormone which plays a key role in controlling iron levels, regulating iron absorption from the gut and mobilizing stored iron. Inflammation also may play a significant role by reducing absorption of iron.
  • Assessing iron status requires measuring serum iron as well as iron-binding capacity.
  • Transferrin saturation is the ratio of iron to total iron-binding capacity and is an early indicator of iron deficiency. Less than 16 percent saturation indicates iron deficiency in the general population. In addition to iron and total iron-binding capacity, it is important to measure ferritin. Ferritin is the storage form of iron and reflects total body iron stores. However, ferritin is an acute phase reactant and may be increased in acute and chronic inflammation.
  • The laboratory assessment of anemia in chronic kidney disease includes a complete blood count as well as iron, TIBC, and ferritin. The anemia that we see in chronic kidney disease is generally normochromic and normocytic.
  • Treatment of anemia in chronic kidney disease may include iron supplementation, either oral or intravenous, and use of erythropoiesis-stimulating agents such as erythropoietin.
  • Initially, many patients receive supplemental oral iron. The amount of iron that's available varies by formulation. A 325 milligram dose of ferrous fumarate has 108 milligrams of elemental iron, ferrous sulfate has 65 milligrams, and ferrous gluconate has 35 milligrams of elemental iron. Absorption is greater when the iron is in the ferrous form.
  • However, oral iron supplements are often poorly absorbed; absorption is reduced by food. The percentage of the dose that's absorbed decreases as the dose increases, and multiple doses may be needed. CDC recommends 50-60 milligrams of elemental iron twice daily for non-pregnant adults. There are fewer GI side effects with extended release forms but less is absorbed.
  • The major problem with oral iron supplements is gastrointestinal side effects. These affect 25 percent of people and include nausea, vomiting, constipation, diarrhea, and abdominal distress. About one-fifth of patients will discontinue supplements due to their side effects.
  • You should be aware that absorption of oral iron supplements may be reduced with caffeinated beverages, when they're taken along with supplemental calcium or calcium containing antacids and in patients who take H2-receptor blockers or proton pump inhibitors. You should consider starting with half of the recommended dose and gradually increase to avoid the GI side effects. Patients may have fewer side effects if they take iron with food. You may try different preparations if the patient doesn't tolerate one preparation. Iron may be better tolerated if taken in divided doses, and stool softeners may reduce constipation. 4-15 version of Module 3
  • It is particularly important to take iron supplements separate from calcium-based phosphate binders. Calcium supplements, which may be prescribed with meals to bind phosphorus, can interfere with iron absorption. However, many patients have been instructed to take iron with meals to reduce the GI side effect. Despite this, patients taking calcium may need to take their iron in between meals. Iron absorption is increased when it's taken between meals and separate from phosphate binders but may have more GI side effects. In addition, if the patient is already on multiple medications, the oral iron supplement may increase the complexity of their regimen.
  • Parenteral iron may be used, especially in dialysis; because free iron is toxic, parenteral iron is administered as an iron-carbohydrate complex. The carbohydrates may shield the body from oxidation, allowing safe delivery of iron.
  • Parenteral iron is a potent oxidant and may be toxic to the renal tubule. In addition, IV iron may increase the risk of infection through suppression of phagocytosis of bacteria by leukocytes.
  • There are several erythropoiesis-stimulating agents available. The most commonly used is recombinant erythropoietin; it's an injectable medication, used since the late '80s. ESAs may potentially benefit patients, including reducing the need for transfusion. However, there is risk associated with their use and it's required that all patients receiving ESAs be advised of the risks.
  • Anemia in dialysis patients is frequently treated with ESAs. The current role of ESAs for people with CKD is unclear. The FDA recently produced an advisory which suggested that ESAs not be used in CKD in patients with hemoglobin level over 10.
  • Let’s apply the information to Joseph. Joseph is a 40-year-old man with type 2 diabetes since 1997. Initial eGFR was 21. His Up/Uc was very elevated, at 6.6 grams per day. He is morbidly obese with a BMI of 45.8. He needs to have a BMI less than 30 to be considered for a kidney transplant. He attends weight loss classes at an endocrinologist’s office. Anemia is discussed first because Joseph’s personal goal is weight loss. The physician referred him for hyperkalemia. He received information about potassium at the nephrologist’s office. Joseph wants to walk for weight loss. He is anemic and fatigues easily.
  • This is the same format used in assessment in module 2. Joseph eats twice a day. He is restricting dietary potassium. His current intake for breakfast includes three eggs, one to two slices of dry toast, and a sugar-free beverage. His supper is generally fast foods. He stopped drinking iced tea due to the potassium content. He eats more rice and noodles and fewer potatoes to help control potassium. He snacks on salted jerky or corn chips. Since we are focusing on anemia first, pertinent medications are listed. He is supposed to take ferrous sulfate, 325 milligrams twice a day. He is not taking iron supplements, he feels he is taking too many medications. He takes lisinopril 80 milligrams per day and he knows this medication may increase serum potassium. The endocrinologist stopped pioglitazone and glyburide and started 50 units of glargine at bedtime. Joseph reports postprandial glucose levels are less than 150. They were 200 to 300. He recently started 0.25 micrograms of calcitriol, or active vitamin D, last month. The medications are listed to help you see why he feels he is taking too many medications. The current diet prescription, from the endocrinologist’s office, is 1,700 to 2,000 calories per day, with 96 grams of protein. The nephrologist added a potassium restriction. Joseph has not been instructed to restrict sodium. He played football in high school and he is not active now. He lives at a high altitude, 5,000 feet. He was very short of breath as he walked down the hall to the office. He reports being fatigued, yet he wants to walk more. He learned about treatment options for kidney failure at the nephrologist’soffice. His height is 69 inches; his weight was 310 pounds at the first visit. He has lost 25 pounds since September.
  • Initial eGFR is 21, potassium is 5.0. His hemoglobin is 10.5, transferrin saturation or T-SAT is 19, serum ferritin is 134. He is 40 years old, and studies criminology at the university. He does not use tobacco or alcohol. His chief complaint is being miserable due to too few calories in his current diet. The potassium restriction has been very difficult. He has had diabetes for over 13 years, and his blood pressure was 142/80. His wife reports she is trying to lose weight as well. They are both up late doing homework. Fast foods are convenient for supper. The wife is struggling with the potassium restriction as well because she is trying to eat what he eats.
  • Joseph already knows about potassium restriction. He is anemic and is not taking supplemental iron as prescribed. He didn’t know he should be restricting sodium. The diagnoses could be inadequate iron intake and nutrition-related knowledge deficit.
  • He needs nutrition education. He learned about the kidneys and anemia, and the importance of the iron supplement. He also learned about the injectable erythropoiesis-stimulating agents. That medication may be added in the future. He learned about sodium and blood pressure. He received the National Kidney Disease Education Program handout on sodium. Used Your Kidney Test Results to show hemoglobin level and other data. One of his goals was to take the iron supplement with breakfast and supper as prescribed. His other goals were to read Nutrition Facts labels for sodium and choose foods with less sodium.
  • Joseph’s hemoglobin is low. The oral iron alone did not improve the hemoglobin level. An erythropoiesis-stimulating agent was prescribed in May. His hemoglobin increased as a result. The box on the right shows iron studies, including percent transferrin saturation and ferritin. Joseph’s TSAT was 19 percent in February and 20 percent in May. Joseph’s ferritin was 134 in February and May.
  • To summarize this section, monitor hemoglobin levels and assess iron status prior to starting an iron supplement. Transferrin saturation provides information about available iron; ferritin levels provides information about storage iron. Iron supplements have side effects and many people do not take them as prescribed. In CKD, iron supplements may be most effective when taken between meals, particularly if someone is taking a phosphorus-binding medication. Joseph was told to take the iron supplement with meals to decrease side effects and increase adherence. People with anemia may receive erythropoiesis-stimulating agents and some may receive parenteral iron if they cannot tolerate oral iron supplements.
  • The second complication of chronic kidney disease that we'll discuss is hyperkalemia. It is important to recall that potassium excretion is regulated by the renin-angiotensin-aldosterone system, and perturbations of this system may result in hyperkalemia.
  • As we showed in the previous module, serum potassium tends to increase as the GFR declines. Nearly half of patients with eGFR less than 30 have serum potassium greater than 4.5.
  • In this module we'll talk about potassium balance and hyperkalemia.
  • Joseph's diet and medications play a role in his hyperkalemia. As his eGFR declined, his potassium increased.
  • Serum potassium levels affect muscle function and both elevated and depressed levels of potassium can cause significant abnormalities. Hypokalemia is associated with cardiac arrhythmias, muscle weakness, and glucose intolerance. Hyperkalemia is also associated with cardiac arrhythmias and muscle weakness.
  • Hyperkalemia is the potassium disorder that we're most concerned with in patients with chronic kidney disease. This is a potentially life threatening complication. The general reference range for potassium for most labs is 3.5 to 5. Susceptibility to hyperkalemia depends on the calcium level and other factors which determine transmembrane potential. Higher calcium levels may be relatively protective against hyperkalemia. Cardiac arrhythmias and cardiac arrest are possible if severe hyperkalemia is not recognized and treated.
  • The kidneys play a critical role in maintaining potassium balance. About 85 percent of ingested potassium is absorbed; potassium is freely filtered by the glomerulus, and the proximal tubule absorbs about 70 to 80 percent of filtered potassium. Potassium secretion occurs in the distal tubule and the collecting duct and may occur as an adaptation to high intake. A small amount of potassium is excreted in the feces.
