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CHRONIC RENAL FAILURECHRONIC RENAL FAILURE
Valerie Kolmer Valerie Kolmer RN BSN BCRN BSN BCMSN 621MSN 621
Alverno CollegeAlverno College
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ObjectivesObjectives
Upon completion of this tutorial the learner Upon completion of this tutorial the learner will:will:
Have an increased understanding of the Have an increased understanding of the pathophysiology of Chronic Renal Failure pathophysiology of Chronic Renal Failure
Recognize the signs and symptoms of Recognize the signs and symptoms of Chronic Renal Failure Chronic Renal Failure
Identify the disease progression and Identify the disease progression and treatment interventionstreatment interventions
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Chronic Renal FailureChronic Renal Failure Tutorial GuideTutorial Guide
Return to the main menu at any time by Return to the main menu at any time by pushing the button.pushing the button.
Hyperlinks to outside sources, for in-depth Hyperlinks to outside sources, for in-depth information, are available on various information, are available on various slides. Just push on the slides. Just push on the button. Click back button to return.button. Click back button to return.
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Chronic Renal FailureChronic Renal Failure Main MenuMain Menu
Tutorial GuideTutorial Guide DefinitionsDefinitions Renal Physiology ReviewRenal Physiology Review PathophysiologyPathophysiology CausesCauses Signs & SymptomsSigns & Symptoms Hyperlipidemia in CRFHyperlipidemia in CRF InflammationInflammation PharmacologyPharmacology Case Study/QuizCase Study/Quiz ReferencesReferences
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DefinitionsDefinitions CRF = Chronic Renal Failure – permanent loss of nephrons = Chronic Renal Failure – permanent loss of nephrons
and renal functionand renal function Erythropoietin = Hormone produced by kidneys and = Hormone produced by kidneys and
regulates production of RBC’sregulates production of RBC’s FiltrateFiltrate = Liquid entering the nephron= Liquid entering the nephron FiltrationFiltration = Movement of liquid through a membrane (like a = Movement of liquid through a membrane (like a
sieve), allows only small molecules & liquids to pass sieve), allows only small molecules & liquids to pass through. Movement is from higher to lower pressurethrough. Movement is from higher to lower pressure
GFRGFR = Glomerular Filtration Rate – amount of filtrate = Glomerular Filtration Rate – amount of filtrate produced each minuteproduced each minute
GlomerulusGlomerulus = Filtration system of the nephron, composed = Filtration system of the nephron, composed of capillaries surrounded by a thin double-walled capsule, of capillaries surrounded by a thin double-walled capsule, called Bowman’s Capsulecalled Bowman’s Capsule
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DefinitionsDefinitions LysosomeLysosome = Membrane bound organelles, within = Membrane bound organelles, within
the cell, containing hydrolytic enzymes - involved the cell, containing hydrolytic enzymes - involved in intra & extracellular digestionin intra & extracellular digestion
Mesangial CellsMesangial Cells = Supporting cells of glomeruli- = Supporting cells of glomeruli- produce intracellular substancesproduce intracellular substances
Nephron Nephron = Functional unit of the kidney= Functional unit of the kidney ReabsorptionReabsorption = Movement of substances from the = Movement of substances from the
filtrate back into the bloodfiltrate back into the blood Renal Corpuscle Renal Corpuscle = Glomerulus and surrounding = Glomerulus and surrounding
epithelial capsule.epithelial capsule. SecretionSecretion = Active transport of solutes into the = Active transport of solutes into the
nephronnephron
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Renal Physiology ReviewRenal Physiology ReviewThe Kidneys:The Kidneys:
a.a. Control the fluid/electrolyte balance for the Control the fluid/electrolyte balance for the bodybody
b.b. Remove metabolic wastes from the blood & Remove metabolic wastes from the blood & excrete them to the outsideexcrete them to the outside
c.c. Regulate red-blood cell productionRegulate red-blood cell production
d.d. Regulate blood-pressureRegulate blood-pressure
e.e. Important in calcium ion absorptionImportant in calcium ion absorption
f.f. Control volume, composition and pH of the Control volume, composition and pH of the bloodblood
Link: Renal Physiology
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Renal Hormone RegulationRenal Hormone Regulation
Synthesis and activation of hormones by Synthesis and activation of hormones by the kidney include:the kidney include:
• Active form of Vitamin DActive form of Vitamin D• ErythropoietinErythropoietin
Renal blood flow regulated by:Renal blood flow regulated by:
Renin-angiotensin aldosterone system Renin-angiotensin aldosterone system (RAAS)(RAAS)
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Fluid and Electrolyte ControlFluid and Electrolyte ControlMechanismsMechanisms
RAAS – Renin-Angiotensin Aldosterone RAAS – Renin-Angiotensin Aldosterone SystemSystem
AldosteroneAldosterone ADH – Anti-Diuretic HormoneADH – Anti-Diuretic Hormone
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How the RAAS Pathway WorksHow the RAAS Pathway Works
Valerie KolmerValerie Kolmer
20062006
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Aldosterone
Increases rate of sodium ion absorptionIncreases rate of sodium ion absorption Chloride moves along with sodium Chloride moves along with sodium
because of + charge of sodiumbecause of + charge of sodium Increases rate of potassium & hydrogen Increases rate of potassium & hydrogen
ion secretionion secretion
Result:Result:
Fluid and sodium retention increases blood-Fluid and sodium retention increases blood-pressurepressure
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ADH (Anti-Diuretic Hormone)
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Quick QuizQuick Quiz
Pick the correct pathway of the RAASPick the correct pathway of the RAAS
1.1. Renin – Angiotensin II – ACE – ADH – AlRenin – Angiotensin II – ACE – ADH – Aldosteronedosterone
2.2. Renin – Angiotensin I – Aldosterone – ARenin – Angiotensin I – Aldosterone – ADH –ACE DH –ACE
3.3. Renin – Angiotensin I – ACE – Renin – Angiotensin I – ACE – Angiotensin II – Aldosterone Angiotensin II – Aldosterone
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Answer 1.Answer 1.
