CHRONIC RENAL FAILURE

Valerie Kolmer RN BSN BC

MSN 621 Alverno College
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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
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Chronic Renal Failure Tutorial Guide

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to the main menu at any time by pushing the Main Menu button.  Hyperlinks to outside sources, for in-depth ininformation, 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
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Chronic Renal Failure Main Menu

          

Tutorial Guide Definitions Renal Physiology Review Pathophysiology Causes Signs & Symptoms Hyperlipidemia in CRF Inflammation Pharmacology Case Study/Quiz References
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Definitions
   

 

CRF = Chronic Renal Failure permanent loss of nephrons and renal function Erythropoietin = Hormone produced by kidneys and regulates production of RBCs 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, doublecalled Bowmans Capsule

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Definitions


    

Lysosome = Membrane bound organelles, within the cell, containing hydrolytic enzymes - involved in intra & extracellular digestion Mesangial Cells = Supporting cells of glomeruliglomeruliproduce 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
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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 redRegulate blood-pressure bloodImportant in calcium ion absorption Control volume, composition and pH of the blood
Link: Renal Physiology
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Renal Hormone Regulation

Synthesis and activation of hormones by the kidney include: Active form of Vitamin D Erythropoietin Renal blood flow regulated by: ReninRenin-angiotensin aldosterone system (RAAS)
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Fluid and Electrolyte Control Mechanisms

 RAAS

Renin-Angiotensin Aldosterone ReninSystem  Aldosterone  ADH Anti-Diuretic Hormone Anti-

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How the RAAS Pathway Works

Valerie Kolmer 2006

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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 bloodbloodpressure
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ADH (Anti-Diuretic Hormone)

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Quick Quiz
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
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1. 2. 3.

Answer 1.
Renin Angiotensin II- ACE- ADH Aldosterone II- ACEThat is not correct Please try again

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Answer 2.
Renin Angiotensin I Aldosterone ADH - ACE

1.

That is not correct Please Try Again

2.

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Answer 3.
Renin Angiotensin I ACE Angiotensin II Aldosterone You are RIGHT!

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Renal Structure
 Each

kidney has a renal pelvis (divided into major & minor calyces), renal cortex calyces), (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
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(a) Nephron (b) Renal Pyramid with Nephrons (c) Section of Kidney

Shier,D., Butler, J., Lewis, R (1999). Holes human anatomy and physiology.(8th ed.). The McGraw-Hill Co, Inc. Used with permission: The McGraw-Hill Companies

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The Nephron
Each kidney contains approximately a million nephrons 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
.
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1. 2. 3. 4.

Shier, D., Butler, J., Lewis, R. (1999). Holes human anatomy & physiology(8th ed.). The McGraw-Hill Co., Inc

Nephron & Blood Supply

Shier,D., Butler, J., Lewis, R (1999). Holes human anatomy and physiology.(8th ed.). The McGraw-Hill Co, Inc. Used with permission: The McGraw-Hill Companies

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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). Holes human anatomy & physiology(8th ed.). The McGraw-Hill Co., Inc. McGraw-

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What is Glomerular Filtration Rate (GFR)?

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 CockcroftCockcroftGault equation that estimates creatinine clearance
 The
Link: GFR Info
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Urine Formation
Name Glomerular Filtration Tubular Reabsorption Tubular Secretion Reabsorption of Water Process Blood Pressure pushes sm. molecules from glomerulus into glomerular capsule Diffusion/active transport take molecules to blood-at the bloodproximal tubule Active transport takes molecules from blood into distal convoluted tubule All along nephron length, mainly Loop of Henle & collecting ductductH2O returns by osmosis after reabsorption of Na Urine formation rids body of metabolic wastes Molecule Example Water,glucose,salts,urea, creatinine,amino acids,uric acid Water, glucose, amino acids, salts Uric acid, creatinine, hydrogen ions, ammonia

Salt & water

Excretion

Water, salts, urea, uric acid, ammonium, creatinine

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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

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Pathophysiology of CRF
What is Chronic Renal Failure? It is progressive tissue destruction with permanent loss of nephrons and renal function.