  • The renin-angiotensin-aldosterone system plays a major role in potassium regulation. Activation of the renin-angiotensin-aldosterone system increases potassium excretion in response to aldosterone. Medications that inhibit this system increase the risk for hyperkalemia.
  • Shifts between the intracellular and extracellular compartments are reflected in serum potassium. Remember that 98 percent of potassium is intracellular, and about 75 percent is in the muscles. Only two percent of potassium is extracellular. The transcellular electrical potential generated by the sodium-potassium exchange is responsible for the voltage gradient across cell membranes. This gradient difference is needed for muscle and nerve activation.
  • Several factors can drive potassium to shift between the intracellular and extracellular compartments; insulin tends to move potassium into the cells; insulin deficiency can result in hyperkalemia. Acid-base status also affects the balance between intracellular and extracellular potassium. Metabolic acidosis, which basically means excessive hydrogen ion in the plasma, may drive potassium out of the cells as hydrogen ion is buffered intracellularly.
  • As a result, treating both hyperglycemia and acidemia may lower serum potassium. Controlling hyperglycemia with adequate insulin will drive potassium into the cells along with glucose. Treating acidosis may also lower potassium. In some patients with CKD, treatment of the acidosis may allow continued use of blood pressure medications that are reno-protective. That is, if a patient on an angiotensin-converting enzyme inhibitor or an angiotensin receptor blocker has hyperkalemia and acidosis, treating the acidosis may lower potassium and allow continuation of the RAAS antagonist.
  • Medication-induced hyperkalemia is a concern in patients using ACE inhibitors, angiotensin receptor blockers, potassium-sparing diuretics, and nonsteroidal anti-inflammatory drugs. In addition, tacrolimus and cyclosporine – anti-rejection drugs used by kidney transplant recipients – may raise potassium.
  • Despite all these concerns, routine restriction of potassium in chronic kidney disease patients is not indicated in the absence of hyperkalemia. There is no specific level of eGFR which precipitates potassium restriction. We restrict the dietary potassium to achieve and maintain safe potassium levels. Potassium restriction should be individualized.
  • In Joseph's case, potassium may be elevated due to transcellular shifts. He had metabolic acidosis which can cause potassium to move out of the cells as hydrogen ion moves intracellularly. Joseph’s nephrologist changed his medications; he stopped his ACE inhibitor, and he is trying an angiotensin receptor blocker which may be less associated with hyperkalemia. He added a loop diuretic to increase potassium excretion, and he added sodium bicarbonate to treat his acidemia.
  • Following treatment of metabolic acidosis, Joseph's potassium decreased.
  • This is a reassessment. Joseph met his goals. He takes iron and reads Nutrition Facts labels for sodium. He reports less fatigue and is walking more. He eats the same breakfast. He added a small lunch. Dinner includes green beans, rice, and a small piece of meat. He eats fewer fast foods and salted snacks. He brings a diet beverage with him to the office. He had not read the ingredient list before. He was upset when he saw potassium acesulfame on the ingredient list. He attends diabetes cooking classes with his wife. They use the recipes from those classes. He still has trouble following the potassium restriction. His wife helps him with the sodium restriction. He reports walking 10 to 15 minutes a day and reports less shortness of breath. His weight is 296 pounds. His eGFR is now 18. The urine protein-to-urine creatinine ratio is 5.6 down from 6.6. His potassium is up to 5.5, serum bicarbonate level is down to 16.2, and hemoglobin is 10.6. His phosphorus is 5.2, which is considered high. Labs are pending. He continues to receive darbepoetin to treat anemia. The nephrologist discontinued lisinopril and added losartan 50 milligrams and furosemide 80 milligrams last week due to hyperkalemia. He also added sodium bicarbonate, 650 milligrams twice a day. The blood pressure was 138/85. He needs to have a tooth extracted.
  • The nutrition diagnoses include altered nutrition-related laboratory value and decreased need for dietary phosphorus. He is hyperkalemic due to reduced renal excretion, medication, metabolic acidosis, and dietary intake. His serum phosphorus is now elevated, at 5.2. He needs to restrict phosphorus. The level may be higher due to vitamin D supplementation. Vitamin D enhances phosphorus absorption.
  • The intervention includes nutrition education. He wanted to review his lab results and was happy the hemoglobin level improved from 10.3 to 10.5. He heard about dietary potassium again and how sodium bicarbonate may help lower potassium level. His dietitian started discussing dietary phosphorus with him. He learned he may have to take another medication to help control phosphorus. He also learned how vitamin D may increase the phosphorus level. He added a few new goals. He will start reading ingredient lists to help choose foods without added phosphorus and potassium. He is still struggling with number of medications he takes. He plans to take the new medications prescribed by the nephrologist.
  • The next complication we're going to discuss is hypoalbuminemia. Serum albumin is a marker for nutritional status and inflammation.
  • We're going to discuss serum albumin and the relationship between inflammation and poor oral intake and hypoalbuminemia. We'll also discuss metabolic acidosis and hypoalbuminemia.
  • Joseph was hypoalbuminemic, but his albumin level did improve with interventions that will be described shortly.
  • Let’s briefly review how the kidney handles albumin. Normally very little albumin crosses the glomerulus and most of what does cross is reabsorbed by the tubule. However, damaged kidneys allow albumin to cross the filtration barrier into the urine in quantities which exceed the tubule’s capacity to reabsorb. As a result, elevated levels appear in the urine.
  • Recall that serum albumin helps maintain oncotic pressure and blood volume. It acts as a buffer and binds calcium, magnesium, hormones, vitamins, and medications. Serum albumin is also a marker for nutritional status and decreases in the presence of inflammation.
  • We know that serum albumin level at the time of dialysis initiation is an independent risk factor for mortality. Serum albumin greater than four grams per deciliter at initiation of dialysis is associated with reduced mortality risk. Unfortunately, only 11 percent of new dialysis patients in a recent study had serum albumin greater than four grams per deciliter.
  • Hypoalbuminemia occurs in chronic kidney disease as a result of multiple factors. Both acute and chronic inflammation are associated with reduced albumin synthesis. Loss of albumin in the urine in large quantities will reduce albumin. Metabolic acidosis, insulin resistance, and a decrease in intake in high protein foods are all additional factors contributing to low serum albumin.
  • The prevalence of hypoalbuminemia increases as GFR declines and in association with acidemia, defined as a serum bicarbonate less than 22 and inflammation as reflected in elevated C-reactive protein.
  • Joseph’s serum albumin increased as the eGFR decreased. Weight loss and sodium restriction may have been beneficial.
  • Joseph had two teeth removed in June. After the teeth were removed, the albumin level increased from 3.3 to 3.5. He started taking sodium bicarbonate in June. Reducing inflammation and correcting acidosis may help improve albumin levels.
  • Joseph returned for reassessment. He met his goals. He takes medications as prescribed; he reads ingredient lists for phosphorus and potassium. Of note, he needs to plan when he takes the diuretic. He cannot take it on days he is in the classroom. He feels more confident with sodium, potassium, and calorie restrictions. He was surprised about added phosphorus in foods. He saw the nephrologist two weeks ago. Calcium acetate, 667 milligrams per day with meals, was added as a phosphorus binder. Joseph was happy he knew why this medication was added. He wasn’t walking as often. His eGFR is stable. Potassium is 4.9. Dietary restriction and treating metabolic acidosis may have helped lower his serum potassium level. His CO2 is still low at 18.5, but improved. His phosphorus is up to 5.3. That is why the nephrologist added calcium acetate as a phosphorus binder. His corrected calcium is 8.5. The vitamin D level is 25. The iPTH is down to 130 from 207. Serum albumin is 3.5. Patient history includes dental extractions. Blood pressure is 136/85. He was tearful when he discussed the possibility of needing dialysis before getting on the transplant list. His eGFR is 18. Joseph may not be able to achieve a BMI less than 30 prior to needing dialysis.
  • One possible diagnosis could be an altered nutrient-related laboratory value. He has elevated phosphorus. He just started taking the phosphorus binding medication two weeks ago.
  • Follow-up counseling included use of Your Kidney Test Results handout. The nephrologist is discussing treatment options other than a kidney transplant. His eGFR is 18, which is close to kidney failure. The dietitian discussed diet requirements for dialysis. People should know the diet will change depending on the chosen option. His new goals include continuing sodium, potassium, and phosphorus restrictions; continue medications as prescribed, including calcium acetate with meals.
  • To summarize this section, treating inflammation or infection may help improve serum albumin levels. A serum albumin greater than four grams per deciliter at the time of initiation of dialysis is associated with reduced mortality. Blood pressure control, adequate protein, and calories are important too. A serum bicarbonate level greater than 22 may be beneficial in helping improve hypoalbuminemia. Nutrition interventions may include protein reduction. Animal proteins are a source of metabolic acids and eating less protein will reduce acid loads. The physician may prescribe certain medications to treat metabolic acidosis.
  • The next complication we'll discuss is metabolic acidosis, which is usually defined as serum bicarbonate level less than 22.
  • The prevalence of decreased serum bicarbonate increases as GFR declines. Nearly a quarter of patients with eGFR less than 30 have a serum bicarbonate less than 20.5.
  • The topics discussed in this segment include metabolic acidosis, its adverse effects, and interventions to treat metabolic acidosis.