Renin – Angiotensin II- ACE- ADH – AldosteroneRenin – Angiotensin II- ACE- ADH – Aldosterone
That is not correctThat is not correct
Please try againPlease try again
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Answer 2.Answer 2.
Renin – Angiotensin I – Aldosterone – ADH - ACERenin – Angiotensin I – Aldosterone – ADH - ACE
1.1. That is not That is not correctcorrect
2.2. Please Try Please Try AgainAgain
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Answer 3.Answer 3.Renin – Angiotensin I – ACE – Renin – Angiotensin I – ACE –
Angiotensin II – AldosteroneAngiotensin II – AldosteroneYou are RIGHT!You are RIGHT!
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Renal StructureRenal Structure Each kidney has a renal pelvis Each kidney has a renal pelvis (divided (divided
into major & minor calyces)into major & minor calyces),, renal cortex renal cortex (the outer portion)(the outer portion) & renal medulla & renal medulla (lies (lies under the cortex)under the cortex)
Within the renal medulla there are many Within the renal medulla there are many renal pyramids that consist of multiple renal pyramids that consist of multiple nephrons nephrons (the functional units of the (the functional units of the kidney)kidney)
The renal pelvis collects the urine & The renal pelvis collects the urine & passes it to the ureterpasses it to the ureter
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(a)(a) NephronNephron(b) Renal Pyramid with Nephrons(b) Renal Pyramid with Nephrons
(c) Section of Kidney(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
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The NephronThe Nephron
Each kidney contains approximately a Each kidney contains approximately a million nephron’smillion nephron’s
Filtered fluid from the blood enters:Filtered fluid from the blood enters:1.1. The renal corpuscle The renal corpuscle (consisting of the (consisting of the
glomerulus)glomerulus)2.2. Proximal convoluted tubuleProximal convoluted tubule3.3. Loop of Henle Loop of Henle (descending & ascending (descending & ascending
limb)limb)4.4. Distal convoluted tubuleDistal convoluted tubule
Shier, D., Butler, J., Lewis, R. (1999). Hole’s human anatomy & physiology(8th ed.). The McGraw-Hill Co., Inc.
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Nephron & Blood SupplyNephron & Blood Supply
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
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Urine Formation Efferent arteriole constriction causes the Efferent arteriole constriction causes the
blood in the glomerulus to be under high blood in the glomerulus to be under high pressure. pressure.
Filtrate: the water and other small Filtrate: the water and other small molecules that move into the glomerular molecules that move into the glomerular capsule. Approximately 45 gallons of filtrate capsule. Approximately 45 gallons of filtrate are produced each day. Most of the water are produced each day. Most of the water and molecules are reabsorbed along the and molecules are reabsorbed along the tubules as the filtrate passes through.tubules as the filtrate passes through.
Shier, D., Butler, J., Lewis, R. (1999). Shier, D., Butler, J., Lewis, R. (1999). Hole’s Hole’s human anatomy & physiology(8human anatomy & physiology(8thth ed.). ed.). The McGraw-Hill Co., Inc.The McGraw-Hill Co., Inc.
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What is Glomerular Filtration Rate
(GFR)? The GFR is the measurement of the The GFR is the measurement of the
kidneys ability to filter waste productskidneys ability to filter waste products It shows the volume of H2O and solutes It shows the volume of H2O and solutes
filtered out of blood plasma through the filtered out of blood plasma through the glomeruli over a period of timeglomeruli over a period of time
Common measurement is the Cockcroft-Common measurement is the Cockcroft-Gault equation that estimates creatinine Gault equation that estimates creatinine clearanceclearance
Link: GFR Info
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Urine FormationUrine Formation
NameName ProcessProcess Molecule ExampleMolecule Example
GlomerularGlomerular
FiltrationFiltration
Blood Pressure pushes sm. Blood Pressure pushes sm. molecules from glomerulus into molecules from glomerulus into glomerular capsuleglomerular capsule
Water,glucose,salts,urea,Water,glucose,salts,urea,
creatinine,amino acids,uric creatinine,amino acids,uric acidacid
TubularTubular
ReabsorptionReabsorption
Diffusion/active transport take Diffusion/active transport take molecules to blood-at the molecules to blood-at the proximal tubuleproximal tubule
Water, glucose, amino acids, Water, glucose, amino acids, saltssalts
Tubular Tubular
SecretionSecretion
Active transport takes molecules Active transport takes molecules from blood into distal convoluted from blood into distal convoluted tubuletubule
Uric acid, creatinine, Uric acid, creatinine, hydrogen ions, ammoniahydrogen ions, ammonia
Reabsorption ofReabsorption of
WaterWater
All along nephron length, mainly All along nephron length, mainly Loop of Henle & collecting duct- Loop of Henle & collecting duct- H2O returns by osmosis after H2O returns by osmosis after reabsorption of Nareabsorption of Na
Salt & waterSalt & water
ExcretionExcretion Urine formation rids body of Urine formation rids body of metabolic wastesmetabolic wastes
Water, salts, urea, uric acid, Water, salts, urea, uric acid, ammonium, creatinineammonium, creatinine
Modified from: Shier, D., Butler, J., Lewis, R. (1999). Modified from: Shier, D., Butler, J., Lewis, R. (1999). Hole’s human anatomy & physiology(8th ed.). The McGraw-Hill Co.,Hole’s human anatomy & physiology(8th ed.). The McGraw-Hill Co., Inc.Inc.
