Transcript Chronic Renal Failure - Alverno College Faculty

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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Chronic Renal Failure
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
Tutorial Guide
 Definitions
 Renal Physiology Review
 Pathophysiology
 Causes
 Signs & Symptoms
 Hyperlipidemia in CRF
 Inflammation
 Pharmacology
 Case Study/Quiz
 References
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Definitions
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

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
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Definitions
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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
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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
Regulate blood-pressure
Important 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:
Renin-angiotensin aldosterone system
(RAAS)
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Fluid and Electrolyte Control
Mechanisms
– Renin-Angiotensin Aldosterone
System
 Aldosterone
 ADH – Anti-Diuretic Hormone
 RAAS
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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 bloodpressure
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ADH (Anti-Diuretic Hormone)
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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
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Answer 1.
Renin – Angiotensin II- ACE- ADH – Aldosterone
That is not correct
Please try again
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Answer 2.
Renin – Angiotensin I – Aldosterone – ADH - ACE
1.
That is not
correct
2.
Please Try
Again
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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
(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). 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 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
.
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Nephron & Blood Supply
Shier,D., Butler, J., Lewis, R (1999). Hole’s human anatomy and
physiology.(8th ed.). The McGraw-Hill Co, Inc. Used
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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). Hole’s
human anatomy & physiology(8th ed.).
The McGraw-Hill Co., Inc.
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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
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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
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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
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
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
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Chronic vs. Acute Renal Failure

a.
b.
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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
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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
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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
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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
Healthy Glomerulus
Damaged Glomerulus
Valerie Kolmer 2006
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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
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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.
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
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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.
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
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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
(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
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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
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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
 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
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
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Metabolic Impact
 Hyperlipidemia
common in CRFespecially in Nephrotic Syndrome
 Excessive lipids accelerate progression of
renal disease
 Cholesterol increases glomerular injury
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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
 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
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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
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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
wall-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, 1998
Porth, 1998
h
,
1
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Chronic Glomerulonephritis

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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 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
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.
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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.
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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
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.
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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)
(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)
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Other Tests
Urinalysis:
Protein-100
RBC – 1-2
CXR:
Moderately enlarged heart
EKG:
Sinus rhythm with
occasional PVC’s
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
Elevated creatinine
: all 3 indicative of renal failure
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?
1.
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 –
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.
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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
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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
2. 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
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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.
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References
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

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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/
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References
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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
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References
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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
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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
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]
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