  • Metabolic acidosis means excessive hydrogen ions are in the blood and results when acid production exceeds acid excretion. Increased hydrogen ions are buffered by plasma bicarbonate. Decreased plasma bicarbonate occurs when hydrogen ions are elevated. The reference range for serum bicarbonate is generally 21 through 28. Maintaining serum bicarbonate may be associated with slower progression of kidney disease as well as reduced malnutrition.
  • The kidney tubules play an important role in acid-base balance. The tubules reabsorb filtered bicarbonate and synthesize bicarbonate to neutralize the acid load. About 80 to 85 percent of filtered bicarbonate is reabsorbed in the proximal tubule. Patients with CKD have fewer functioning nephrons, less hydrogen ion is excreted, and the capacity to reabsorb and synthesize bicarbonate is reduced. As a result, chronic kidney disease may be associated with chronic metabolic acidosis.
  • Chronic metabolic acidosis is associated with accelerated muscle degradation, reduced albumin synthesis, exacerbation of metabolic bone disease, impaired glucose tolerance, and acceleration of CKD progression. It also may be associated with increased inflammation.
  • Animal protein may be a source of acid load. Fruits and vegetables are not sources of acid load. Serum bicarbonate levels may increase as dietary protein decreases.
  • Interventions to treat chronic metabolic acidosis include adequate, not excessive, intake of animal protein and the physician may prescribe a supplemental base, such as sodium bicarbonate. One 650 milligram tablet has 179 milligrams of sodium. Reemphasize dietary salt restriction when sodium bicarbonate is prescribed. Some people may need an additional diuretic to help remove the extra sodium.
  • You have seen this slide before. Joseph’s albumin level improved with weight loss, sodium restriction, and dental extractions. Treating low bicarbonate levels, that is treating acidosis, may have helped. His serum bicarbonate was 16.2 and increased to 18.5.
  • To summarize this section, a serum bicarbonate level less than 22 milliequivalents per liter may indicate metabolic acidosis, and animal protein intake may increase the acid load. Reducing protein intake may help increase serum bicarbonate level. A supplemental base may be prescribed. If sodium bicarbonate is added, review sodium and salt restriction. Improving serum bicarbonate may help improve serum albumin levels.
  • The next complication we're going to discuss is the mineral and bone disorders associated with chronic kidney disease, when the kidneys fail to maintain serum calcium and phosphorus levels.
  • We will discuss CKD bone disorders, vitamin D, phosphorus, calcium, PTH, and fibroblast growth factor 23. FGF-23 may be new to you but may become important clinically in the future.
  • As eGFR declines, the prevalence of hypocalcemia and hyperphosphatemia increase. Over 20 percent of patients with eGFR less than 30 have serum calcium less than 8.9 and over 30 percent have serum phosphorus greater than 4.7.
  • What are the chronic kidney disease bone disorders? These are systemic disorders of mineral and bone metabolism associated with chronic kidney disease. They are reflected in abnormalities in calcium, phosphorus, PTH and vitamin D metabolism. These derangements result in abnormalities in bone turnover, bone mineralization, bone volume, linear growth or strength. They may be associated with vascular or other soft tissue calcification.
  • Our friend Joseph has abnormalities in calcium and phosphorus associated with his progressive kidney disease.
  • The mineral and bone disorders in chronic kidney disease comprise a range of disorders. They include high bone turnover disease, also known as secondary hyperparathyroidism; low bone turnover disease, which includes adynamic bone disease, seen more frequently in diabetes and osteomalacia; and, finally, mixed bone disease, which has features of both high and low turnover.
  • It's very difficult to determine which of these kinds of bone disease a patient has in the absence of a bone biopsy.
  • There are several laboratory indicators of bone disease with which you should be familiar. These include serum levels of calcium and phosphorus, intact parathyroid hormone, and alkaline phosphatase. These measures vary depending on the type of bone disease. In secondary hyperparathyroidism, we generally see elevated calcium and phosphorus, PTH, and alkaline phosphatase. In adynamic bone disease, you may see normal or elevated calcium and phosphorus, and normal to low parathyroid hormone and alkaline phosphatase. In osteomalacia, you may see elevated calcium, normal or elevated phosphorus, PTH, and alkaline phosphatase.
  • We will now discuss 1,25-dihydroxy vitamin D, calcium, phosphorus, parathyroid hormone, and fibroblastic growth factor-23.
  • The kidneys activate vitamin D. At the top, you see 7-dehydrocholesterol on the left and vitamin D2 or ergocalciferol on the right. Both can be converted to vitamin D3. An enzyme in the liver converts vitamin D3 to 25-hydroxy vitamin D. An enzyme in the kidney converts 25-hydroxy vitamin D to 1,25-dihydroxy vitamin D.
  • Use 25-hydroxy vitamin D to assess vitamin D status. An adequate level is equal to or greater than 20 nanograms per milliliter. In November 2010, the Institute of Medicine changed the level considered as adequate for health from 30 to 20. An adequate level has not been established for CKD.
  • Active vitamin D, also known as calcitriol, helps maintain serum calcium levels by enhancing tubular calcium reabsorption. In the intestines, active vitamin D increases both calcium and phosphorus absorption. Vitamin D increases calcium deposition in the bone.
  • The parathyroid hormone helps maintain serum calcium levels. The parathyroid gland has calcium-sensing receptors and parathyroid hormone levels may increase in response to low serum calcium levels. This hormone stimulates the enzyme in the kidney tubules to increase the active vitamin D level and enhance calcium absorption. PTH may increase calcium resorption from the bone, potentially causing bone strength issues.
  • PTH reduces phosphorus reabsorption in the tubule and increases phosphorus excretion by the tubule. As a result, serum phosphorus may be within the normal range. PTH helps maintain serum calcium levels and indirectly helps maintain serum phosphorus levels.
  • Providers may assess intact PTH or iPTH level. The normal serum level of iPTH is thought to be less than 65 picograms per deciliter. Levels will vary by kidney function and type of bone disease. The assay for iPTH is not standardized and results may not be comparable from lab to lab.
  • The role of fibroblastic growth factor-23, or FGF-23, is under intense investigation. FGF-23 is thought to control serum phosphorus levels. FGF-23 is produced by bone in response to high serum phosphorus levels. FGF-23 inhibits the activation of vitamin D. Active vitamin D increases phosphorus absorption and lower levels result in a reduction in intestinal absorption of phosphorus. FGF-23 also reduces the reabsorption of phosphorus within the tubule and more phosphorus is excreted into the urine. Serum phosphorus may be within normal range until CKD is advanced. Serum phosphorus is reduced by the actions of PTH and FGF-23.
  • This is a very complex system of interactions. In the green arrow, you see active vitamin D increases both calcium and phosphorus absorption by the intestines, increases calcium deposition in the bone, and increases calcium reabsorption by the kidneys. Vitamin D helps maintain serum calcium levels and bone strength. PTH, shown within the gold arrow, helps maintain serum calcium levels. PTH stimulates the enzyme in the kidney that converts 25-hydroxy vitamin D to 1,25-dihydroxy vitamin D. Increased levels of active vitamin D in the intestines means an increase in calcium and phosphorus absorption. PTH increases calcium resorption from the bones. This means calcium may come out of the bone and move into the blood. Bone strength may be affected. Within the kidneys, PTH stimulates calcium reabsorption by the tubule and increases phosphorus excretion. PTH helps maintain serum calcium, and for some people, at the expense of the bone. FGF-23 shown in the maroon arrow is thought to control serum phosphorus. Levels may increase as serum phosphorus increases. FGF-23 is produced by the bone and may inhibit the enzyme that activates vitamin D. Lower levels of active vitamin D result in a reduction in phosphorus and calcium absorption by the intestines. High levels of serum phosphorus stimulate FGF-23 production by the bones. FGF-23 is thought to increase phosphorus excretion by the kidneys. Repleting vitamin D levels may help lower PTH levels.
  • You may have noticed Joseph’s corrected calcium levels have been included in the biochemical data within the assessments. The total calcium levels vary with the level of serum albumin, as calcium is bound to albumin. When someone has a serum albumin less than 4.0, we use a formula to correct calcium level. The formula is shown in the box. This formula is used when an ionized calcium level is not available.
  • Here is an example. Serum calcium is 8.0, shown in blue. Serum albumin is 3.0, shown in red font. The corrected calcium level is 8.8. Many of us are familiar with this correction. However, if you are not, the next activity is to use the formula to correct calcium.
  • Take a few minutes and do the math. Use the serum calcium and serum albumin level listed to calculate the corrected calcium. When you see hypoalbuminemia and a low serum calcium level, use the formula to assess corrected calcium.
  • Interventions for bone disease include dietary phosphorus restriction, adequate protein intake instead of excessive protein intake, phosphorus-binding medications, and vitamin D. Most protein-rich foods are also rich in phosphorus. If people reduce dietary protein, they reduce dietary phosphorus.
  • You heard this information before, but it is worth repeating. Phosphorus absorption varies based on the source. Limiting phosphorus food additives may be good place to start, as the phosphorus is absorbed at a much higher rate compared to phosphorus in whole foods. Phosphorus additives can be identified by reading the ingredient list for PHOS.
  • There are several calcium-based phosphorus binders; calcium carbonate is most commonly used. It is 40 percent elemental calcium, which means that a 1,250 milligram tablet will contain 500 milligrams of elemental calcium. Calcium acetate is 25 percent elemental calcium, so a 667 milligram capsule will contain 169 milligrams of elemental calcium. Calcium citrate is not recommended for phosphorus binding in CKD because of the risk for increasing aluminum absorption.