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Nephron Component FunctionsNephron Component Functions
Reabsorption of glucose, calcium, K+, Na, proteins and H2O
Filtration of H2O and dissolved substances from the plasma Reabsorption of Na ions,
Water, Secretion of hydrogen ions and K+ ions
Reabsorption of Na, K+ & Chloride ions
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
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Pathophysiology of CRFPathophysiology of CRF
What is Chronic Renal Failure?What is Chronic Renal Failure?
It is progressive tissue destruction with It is progressive tissue destruction with
permanent loss of nephrons and renal permanent loss of nephrons and renal function.function.
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Risk Factors
AgeAge > 60 years > 60 years Race or ethnic backgroundRace or ethnic background African-AmericanAfrican-American HispanicHispanic American IndianAmerican Indian AsianAsian History of exposure to chemicals/toxinsHistory of exposure to chemicals/toxins Cigarette smokeCigarette smoke Heavy metalsHeavy metals Family history of chronic kidney diseaseFamily history of chronic kidney disease
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Chronic vs. Acute Renal FailureChronic vs. Acute Renal Failure
Acute Renal Failure (ARF):Acute Renal Failure (ARF):
a.a. Abrupt onsetAbrupt onset
b.b. Potentially reversiblePotentially reversible Chronic Renal Failure (CRF):Chronic Renal Failure (CRF):
a.a. Progresses over at least 3 monthsProgresses over at least 3 months
b.b. Permanent- non-reversible damage to Permanent- non-reversible damage to nephronsnephrons
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Pathophysiology of CRFPathophysiology of CRF
Progressive destruction of nephrons leads to:Progressive destruction of nephrons leads to:
a.a. Decreased Decreased glomerularglomerular filtration, tubular reabsorption filtration, tubular reabsorption & & renal hormone regulation renal hormone regulation
b.b. Remaining functional nephrons compensate Remaining functional nephrons compensate
c.c. FunctionalFunctional and and structuralstructural changes occur changes occur
d.d. Inflammatory response triggeredInflammatory response triggered
e.e. Healthy glomeruli so overburdened they Healthy glomeruli so overburdened they become stiff, sclerotic and necroticbecome 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 CRFFunctional Changes of CRF
The Kidneys are unable to:The Kidneys are unable to: Regulate fluids and electrolytesRegulate fluids and electrolytes Balance fluid volume and Balance fluid volume and
renin-angiotensin systemrenin-angiotensin system Control blood pressureControl blood pressure Eliminate nitrogen and other wastesEliminate nitrogen and other wastes Synthesize Synthesize erythropoietinerythropoietin Regulate serum phosphate and calcium levelsRegulate serum phosphate and calcium levels
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Structural Changes of CRFStructural Changes of CRF
Epithelial damageEpithelial damage Glomerular and parietal Glomerular and parietal
basement membrane basement membrane damagedamage
Vessel wall thickeningVessel wall thickening Vessel lumen narrowing Vessel lumen narrowing
leading to stenosis of leading to stenosis of arteries and capillariesarteries and capillaries
Sclerosis of membranes, Sclerosis of membranes, glomeruli and tubulesglomeruli and tubules
Reduced glomerular Reduced glomerular filtration ratefiltration rate
Nephron destructionNephron destruction
Healthy Glomerulus
Damaged Glomerulus
Valerie Kolmer 2006Valerie Kolmer 2006
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4 Stages of CRF4 Stages of CRF
1.1. Reduced Renal Reserve (Silent):Reduced Renal Reserve (Silent): no no symptoms evident- GFR up to 50ml/minsymptoms evident- GFR up to 50ml/min
2.2. Renal Insufficiency:Renal Insufficiency: ½ function of both ½ function of both kidneys lost- GFR 25-50 ml/minkidneys lost- GFR 25-50 ml/min
3.3. Renal Failure:Renal Failure: GFR 5-25 ml/min GFR 5-25 ml/min
4.4. End Stage Renal Disease:End Stage Renal Disease: GFR less GFR less than 5 ml/minthan 5 ml/min
Link: GFR Info
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Quick QuizQuick Quiz
Chronic Renal Failure is reversible.Chronic Renal Failure is reversible.