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Risk Factors
 

Age > 60 years Race or ethnic background AfricanAfrican-American Hispanic American Indian Asian History of exposure to chemicals/toxins Cigarette smoke Heavy metals Family history of chronic kidney disease
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Chronic vs. Acute Renal Failure

Acute Renal Failure (ARF): a. Abrupt onset b. Potentially reversible  Chronic Renal Failure (CRF): a. Progresses over at least 3 months b. Permanent- non-reversible damage to Permanent- nonnephrons

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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

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Functional Changes of CRF

The Kidneys are unable to: Regulate fluids and electrolytes Balance fluid volume and renin-angiotensin reninsystem Control blood pressure Eliminate nitrogen and other wastes Synthesize erythropoietin Regulate serum phosphate and calcium levels
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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
Valerie Kolmer 2006

Healthy Glomerulus

Damaged Glomerulus Main Menu

4 Stages of CRF
1. 2. 3. 4.

Reduced Renal Reserve (Silent): no symptoms evident- GFR up to 50ml/min evidentRenal Insufficiency: function of both kidneys lost- GFR 25-50 ml/min lost25Renal Failure: GFR 5-25 ml/min 5End Stage Renal Disease: GFR less than 5 ml/min
Link: GFR Info
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Quick Quiz Chronic Renal Failure is reversible.

True

False

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Sorry! That is not correct.

The answer is false. Nephron damage is permanent & progressive in CRF Please continue.

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You are right!

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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
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SIGNS & SYMPTOMS Lab Value Cues

1.

2.

3.

Anemias - d/t decreased erythropoietin secretion & uremic toxin damage to RBCs Azotemia (elevated nitrogen) d/t retention of nitrogenous wastes Creatinine a component of muscle & its 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

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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.

6.

7.

Hyperlipidemia decreased serum albumin leads to increased synthesis of LDLs & cholesterol by the liver, contributing to elevated lipid levels Proteinuria increased protein filtration d/t glomeruli damage

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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
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Signs & Symptoms at a Glance

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Genetics of Kidney Disease

Genetic diseases that cause CRF:


Polycystic Kidney Disease (PKD)

Nephropathic Cystinosis (Fanconis Syndrome)

Alport Syndrome
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Sanford, R. (2004). Autosomal dominant polycystic kidney disease. Retrieved February 8, 2006, http://www.cgkp.org.uk/topics/camhttp://www.cgkp.org.uk/topics/camgenetics/sanford.htm

Polycystic Kidney Disease

 

 

Most Common Genetic Disorder Numerous fluid-filled fluidcysts in kidneys and renal tubules Normal renal tissue replaced by cysts Decreased function leads to end-stage endrenal disease

Polycystic jpg 58_001.connection.ww.com//Ch58/jpg/58_001.jpg

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Two Major Forms PKD



Autosomal Dominant PKD Autosomal Recessive PKD

Only treatment for both = dialysis and kidney transplantation

Used with permission: Lippincott Williams & Wilkins

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Autosomal Dominant PKD

 90%

of the cases of PKD are this form  4th leading cause of renal failure age 40-60 40 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
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Autosomal Recessive PKD

 Rare

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
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Metabolic Impact
common in CRFCRFespecially in Nephrotic Syndrome  Excessive lipids accelerate progression of renal disease  Cholesterol increases glomerular injury
 Hyperlipidemia

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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
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Mesangial Cell Contribution

Valerie Kolmer 2006

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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
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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
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Inflammation- (Cont.)
Renal Failure- prolongs inflammatory reactions Failure 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 AJN,105(6),40-

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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 AJN,105(6),40-

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Angiotensin II in the Inflammatory Process

Inflammatory mediator causing:

Increased vascular permeability Increased leukocyte infiltration (monocytes, macrophages) Cell proliferation & hypertrophy

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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.

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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
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Nephritic Syndromes
Glomerulonephritis An inflammatory response in the endothelial, epithelial & mesangial cells of the glomeruli Inflammatory process damages the capillary wallwall-allowing RBCs into the urine Symptoms: 1st oliguria, followed by hematuria, azotemia, low GFR (d/t hemodynamic changes), hypertension
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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
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P o r t Porth, Porth, 1998 1998 h , 1

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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
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Pharmacology in CRF
Pharmacokinetics drug absorption, distribution, metabolism & excretion Pharmacodynamics A drugs mechanism of action and effect at the target site

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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 PDecreased glomerular filtration rate affects drug excretion
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Campoy, S, Elwell, R.(2005). Pharmacology & CKD. AJN, 105(9),60-72.