  • Other, non-calcium, containing phosphorus binders are commonly used in dialysis. These include sevelamer bicarbonate, which is a resin which may also reduce LDL cholesterol and increase bicarbonate level. However, it's quite expensive. Lanthanum carbonate is a rare earth metal and expensive. Aluminum hydroxide is a very effective phosphorus binder but is no longer widely used due to the potential of aluminum toxicity.
  • There are a range of vitamin D supplements available. In CKD, patients with low 25-hydroxy vitamin D levels may receive ergocalciferol or cholecalciferol. Patients with end-stage renal disease are more likely to receive active vitamin D including calcitriol. They also may receive one of the vitamin D analogues including alfacalcidol, doxercalciferol or paricalcitol.
  • Bone disease in people with CKD is complex, and interpreting the lab results is difficult. There are observational data supporting correction of the metabolic abnormalities but a shortage of high quality evidence supporting intervention. As was discussed earlier, it may be important to look at a corrected calcium which compensates for changes in serum albumin. Phosphorus restriction may be implemented while trying to maintain adequate protein intake. Phosphorus binding medications are generally prescribed with meals in order to prevent absorption of phosphorus. As mentioned earlier, patients who have low 25-hydroxy vitamin D levels may receive ergocalciferol or cholecalciferol. Patients with elevated PTH may be managed with vitamin D and phosphorus restriction.
  • Correcting serum calcium for Joseph's depressed albumin level places his calcium in the low normal range rather than the hypocalcemic range.
  • Joseph received vitamin D, and as this was administered, his PTH gradually decreased over time.
  • However, the supplemental vitamin D was associated with increased phosphorus absorption and an elevation in his serum phosphorus.
  • Active vitamin D increases the risk for hypercalcemia and hyperphosphatemia. Vitamin D may lower PTH but at the same time may increase calcium absorption. Vitamin D may need to be discontinued due to hypercalcemia. It may also increase phosphate absorption, and may need to be discontinued due to hyperphosphatemia.
  • Bone disease is a complex complication of CKD. The types include high turnover, low turnover, and mixed bone diseases. Vitamin D and PTH levels are inversely related to each other. Phosphorus restriction and phosphorus-binding medication may be beneficial.
  • A brief review of module content may be helpful. Complications may increase in frequency and severity as kidney function declines. People may become anemic due to inadequate levels of the hormone erythropoietin. Monitor hemoglobin levels. Assess iron status prior to use of iron supplements. Supplemental iron is available in oral or parenteral formulations. Oral iron is used frequently in CKD and has numerous side effects making adherence problematic. An injectable form of recombinant erythropoietin is available and is more commonly used in dialysis patients. Iron supplements should be taken between meals and phosphorus-binding medication should be taken with meals. Serum potassium levels may increase as eGFR decreases. Dietary intake, medications that block the renin-angiotensin-aldosterone system such as ACE inhibitors and ARBS, transcellular shifts, and lack of insulin all affect serum potassium levels. Restrict dietary potassium when the serum level is elevated. The level of the eGFR does not determine the need for a potassium restriction.
  • Hypoalbuminemia in CKD is multi-factorial. Hypoalbuminemia is used as a marker of nutritional status and may reflect inflammation. People who begin dialysis with an albumin greater than 4.0 have a lower risk of mortality. Treating metabolic acidosis may improve serum albumin levels. Treating infections, such as diabetic foot ulcer or removing an infected tooth, may reduce inflammation and improve serum albumin levels. Maintaining serum bicarbonate level above 22 milliequivalents per liter may be beneficial. A low level is considered metabolic acidosis. Animal protein may be a source of metabolic acid and reducing protein intake reduces acid load. The physician may prescribe sodium bicarbonate to help increase serum bicarbonate levels. Review information about sodium when this medication is prescribed.
  • We just discussed mineral and bone disorders. The kidneys activate vitamin D. As kidney function declines, a cascade of reactions may occur that result in mineral and bone disorders. Vitamin D, parathyroid hormone, FGF-23, calcium, and phosphorus are involved. Although not shown on this slide, multiple medications may be taken at different times of the day, making self-management more challenging. Medications may include 3 or more blood pressure medications, diabetes medications, iron supplements between meals, phosphorus binders with meals, sodium bicarbonate, weekly vitamin D, medications to treat dyslipidemia, hypothyroidism, and other medications as indicated. Please keep this in mind as you work with people with CKD.
  • At the beginning of the module we asked you to download and print Your Kidney Test Results. Use this as a guide to help you keep track of the data used to monitor kidney function and CKD complications. Does your lab automatically report estimated glomerular filtration rates, or do you need to use the GFR calculator? Do you have access to a urine albumin-to-creatinine ratio to assess kidney damage? Do you have access to the other labs used to assess and monitor the numerous complications? You may need to look beyond the ABCs for diabetes. Diabetes is the leading cause of kidney failure. This handout was designed to be used with patients by all health care professionals to help the CKD patient keep track of their lab values not only when at a visit with the dietitian. This reinforcement by multiple providers at multiple visits helps them understand their CKD better. Help to introduce it to all providers you work with. Many people are interested in their laboratory results. Keep in mind, not every lab result is discussed at every visit. If a level is high or low, start with that one. Help your patients become familiar with the language of kidney disease.
  • The National Kidney Disease Education Program has another resource that may be of interest to you. The Chronic Kidney Disease (CKD) and Diet: Assessment, Management and Treatment overview guide was developed specifically for dietitians. Keep this one in mind as you work with kidney disease patients. You may not see kidney disease patients every day and much of the information discussed here is included in the guide. 4-15 version of Module 3
  • Consider how overwhelmed the person with CKD may feel. They learn they have a chronic disease that may result in kidney failure. Ideally, information is shared over time.
  • This continuing education opportunity was developed in partnership with 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.

CKD MNT Module 3: Complications CKD MNT Module 3: Complications Presentation Transcript

  • Module 3: Complications Complications May Increase as Kidney Function Declines
  • 1. Use laboratory parameters to assess anemia in chronic kidney disease (CKD) 2. Associate increased risk for hyperkalemia with hyperglycemia and metabolic acidosis in CKD 3. Use and interpret laboratory parameters to assess hypoalbuminemia in CKD 4. Use and interpret laboratory parameters to assess metabolic acidosis in CKD 5. Use and interpret laboratory parameters to assess CKD bone disorders Participants will be able to:
  •  Fewer functioning nephrons may mean: − Inadequate erythropoietin (anemia) − Accumulation of potassium (K) − Accumulation of hydrogen ion (metabolic acidosis) − Inadequate activation of vitamin D (bone disease) − Accumulation of phosphorus (P) − Accumulation of pro-inflammatory cytokines  Toxins build up in the blood. Complications increase as kidney function declines
  • Complications may increase as estimated glomerular filtration rate (eGFR) decreases Reference: Adapted from USRDS 2010 Annual Data Report (NIDDK, 2010)
  •  Joseph is a 40-year-old man with numerous medical issues, including morbid obesity and type 2 diabetes.  His eGFR is 21 mL/min/1.73 m2 at initial visit.  His urine protein-to-creatinine ratio (Up/Uc) is 6.6 grams/day. Let’s meet Joseph
  • Date Weight (lb) Blood pressure A1C Urine protein/urine creatinine (g/day) 2/16 310 140/82 10.5 6.6 4/6 306 128/80 9.0 5/20 299 135/80 8.0 5.6 6/22 296 128/83 7/29 293 127/80 7.7 3.0 Test Reference 2/16 4/6 6/22 7/29 WBC 4.8-10.8 10.6 10.2 12.6 H 11.8 H RBC 4.7-6.1 3.83 L 3.7 L 3.82 L 3.93 L HGB 14-18 10.5 L 10.3 L 10.6 L 10.9 L HCT 42-52 30.3 L 29.9 L 30.8 L 31.6 L MCV 80-94 80.6 80.9 80.7 80.2 MCH 28-32 27.8 L 27.9 L 27.8 L 27.8 L MCHC 32-36 34.6 34.5 34.5 34.6 RDW 11.5-14.5 14.5 14.8 H 14.6 H 15.1 H PLT 140-440 398 335 332 377 Joseph: The man with many complications
  • Joseph: The man with many complications Test Reference 2/16 4/6 5/20 6/22 7/29 Glucose 70. -100 301 174 H 103 H 174 H 157 H BUN 7-18 72 H 58 H 69 H 88 H 87 H Creatinine 0.8-1.3 3.5 H 3.4 H 3.5 H 4.0 H 4.6 H eGFR > 60 21 22 21 18 15 Sodium 135-145 136 140 139 136 138 Potassium 3.5- 5.0 5.0 4.7 5.3 H 5.5 H 4.9 Chloride 101-111 108 110 111 104 108 CO2 21-32 20.2 L 23.8 18.0 L 16.2 L 18.5 L Phosphorus 2.5-4.9 4.8 4.2 5.2 H 5.3 H Calcium 8.5-10.0 7.4 L 8.3 L 8.1 L 8.0 L 8.1 L Albumin 3.5-5.0 3.1 L 3.0 L 3.2 L 3.3 L 3.5 Cholesterol 0-200 155 - - - - Triglyceride 30-200 214 - - - - HDL 35 26 - - - - LDL 0-170 86.2 - - - -
  •  Anemia  Hyperkalemia  Hypoalbuminemia − Marker for malnutrition and/or inflammation  Metabolic acidosis  Mineral and bone disorders Topics
  • You may want to download this PDF to use with this module. Reference: http://www.nkdep.nih.gov/resources/nkdep-kidney-test-results-508.pdf
  • ANEMIA Anemia may start early in the course of CKD due to inadequate erythropoietin synthesis
  • Anemia may develop as eGFR declines Reference: Adapted from USRDS Annual Data Report (NIDDK, 2009)
  •  Anemia may develop as a result of inadequate erythropoietin synthesis.  May develop early and worsens as CKD progresses.  May develop earlier in people with diabetes.  May involve inadequate iron intake or impaired iron absorption as well. Anemia is a complication of CKD
  • Joseph’s anemia worsened as eGFR declined; treatment improved Hgb levels
  •  Decreased responsiveness to erythropoietin  Uremia  Chronic inflammation  Severe hyperparathyroidism  Folate deficiency Additional factors for anemia in CKD
  • Observational data show association with:  Coronary artery disease  Hospitalization for cardiac disease  Death from congestive heart failure  All-cause mortality  Left ventricular hypertrophy Anemia in CKD is associated with morbidity and mortality Reference: Toto. Kidney Int 2003; 64(suppl 87):S20–S23.