True False
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Sorry! That is not correct.Sorry! That is not correct. The answer is false.The answer is false.Nephron damage is permanentNephron damage is permanent & progressive in CRF& progressive in CRF
Please continue. Please continue.
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You are right!You are right!
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Causes of CRFCauses of CRF
1)1) Diabetic Nephropathy Diabetic Nephropathy 2)2) HypertensionHypertension3)3) Vascular DiseaseVascular Disease4)4) Polycystic Kidney Disease/GeneticsPolycystic Kidney Disease/Genetics5)5) Chronic InflammationChronic Inflammation6)6) ObstructionObstruction7)7) Glomerular Disorders/ Glomerular Disorders/
GlomerulonephritisGlomerulonephritis
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SIGNS & SYMPTOMS Lab Value Cues
1. Anemia’s - d/t decreased erythropoietin secretion & uremic toxin damage to RBC’s
2. Azotemia – (elevated nitrogen) d/t retention of nitrogenous wastes
3. 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.
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SIGNS & SYMPTOMS Lab Value Cues
4. Hypocalcemia – impaired regulation of Vitamin D leads to decreased absorption & low calcium levels. High phosphorus levels also cause low serum calcium levels.
5. Hyperkalemia – impaired excretion of potassium by the kidneys leads to elevated potassium levels.
6. Hyperlipidemia – decreased serum albumin leads to increased synthesis of LDL’s & cholesterol by the liver, contributing to elevated lipid levels
7. Proteinuria – increased protein filtration d/t glomeruli damage
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SIGNS & SYMPTOMSSIGNS & SYMPTOMSVisual / Verbal CuesVisual / Verbal Cues
1)1) Dry mouth, fatigue, Dry mouth, fatigue, nauseanausea – d/t – d/t hyponatremia & uremiahyponatremia & uremia
2)2) HypertensionHypertension – d/t – d/t sodium & water sodium & water retentionretention
3)3) Hypervolemia Hypervolemia – d/t – d/t sodium & water sodium & water retentionretention
4)4) Gray/yellow skinGray/yellow skin – d/t – d/t accumulated urine accumulated urine pigmentspigments
5)5) Cardiac irritabilityCardiac irritability – d/t – d/t hyperkalemiahyperkalemia
6)6) Muscle crampsMuscle cramps – d/t – d/t hypocalcemiahypocalcemia
7)7) Bone & muscle painBone & muscle pain – d/t – d/t hypocalcemia / hypocalcemia / hyperphosphatemia hyperphosphatemia
8)8) Restless leg syndromeRestless leg syndrome – – d/t toxins’ effects on the d/t toxins’ effects on the nervous systemnervous system
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Signs & Symptoms at a Glance
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Genetics of Kidney DiseaseGenetics of Kidney Disease
Genetic diseases that Genetic diseases that cause CRF:cause CRF:
Polycystic Kidney Polycystic Kidney Disease (PKD)Disease (PKD)
Nephropathic CystinosisNephropathic Cystinosis (Fanconi’s Syndrome)(Fanconi’s Syndrome)
Alport SyndromeAlport Syndrome
Sanford, R. (2004). Sanford, R. (2004). Autosomal dominant polycystic kidney disease.Autosomal dominant polycystic kidney disease. Retrieved February 8, 2006, http://www.cgkp.org.uk/topics/cam-Retrieved February 8, 2006, http://www.cgkp.org.uk/topics/cam-genetics/sanford.htmgenetics/sanford.htm
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Polycystic Kidney DiseasePolycystic Kidney Disease
Most Common Most Common Genetic DisorderGenetic Disorder
Numerous fluid-filled Numerous fluid-filled cysts in kidneys and cysts in kidneys and renal tubulesrenal tubules
Normal renal tissue Normal renal tissue replaced by cystsreplaced by cysts
Decreased function Decreased function leads to end-stage leads to end-stage renal diseaserenal disease Polycystic jpg 58_001.connection.ww.com/…/Ch58/jpg/58_001.jpg
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Two Major Forms PKDTwo Major Forms PKD
Autosomal Dominant Autosomal Dominant PKDPKD
Autosomal Recessive Autosomal Recessive PKDPKD
Only treatment for both = Only treatment for both = dialysis and kidney dialysis and kidney transplantationtransplantation
Used with permission: Lippincott Williams & Wilkins
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Autosomal Dominant PKDAutosomal Dominant PKD
90% of the cases of PKD are this form90% of the cases of PKD are this form 44thth leading cause of renal failure age 40-60 leading cause of renal failure age 40-60 Undetected for years until symptoms Undetected for years until symptoms
developdevelop Occurs equally males and females, mainly Occurs equally males and females, mainly
CaucasiansCaucasians One parent with ADPKD gene = 50% One parent with ADPKD gene = 50%
chance children will inherit diseasechance children will inherit disease Gene mutation on chromosome 16 or 4Gene mutation on chromosome 16 or 4
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Autosomal Recessive PKDAutosomal Recessive PKD
Rare form – occurs in 1 in 4 babies (of Rare form – occurs in 1 in 4 babies (of parents with mutation)parents with mutation)
Worst cases die within hours of birthWorst cases die within hours of birth Both parents with gene mutationBoth parents with gene mutation Mutation on chromosome 6Mutation on chromosome 6 25% chance children will inherit disease25% chance children will inherit disease
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Metabolic ImpactMetabolic Impact
Hyperlipidemia common in CRF- Hyperlipidemia common in CRF- especially in Nephrotic Syndromeespecially in Nephrotic Syndrome
