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CHRONIC RENAL FAILURE. Valerie Kolmer RN BSN BC MSN 621 Alverno College. 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

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chronic renal failure


Valerie Kolmer RN BSN BC

MSN 621

Alverno College


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
chronic renal failure tutorial guide
Chronic Renal FailureTutorial Guide
  • Return to the main menu at any time by pushing the button.
  • Hyperlinks to outside sources, for in-depth information, are available on various slides. Just push on the button. Click back button to return.
  • Easy navigation forward or backward using the or buttons.
  • Within text - highlighted words link to definitions - then return with button

Main Menu


chronic renal failure main menu
Chronic Renal FailureMain Menu
  • Tutorial Guide
  • Definitions
  • Renal Physiology Review
  • Pathophysiology
  • Causes
  • Signs & Symptoms
  • Hyperlipidemia in CRF
  • Inflammation
  • Pharmacology
  • Case Study/Quiz
  • References
  • 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
  • Lysosome = Membrane bound organelles, within the cell, containing hydrolytic enzymes - involved in intra & extracellular digestion
  • Mesangial Cells = Supporting cells of glomeruli- produce 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
renal physiology review
Renal Physiology Review

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

renal hormone regulation
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)

fluid and electrolyte control mechanisms
Fluid and Electrolyte ControlMechanisms
  • RAAS – Renin-Angiotensin Aldosterone System
  • Aldosterone
  • ADH – Anti-Diuretic Hormone
how the raas pathway works
How the RAAS Pathway Works

Valerie Kolmer


  • Increases rate of sodium ion absorption
  • Chloride moves along with sodium because of + charge of sodium
  • Increases rate of potassium & hydrogen ion secretion


Fluid and sodium retention increases blood-pressure

quick quiz
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
answer 2
Answer 2.

Renin – Angiotensin I – Aldosterone – ADH - ACE

That is not correct

Please Try Again

answer 3
Answer 3.

Renin – Angiotensin I – ACE –

Angiotensin II – Aldosterone

You are RIGHT!

renal structure
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
nephron b renal pyramid with nephrons c section of kidney
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

the nephron
The Nephron

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.

nephron blood supply
Nephron & 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

urine formation
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.

what is glomerular filtration rate gfr
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 Cockcroft-Gault equation that estimates creatinine clearance

Link: GFR Info

urine formation23
Urine Formation

Modified from: Shier, D., Butler, J., Lewis, R. (1999). Hole’s human anatomy & physiology(8th ed.). The McGraw-Hill Co.,Inc.

nephron component functions
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

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

pathophysiology of crf
Pathophysiology of CRF

What is Chronic Renal Failure?

It is progressive tissue destruction with

permanent loss of nephrons and renal function.

risk factors
Risk Factors
  • Age > 60 years
  • Race or ethnic background



American Indian


  • History of exposure to chemicals/toxins

Cigarette smoke

Heavy metals

  • Family history of chronic kidney disease
chronic vs acute renal failure
Chronic vs. Acute Renal Failure
  • Acute Renal Failure (ARF):
  • Abrupt onset
  • Potentially reversible
  • Chronic Renal Failure (CRF):
  • Progresses over at least 3 months
  • Permanent- non-reversible damage to nephrons
pathophysiology of crf28
Pathophysiology of CRF

Progressive destruction of nephrons leads to:

  • Decreased glomerular filtration, tubular reabsorption & renal hormone regulation
  • Remaining functional nephrons compensate
  • Functional and structural changes occur
  • Inflammatory response triggered
  • 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

functional changes of crf
Functional Changes of CRF

The Kidneys are unable to:

  • Regulate fluids and electrolytes
  • Balance fluid volume and renin-angiotensin system
  • Control blood pressure
  • Eliminate nitrogen and other wastes
  • Synthesize erythropoietin
  • Regulate serum phosphate and calcium levels
structural changes of crf
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

4 stages of crf
4 Stages of CRF
  • 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

Quick Quiz

Chronic Renal Failure is reversible.



sorry that is not correct
Sorry! That is not correct.

The answer is false.

Nephron damage is permanent

& progressive in CRF

Please continue.

causes of crf
Causes of CRF
  • Diabetic Nephropathy
  • Hypertension
  • Vascular Disease
  • Polycystic Kidney Disease/Genetics
  • Chronic Inflammation
  • Obstruction
  • Glomerular Disorders/ Glomerulonephritis
signs symptoms lab value cues

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.

signs symptoms lab value cues37
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.

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


signs symptoms visual verbal cues
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

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

SIGNS & SYMPTOMSVisual / Verbal Cues

genetics of kidney disease
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,

polycystic kidney disease
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…/Ch58/jpg/58_001.jpg

two major forms pkd
Two Major Forms PKD
  • Autosomal Dominant PKD
  • Autosomal Recessive PKD

Only treatment for both = dialysis and kidney transplantation

Used with permission: Lippincott Williams & Wilkins

autosomal dominant pkd
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
autosomal recessive pkd
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
metabolic impact
Metabolic Impact
  • Hyperlipidemia common in CRF- especially in Nephrotic Syndrome
  • Excessive lipids accelerate progression of renal disease
  • Cholesterol increases glomerular injury
contributing mechanisms
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
mesangial cell contribution
Mesangial Cell Contribution

Valerie Kolmer 2006

albumin contribution
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
  • 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
inflammation cont
Inflammation- (Cont.)