  •  Renal tissue hypoxia triggers erythropoietin production.  Erythropoietin stimulates erythrocyte (red blood cell) synthesis in bone marrow.  Hemoglobin is the primary iron-containing protein in erythrocytes that transports and delivers oxygen to tissues.  Both erythropoietin and iron are required to produce hemoglobin (Hgb) and correct hypoxia. Kidneys act as oxygen sensors in the body
  • Iron transport and storage Reference: http://www.cdc.gov/ncbddd/hemochromatosis/training/pathophysiology/iron_cycle_popup.htm
  •  Increased absorption with: − Decreased iron stores (ferritin) − Increased erythropoiesis − Anemia (low hemoglobin) − Hypoxia − Absence of inflammatory cytokines  Reduced absorption with: − Inflammation or infection Many factors influence iron absorption
  •  Both a spontaneous decrease in intake and aversion to foods with protein may occur as eGFR declines.  Hepcidin may accumulate in CKD. − Hepcidin is the hormone that controls iron levels. − This hormone regulates iron absorption in the gut and mobilization of stored iron.  Inflammation may reduce absorption of iron. Additional factors for inadequate iron in CKD References: Kopple et al. Kidney Int 2000; 57(4):1688–1703; Young et al. Clin J Am Soc Nephrol 2009;4(8):1384–1387.
  •  Serum iron − Measures ferric iron (Fe+3 ) − Decreases with iron deficiency and inflammation  Total iron-binding capacity (TIBC) − TIBC measures serum transferrin after saturation of all available binding sites with iron.  Tends to be increased with iron deficiency  Tends to be decreased with chronic inflammation − More than 400 µg/dL indicates storage iron depletion. Assessing iron status Reference: http://www.cdc.gov/nutritionreport/report.html
  •  Transferrin saturation (TSAT) − Transferrin transports iron − Ratio of serum iron/TIBC x 100 = TSAT − Early functional iron deficiency: < 16% may indicate iron-deficiency anemia in general population (IOM)  Ferritin − Storage iron − Acute phase reactant (↑acute & chronic inflammation) − Depleted stores: < 12 ng/mL may indicate iron depletion in general population (Institute of Medicine) Assessing iron status Reference: http://www.cdc.gov/nutritionreport/pdf/nutrition_report.pdf
  •  Complete blood count (CBC) − Hemoglobin (Hgb)  Iron indices − Transferrin saturation  Iron available for erythropoiesis − Ferritin  Storage iron  Anemia of CKD is usually normochromic and normocytic. Laboratory assessment for anemia in CKD
  •  Iron supplementation − Oral − Intravenous (parenteral)  Possible oxidant  Erythropoiesis-stimulating agents (ESAs) − Injectable Possible interventions to treat anemia in CKD
  •  A 325 mg dose of: − Ferrous fumarate has 108 mg elemental iron. − Ferrous sulfate has 65 mg elemental iron. − Ferrous gluconate has 35 mg elemental iron.  Absorption: Ferrous+2 iron > ferric+3 iron Amount of elemental iron differs between oral iron supplements Reference: http://www.anemia.org A Physician’s Guide to Oral Iron Supplementation. Nov 2008.
  •  Food reduces iron absorption by 40–66%.  Amount absorbed decreases as dose increases.  Multiple doses may be needed.  CDC recommends 50–60 mg elemental iron twice daily for nonpregnant adults.  Fewer side effects occur with extended release forms, but less is absorbed. Oral iron supplements are poorly absorbed Reference: http://www.anemia.org A Physician’s Guide to Oral Iron Supplementation. Nov 2008.
  •  More than 25% of people experience side effects: − Nausea − Vomiting − Constipation − Diarrhea − Dark-colored stools − Abdominal distress  About 20% of people discontinue supplements due to side effects. Oral iron supplements have gastrointestinal side effects Reference: http://www.anemia.org A Physician’s Guide to Oral Iron Supplementation. Nov 2008.
  • Tips on oral iron supplements Reference: http://www.anemia.org A Physician’s Guide to Oral Iron Supplementation. Nov 2008.
  •  Calcium supplements may be prescribed with meals to bind dietary phosphorus. − Calcium may interfere with iron absorption.  Indications of when to take iron supplements: − Iron absorption is increased when supplement is taken between meals and separate from phosphate binders. − If person is already taking multiple medications, supplement increases complexity of regimen. Take iron supplement separate from calcium-based phosphate binders
  •  Free iron is toxic.  Parenteral iron is transported on iron-carbohydrate complexes: − Dextran (may increase risk of anaphylaxis) − Sucrose − Gluconate − Oligosaccharide  Carbohydrates may “shield” body from oxidation, allowing safe delivery of the iron. Parenteral iron may be used, more common in dialysis Reference: Zager, Clin J Am Soc Nephrol 2006; 1(suppl 1):S24–S31.
  •  Iron is a potent oxidant.  Parenteral iron may injure renal tubules.  Iron may increase risk of infection.  Parenteral iron may suppress phagocytosis of bacteria. Risks with parenteral iron References: Zager et al. Kidney Int 2004; 66(1):144–156; Zager, Clin J Am Soc Nephrol 2006; 1(suppl 1):S24–S31; Hörl, J Am Soc Nephrol 2007; 18(2):382–393.
  •  Genetically engineered forms of erythropoietin  Injectable medication  Approved in 1989 to treat anemia in end-stage renal disease (ESRD)  Must advise patient of risks and benefits Erythropoiesis-stimulating agents (ESAs) are available Reference: http://www.fda.gov/drugs/drugsafety/postmarketdrugsafetyinformationforpatientsandproviders/ucm200297.htm
  •  Therapy may include ESAs to increase red blood cell production and prevent need for transfusion. ESAs may be beneficial, although their exact role is still being defined.  FDA black box warning for ESAs was released as a result of recent trials which showed an increased risk for stroke, blood clot, heart attack, and death when ESAs were prescribed to achieve higher Hgb goals (> 12 g/dL).  FDA requires a Medication Guide explaining the risks and benefits of ESAs be provided to all patients receiving ESAs. Treating the anemia of CKD with ESAs
  •  40-year-old male with DM 2 since 1997  His eGFR is 21 at initial visit  Severe kidney damage − Heavy proteinuria  Urine protein/urine creatinine ratio = 6.6 g/day  All protein lost in the urine, not just albumin  Morbidly obese − BMI 45.8 (initial), height 69” − Going to weight-loss classes at endocrinologist’s office  Referred due to history of hyperkalemia − Instructed at nephrologist’s office on potassium restriction Joseph is trying to lose weight to get on kidney transplant list, wants to walk more
  • Food and beverage intake Two meals/day. Working on eating lower potassium foods. Breakfast: 3 eggs, 1–2 slices dry toast, sugar-free beverage. Supper: fast foods. Cut out iced tea, added regular lemon-lime pop or diet cola. Eating more rice, noodles, and fewer potatoes. Snacks on salted jerky or corn chips. Medications FeSO4 325 mg BID ordered, not taking, on “too many medications”; lisinopril 80 mg, knows this makes potassium higher. Endocrinologist stopped pioglitazone and glyburide; now 50 units glargine at bedtime. Reports postprandials < 150, were 200–300. Started 0.25 mcg calcitriol last month. Diet order/ experience 1,700–2,000 Kcal, 96 g protein (per endocrinologist where he attends weight-loss classes); potassium restriction instruction at nephrologist’s office. No sodium restriction per patient and wife. Physical activity Played football in high school. Not active now. Lives at high altitude. Short of breath when walked down hall to office. Very fatigued, wants to walk more. Height & weight Height 69”, weight 310#, down 25 # since Sept. BMI = 45.8. Assessment (2/16)
  • Biochemical data eGFR 21, Up/Uc 6.6, K 5.0, Hgb 10.5, TSAT 19, ferritin 134. A1C 10.5. 25(OH)D 9, intact parathyroid hormone (iPTH) 207, Ca 7.4 (corrected 8.1), P 4.8, Alb 3.1. Personal history 40-year-old male, studying criminology at the university. No tobacco or alcohol use. Patient history Patient’s chief nutrition complaint: “Miserable” due to too few calories in current diet. Dislikes limiting potassium. DM 2 for over 13 years. Blood pressure 142/80 today. Social history Wife is trying to lose weight too. Both attend university; up late with homework. Easier to grab fast food. Wife is struggling with potassium restriction; she tries to eat what he eats. Assessment (2/16) Continued
  •  Inadequate iron intake is related to non- adherence to iron supplementation, as evidenced by not taking FeSO4 and TSAT level.  Nutrition-related knowledge deficit is related to lack of knowledge about need for sodium restriction evidenced by fast food intake, salted snacks. Diagnoses
  •  Nutrition education: Role of kidney disease in anemia; why treating anemia may help with ability to exercise for weight loss; need for FeSO4; may be prescribed ESAs in the future; role of sodium in controlling blood pressure and CKD. Gave him NKDEP’s Sodium handout and used Your Kidney Test Results to show lab results.  Goal: Take 325 mg FeSO4 with breakfast and supper as prescribed. Begin reading Nutrition Facts for sodium information. Choose foods with less sodium. Collaborate with other providers in regard to his CKD. Intervention
  • Joseph developed anemia; he was treated with oral iron and ESAs Iron Studies Reference Anemia 2/16 5/22 % Sat > 20% < 16% 19 20 Ferritin 80–270 mcg/L < 12 mcg/L 134 134
  •  Monitor hemoglobin levels (CBC)  Assess iron status prior to use of supplements − Transferrin saturation − Ferritin  May need iron supplementation − May be most effective between meals  May receive ESAs  May receive parenteral iron Summary: Anemia of CKD
  • HYPERKALEMIA Potassium excretion is regulated by the renin-angiotensin- aldosterone system
  • Serum potassium may increase as eGFR decreases Reference: Adapted from USRDS Annual Data Report (NIDDK, 2009)
  •  Potassium balance − Transcellular shifts  Hyperkalemia − Serum K ≥ 5.0 mEq/L − Interventions Topics
  • Joseph’s diet and medications play a role in his hyperkalemia, but it’s not the entire story
  • Serum potassium levels affect muscle functioning  Hypokalemia − Cardiac arrhythmias − Muscle weakness − Glucose intolerance  Hyperkalemia − Cardiac arrhythmias − Muscle weakness
  •  The reference range for serum potassium level is 3.5–5.0 mEq/L.  Susceptibility to hyperkalemia depends on calcium level and other factors determining transmembrane potential.  Cardiac arrhythmias and cardiac arrest are possible if severe hyperkalemia is not recognized and treated. Hyperkalemia is potentially life threatening
  •  About 85% of dietary potassium is absorbed.  Proximal tubules reabsorb 70–80% of K.  Potassium secretion occurs in distal tubule and collecting duct and may be an “adaptation” to high intake.  A small amount may be excreted in the feces. Potassium balance involves the kidneys Reference: Gennari & Segal, Kidney Int 2002; 62(1):1–9.