Excessive lipids accelerate progression of Excessive lipids accelerate progression of renal diseaserenal disease
Cholesterol increases glomerular injuryCholesterol increases glomerular injury
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Contributing MechanismsContributing Mechanisms
Two known paths of hyperlipidemia Two known paths of hyperlipidemia progression in CRF:progression in CRF:
Hyperlipidemia activates LDL receptors in Hyperlipidemia activates LDL receptors in mesangial cellsmesangial cells
Increased synthesis of lipoproteins in the Increased synthesis of lipoproteins in the liver related to increased albumin liver related to increased albumin productionproduction
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Mesangial Cell ContributionMesangial Cell Contribution
Valerie Kolmer 2006
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Albumin ContributionAlbumin ContributionNormal glomeruli structure limits proteins from filtering Normal glomeruli structure limits proteins from filtering
through the urinethrough the urine
Progression of glomeruli injury leads to increased Progression of glomeruli injury leads to increased capillary filtration of albumincapillary filtration of albumin
The liver compensates and increases albumin production The liver compensates and increases albumin production - to replace albumin lost in urine- to replace albumin lost in urine
This leads to increased synthesis of lipoproteins by the This leads to increased synthesis of lipoproteins by the liver secondary to the compensatory increase in albumin liver secondary to the compensatory increase in albumin production.production.
Results in increased LDL levels – predisposing to Results in increased LDL levels – predisposing to atherosclerosisatherosclerosis
Atherosclerosis further increases glomeruli injury Atherosclerosis further increases glomeruli injury
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InflammationInflammation
Inflammatory response can be triggered Inflammatory response can be triggered by: tissue injury, infections, toxins, immune by: tissue injury, infections, toxins, immune responses and/or Angiotensin IIresponses and/or Angiotensin II
Can be acute or chronicCan be acute or chronic Can affect the renal pelvis and interstitial Can affect the renal pelvis and interstitial
tissue as in pyelonephritistissue as in pyelonephritis Can affect the glomeruli as in Can affect the glomeruli as in
glomerulonephritisglomerulonephritis
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Inflammation- (Cont.)
Renal Failure- prolongs inflammatory reactionsRenal Failure- prolongs inflammatory reactions Adverse effects of chronic inflammation=Adverse effects of chronic inflammation=
Decreased appetiteDecreased appetite
Muscle and fat wastingMuscle and fat wasting
Endothelial damageEndothelial damage
AtherosclerosisAtherosclerosis
HypoalbuminemiaHypoalbuminemia
Increased cardiovascular disease riskIncreased cardiovascular disease risk
Legg, V.(2005). Complications of chronic kidney disease. Legg, V.(2005). Complications of chronic kidney disease. AJN,AJN,105(6),40-105(6),40-5050
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Causes of Inflammation in CRF
InfectionInfection AnemiaAnemia Uremia Uremia – increases oxidation of proteins, – increases oxidation of proteins,
lipids & carbohydrates, leading to vascular lipids & carbohydrates, leading to vascular inflammationinflammation
Malnutrition – Malnutrition – decreases antioxidantsdecreases antioxidants Low serum albumin Low serum albumin – decreases – decreases
antioxidantsantioxidantsLegg, V.(2005). Complications of chronic kidney disease. Legg, V.(2005). Complications of chronic kidney disease. AJN,AJN,105(6),40-50105(6),40-50
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Angiotensin II in theInflammatory Process
Inflammatory mediator causing:Inflammatory mediator causing:
• Increased vascular permeabilityIncreased vascular permeability• Increased leukocyte infiltration Increased leukocyte infiltration
(monocytes, macrophages)(monocytes, macrophages)• Cell proliferation & hypertrophyCell proliferation & hypertrophy
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Glomerular Inflammatory Disorders
Reminder: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 Nephrotic vs. Nephritic SyndromesSyndromes
Nephrotic SyndromesNephrotic Syndromes - glomerular - glomerular disorders that affect the glomerular disorders that affect the glomerular capillary membrane & capillary membrane & increasesincreases permeability to plasma proteinspermeability to plasma proteins
Nephritic SyndromesNephritic Syndromes – glomerular – glomerular disorders that initiate the inflammatory disorders that initiate the inflammatory response within the glomeruli & initially response within the glomeruli & initially decreasesdecreases permeability of the membrane permeability of the membrane
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Nephritic Syndromes
GlomerulonephritisGlomerulonephritis• An inflammatory response in the endothelial, An inflammatory response in the endothelial,
epithelial & mesangial cells of the glomeruliepithelial & mesangial cells of the glomeruli• Inflammatory process damages the capillary Inflammatory process damages the capillary
wall-allowing RBCs into the urinewall-allowing RBCs into the urine
Symptoms:Symptoms:• 1st oliguria, followed by hematuria, azotemia, 1st oliguria, followed by hematuria, azotemia,