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
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Campoy, S, Elwell, R.(2005). Pharmacology & CKD. AJN, 105(9),60-72.

Medication Considerations (Cont.)

Impaired renal excretion leads to toxic drug accumulations with: Diamox Aminoglycoside antibiotics (tobramycin & gentamycin) Atenolol Captopril Lithium Vancomycin Metformin Neurontin Topamax
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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.

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Case Study
Mrs. G. Nephritis is a 42 y/o African-American Africanfemale. 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.
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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.
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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) 8(nl= 0.6-0.9 mg/dL) 0.6(nl= 8.2-10.2 mg/dL) 8.2(nl= 135-145 mEq/L) 135(nl= 12-16 g/dL) 12(nl= 36-48%) 36(nl= 3.5-5 g/dL) 3.5(nl= 6.4-8.3 g/dL) 6.4(nl= <130mg/dL) (nl= 40-85 mg/dL) 40Main Menu

Other Tests
Urinalysis: ProteinProtein-100 RBC 1-2 Moderately enlarged heart Sinus rhythm with occasional PVCs

CXR: EKG:

Blood Pressure: 168/98

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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
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Answer
The correct answer is # 1 chronic renal failure (CRF) Symptoms progressively worsening x several months : all 3 indicative of renal failure Elevated creatinine Elevated BUN

SOB Shoes too tight

:indicating fluid retention

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Question #2
Which compensatory mechanism causes the increased fluid retention, increased sodium and elevated blood-pressure? blood1. 2. 3. 4.

Renin Angiotensin Aldosterone System (RAAS) Bone Marrow suppression Deregulation of baroreceptors Suppression of Sympathetic Nervous System
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Answer
#1 RAAS- Renin Angiotensin RAASAldosterone 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.
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Question #3
Why is this chronic and not acute renal failure? Progressive over long period of time H & H <10 HCT < 30 Sodium of 137

1. 2. 3. 4.

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Answer

#1 is correct Mrs. Nephritis symptoms have progressively worsened over months

http://office.microsoft.com/en-us/tou.aspx

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Question #4
What risk factors in her history could lead to CRF? 1. African-American African2. HTN 3. Smoker 4. Obesity 5. All of the above 6. 1, 2 and 3
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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

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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
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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

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Question # 6
In a patient with renal failure it is important to avoid drugs that are essentially eliminated by the kidneys. True or False?

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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)

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Congratulations!

You have completed the Chronic Renal Failure Tutorial

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References
       

Bowne, P. S. (). . Retrieved February 7, 2006, P. http://faculty.alverno.edu/bowneps/index.html BurrowsBurrows-Hudson, S. (2005). Chronic kidney disease: An overview. American Journal of Nursing, 105(2), 40-50. 105(2), 40Campoy, S. & Elwell, R. (2005, September). Pharmacology & CKD. AJN, 105(9), 60-72. 105(9), 60Cannon, J. (2004). Recognizing chronic renal failure. Nursing 2004, 34(1), 5034(1), 50-53. Castner, D. & Douglas, C. (2005). Now onstage: Chronic kidney disease. Nursing 2005, 35(12), 58-63. 35(12), 58Huether, 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. 105(6), 40Lippincott Williams & Wilkins (2005). Pathophysiology A 2-in-1 2-inreference for nurses (1st ed.). Ambler, Pa.: Lippincott Williams & Wilkins.
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References
 

Microsoft media elements (). . Retrieved February 7, 2006, http://office.microsoft.com/en-us/tou.aspx http://office.microsoft.com/enNational 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/

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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. LippincottPorth, C. M. (2004). Essentials of pathophysiology. Philadelphia, pathophysiology. 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 http://www.cgkp.org.uk/topics/camShier, D. Butler, J. & Lewis, R. (1999). Hole's human anatomy & physiology (8th ed.). pp. 782, 786, 788: The McGraw-Hill McGrawCompanies

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References


Wadhwa, D. (2005). Chronic renal failure. Retrieved February 8, 2006,http://www.uhmc.sunysb.edu/internalmed/nephro/ webpages/Partwebpages/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

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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 McGrawtheir permission to include the wonderful visuals on renal physiology.
Any questions or comments you can contact me at: Valerie Kolmer 1-262-639-4107 262-639or wudwurkr@execpc.com
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