  •  Activation of RAAS increases potassium excretion via aldosterone.  Medications that inhibit RAAS increase risk for hyperkalemia. Renin-angiotensin-aldosterone system (RAAS) affects potassium excretion
  •  98% of potassium is intracellular. − 75% in muscles  2% is extracellular (65–70 mEq).  Transcellular electrical potential generated by sodium-potassium exchange is responsible for voltage gradient across cell membranes.  Gradient difference is needed for muscle and nerve function. K shifts between intracellular and extracellular compartments
  •  Insulin concentration and hyperglycemia − Insulin moves potassium into cells. − Insulin deficiency may lead to hyperkalemia.  Acid-base status − Metabolic acidosis (excessive hydrogen ion in plasma) may drive potassium out of cells, as hydrogen ion is buffered intracellularly. Factors affecting potassium shifts between compartments
  •  Control hyperglycemia with adequate insulin. − Potassium follows glucose into the cells.  Treating acidosis may lower serum potassium. − Treatment may allow continued use of blood pressure medications that help lower urine albumin. − Dietary protein may play a role here. Treating hyperglycemia and acidemia may lower serum potassium Reference: Palmer, N Engl J Med 2004; 351(6):585–592
  •  Impaired K excretion − ACEi − ARBs − K+ -sparing diuretics − Nonsteroidal anti-inflammatory drugs − Tacrolimus or cyclosporine (anti-rejection medication for transplant) Medication-induced hyperkalemia is a concern in CKD
  •  Specific level of eGFR does not determine need for potassium restriction.  Restrict dietary potassium to help achieve and maintain safe level.  Level of potassium restriction should be individualized. Potassium restriction is not indicated in the absence of hyperkalemia
  •  Metabolic acidosis may result in K moving out of the cells to maintain electroneutrality.  His nephrologist changed medications: − Stopped the angiotensin-converting enzyme inhibitor (ACEi), and is trying an angiotensin receptor blocker (ARB) − Added loop diuretic − Added sodium bicarbonate as base to treat the low serum bicarbonate Joseph’s potassium may be elevated due to transcellular shifts
  • Treating metabolic acidosis may have helped lower Joseph’s serum potassium
  • Food/beverage intake Still eating 3 eggs, 1–2 slices of dry white toast. Added “small” lunch―regular burger, apple. Dinner: green beans, rice, small piece of meat. Fewer fast foods and salted snacks. Drinking diet beverage with potassium acesulfame in office. Diet experience Using recipes from cooking classes. Still hard to follow K restriction. Very happy weight < 300#. Wife is helping with Na restriction. Physical activity Walking 10–15 minutes/day with wife; less shortness of breath Height & weight Height 69”, weight 296# Biochemical data eGFR 18 (stable), Up/Ucr 5.6 (↓), K 5.5 (↑), CO2 16.2 (↓), Hgb 10.6 (improved), iron studies next month. Ca 8.0 (corrected 8.5), P 5.2. Vitamin D and intact parathyroid hormone (iPTH) drawn today. Patient history Darbopoeitin injections continue. Saw nephrologist last week. Lisinopril discontinued; added losartan 50 mg, furosemide 80 mg and sodium bicarbonate 650 mg BID. Blood pressure 138/85 today. Has dental appointment tomorrow for tooth extraction. Reassessment (6/30) Met goals: Taking FeSO4 BID. No GI upset. Feels less fatigue, trying to walk more. Iron studies pending. Choosing foods with less sodium.
  •  Altered nutrition-related laboratory value: elevated K due to reduced renal excretion, medication, and acidosis.  Decreased need for dietary phosphorus related to reduced renal excretion and enhanced absorption with use of active vitamin D (calcitriol) evidenced by elevated serum level. Diagnosis
  •  Used Your Kidney Test Results to show improved hemoglobin.  Reviewed dietary potassium; sodium bicarbonate may help lower serum level.  Started discussing phosphorus, binders and calcitriol.  Gave him Phosphorus and How to Read a Food Label handouts. Goals: Read ingredient lists for added phosphorus and potassium. Choose foods without added P and K. Take new medications as prescribed. Intervention: Nutrition education
  • HYPOALBUMINEMIA Serum albumin is a marker for nutritional status and inflammation
  •  Serum albumin  Hypoalbuminemia − Inflammation − Poor oral intake  Metabolic acidosis and hypoalbuminemia Topics
  • Joseph’s hypoalbuminemia improved with various interventions
  •  Very little albumin crosses glomerular basement membrane normally.  Most is reabsorbed by the tubule.  Damaged kidneys allow albumin to cross the filtration barrier into the urine.  The level of albumin in the urine may exceed tubule’s capacity to reabsorb the protein. Review: Renal handling of albumin
  •  Maintains oncotic pressure and blood volume  Acts as buffer  Binds (some examples): − Calcium, magnesium − Hormones − Vitamins (e.g., A, riboflavin, B6, C, and folate) − Medications (e.g., furosemide)  Serum albumin is a marker for nutritional status and inflammation Serum albumin
  •  Serum albumin ≥ 4.0 g/dL at initiation of dialysis is associated with reduced mortality risk.  Only 11% of new dialysis patients had serum albumin ≥ 4.0 g/dL (1999–2005). Serum albumin level at dialysis initiation is an independent risk factor for mortality Reference: Adapted from Kaysen et al. J Renal Nutr 2008; 18(4):323–331.
  •  Inflammation − Acute or chronic, e.g., foot ulcer, infected tooth  Albuminuria  Metabolic acidosis  Insulin resistance  Spontaneous decrease in intake in CKD, particularly for foods high in protein Hypoalbuminemia in CKD is multifactorial
  • Low serum albumin in CKD is associated with inflammation Reference: Eustace et al. Kidney Int 2004; 65(3):1031–1040.
  • Joseph’s weight loss and lower sodium intake may have helped improve albumin
  • Dental extraction and treating metabolic acidosis may have helped improve Joseph’s albumin
  • Reassessment (7/29) Met goal: Reading labels for phosphorus and potassium. Dislikes diuretic, plans when to take; if he has class, takes later in the day. Note: Improved fluid balance with diuretic also may have affected albumin level. Diet experience Feeling more confident with sodium, potassium, and calorie restrictions. Surprised about all the added phosphorus in foods. Medications Nephrologist added calcium acetate 667 mg with meals 2 weeks ago. Glad he knew why he had to take it. Physical activity Not walking as often (summer term). Height & weight Height 69”, weight 293#, down 3# since last month. Labs eGFR 18 (stable), K 4.9 (improved), CO2 18.5 (low but improved), P 5.3 (↑), Ca 8.1, (corrected 8.5), 25(OH)D 25, iPTH 130; Alb 3.5, was 3.3 last month. Patient history Dentist extracted 2 teeth last month, no problems chewing. Blood pressure 136/85. Tearful when discussing eGFR, possible need for dialysis before getting on transplant list. Still not ready to make decision about dialysis option.