low GFR (d/t hemodynamic changes), low GFR (d/t hemodynamic changes), hypertensionhypertension
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Nephrotic Syndromes
Primary causes:Primary causes: Lipoid NephrosisLipoid Nephrosis Focal Segmental Focal Segmental
glomerulosclerosisglomerulosclerosis Membranous Membranous
glomerulonephritisglomerulonephritis
Secondary causes:Secondary causes: Diabetes MellitusDiabetes Mellitus SLESLE AmyloidosisAmyloidosis
Characterized by:Characterized by: Proteinuria > 3.5g/dayProteinuria > 3.5g/day LipiduriaLipiduria HypoalbuminemiaHypoalbuminemia HyperlipidemiaHyperlipidemia
Increased permeability of Increased permeability of glomerular membrane glomerular membrane allows proteins to escape allows proteins to escape into the filtrateinto the filtrate
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Porth, 1998
Porth, 1998Porth, 1998
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Chronic GlomerulonephritisChronic Glomerulonephritis A slow, progressive disease that can be caused A slow, progressive disease that can be caused
by primary ( Nephrotic & Nephritic Syndromes) by primary ( Nephrotic & Nephritic Syndromes) or secondary disorders ( SLE, Good pasture's)or secondary disorders ( SLE, Good pasture's)
Typically develops asymptomatically over many Typically develops asymptomatically over many yearsyears
Hypertension, proteinuria and hematuria Hypertension, proteinuria and hematuria exhibited with progression of diseaseexhibited with progression of disease
Late stages display uremic symptoms of Late stages display uremic symptoms of azotemia, nausea, vomiting, dyspnea and azotemia, nausea, vomiting, dyspnea and pruritispruritis
Leads to CRFLeads to CRF Treatment includes: control of hypertension, Treatment includes: control of hypertension,
control of fluid/electrolyte imbalances, reduce control of fluid/electrolyte imbalances, reduce edema, prevent heart failureedema, prevent heart failure
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Pharmacology in CRF
Pharmacokinetics –
drug absorption, distribution, metabolism & excretion
Pharmacodynamics –
A drug’s mechanism of action and effect at the target site
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Alterations in Drug Responses in CRF
Gastrointestinal impairments affect absorption of Gastrointestinal impairments affect absorption of medicationsmedications
Volume of distribution (VVolume of distribution (Vdd) – the availability of a ) – the availability of a drug distributed in body tissues is increased or drug distributed in body tissues is increased or decreased by alterations in body composition or decreased by alterations in body composition or protein bindingprotein binding
Metabolism of medications altered -the kidneys Metabolism of medications altered -the kidneys produce many enzymes involved in drug produce many enzymes involved in drug metabolism including cytochrome P-450metabolism including cytochrome P-450
Decreased glomerular filtration rate affects drug Decreased glomerular filtration rate affects drug excretionexcretion
Campoy, S, Elwell, R.(2005). Pharmacology & CKD. AJN, 105(9),60-72.
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Medication Considerations in CRF
DilantinDilantin – increased V – increased Vd d related to protein binding related to protein binding changes and low albumin, increasing risk of drug changes and low albumin, increasing risk of drug toxicitytoxicity
DigoxinDigoxin – increased V – increased Vd d leading to toxicity due to leading to toxicity due to decreased renal excretiondecreased renal excretion
InsulinInsulin – metabolism of insulin decreases, – metabolism of insulin decreases, requiring dose reductionrequiring dose reduction
Tylenol and procainamideTylenol and procainamide – liver metabolized – liver metabolized drugs with metabolites that are excreted renally, drugs with metabolites that are excreted renally, can accumulate leading to drug toxicitycan accumulate leading to drug toxicity
Campoy, S, Elwell, R.(2005). Pharmacology & CKD. AJN, 105(9),60-72.
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Medication Considerations (Cont.)
Impaired renal excretion leads to toxic drug accumulations Impaired renal excretion leads to toxic drug accumulations with:with:
DiamoxDiamoxAminoglycoside antibiotics -Aminoglycoside antibiotics -(tobramycin & gentamycin)(tobramycin & gentamycin)
AtenololAtenololCaptoprilCaptoprilLithiumLithium
VancomycinVancomycinMetforminMetforminNeurontinNeurontinTopamaxTopamax
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Over-the-Counter Medicationsand 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 Mrs. G. Nephritis is a 42 y/o African-American female. She has 6 children and has a history female. She has 6 children and has a history of: mild obesity, hypertension, smoker, and of: mild obesity, hypertension, smoker, and chronic fatigue. chronic fatigue.
She comes to the emergency room with c/o She comes to the emergency room with c/o increasing SOB, vertigo, weakness, dry mouth, increasing SOB, vertigo, weakness, dry mouth, and nausea for the last several weeks. She is and nausea for the last several weeks. She is noticing that her shoes fit tightly and that her noticing that her shoes fit tightly and that her urine is concentrated. She also notices that urine is concentrated. She also notices that she only urinates once a day.she only urinates once a day.
