Send the link below via email or IMCopy
Present to your audienceStart remote presentation
- Invited audience members will follow you as you navigate and present
- People invited to a presentation do not need a Prezi account
- This link expires 10 minutes after you close the presentation
- A maximum of 30 users can follow your presentation
- Learn more about this feature in our knowledge base article
Copy of Chronic Kidney Disease
Transcript of Copy of Chronic Kidney Disease
Normochromic normocytic anemia
Anemia is a result of:
inadequate production of erythropoietin
shorter erythrocyte half-life
Anemia causes tissue hypoxia
Common manifestations include
Increased cardiac workload Hematologic Systems Diagnostic testing (lab)
serum creatinine values
Markers of damage:
urine protein (albumin)
Ultrasound, XR, CT show small kidney size
Renal Biopsy confirms diagnosis Decreased Glomerular Filtration Rate (GFR) leads to increased serum creatinine and increased plasma urea concentration
Creatinine increases because there is no compensatory mechanism for level adjustment
Urea is both filtered and absorbed so urea levels are not the best indicator of GFR Creatinine and Urea Clearance By Sarah Ibeling, Tasha Tennessen, &Tricia Borg The two most common causes of CKD are hypertension and diabetes. Prevention is secondary and focuses on treating underlying disease.
Other prevention includes general health management including, diet, exercise, smoking cessation, weight management, and careful use of renally excreted drugs. Prevention Decreased circulating sex hormones
Reduced testosterone in males
May lead to impotence
Oligospermia and germinal cell dysplasia
May result in infertility
Reduced estrogen in females
May cause amenorrhea and inability to maintain pregnancies to term
(McCance et al., 2010, p. 1396) Reproductive System *Neurologic symptoms due to uremic toxicity, chronic hyperkalemic depolarization and anemia
• Impaired concentration, memory loss and impaired judgment Neurologic System Impaired platelet function
Defective platelet aggregation and adhesion to endothelium
Results in increased bleeding tendencies
Alterations of clotting factors, fibrin, thrombin and fibrinolysis put patient at risk for thrombosis, myocardial infarctions and stroke
(McCance et al., 2010, p. 1395) Hematologic Systems * Increased cardiac workload
* Due to decreased erythropoietin and increased
hypoxia from anemia
* Also due to inadequate ventricular filling and
decreased cardiac output
* Due to inflammation from uremic toxins
* Cardiovascular disease advances greatly in the presences of pro-inflammatory mediators, oxidative stress and metabolic imbalances
(McCance et al., 2010, p. 1395) Cardiovascular System * Hypertension
* Due to excess sodium and fluid volume
* Due decreased vessel elasticity and increased
blockage from atheromatous plaque build up and calcium deposits
* Vascular Disease
* Damaged vessels increases the risk of significant
heart disease in patients with uremia Cardiovascular & Pulmonary Proteinuria
Protein in urine that causes increased tubular inflammation and fibrosis, which causes renal damage
(McCance et al., 2010, p. 1395)
Worsening renal function is a factor in insulin resistance, which alters adipokine levels and causes hyperinsulinemia and glucose intolerance.
Increased blood glucose increases oxidative stress, which is attributed to renal tubular and vascular injury thus glomerulosclerosis and further kidney failure.
Insulin resistance also promotes renal endothelial cell proliferations, which increases intrarenal pressure which obstructs urine flow and impairs filtration thus leading to further decrease in kidney function
(McCance et al., 2010, p. 1395)
Uremia results in deficient lipoprotein lipase, which causes high low-density lipoprotein (LDL) and low high-density lipoprotein (HDL).Increased atherosclerosis and vascular calcification also manifest
(McCance et al., 2010, p. 1395). Protein, Carbohydrate and Fat Metabolism Azotemia:
Increased levels of blood urea nitrogen (BUN), serum creatinine and other nitrogenous compounds due to decreasing renal function that causes the kidneys to insufficiently excrete metabolites.
Patient is asymptomatic (despite elevated lab values).
(McCance et al., 2010, p. 1393). Clinical Manifestations Stage 1: GFR>90, normal urea and creatinine, asymptomatic.
Treatment: Try to identify and reverse cause.
Stage II: GFR 60-89, urea and creatinine normal or mildly elevated, asymptomatic
Treatment: Monitor creat, Blood pressure management (<130/80) with ACE, ARB or diuretic, general health, try to slow/stop worsening kidney function
Stage III: GFR 30-59%, increased creatinine and urea, tired, poor appetite, itchy, anemia
Treatment: similar to stage II, continue to try to slow progression, educate on treatment options
Stage IV: GFR 15-29%, increased creatinine and urea, tired, poor appetite, itching may worsen, there is severe kidney damage and the kidneys can barely keep the person alive.
Treatment: access site for dialysis
Stage V: GFR <15%, increased creatinine and urea, difficulty sleeping, difficulty breathing, vomiting
Treatment: Renal Replacement Therapy- transplant or dialysis Stages, Symptoms, & Treatments of CKD Potassium
At first, tubular secretion increases to effectively excrete potassium until the onset of oliguria.
As renal dysfunction significantly increases, potassium levels increase because the kidneys are unable to filtrate it out of the blood.
In early stages, acid excretion and bicarbonate reabsorption increases to maintain normal pH.
Metabolic acidosis occurs when GFR decreases in later stages. Fluid and Electrolyte Balance Phosphate
Phosphate levels increase due to inadequate excretion by the kidneys.
Kidneys are unable to properly synthesize 1,25-vitamin D3, calcitriol so calcium is not absorbed properly
Results in hypocalcemia, which results in hyperparathyroidism
Excess parathyroid hormone stimulates calcium to move out of the bone and into the blood, increasing the risk for bone fractures. Fluid and Electrolyte Balance Sodium
Nephrons become overloaded with sodium resulting in the increase need for excretion and decreased ability for sodium reabsorption.
In early stages, the distal nephron is able to compensate to excrete excess sodium and water, thus maintaining normal levels.
As renal dysfunction worsens, hormones, such as aldosterone, prostaglandins and natriuretic peptides, increase and cause sodium retention and the kidneys are unable to excrete it adequately.
Heart failure and nephrotic syndrome also potentiate sodium retention in patients with ESKD.
Nephrons can maintain water balance until "GFR declines to 15% to 20% of normal with extensive loss of nephron and tubular function" (McCance, et al., 2010, p. 1394).
As GFR decreases, body is unable to concentrate and dilute urine. Fluid and Electrolyte Balance Regardless of initial disease, CKD is associated with:
Glomerular hypertension, hyperfiltration and hypertorphy
Tubulointerstitial inflammation and fibrosis
(McCance et al., 2010, p. 1392) Progression of CKD According to the National Kidney Foundation, kidney damage is more specifically defined as a “Glomerular Filtration Rate (GFR) less than 60 mL/min/1.73m 2 for 3 months or more, irrespective of cause” (McCance et al., 2010, p. 1389).
GFR and tubular functions decrease and organ system changes manifest throughout body. Symptomatic changes usually do not become evident until renal function declines to less than 25% (McCance et al., 2010, p. 1390). Kidney Damage A progressive loss of renal function. Plasma creatine levels gradually become elevated as GFR declines, sodium is lost in the urine, potassium is retained, acidosis develops, calcium metabolism and phosphate metabolism are altered and erythropoietin production is diminished. All organs systems are affected by CKD. (McCance et al., 2010, p. 1397). CKD definition Dialysis
Renal transplant Treatment for End Stage Kidney Disease Dietary Control:
Calcium &Vitamin D supplements
low sodium diet
adequate caloric intake
ACE inhibitor or receptor blockers to control systemic hypertension
loop diuretics (lasix)
cation exchange resins (Kayexalate)
tight glycemic control in diabeties
management of dyslipidemias
erythropoietin PRN CKD Management Insulin resistance (related to uremia and/or systemic inflammation and oxidative stress)
Kidneys are unable to breakdown insulin and insulin’s half-life is increased
Causes low thyroid hormone levels
Uremia causes reduction of conversion of T3 to T4
Anemia causes bleeding into the skin (ecchymosis)
Uremic skin residues cause itching and scratching (uremic frost)
Skin has an increased risk for infection
(McCance et al., 2010, p. 1396)
Endocrine/Integumentary Systems Uremic gastroenteritis
Causes bleeding ulcers and blood loss
Constipation or diarrhea
Aka “uremic fetor” caused by breakdown of urea by salivary enzymes
(McCance et al., 2010, p. 1396) Gastrointestinal System Immunosuppression
Increased risk for infection
Inadequate response to vaccinations
Suppression of chemotaxis, phagocytosis, anti-body production and cell-mediated immune responses
Immunosuppression worsened with malnutrition, metabolic acidosis and hyperglycemia
(McCance et al., 2010, p. 1396) Immune System Uremia
A pro-inflammatory state in which renal function worsens and systemic effects manifest
Decline in renal function causes an increased accumulation of urea and other nitrogenous compound toxins, which cause systemic manifestations
Accumulation of end products of protein metabolism, alterations in fluid and electrolytes, metabolic acidosis, intestinal absorption of toxins produced by gut bacteria and results of altered renal hormone synthesis (anemia, hyperphosphatemia and hypocalcemia)
(McCance et al., 2010, p. 1393). Clinical Manifestations Diagnosis/Lab Values Glomerular hyperfiltration and increased glomerular capillary permeability
lead to . . .
so then . . .
proteinuria builds up in interstitial space
and then . . .
activates complement proteins and other mediators and cells
which promotes . . .
inflammation and progressive fibrosis
which contributes . . .
to tubulointerstitial injury
(McCance et al., 2010, p. 1393) Effects of Proteinuria in CKD Trade-off Hypothesis Loss of nephron mass and adaptive hyperfiltration (increased glomerular pressure)
uremia and end-stage renal failure
(McCance et al., 2010, p. 1392) Elevated Angiotensin II
activity of inflammatory cells and growth factors
that contribute to
tubulointerstitial fibrosis and scarring
(McCance et al., 2010, p. 1393) More Effects of Angiotensin II Nephron loss or injury
leads to . . .
elevated Angiotensin II
which causes . . .
efferent arteriolar vasoconstriction and promotes systemic hypertension
that leads to . . .
glomerular hypertension and hyperfiltration
so then . . .
chronic increased intraglomerular pressure
in turn increases . . .
glomerular capillary permeability
which contributes to . . .
proteinuria Effects of Angiotensin II in CKD Loss of nephron mass with progressive kidney damage
causes . . .
Surviving nephrons to sustain normal kidney function
by . . .
compensatory hypertrophy and expansion or hyperfunction in rates of filtration, resorption and secretion . . .
maintaining constant rates of excretion in the presence of overall declining GFR
*Note: Major end products of urinary excretion are similar to end products of normally functioning kidneys until advanced stage.
(McCance et al., 2010, p. 1390) Intact Nephron Hypothesis Case Study: "J.M., a 34-year-old African American man, came to the emergency department with a 6-day history of increasing swelling in both lower extremities. A similar swelling had occurred once before recently but had cleared up spontaneously. J.M. said he had no history of headaches, hypertension, nausea, vomiting or diarrhea, fever and chills, shortness of breath, chest pain, urinary problems, weight loss, confusion or other neurological changes, or exposure to toxic substances. He also stated that he was not taking any medication. On physical examination, his blood pressure was 222/142 mm Hg, his heart rate was 110/min with S3 and S4 gallops, and his respiratory rate was 24/min with bibasilar crackles. Electrocardiography showed left ventricular hypertrophy and ST-T waves consistent with a strain pattern. A funduscopic examination showed bilateral chronic and new hemorrhages (cotton wool hemorrhages and exudates), arteriolar narrowing, and arteriovenous nicking. Laboratory results are reported in table below. J.M. was admitted to the intensive care unit with a diagnosis of ESRD due to hypertension with hypertensive crisis and metabolic acidosis" (Critical Care Nurse, 2006) CKD Overview Left Side of Line Diagram Demonstration Case Study Questions 1. What physical exam findings indicate that J.M. has CKD?
2. On admission, what lab values indicate that J.M. has CKD?
3. As a nurse practitioner, how would you explain to your patient why managing their diabetes and/or hypertension is important?
4. J.M. has just gotten married and wants to start a family. How might CKD affect this?
5. J.M. is 34-years-old. How would you explain his treatment options to him? What if he was 75-years-old? What if you were an NP on a mission trip in a developing country such as India or Nigeria and J.M. was your patient? How would this affect his treatment options? What kind of education would you give J.M. and his family in this situation?
6. J.M. has 20 family members visiting him at the hospital. They are all worried that they might get CKD too. They are asking you how to prevent this disease. What would you tell them?
7. J.M. likes to drink beer on the weekends with his friends, enjoys ham sandwiches, and eating fast food. His wife is asking you about which foods she should be cooking for him. What dietary counseling are you going to give them? What is a sample menu you could prepare for them? What if J.M. was also diabetic?
8. As a nurse practitioner, what medications will you be prescribing to manage J.M.'s CKD? What kinds of medications would you avoid?
9. As a nurse practitioner, what resources might J.M. need with coping this disease?
* Please choose a couple of questions and give a qualitative versus quantitative post. Practice Quiz Questions Renal Clearance: renal clearance refers to how much of a substance the kidneys can be clear from the blood during a given unit of time. This give us an indirect measure of Glomerular Filtration Rate (GFR.)
GFR: Factors that determine GFR are directly related to the pressures that favor or oppose filtration. Changes in the afferent or efferent arteriolar resistance will alter GFR.
Creatinine is a substance produced at a constant rate by muscle and is released into blood where it is filtered by the glomerulus. Because it is produced at a constant rated, the amount of creatinine filtered by the glomerulus is approximately equal to the amount excreted. Normal plasma creatinine is 0.7-1.2 mg/dl.
Plasma Creatinine and GFR are inversely related. As GFR declines, Plasma Creatinine increased proportionately. If GFR decreases 50%, the filtration and excretion of creatine decreased 50%, causing creatinine values to double. 1. Which one of these statements is false?
a) As GFR decreases, the body is unable to concentrate and dilute urine
b) Headaches, drowsiness, and insomnia are all neurologic symptoms of CKD.
c) Chronic intraglomerular pressure causes increased glomerular permeability which contributes to proteinuria.
d) As CKD develops, sodium is lost, potassium is retained, acidosis develops and erythropoietin is increased Practice Quiz Questions 2. Which one of these statements is false?
a) CKD patients are at risk for both bleeding and clots.
b) Decreased GFR in ESRD causes decreased erythropoietin, increased potassium, increased calcium, and decreased phosphorus
c) Decreased GFR causes an increase in Creatinine and BUN.
d) Proper management of diabetes and hypertension can reduce your risk of CKD. Quiz Answers 1) d This is false because erythropoietin is decreased not increased. Make sure all parts of the sentence are correct. 2) b This is false because calcium is decreased and phosphorus is increased. Make sure anything that is "increased" or "decreased" is actually correct. References McCance, K.L., Huether, S.E., Brashers, V.L., & Rote, N.S. (2010). Pathophysiology: The Biologic
Basis for Disease in Adults and Children (6th ed.). Maryland Heights, MO: Mosby/Elsevier . J.M.'s Lab Values (Critical Care Nurse, 2006) Procedures & Testing • Dyspnea
• Pulmonary edema
• Kussmaul respirations (due to metabolic acidosis)
*Most complications related to fluid overload and congestive heart failure
(McCance et al., 2010, p. 1395) Neuromuscular irritation
Causes hiccups, muscle cramps and muscle twitching
Causes decreased tendon reflexes, muscle weakness and muscle atrophy
Seizures and coma (in advanced stages)
(McCance et al., 2010, p. 1396) Managing CKD: the Diet Avoid foods high in salt: soy sauce, most canned foods, some frozen foods, take-out, processed meats: bacon, cold-cuts, sausage, ham, canned or dehydrated soups, DO NOT USE SALT SUBSTITUTES--THESE ARE HIGH IN K
Avoid foods high in phosphorus: milk, cheese, pudding, yogurt, ice cream, dried beans and peas, nuts, peanut butter, hot chocolate, beer, and dark cola drinks (National Kidney Foundation, 2006) Avoid foods high in potassium: oranges, nectarines, kiwis,bananas, asparagus, potatoes, tomatoes, winter squash, pumpkin, and cooked spinach What can you eat ? 1. Try dried herbs and spices, dash of hot pepper sauce, or a squeeze of lemon juice for flavorings
2. Use non-dairy creamers and milk substitutes instead of milk (National Kidney Foundation, 2006).
3. Choose fruits and vegetables low in potassium: peaches, pears, cherries, apples, broccoli, carrots, green beans, and zucchini
4. Replace calories from protein with carbohydrates such as breads and grains. If not overweight or diabetic, may have certain high calorie desserts (MedLine Plus, 2012). Chronic kidney disease: Acute manifestations and role of
critical care nurses. (2006, August). Critical Care Nurse, 26, 17-27. Retrieved October 10, 2012 from
http://ccn.aacnjournals.org/content/26/4/17.full Plumbline films. (2009, Feb 11). Davita dialysis center.
[Video]. Retrieved from:
www.youtube.com/watch?v=MMSYoh4jfWA&feature=related (McCance et. al., 2010, p. 1393)
(Journal of the American Society of Nephrology, 2006) How does proteinuria cause progressive renal
damage? (2006, Oct 11). Journal of the American Society of Nephrology, 17, 2974-2984. Retrieved November 4, 2012 from http://jasn.asnjournals.org/content/17/11/2974.full What is chronic kidney disease? (n.d.).
Retrieved October 25, 2012 from
http://www.kidney.ca/page.aspx?pid=320 Nutrition and chronic kidney disease. (2006).
National Kidney Foundation.
Retrieved November 2, 2012 from http://www.kidney.org/atoz/pdf/nutri_chronic.pdf Limit foods high in protein: poultry, pork, beef, fish and eggs
Avoid foods high in water: jello, popsicles, grapes, melon, and lettuce (Medline Plus, 2012) Diet-chronic kidney disease. (2012). MedLine Plus.
Retrieved November 2, 2012 from http://www.nlm.nih.gov/medlineplus/ency/article/002442.htm Picture is Shemar Moore, taken from www.askactor.com Graph obtained from http://users.atw.hu/blp6/BLP6/HTML/C0329780323045827.htm Pictures from: http://cigdemtepetveeml.k12.tr/resimler/uremic-frost-photos and http://www.kmle.co.kr Pictures taken from: http://somanorodom.wordpress.com/2010/06/30/a-day-with-dad-and-dialysis-treatment/, http://healthyworldblog.org/hospice/, and http://www.sciencephoto.com/media/86282/enlarge