  •  Altered nutrient-related laboratory value: Elevated phosphorus; just started phosphorus- binding medication 2 weeks ago. NCP diagnosis
  •  Nutrition education: Used Your Kidney Test Results to re-explain why nephrologist is discussing dialysis options. Discussed diet requirements for different treatment options. Goals: Continue sodium, potassium, phosphorus restrictions. Continue medications as prescribed, including calcium acetate with meals (phosphorus binder). Intervention
  •  Reduce inflammation, treat infections  Serum albumin ≥ 4.0 g/dL at initiation of dialysis associated with lower risk of mortality  Control blood pressure to slow progression  Provide adequate protein and calories  Treat metabolic acidosis − Eating less protein may reduce acid load. − Physician may prescribe medication to treat. Summary: Hypoalbuminemia in CKD
  • METABOLIC ACIDOSIS A serum bicarbonate level < 22 mEq/L may indicate metabolic acidosis
  • Serum bicarbonate may decrease as eGFR decreases Reference: Adapted from USRDS Annual Data Report (NIDDK, 2009)
  •  Metabolic acidosis (chronic)  Possible adverse effects of metabolic acidosis  Interventions Topics
  •  Acid production exceeds acid loss  CO2 + H2O HCO3 + H+  The reference range for serum HCO3 is 21–28 mEq/L.  Maintaining normal serum HCO3 may be beneficial. Metabolic acidosis = excessive hydrogen ions in the blood
  •  Tubules reabsorb filtered HCO3 and synthesize HCO3 to neutralize acid load. − About 80–85% is reabsorbed within the proximal tubules.  Patients with CKD have fewer functioning nephrons. − Less hydrogen ion (acid) is excreted. − Capacity to reabsorb and synthesize HCO3 is reduced. − Condition may lead to chronic metabolic acidosis. Kidney tubules help maintain normal acid-base balance
  •  Accelerates muscle degradation  Reduces albumin synthesis  Exacerbates pre-existing bone disease  May impair glucose tolerance due to interference with insulin actions  May accelerate CKD progression  May stimulate inflammation Chronic metabolic acidosis
  •  Endogenous acid production correlates to animal protein intake, primarily due to the catabolism of sulfur-containing amino acids.  Fruit and vegetables are not sources of acid load.  Reducing dietary protein may result in increasing bicarbonate levels. Animal protein may be a source of acid load References: Remer & Manz, J Am Diet Assoc 1995; 95(7):791–797; Gennari et al. Clin J Am Soc Nephrol 2006; 1(1):52–57
  •  Adequate, not excessive, intake of animal protein  Supplemental base may be prescribed to balance the acid  Sodium bicarbonate may be prescribed, 650 mg tablet has 179 mg sodium  Re-emphasize dietary salt restriction, if used  May require higher dose of diuretic Interventions for chronic metabolic acidosis Reference: Kraut & Madias, Nat Rev Nephrol 2010; 6(5):274–285
  • Treating metabolic acidosis may have helped improve Joseph’s albumin
  •  Serum bicarbonate (HCO3) level < 22 mEq/L may indicate metabolic acidosis.  Animal protein may increase acid load.  Reducing protein may increase serum HCO3.  Supplemental base may be prescribed to treat. Sodium bicarbonate will increase sodium intake. Review salt restriction, if prescribed.  Treatment may improve serum albumin levels. Summary: Metabolic acidosis
  • CKD MINERAL AND BONE DISORDERS Kidneys fail to maintain serum calcium and phosphorus levels
  •  CKD bone disorders  Vitamin D  Phosphorus  Calcium  Parathyroid hormone (PTH)  Fibroblastic growth factor-23 (FGF-23) Topics
  • Lower serum calcium, higher serum phosphorus may be seen as eGFR declines Reference: Adapted from USRDS Annual Data Report (NIDDK, 2009)
  •  Systemic disorder of mineral and bone metabolism due to CKD is identified by: − Abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism − Abnormalities in bone turnover, mineralization, volume, linear growth, or strength − Vascular or other soft-tissue calcification CKD mineral and bone disorders Reference: Kidney International (suppl 113), 2009
  • Joseph’s kidneys failed to maintain serum calcium and phosphorus levels
  •  High bone turnover disease − Also known as secondary hyperparathyroidism  Low bone turnover disease − Adynamic  May be seen more frequently with diabetes − Osteomalacia  Mixed bone disease − Features of both high and low types A range of bone disorders occur in CKD
  • Bone biopsy is the gold standard for diagnosing bone disease in CKD
  •  Serum levels of calcium, phosphorus, intact parathyroid hormone (iPTH), and alkaline phosphatase (alk phos) vary by type of bone disease. − Secondary hyperparathyroidism may see:  Elevated Ca, P, iPTH, alk phos − Adynamic bone disease may see:  Normal or elevated Ca and P; normal to low iPTH and alk phos − Osteomalacia may see:  Elevated Ca; normal or elevated P, iPTH, alk phos Laboratory indicators in bone disease Reference: Martin & Gozalez, J Am Soc Nephrol 2007; 18(3):875–885.
  •  1,25(OH)2 D  Calcium  Phosphorus  Parathyroid hormone (PTH)  Fibroblastic growth factor-23 (FGF-23) Bone disease results from complex interactions
  • 7-dehydrocholesterol D2 Ergocalciferol (plants) D3 Cholecalciferol (animals) Ultraviolet B D3 Liver 25(OH)D Kidneys 1,25(OH)2 D (Calcitriol) 1-alpha-hydroxylase 25-hydroxylase Major form in circulation, used to assess status The kidneys activate vitamin D
  •  The major circulating form of vitamin D is 25(OH)D.  The “adequate” level is > 20 ng/mL (> 50 nmol/L).  Levels for CKD have not been established. 25(OH)D is used to assess vitamin D status Reference: Institute of Medicine (November 2010)
  •  Kidneys − 1-alpha-hydroxylase enzyme in tubules stimulates conversion of 25(OH)D to 1,25 (OH)2 D − 1,25 (OH)2 D enhances tubular calcium reabsorption  Intestines − 1,25 (OH)2 D increases calcium absorption and increases phosphorus absorption  Bone formation − 1,25 (OH)2 D increases calcium deposition Calcitriol helps maintain serum calcium levels
  •  Calcium-sensing receptors are located in the parathyroid gland.  Low serum calcium stimulates PTH secretion from the parathyroid.  PTH stimulates the 1-alpha-hydroxylase enzyme in the tubule increasing 1,25(OH)2D which enhances calcium absorption.  PTH increases calcium resorption from bone. Parathyroid hormone helps maintain serum calcium levels
  •  PTH reduces phosphorus reabsorption and increases phosphorus excretion by tubule.  Serum phosphorus may remain in the normal range as a result of higher PTH levels. PTH stimulates phosphorus excretion
  •  Normal serum level is thought to be < 65 pg/dL.  Levels vary by kidney function and type of bone disease.  iPTH is not standardized, and levels may not be comparable. Intact PTH (iPTH) may be used to monitor PTH levels Reference: Martin & Gozalez, J Am Soc Nephrol 2007; 18(3):875–885.
  •  FGF-23 is produced by bone osteoclasts and osteoblasts and is stimulated by high serum phosphorus levels.  FGF-23 inhibits 1,25(OH)2D formation, which decreases intestinal P absorption.  FGF-23 increases urinary phosphorus excretion.  Serum phosphorus is within “normal range.” FGF-23 may maintain serum phosphorus levels Reference: Ramon et al. Eur J Endocrinol 2010; 162(1):1–10.
  • CKD-MBD: Complex interactions involving numerous systems
  •  Normal serum level: 8.5–10.2 mg/dL  40% transported on albumin  If hypoalbuminemia, use corrected calcium Corrected calcium (mg/dL) = serum calcium (mg/d) + 0.8(4.0 – serum albumin g/dL) Correct calcium for albumin level Reference: http://www.mdcalc.com/calcium-correction-for-hypoalbuminemia
  •  Serum Ca 8.0  Serum albumin 3.0 Corrected calcium (mg/dL) = serum calcium (mg/dL) + 0.8(4.0 – serum albumin g/dL) Corrected calcium = 8.0 + 0.8 (4.0 – 3.0) = 8.8 Example of calculation to correct calcium
  • Activity: Corrected calcium Serum calcium Serum albumin Corrected calcium 7.4 2.3 - 8.1 2.9 - 8.3 3.0 - Corrected calcium (mg/dL) = serum calcium (mg/dL) + 0.8(4.0 – serum albumin g/dL)
  •  Phosphorus restriction  Adequate, not excessive protein  Phosphorus-binding medication − Usually calcium-based salts in CKD  Vitamin D (CKD) and vitamin D analogs Interventions for bone disease in CKD
  •  Phosphorus absorption differs between food sources. − Food additives > animal sources > plant sources  Reducing dietary protein reduces phosphorus.  Phosphorus food additives can be identified by reading ingredient list for phosphorus. − Limit or avoid these foods.  Phosphorus in plants is not well absorbed due to phytates (last ones to limit). Dietary phosphorus restriction may be beneficial
  •  Calcium carbonate − 40% elemental calcium − 1,250 mg tablet = 500 mg elemental calcium  Calcium acetate − 25% elemental calcium − 667 mg capsule = 169 mg elemental calcium  Calcium citrate − NOT RECOMMENDED for CKD because of risk for increased aluminum absorption. Calcium-based phosphorus binders
  •  Sevalemer bicarbonate − Resin − May also help lower low-density lipoprotein (LDL), increase HCO3 level − Expensive  Lanthanum carbonate − Rare earth metal − Expensive  Aluminum hydroxide − Not recommended, used rarely Other phosphorus binders are commonly used in dialysis
  •  CKD − Ergocalciferol  50,000 IU weekly − Cholecalciferol  End-stage renal disease (ESRD) − Calcitriol (risk for hypercalcemia and hyperphosphatemia) − Vitamin D analogs  Alfacalcidol (1α-hydroxyvitamin D3)  Doxercalciferol (1α-hydroxyvitamin D2)  Paricalcitol (19-nor-1,25-dihydroxyvitamin D3) Vitamin D supplements Reference: Palmer et al. Cochrane Database Syst Rev 2009; October 7(4);CD008175.
  • - Normal Levels Notes Calcium 8.5–10.2 mg/dL If hypoalbuminemia, use corrected calcium Corrected Ca = serum Ca + 0.8(4.0 – serum albumin) Phosphorus 2.7–4.6 mg/dL Phosphorus restriction • Adequate protein, not excessive intake Phosphorus-binding medication with meals • Calcium based • Non-calcium based 25(OH)D > 20 ng/mL Ergocalciferol (D2) Cholecalficerol (D3) iPTH < 65 pg/dL Assess level Vitamin D suppresses PTH Phosphorus restriction Bone disease results from complex interactions
  • Using corrected calcium makes a difference when assessing Joseph’s Ca levels
  • As vitamin D increased, iPTH decreased
  • Supplemental vitamin D may increase phosphorus absorption
  •  Vitamin D may lower iPTH.  Vitamin D increases calcium absorption and may be discontinued with hypercalcemia.  Vitamin D increases phosphorus absorption and may be discontinued with hyperphosphatemia. Active vitamin D increases risk for hypercalcemia and hyperphosphatemia
  •  Different types of renal bone diseases − High turnover, low turnover, mixed  25(OH)D and iPTH levels − Inversely related to each other  Serum phosphorus normal until advanced CKD − May need dietary phosphorus restriction − May need phosphate binders with meals Summary: Bone disease in CKD
  •  Anemia (inadequate erythropoietin) − Monitor hemoglobin, transferrin saturation, ferritin − May be treated with oral or parenteral iron; erythropoietic-stimulating agents − Take oral iron supplements at different times than phosphate-binding medications  Hyperkalemia − May involve dietary intake, use of medications that block the RAAS, and transcellular shifts − Limit dietary potassium when serum level elevated Take-home messages: Complications increase as kidney function declines
  •  Hypoalbuminemia − Marker indicates nutritional status and inflammation. − Serum albumin > 4.0 g/dL at times of initiation of dialysis reduces risk of mortality. − Treating metabolic acidosis may improve serum albumin.  Metabolic acidosis − Maintaining normal serum HCO3 > 22 mEq/L may be beneficial. − Animal protein may be a source of metabolic acid. − Condition may be treated with base such as sodium bicarbonate. Take-home messages: Complications increase as kidney function declines
  •  Mineral and bone disorders − Inadequate activation of Vitamin D  Check 25(OH)D  May be treated with supplemental vitamin D − Increases both calcium and phosphorus absorption − May be discontinued with hypercalcemia, hyperphosphatemia − Accumulation of phosphorus  iPTH and FGF-23 enhance excretion  May need phosphorus restriction  May need phosphate binders with meals Take-home messages: Complications increase as kidney function declines
  • You may find this helpful when you counsel patients Reference: http://nkdep.nih.gov/resources/nkdep-kidney-test-results-508.pdf
  • You may find this guide helpful Reference: http://www.nkdep.nih.gov/resources/nkdep-ckd-amt-guide-508.pdf
  • If you think you are overwhelmed…consider the person with CKD!
  • 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 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
  • American Dietetic Association. International Dietetics and Nutrition Terminology (IDNT) Reference Manual. Standardized Language for the Nutrition Care Process. 3rd ed. Chicago, IL: American Dietetic Association; 2011. A physician’s guide to oral iron supplements. National Anemia Action Council website. http://www.anemia.org/professionals/feature- articles/content.php?contentid=306&sectionid=15 November 2008. Accessed June 14, 2011. Besarab A, Coyne DW. Iron supplementation to treat anemia in patients with chronic kidney disease. Nature Reviews Nephrology. 2010;6(12):699–710. Drueke TB, Locatelli F, Clyne N, et al. Normalization of hemoglobin levels in patients with chronic kidney disease and anemia. New England Journal of Medicine. 2006;355(20):2071–2084. References: Anemia
  • FDA Drug Safety Communication: Erythropoiesis-stimulating agents (ESAs): Procrit, Epogen and Aranesp. U.S. Food and Drug Administration website. http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInfo rmationforPatientsandProviders/ucm200297.htm . February 26, 2010. Accessed September 8, 2011. FDA Drug Safety Communication: Modified dosing recommendations to improve the safe use of erythropoiesis-stimulating agents (ESAs) in chronic kidney disease. U.S. Food and Drug Administration website. http://www.fda.gov/Drugs/DrugSafety/ucm259639.htm . June 24, 2011. Accessed September 7, 2011. Fleming RE, Bacon BR. Orchestration of iron homeostasis. New England Journal of Medicine. 2005;352(17):1741–1744. Ganz, T. Molecular control of iron transport. Journal of the American Society of Nephrology. 2007;18(2):394–400. References: Anemia
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  • Gennari FJ, Segal AS. Hyperkalemia: an adaptive response in chronic renal insufficiency. Kidney International. 2002;62(1):1–9. Institute of Medicine. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, D.C.: National Academy Press; 2004. Institute of Medicine website. http://iom.edu/Reports/2004/Dietary-Reference-Intakes-Water- Potassium-Sodium-Chloride-and-Sulfate.aspx. Accessed June 13, 2011. Palmer BF. Managing hyperkalemia caused by inhibitors of the renin- angiotensin-aldosterone system. New England Journal of Medicine. 2004; 351(6):585–592. Schaefer TJ, Wolford RW. Disorders of potassium. Emergency Medicine Clinics of North America. 2005;23(3):723–747. References: Hyperkalemia
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  • Remer T, Manz F. Potential renal acid load of foods and its influence on urine pH. Journal of the American Dietetic Association. 1995; 95(7):791–797. U.S. Renal Data System. USRDS 2009 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2009. United States Renal Data System website. http://www.usrds.org/adr.htm . Accessed August 31, 2011. References: Metabolic Acidosis
  • Dietary supplements fact sheet: vitamin D. Office of Dietary Supplements, National Institutes of Health website. http://ods.od.nih.gov/factsheets/VitaminD/. Reviewed June 24, 2011. Accessed August 31, 2011. Doorenbos CRC, van den Born J, Navis G, de Borst MH. Possible renoprotection by vitamin D in chronic renal disease: beyond mineral metabolism. Nature Reviews Nephrology. 2009;5(12):691–700. Emmett M. A comparison of clinically useful phosphorus binders for patients with chronic kidney failure. Kidney International. 2004;66(suppl 90):S25–S32. Fadem SZ, Moe SM. Management of chronic kidney disease mineral- bone disorder. Advances in Chronic Kidney Disease. 2007;14(1):44–53. References: Mineral and Bone Disorders
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  • Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention and treatment of chronic kidney disease- mineral and bone disorder (CKD-MBD). Kidney International. 2009;76(suppl 113):S1–S130. Kidney Disease Improving Global Outcomes website. http://www.kdigo.org/guidelines/mbd/index.html . Accessed August 31, 2011. Liu S, Quarles LD. How fibroblastic growth factor 23 works. Journal of the American Society of Nephrology. 2007;18(6):1637–1647. Martin KJ, Gonzalez EA. Metabolic bone disease in chronic kidney disease. Journal of the American Society of Nephrology. 2007;18(3):875–885. References: Mineral and Bone Disorders
  • National Kidney and Urologic Diseases Information Clearinghouse. Chronic kidney disease—Mineral and bone disorder. February 2009. NIH publication 09–4630. National Kidney and Urological Diseases Information Clearinghouse website. http://www.kidney.niddk.nih.gov/kudiseases/pubs/CKD_Mineral_ Bone . Accessed June 14, 2011. National Kidney Disease Education Program. Chronic kidney disease (CKD) and diet: assessment, management and treatment. Treating CKD patients who are not on dialysis. An overview guide for dietitians. Revised September 2011. National Kidney Disease Education Program website. http://nkdep.nih.gov/resources/nkdep-ckd-amt-guide-508.pdf. Accessed September 8, 2011. Palmer SC, McGregor DO, Craig JC, Elder G, Macaskill P, Strippoli GF. Vitamin D compounds for people with chronic kidney disease not requiring dialysis. Cochrane Database of Systematic Reviews. 2009;October 7(4);CD008175. References: Mineral and Bone Disorders
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  • U.S. Renal Data System. USRDS 2009 Annual Data Report: Atlas of Chronic Kidney Disease and End-Stage Renal Disease in the United States. Bethesda, MD: National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases; 2009. United States Renal Data System website. http://www.usrds.org/adr.htm . Accessed August 31, 2011. References: Mineral and Bone Disorders