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Case Study (cont.)
She recently moved here from Texas. Mrs. She recently moved here from Texas. Mrs. Nephritis experienced the same symptoms Nephritis experienced the same symptoms when in Texas and was told to follow up in when in Texas and was told to follow up in several weeks. She became busy with the several weeks. She became busy with the move and relates she was “too busy to move and relates she was “too busy to find a new physician”. Now months later find a new physician”. Now months later the symptoms have progressively the symptoms have progressively worsened.worsened.
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Significant Lab Work
BUN 37 (nl= 8-20 mg/dL)BUN 37 (nl= 8-20 mg/dL)Creatinine 4.7 (nl= 0.6-0.9 mg/dL)Creatinine 4.7 (nl= 0.6-0.9 mg/dL)Calcium 7.6 (nl= 8.2-10.2 mg/dL)Calcium 7.6 (nl= 8.2-10.2 mg/dL)Sodium 137 (nl= 135-145 mEq/L)Sodium 137 (nl= 135-145 mEq/L)Hemoglobin 8.5 (nl= 12-16 g/dL)Hemoglobin 8.5 (nl= 12-16 g/dL)Hematocrit 28.9 (nl= 36-48%)Hematocrit 28.9 (nl= 36-48%)Albumin 2.5 (nl= 3.5-5 g/dL)Albumin 2.5 (nl= 3.5-5 g/dL)Total Protein 6.2 (nl= 6.4-8.3 g/dL)Total Protein 6.2 (nl= 6.4-8.3 g/dL)LDL 156 (nl= <130mg/dL)LDL 156 (nl= <130mg/dL)HDL 32 (nl= 40-85 mg/dL)HDL 32 (nl= 40-85 mg/dL)
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Other Tests
Urinalysis: Protein-100Urinalysis: Protein-100 RBC – 1-2RBC – 1-2
CXR: Moderately enlarged heartCXR: Moderately enlarged heart
EKG: Sinus rhythm with EKG: Sinus rhythm with occasional PVC’soccasional PVC’s
Blood Pressure: 168/98Blood Pressure: 168/98
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Question #1
Based on this persons symptoms, history Based on this persons symptoms, history and lab work – What do you think her and lab work – What do you think her diagnosis would be?diagnosis would be?
1.1. CRFCRF
2.2. ARFARF
3.3. CHFCHF
4.4. Influenza Influenza
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Answer
The correct answer is # 1 chronic renal failure (CRF)
Symptoms progressively worsening x several monthsSymptoms progressively worsening x several monthsElevated creatinine Elevated creatinine : all 3 indicative of renal failure: all 3 indicative of renal failureElevated BUN Elevated BUN
SOBSOBShoes too tight Shoes too tight :indicating fluid retention:indicating fluid retention
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Question #2
Which compensatory mechanism causes the Which compensatory mechanism causes the increased fluid retention, increased sodium increased fluid retention, increased sodium
and elevated blood-pressure?and elevated blood-pressure?
1.1. Renin – Angiotensin – Aldosterone System Renin – Angiotensin – Aldosterone System (RAAS)(RAAS)
2.2. Bone Marrow suppressionBone Marrow suppression
3.3. Deregulation of baroreceptorsDeregulation of baroreceptors
4.4. Suppression of Sympathetic Nervous SystemSuppression of Sympathetic Nervous System
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Answer
#1 RAAS- Renin – Angiotensin – Aldosteron#1 RAAS- Renin – Angiotensin – Aldosterone System is correcte 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?
1. Progressive over long period of time
2. H & H <10
3. HCT < 30
4. Sodium of 137
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Answer
#1 is correct#1 is correct
Mrs. Nephritis’ Mrs. Nephritis’ symptoms have symptoms have progressively progressively
worsened over worsened over monthsmonths
http://office.microsoft.com/en-us/tou.aspx
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Question #4
What risk factors in her history could lead to What risk factors in her history could lead to CRF?CRF?
1.1. African-AmericanAfrican-American2.2. HTNHTN3.3. SmokerSmoker4.4. ObesityObesity5.5. All of the aboveAll of the above6.6. 1, 2 and 31, 2 and 3
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Answer
#5 All of the above is the correct answer.#5 All of the above is the correct answer.
Mrs. Nephritis has an increased risk of Mrs. Nephritis has an increased risk of renal failure related to her race and the renal failure related to her race and the smoking, HTN and obesity worsen the smoking, HTN and obesity worsen the disease processdisease process
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Question #5
Her risk factors as identified resulted in what Her risk factors as identified resulted in what happening to her kidneys?happening to her kidneys?
1.1. Nephron destructionNephron destruction
2.2. Vessel stenosisVessel stenosis
3.3. Sclerosis of the glomeruliSclerosis of the glomeruli
4.4. All of the aboveAll of the above
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Answer
#4 is correct – all of the above#4 is correct – all of the above
Renal failure progresses as nephrons are Renal failure progresses as nephrons are destroyed. Epithelial damage leads to destroyed. Epithelial damage leads to sclerosis of the glomeruli and stenosis of sclerosis of the glomeruli and stenosis of the vessel wallsthe vessel walls
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Question # 6
In a patient with renal failure it is important In a patient with renal failure it is important to avoid drugs that are essentially to avoid drugs that are essentially
eliminated by the kidneys.eliminated by the kidneys.
True or False?True or False?
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Answer
The answer is true.The answer is true.
It is important to know how drugs are It is important to know how drugs are excreted, especially if by the kidneys and it excreted, especially if by the kidneys and it is important to know or monitor the is important to know or monitor the glomerular filtration rate (GFR)glomerular filtration rate (GFR)
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Congratulations!
You have completed the Chronic Renal You have completed the Chronic Renal Failure TutorialFailure Tutorial
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ReferencesReferences
Microsoft media elements (). . Retrieved February 7, 2006, Microsoft media elements (). . Retrieved February 7, 2006, http://office.microsoft.com/en-us/tou.aspxhttp://office.microsoft.com/en-us/tou.aspx National Kidney and Urologic Diseases Information National Kidney and Urologic Diseases Information Clearinghouse (2004, December). Clearinghouse (2004, December). Polycystic Polycystic kidney disease. kidney disease. Retrieved March 3, 2006, Retrieved March 3, 2006, http://kidney.niddk.nih.gov/kudiseases/pubs /polycystic/http://kidney.niddk.nih.gov/kudiseases/pubs /polycystic/ Nephrology Channel (2005, February 8). Nephrology Channel (2005, February 8). Chronic renal Chronic renal failure. failure. Retrieved March 7, 2006, Retrieved March 7, 2006, http://www.nephrologychannel.com/crf/http://www.nephrologychannel.com/crf/ Nephrology Channel (2005, February 8). Nephrology Channel (2005, February 8). Nephrotic Nephrotic syndrome. syndrome. Retrieved March 7, 2006Retrieved March 7, 2006 http://www.nephrologychannel.com/nephrotic/http://www.nephrologychannel.com/nephrotic/
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ReferencesReferences
Nephrology Channel (2005, February 8). Nephrology Channel (2005, February 8). Polycystic Polycystic kidney disease. kidney disease. Retrieved March 7, 2006, Retrieved March 7, 2006, http://nephrologychannel.com/polycystic/http://nephrologychannel.com/polycystic/ Porth, C. M. (1998). Porth, C. M. (1998). Pathophhysiology Concepts of Altered Health Pathophhysiology Concepts of Altered Health States States (5th ed.). Philadelphia, Pa.: Lippincott-Raven.(5th ed.). Philadelphia, Pa.: Lippincott-Raven. Porth, C. M. (2004). Porth, C. M. (2004). Essentials of pathophysiologyEssentials of pathophysiology. Philadelphia, . Philadelphia, Pa.: Lippincott Williams & Wilkins.Pa.: Lippincott Williams & Wilkins. Sanford, R. (2004, May 25). Sanford, R. (2004, May 25). Autosomal dominant polycystic kidney Autosomal dominant polycystic kidney disease. disease. Retrieved February 8, 2006, Retrieved February 8, 2006, http://www.cgkp.org.uk/topics/cam-genetics/sanford.htmhttp://www.cgkp.org.uk/topics/cam-genetics/sanford.htm Shier, D. Butler, J. & Lewis, R. (1999). Shier, D. Butler, J. & Lewis, R. (1999). Hole's human anatomy & Hole's human anatomy & physiology physiology (8th ed.). pp. 782, 786, 788: The McGraw-Hill (8th ed.). pp. 782, 786, 788: The McGraw-Hill CompaniesCompanies
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References
Wadhwa, D. (2005). Wadhwa, D. (2005). Chronic renal failure. Chronic renal failure. Retrieved February 8, Retrieved February 8, 2006,http://www.uhmc.sunysb.edu/internalmed/nephro/2006,http://www.uhmc.sunysb.edu/internalmed/nephro/ webpages/Part-G.htmwebpages/Part-G.htm Yale Medical Group (2005, October 28). Yale Medical Group (2005, October 28). Overview of renal failure. Overview of renal failure. Retrieved February 8, 2006, http://ymghealthinfo.org/contentRetrieved February 8, 2006, http://ymghealthinfo.org/content asp?pageid=PO3111asp?pageid=PO3111 eMedicine (2003, march 25). eMedicine (2003, march 25). Cystinosis. Cystinosis. Retrieved March 3, 2006, Retrieved March 3, 2006, http://www.emedicine.com/ped/topic538.htmhttp://www.emedicine.com/ped/topic538.htm
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Thank You!
I appreciate your time spent viewing this tutorial and I hope I appreciate your time spent viewing this tutorial and I hope you enjoyed it!you enjoyed it!
I would like to thank Pat Bowne and Lee Jeske for all of I would like to thank Pat Bowne and Lee Jeske for all of their guidance in the development of this tutorial.their guidance in the development of this tutorial.
I would also like to thank the McGraw-Hill companies for I would also like to thank the McGraw-Hill companies for their permission to include the wonderful visuals on renal their permission to include the wonderful visuals on renal physiology.physiology.
Any questions or comments you can contact me at:Any questions or comments you can contact me at:Valerie KolmerValerie Kolmer1-262-639-41071-262-639-4107
[email protected]@execpc.com