Renal Failure- prolongs inflammatory reactions

  • Adverse effects of chronic inflammation=

Decreased appetite

Muscle and fat wasting

Endothelial damage



Increased cardiovascular disease risk

Legg, V.(2005). Complications of chronic kidney disease. AJN,105(6),40-50

causes of inflammation in crf
Causes of Inflammation in CRF
  • Infection
  • Anemia
  • Uremia – increases oxidation of proteins, lipids & carbohydrates, leading to vascular inflammation
  • Malnutrition – decreases antioxidants
  • Low serum albumin – decreases antioxidants

Legg, V.(2005). Complications of chronic kidney disease. AJN,105(6),40-50

angiotensin ii in the inflammatory process
Angiotensin II in theInflammatory Process

Inflammatory mediator causing:

  • Increased vascular permeability
  • Increased leukocyte infiltration (monocytes, macrophages)
  • Cell proliferation & hypertrophy
glomerular inflammatory disorders
Glomerular Inflammatory Disorders


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.

nephrotic vs nephritic syndromes
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
nephritic syndromes
Nephritic Syndromes


  • An inflammatory response in the endothelial, epithelial & mesangial cells of the glomeruli
  • Inflammatory process damages the capillary wall-allowing RBCs into the urine


  • 1st oliguria, followed by hematuria, azotemia, low GFR (d/t hemodynamic changes), hypertension
nephrotic syndromes
Primary causes:

Lipoid Nephrosis

Focal Segmental glomerulosclerosis

Membranous glomerulonephritis

Secondary causes:

Diabetes Mellitus



Characterized by:

Proteinuria > 3.5g/day




Increased permeability of glomerular membrane allows proteins to escape into the filtrate

Nephrotic Syndromes

Porth, 1998


Porth, 1998

chronic glomerulonephritis
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
pharmacology in crf
Pharmacology in CRF

Pharmacokinetics –

drug absorption, distribution, metabolism & excretion

Pharmacodynamics –

A drug’s mechanism of action and effect at the target site

alterations in drug responses in crf
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.

medication considerations in crf
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.

medication considerations cont
Medication Considerations (Cont.)

Impaired renal excretion leads to toxic drug accumulations with:


Aminoglycoside antibiotics -

(tobramycin & gentamycin)








over the counter medications and crf
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.

case study
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.

case study cont
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.

significant lab work
Significant Lab Work

BUN 37 (nl= 8-20 mg/dL)

Creatinine 4.7 (nl= 0.6-0.9 mg/dL)

Calcium 7.6 (nl= 8.2-10.2 mg/dL)

Sodium 137 (nl= 135-145 mEq/L)

Hemoglobin 8.5 (nl= 12-16 g/dL)

Hematocrit 28.9 (nl= 36-48%)

Albumin 2.5 (nl= 3.5-5 g/dL)

Total Protein 6.2 (nl= 6.4-8.3 g/dL)

LDL 156 (nl= <130mg/dL)

HDL 32 (nl= 40-85 mg/dL)

other tests
Other Tests

Urinalysis: Protein-100

RBC – 1-2

CXR: Moderately enlarged heart

EKG: Sinus rhythm with

occasional PVC’s

Blood Pressure: 168/98

question 1
Question #1

Based on this persons symptoms, history and lab work – What do you think her diagnosis would be?

  • CRF
  • ARF
  • CHF

4. Influenza


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


Shoes too tight :indicating fluid retention

question 2
Question #2

Which compensatory mechanism causes the increased fluid retention, increased sodium and elevated blood-pressure?

  • Renin – Angiotensin – Aldosterone System (RAAS)
  • Bone Marrow suppression
  • Deregulation of baroreceptors
  • Suppression of Sympathetic Nervous System

#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.

question 3
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 is correct

Mrs. Nephritis’ symptoms have progressively worsened over months

question 4
Question #4

What risk factors in her history could lead to CRF?

  • African-American
  • HTN
  • Smoker
  • Obesity
  • All of the above
  • 1, 2 and 3

#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

question 5
Question #5

Her risk factors as identified resulted in what happening to her kidneys?

  • Nephron destruction
  • Vessel stenosis
  • Sclerosis of the glomeruli
  • All of the above

#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

question 6
Question # 6

In a patient with renal failure it is important to avoid drugs that are essentially eliminated by the kidneys.

True or False?


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)


You have completed the Chronic Renal Failure Tutorial

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American Journal of Nursing, 105(2), 40-50.

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AJN, 105(9), 60-72.

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34(1), 50-53.

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disease. Nursing 2005, 35(12), 58-63.

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AJN, 105(6), 40-50.

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reference for nurses (1st ed.). Ambler, Pa.: Lippincott Williams

& Wilkins.

  • Microsoft media elements (). . Retrieved February 7, 2006,

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Clearinghouse (2004, December). Polycystic

kidney disease. Retrieved March 3, 2006, /polycystic/

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failure. Retrieved March 7, 2006,

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syndrome. Retrieved March 7, 2006

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kidney disease. Retrieved March 7, 2006,

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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,

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physiology (8th ed.). pp. 782, 786, 788: The McGraw-Hill


  • Wadhwa, D. (2005). Chronic renal failure. Retrieved February 8,



  • Yale Medical Group (2005, October 28). Overview of renal failure.

Retrieved February 8, 2006,


  • eMedicine (2003, march 25). Cystinosis. Retrieved March 3, 2006,

thank you
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