Renal I - MED 115 Syllabus

Kansas City University of Medicine and Biosciences

College of Osteopathic Medicine

COURSE DESCRIPTION
This course utilizes a multidisciplinary approach to prepare students with a foundational
understanding of the normal structure and function of the renal system. It includes a review of
the basic functional principles of the organs of urine production and excretion including the
gross anatomy, histology, and embryology of the kidney and urinary tract. A thorough
investigation of the essential physiology of kidney function will include the primary renal
processes, urine formation, and renal blood flow. In addition, the renal system’s role in ion
regulation, acid-base balance, fluid volume, and salt-water balance will be examined along with
the regulatory control mechanisms of these functions. An understanding of the renal system will
be accomplished through student involvement in lectures, directed student assignments, and
relevant interactive clinical correlation sessions.

Course Goals Core Competency EPA

1. Describe the normal structure and development of the urinary 1, 2, 3,

system. I, II, III
12

2. Describe the role of the kidneys in body fluid volume, homeostasis of II, III
2, 3,
ions, and acid-base balance. 10

3. Correlate and apply information acquired in this course to relevant

clinical presentations. I, II, III 2, 3

COURSE SCHEDULE, LECTURE OBJECTIVES, AND ASSIGNMENTS

Please refer to the posted Outlook Student Calendar to view the course schedule. Links to
learning objectives, reading assignments, and required materials are posted within each
scheduled activity. Communication of important course information may occur through KCU
email and/or Blackboard.

It is the student’s responsibility to check both email and Blackboard daily.

COURSE MATERIALS
See the below required textbook list. Many of the required text books are available free online
through the library.

POLICIES
Please refer to student handbook and catalog for KCU-COM academic and course policies.

ATTENDANCE
Attendance of lectures and laboratories is based on the university’s stated attendance policy.
Refer to the student handbook for more information.

CLASSROOM BEHAVIOR AND ATTIRE

Date modified: 08/28/2018

If a student is determined to demonstrate unprofessional behavior or wear unprofessional or
inappropriate attire, he/she may be subject to disciplinary action per Kansas City University of
Medicine and Biosciences policy.

EVALUATION
The student will receive a numerical grade in the form of a percent and letter grade at the end of
the course. The student must achieve a cumulative grade of 70% or higher on graded
assessments to pass the course.

POINT ALLOTMENT
The following table is a breakdown of the allotment of points. These values are subject to
change with notice.

Activity Point Value

Quiz 1 5

Exam 1 60

Exam 2 60

Total points 125

Date modified: 08/28/2018

Required Textbooks and Other Resource Material
PHYSIOLOGY
Renal Physiology (6th ed.) / Koeppen, Bruce M., Stanton, Bruce A.
Elsevier/Mosby, c2018.
ISBN: 978-0323086912 (paperback)

ANATOMY
Histology: A Text and Atlas with Correlated Cell and Molecular Biology (7th ed.), Pawlina, W.,
Wolters Kluwer, c. 2016.
ISBN: 978-1-4511-8742-7.

The Developing Human: Clinically Oriented Embryology (10th ed.), Moore, K.L., Persaud,
T.V.N., and,Torchia, M.G., Elsevier, c 2016.
ISBN: 978-0-323-31338-4. Available on Clinical Key.

Clinically Oriented Anatomy (8th ed), Moore, K.L., Dalley, A.F.,and Agur, A.M.R., Lippincott
Williams & Wilkins, c 2018.
ISBN: 978-1-4963-4721-3. (paperback); E-ISBN: 978-1-4963-8942-8 (digital)

OPTIONAL
BRS Physiology (Board Review Series) (6th ed.) / Costanzo, Linda.
Wolters Kluwer Health, c2014.
ISBN: 978-1451187953 (paperback)
2017-2018 OMS I Textbook List

Guyton and Hall Physiology Review (3rd ed.) / Hall, John.

Elsevier, c2015.
ISBN: 978-1455770076 (paperback)

Endocrine and Reproductive Physiology (4th ed.) / White, Bruce; Porterfield, Susan P.
Elsevier/Mosby, c2013.
ISBN: 978-0323087049 (paperback)
E-ISBN: 978-0323088282

Renal Pathophysiology (4th ed.) / Rennke, Helmut G., Denker, Bradley M.

Lippincott Williams & Wilkins, c2014.
ISBN: 978-1451173383 (paperback)

Larsen’s Human Embryology (5th ed.), Schoenwolf, G.C., Bleyl, S.B., Brauer, P.R., and Francis-
West, P.H., Elsevier Churchill Livingstone, c. 2015.
ISBN: 978-1-4557-0684-6. Available on Clinical Key.

Moore’s Anatomy Review PrepU for Clinically Oriented Anatomy, Lippincott Williams & Wilkins,
c2018.
ISBN: 978-1-4963-9916-8

Date modified: 08/28/2018

Contact Information
Kansas City Joplin

Robert (Jason) Walker, PhD (Course Angela Pierce, DC, PhD (Course Director/Phase II
Director/Phase I Director) Director)
Office SEP 453 Office 2616
816-654-7208 417-208-0656
RWalker@kcumb.edu APierce@kcumb.edu
Sarah Keim Philip Brauer, PhD
Office SEP 239 Office 2606
816-654-7546 417-208-0666
SKeimJanssen@kcumb.edu PBrauer@kcumb.edu

Ryan Sheehy, PhD Jennifer Dennis, PhD

Office SEP 226 Office 2612
816-654-7613 417-208-0672
RSheehy@kcumb.edu JDennis@kcumb.edu

Alex Shnyra, MD, PhD Monica Kinde, PhD

Office SEP 228 Office 2622
816-654-7635 417-208-0648
AShnyra@kcumb.edu MKinde@kcumb.edu

Dennis Wolff, PhD

Office 2617
417-208-0701
DWolff@kcumb.edu

Date modified: 08/28/2018

Lecture Topic: Renal Anatomy and Histology (Brauer)
Reference Reading: Pawlina W., Histology: A Text and Atlas, 7th ed., Chapter 20; Moore’s
Clinical Oriented Anatomy 8th ed., pp. 515-523.

Objectives: After reading the text, attending the lecture, and using online resources, the
student physician should be able to:

1. Describe the location and relationship of the kidneys and ureters to neighboring structures at
the gross anatomy level. 


2. Describe the major nerve and blood supply to the kidneys and the vascular branches found
within the kidney.

3. Describe and identify the basic internal gross anatomy of the kidney.

4. Describe the location and morphological characteristics of uriniferous tubules and renal
corpuscles.

5. Describe and identify the structural features and role of the glomerulus, Bowman’s capsule,
podocytes and mesangial cells.

6. Describe the renal filtration barrier.

7. Describe the location, morphological characteristics, and general functions of the proximal
convoluted and straight tubules, loop of Henle, distal convoluted tubules, and collecting
ducts.

8. Identify the targets of aldosterone and antidiuretic hormone within the uriniferous tubules.

9. Describe the vasculature surrounding the uriniferous tubules.

10. Describe the microscopic appearance of the juxtaglomerular apparatus and describe its
basic function.

11. List the components of the urinary tract. Describe transitional epithelium and its unique
characteristics and explain where this epithelium is found.

12. