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CHRONIC RENAL FAILURE Valerie Kolmer RN BSN BC MSN 621 Alverno College Main Menu Objectives Upon completion of this tutorial the learner will: Have an increased understanding of the pathophysiology of Chronic Renal Failure Recognize the signs and symptoms of Chronic Renal Failure Identify the disease progression and treatment interventions Main Menu Chronic Renal Failure Tutorial Guide Return to the main menu at any time by pushing the Main Menu button. Hyperlinks to outside sources, for in-depth information, are available on various slides. Just push on the Link button. Click back button to return. Easy navigation forward or backward using the or buttons. Within text - highlighted words link to definitions - then return with button Main Menu Chronic Renal Failure Main Menu Tutorial Guide Definitions Renal Physiology Review Pathophysiology Causes Signs & Symptoms Hyperlipidemia in CRF Inflammation Pharmacology Case Study/Quiz References Main Menu Definitions CRF = Chronic Renal Failure – permanent loss of nephrons and renal function Erythropoietin = Hormone produced by kidneys and regulates production of RBC’s Filtrate = Liquid entering the nephron Filtration = Movement of liquid through a membrane (like a sieve), allows only small molecules & liquids to pass through. Movement is from higher to lower pressure GFR = Glomerular Filtration Rate – amount of filtrate produced each minute Glomerulus = Filtration system of the nephron, composed of capillaries surrounded by a thin double-walled capsule, called Bowman’s Capsule Main Menu Definitions Lysosome = Membrane bound organelles, within the cell, containing hydrolytic enzymes - involved in intra & extracellular digestion Mesangial Cells = Supporting cells of glomeruliproduce intracellular substances Nephron = Functional unit of the kidney Reabsorption = Movement of substances from the filtrate back into the blood Renal Corpuscle = Glomerulus and surrounding epithelial capsule. Secretion = Active transport of solutes into the nephron Main Menu Renal Physiology Review a. b. c. d. e. f. The Kidneys: Control the fluid/electrolyte balance for the body Remove metabolic wastes from the blood & excrete them to the outside Regulate red-blood cell production Regulate blood-pressure Important in calcium ion absorption Control volume, composition and pH of the blood Link: Renal Physiology Main Menu Renal Hormone Regulation Synthesis and activation of hormones by the kidney include: • Active form of Vitamin D • Erythropoietin Renal blood flow regulated by: Renin-angiotensin aldosterone system (RAAS) Main Menu Fluid and Electrolyte Control Mechanisms – Renin-Angiotensin Aldosterone System Aldosterone ADH – Anti-Diuretic Hormone RAAS Main Menu How the RAAS Pathway Works Valerie Kolmer 2006 Main Menu Aldosterone Increases rate of sodium ion absorption Chloride moves along with sodium because of + charge of sodium Increases rate of potassium & hydrogen ion secretion Result: Fluid and sodium retention increases bloodpressure Main Menu ADH (Anti-Diuretic Hormone) Main Menu Quick Quiz 1. 2. 3. Pick the correct pathway of the RAAS Renin – Angiotensin II – ACE – ADH – Aldosterone Renin – Angiotensin I – Aldosterone – ADH –ACE Renin – Angiotensin I – ACE – Angiotensin II – Aldosterone Main Menu Answer 1. Renin – Angiotensin II- ACE- ADH – Aldosterone That is not correct Please try again Main Menu Answer 2. Renin – Angiotensin I – Aldosterone – ADH - ACE 1. That is not correct 2. Please Try Again Main Menu Answer 3. Renin – Angiotensin I – ACE – Angiotensin II – Aldosterone You are RIGHT! Main Menu Renal Structure Each kidney has a renal pelvis (divided into major & minor calyces), renal cortex (the outer portion) & renal medulla (lies under the cortex) Within the renal medulla there are many renal pyramids that consist of multiple nephrons (the functional units of the kidney) The renal pelvis collects the urine & passes it to the ureter Main Menu (a) Nephron (b) Renal Pyramid with Nephrons (c) Section of Kidney Shier,D., Butler, J., Lewis, R (1999). Hole’s human anatomy and physiology.(8th ed.). The McGraw-Hill Co, Inc. Used with permission: The McGraw-Hill Companies Main Menu The Nephron 1. 2. 3. 4. Each kidney contains approximately a million nephron’s Filtered fluid from the blood enters: The renal corpuscle (consisting of the glomerulus) Proximal convoluted tubule Loop of Henle (descending & ascending limb) Distal convoluted tubule Shier, D., Butler, J., Lewis, R. (1999). Hole’s human anatomy & physiology(8th ed.). The McGraw-Hill Co., Inc . Main Menu Nephron & Blood Supply Shier,D., Butler, J., Lewis, R (1999). Hole’s human anatomy and physiology.(8th ed.). The McGraw-Hill Co, Inc. Used Main Menu Urine Formation Efferent arteriole constriction causes the blood in the glomerulus to be under high pressure. Filtrate: the water and other small molecules that move into the glomerular capsule. Approximately 45 gallons of filtrate are produced each day. Most of the water and molecules are reabsorbed along the tubules as the filtrate passes through. Shier, D., Butler, J., Lewis, R. (1999). Hole’s human anatomy & physiology(8th ed.). The McGraw-Hill Co., Inc. Main Menu What is Glomerular Filtration Rate (GFR)? The GFR is the measurement of the kidneys ability to filter waste products It shows the volume of H2O and solutes filtered out of blood plasma through the glomeruli over a period of time Common measurement is the CockcroftGault equation that estimates creatinine clearance Link: GFR Info Main Menu Urine Formation Name Process Molecule Example Glomerular Filtration Blood Pressure pushes sm. molecules from glomerulus into glomerular capsule Water,glucose,salts,urea, creatinine,amino acids,uric acid Tubular Reabsorption Diffusion/active transport take molecules to blood-at the proximal tubule Water, glucose, amino acids, salts Tubular Secretion Active transport takes molecules from blood into distal convoluted tubule Uric acid, creatinine, hydrogen ions, ammonia Reabsorption of Water All along nephron length, mainly Loop of Henle & collecting ductH2O returns by osmosis after reabsorption of Na Salt & water Excretion Urine formation rids body of metabolic wastes Water, salts, urea, uric acid, ammonium, creatinine Main Menu Nephron Component Functions Filtration of H2O and dissolved substances from the plasma Reabsorption of Na ions, Water, Secretion of hydrogen ions and K+ ions Reabsorption of glucose, calcium, K+, Na, proteins and H2O Reabsorption of Na, K+ & Chloride ions Main Menu Pathophysiology of CRF What is Chronic Renal Failure? It is progressive tissue destruction with permanent loss of nephrons and renal function. Main Menu Risk Factors Age > 60 years Race or ethnic background African-American Hispanic American Indian Asian History of exposure to chemicals/toxins Cigarette smoke Heavy metals Family history of chronic kidney disease Main Menu Chronic vs. Acute Renal Failure a. b. a. b. Acute Renal Failure (ARF): Abrupt onset Potentially reversible Chronic Renal Failure (CRF): Progresses over at least 3 months Permanent- non-reversible damage to nephrons Main Menu Pathophysiology of CRF Progressive destruction of nephrons leads to: a. Decreased glomerular filtration, tubular reabsorption & renal hormone regulation b. Remaining functional nephrons compensate c. Functional and structural changes occur d. Inflammatory response triggered e. Healthy glomeruli so overburdened they become stiff, sclerotic and necrotic Lippincott Williams & Wilkins (2005). Pathophysiology A 2-1 reference for nurses (1st ed.) Ambler, Pa.:Lippincott Williams & Wilkins Main Menu Functional Changes of CRF The Kidneys are unable to: Regulate fluids and electrolytes Balance fluid volume and renin-angiotensin system Control blood pressure Eliminate nitrogen and other wastes Synthesize erythropoietin Regulate serum phosphate and calcium levels Main Menu Structural Changes of CRF Epithelial damage Glomerular and parietal basement membrane damage Vessel wall thickening Vessel lumen narrowing leading to stenosis of arteries and capillaries Sclerosis of membranes, glomeruli and tubules Reduced glomerular filtration rate Nephron destruction Healthy Glomerulus Damaged Glomerulus Valerie Kolmer 2006 Main Menu 4 Stages of CRF 1. 2. 3. 4. Reduced Renal Reserve (Silent): no symptoms evident- GFR up to 50ml/min Renal Insufficiency: ½ function of both kidneys lost- GFR 25-50 ml/min Renal Failure: GFR 5-25 ml/min End Stage Renal Disease: GFR less than 5 ml/min Link: GFR Info Main Menu Quick Quiz Chronic Renal Failure is reversible. True False Main Menu Sorry! That is not correct. The answer is false. Nephron damage is permanent & progressive in CRF Please continue. Main Menu You are right! Main Menu Causes of CRF 1) 2) 3) 4) 5) 6) 7) Diabetic Nephropathy Hypertension Vascular Disease Polycystic Kidney Disease/Genetics Chronic Inflammation Obstruction Glomerular Disorders/ Glomerulonephritis Main Menu SIGNS & SYMPTOMS Lab Value Cues 1. 2. 3. Anemia’s - d/t decreased erythropoietin secretion & uremic toxin damage to RBC’s Azotemia – (elevated nitrogen) d/t retention of nitrogenous wastes Creatinine – a component of muscle & it’s non-protein waste product. Normally filtered in the glomerulus & lost in the urine. Glomerular damage increases reabsorption into the blood. Serum creatinine 3 x normal shows a 75% loss of renal function. http://office.microsoft.com/en-us/tou.aspx Main Menu SIGNS & SYMPTOMS Lab Value Cues 4. 5. Hypocalcemia – impaired regulation of Vitamin D leads to decreased absorption & low calcium levels. High phosphorus levels also cause low serum calcium levels. Hyperkalemia – impaired excretion of potassium by the kidneys leads to elevated potassium levels. http://office.microsoft.com/en-us/tou.aspx 6. 7. Hyperlipidemia – decreased serum albumin leads to increased synthesis of LDL’s & cholesterol by the liver, contributing to elevated lipid levels Proteinuria – increased protein filtration d/t glomeruli damage Main Menu SIGNS & SYMPTOMS Visual / Verbal Cues 1) 2) 3) 4) Dry mouth, fatigue, nausea – d/t hyponatremia & uremia Hypertension – d/t sodium & water retention Hypervolemia – d/t sodium & water retention Gray/yellow skin – d/t accumulated urine pigments http://office.microsoft.com/en-us/tou.aspx 5) 6) 7) 8) Cardiac irritability – d/t hyperkalemia Muscle cramps – d/t hypocalcemia Bone & muscle pain – d/t hypocalcemia / hyperphosphatemia Restless leg syndrome – d/t toxins’ effects on the nervous system Main Menu Signs & Symptoms at a Glance Main Menu Genetics of Kidney Disease Genetic diseases that cause CRF: Polycystic Kidney Disease (PKD) Nephropathic Cystinosis (Fanconi’s Syndrome) Alport Syndrome Sanford, R. (2004). Autosomal dominant polycystic kidney disease. Retrieved February 8, 2006, http://www.cgkp.org.uk/topics/camgenetics/sanford.htm Main Menu Polycystic Kidney Disease Most Common Genetic Disorder Numerous fluid-filled cysts in kidneys and renal tubules Normal renal tissue replaced by cysts Decreased function leads to end-stage renal disease Polycystic jpg 58_001.connection.ww.com/…/Ch58/jpg/58_001.jpg Main Menu Two Major Forms PKD Autosomal Dominant PKD Autosomal Recessive PKD Only treatment for both = dialysis and kidney transplantation Used with permission: Lippincott Williams & Wilkins Main Menu Autosomal Dominant PKD 90% of the cases of PKD are this form 4th leading cause of renal failure age 40-60 Undetected for years until symptoms develop Occurs equally males and females, mainly Caucasians One parent with ADPKD gene = 50% chance children will inherit disease Gene mutation on chromosome 16 or 4 Main Menu Autosomal Recessive PKD form – occurs in 1 in 4 babies (of parents with mutation) Worst cases die within hours of birth Both parents with gene mutation Mutation on chromosome 6 25% chance children will inherit disease Rare Main Menu Metabolic Impact Hyperlipidemia common in CRFespecially in Nephrotic Syndrome Excessive lipids accelerate progression of renal disease Cholesterol increases glomerular injury Main Menu Contributing Mechanisms Two known paths of hyperlipidemia progression in CRF: Hyperlipidemia activates LDL receptors in mesangial cells Increased synthesis of lipoproteins in the liver related to increased albumin production Main Menu Mesangial Cell Contribution Valerie Kolmer 2006 Main Menu Albumin Contribution Normal glomeruli structure limits proteins from filtering through the urine Progression of glomeruli injury leads to increased capillary filtration of albumin The liver compensates and increases albumin production - to replace albumin lost in urine This leads to increased synthesis of lipoproteins by the liver secondary to the compensatory increase in albumin production. Results in increased LDL levels – predisposing to atherosclerosis Atherosclerosis further increases glomeruli injury Main Menu Inflammation Inflammatory response can be triggered by: tissue injury, infections, toxins, immune responses and/or Angiotensin II Can be acute or chronic Can affect the renal pelvis and interstitial tissue as in pyelonephritis Can affect the glomeruli as in glomerulonephritis Main Menu Inflammation- (Cont.) Renal Failure- prolongs inflammatory reactions Adverse effects of chronic inflammation= Decreased appetite Muscle and fat wasting Endothelial damage Atherosclerosis Hypoalbuminemia Increased cardiovascular disease risk Legg, V.(2005). Complications of chronic kidney disease. AJN,105(6),40-50 Main Menu Causes of Inflammation in CRF Infection Anemia – increases oxidation of proteins, lipids & carbohydrates, leading to vascular inflammation Malnutrition – decreases antioxidants Low serum albumin – decreases antioxidants Uremia Legg, V.(2005). Complications of chronic kidney disease. AJN,105(6),40-50 Main Menu Angiotensin II in the Inflammatory Process Inflammatory mediator causing: • • • Increased vascular permeability Increased leukocyte infiltration (monocytes, macrophages) Cell proliferation & hypertrophy Main Menu Glomerular Inflammatory Disorders Reminder: The glomeruli filter blood & form urine filtrate. The selectively permeable, capillary membrane allows H2O and small particles (i.e. glucose) to leave the capillary membrane. Large particles (i.e. proteins & blood cells) stay in the blood. Main Menu Nephrotic vs. Nephritic Syndromes Nephrotic Syndromes - glomerular disorders that affect the glomerular capillary membrane & increases permeability to plasma proteins Nephritic Syndromes – glomerular disorders that initiate the inflammatory response within the glomeruli & initially decreases permeability of the membrane Main Menu Nephritic Syndromes Glomerulonephritis • An inflammatory response in the endothelial, epithelial & mesangial cells of the glomeruli • Inflammatory process damages the capillary wall-allowing RBCs into the urine Symptoms: • 1st oliguria, followed by hematuria, azotemia, low GFR (d/t hemodynamic changes), hypertension Main Menu Nephrotic Syndromes Primary causes: Lipoid Nephrosis Focal Segmental glomerulosclerosis Membranous glomerulonephritis Secondary causes: Diabetes Mellitus SLE Amyloidosis Characterized by: Proteinuria > 3.5g/day Lipiduria Hypoalbuminemia Hyperlipidemia Increased permeability of glomerular membrane allows proteins to escape into the filtrate Main Menu P o r t Porth, 1998 Porth, 1998 h , 1 Main Menu Chronic Glomerulonephritis A slow, progressive disease that can be caused by primary ( Nephrotic & Nephritic Syndromes) or secondary disorders ( SLE, Good pasture's) Typically develops asymptomatically over many years Hypertension, proteinuria and hematuria exhibited with progression of disease Late stages display uremic symptoms of azotemia, nausea, vomiting, dyspnea and pruritis Leads to CRF Treatment includes: control of hypertension, control of fluid/electrolyte imbalances, reduce edema, prevent heart failure Main Menu Pharmacology in CRF Pharmacokinetics – drug absorption, distribution, metabolism & excretion Pharmacodynamics – A drug’s mechanism of action and effect at the target site Main Menu Alterations in Drug Responses in CRF Gastrointestinal impairments affect absorption of medications Volume of distribution (Vd) – the availability of a drug distributed in body tissues is increased or decreased by alterations in body composition or protein binding Metabolism of medications altered -the kidneys produce many enzymes involved in drug metabolism including cytochrome P-450 Decreased glomerular filtration rate affects drug excretion Campoy, S, Elwell, R.(2005). Pharmacology & CKD. AJN, 105(9),60-72. Main Menu Medication Considerations in CRF Dilantin – increased Vd related to protein binding changes and low albumin, increasing risk of drug toxicity Digoxin – increased Vd leading to toxicity due to decreased renal excretion Insulin – metabolism of insulin decreases, requiring dose reduction Tylenol and procainamide – liver metabolized drugs with metabolites that are excreted renally, can accumulate leading to drug toxicity Campoy, S, Elwell, R.(2005). Pharmacology & CKD. AJN, 105(9),60-72. Main Menu Medication Considerations (Cont.) Impaired renal excretion leads to toxic drug accumulations with: Diamox Aminoglycoside antibiotics (tobramycin & gentamycin) Atenolol Captopril Lithium Vancomycin Metformin Neurontin Topamax Main Menu Over-the-Counter Medications and CRF NSAIDS – inhibit prostaglandins decreasing GFR and reduced sodium excretion Decongestants – elevate blood-pressure and increase renal damage Antacids and laxatives (containing magnesium & aluminum) – causes mineral accumulation and metabolic complications Herbal Remedies – (juniper berry, buckthorn bark, cascara bark, licorice root) can cause electrolyte imbalances which worsen with diuretic therapy Campoy, S, Elwell, R.(2005). Pharmacology & CKD. AJN, 105(9),60-72. Main Menu Case Study Mrs. G. Nephritis is a 42 y/o African-American female. She has 6 children and has a history of: mild obesity, hypertension, smoker, and chronic fatigue. She comes to the emergency room with c/o increasing SOB, vertigo, weakness, dry mouth, and nausea for the last several weeks. She is noticing that her shoes fit tightly and that her urine is concentrated. She also notices that she only urinates once a day. Main Menu Case Study (cont.) She recently moved here from Texas. Mrs. Nephritis experienced the same symptoms when in Texas and was told to follow up in several weeks. She became busy with the move and relates she was “too busy to find a new physician”. Now months later the symptoms have progressively worsened. Main Menu Significant Lab Work BUN 37 Creatinine 4.7 Calcium 7.6 Sodium 137 Hemoglobin 8.5 Hematocrit 28.9 Albumin 2.5 Total Protein 6.2 LDL 156 HDL 32 (nl= 8-20 mg/dL) (nl= 0.6-0.9 mg/dL) (nl= 8.2-10.2 mg/dL) (nl= 135-145 mEq/L) (nl= 12-16 g/dL) (nl= 36-48%) (nl= 3.5-5 g/dL) (nl= 6.4-8.3 g/dL) (nl= <130mg/dL) (nl= 40-85 mg/dL) Main Menu Other Tests Urinalysis: Protein-100 RBC – 1-2 CXR: Moderately enlarged heart EKG: Sinus rhythm with occasional PVC’s Blood Pressure: 168/98 Main Menu Question #1 Based on this persons symptoms, history and lab work – What do you think her diagnosis would be? 1. CRF 2. ARF 3. CHF 4. Influenza Main Menu Answer The correct answer is # 1 chronic renal failure (CRF) Symptoms progressively worsening x several months Elevated creatinine : all 3 indicative of renal failure Elevated BUN SOB Shoes too tight :indicating fluid retention Main Menu Question #2 Which compensatory mechanism causes the increased fluid retention, increased sodium and elevated blood-pressure? 1. 2. 3. 4. Renin – Angiotensin – Aldosterone System (RAAS) Bone Marrow suppression Deregulation of baroreceptors Suppression of Sympathetic Nervous System Main Menu Answer #1 RAAS- Renin – Angiotensin – Aldosterone System is correct Reduced renal blood flow due to HTN, epithelial damage and stenosis causes the kidneys to secrete renin activating the system over and over- the end result is fluid and sodium retention which further increases blood pressure. Main Menu Question #3 1. 2. 3. 4. Why is this chronic and not acute renal failure? Progressive over long period of time H & H <10 HCT < 30 Sodium of 137 Main Menu Answer #1 is correct Mrs. Nephritis’ symptoms have progressively worsened over months http://office.microsoft.com/en-us/tou.aspx Main Menu Question #4 What risk factors in her history could lead to CRF? 1. African-American 2. HTN 3. Smoker 4. Obesity 5. All of the above 6. 1, 2 and 3 Main Menu Answer #5 All of the above is the correct answer. Mrs. Nephritis has an increased risk of renal failure related to her race and the smoking, HTN and obesity worsen the disease process Main Menu Question #5 Her risk factors as identified resulted in what happening to her kidneys? 1. 2. 3. 4. Nephron destruction Vessel stenosis Sclerosis of the glomeruli All of the above Main Menu Answer #4 is correct – all of the above Renal failure progresses as nephrons are destroyed. Epithelial damage leads to sclerosis of the glomeruli and stenosis of the vessel walls Main Menu Question # 6 In a patient with renal failure it is important to avoid drugs that are essentially eliminated by the kidneys. True or False? Main Menu Answer The answer is true. It is important to know how drugs are excreted, especially if by the kidneys and it is important to know or monitor the glomerular filtration rate (GFR) Main Menu Congratulations! You have completed the Chronic Renal Failure Tutorial Main Menu References Bowne, P. S. (). . Retrieved February 7, 2006, http://faculty.alverno.edu/bowneps/index.html Burrows-Hudson, S. (2005). Chronic kidney disease: An overview. American Journal of Nursing, 105(2), 40-50. Campoy, S. & Elwell, R. (2005, September). Pharmacology & CKD. AJN, 105(9), 60-72. Cannon, J. (2004). Recognizing chronic renal failure. Nursing 2004, 34(1), 50-53. Castner, D. & Douglas, C. (2005). Now onstage: Chronic kidney disease. Nursing 2005, 35(12), 58-63. Huether, S. E., & McCance, K. L. (2000). Understanding pathophysiology (2nd ed.). St Louis, Mo: Mosby, Legg, V. (2005, June). Complications of chronic kidney disease. AJN, 105(6), 40-50. Lippincott Williams & Wilkins (2005). Pathophysiology A 2-in-1 reference for nurses (1st ed.). Ambler, Pa.: Lippincott Williams & Wilkins. Main Menu References Microsoft media elements (). . Retrieved February 7, 2006, http://office.microsoft.com/en-us/tou.aspx National Kidney and Urologic Diseases Information Clearinghouse (2004, December). Polycystic kidney disease. Retrieved March 3, 2006, http://kidney.niddk.nih.gov/kudiseases/pubs /polycystic/ Nephrology Channel (2005, February 8). Chronic renal failure. Retrieved March 7, 2006, http://www.nephrologychannel.com/crf/ Nephrology Channel (2005, February 8). Nephrotic syndrome. Retrieved March 7, 2006 http://www.nephrologychannel.com/nephrotic/ Main Menu References Nephrology Channel (2005, February 8). Polycystic kidney disease. Retrieved March 7, 2006, http://nephrologychannel.com/polycystic/ Porth, C. M. (1998). Pathophhysiology Concepts of Altered Health States (5th ed.). Philadelphia, Pa.: Lippincott-Raven. Porth, C. M. (2004). Essentials of pathophysiology. Philadelphia, Pa.: Lippincott Williams & Wilkins. Sanford, R. (2004, May 25). Autosomal dominant polycystic kidney disease. Retrieved February 8, 2006, http://www.cgkp.org.uk/topics/cam-genetics/sanford.htm Shier, D. Butler, J. & Lewis, R. (1999). Hole's human anatomy & physiology (8th ed.). pp. 782, 786, 788: The McGraw-Hill Companies Main Menu References Wadhwa, D. (2005). Chronic renal failure. Retrieved February 8, 2006,http://www.uhmc.sunysb.edu/internalmed/nephro/ webpages/Part-G.htm Yale Medical Group (2005, October 28). Overview of renal failure. Retrieved February 8, 2006, http://ymghealthinfo.org/content asp?pageid=PO3111 eMedicine (2003, march 25). Cystinosis. Retrieved March 3, 2006, http://www.emedicine.com/ped/topic538.htm Main Menu Thank You! I appreciate your time spent viewing this tutorial and I hope you enjoyed it! I would like to thank Pat Bowne and Lee Jeske for all of their guidance in the development of this tutorial. I would also like to thank the McGraw-Hill companies for their permission to include the wonderful visuals on renal physiology. Any questions or comments you can contact me at: Valerie Kolmer 1-262-639-4107 or [email protected] Main Menu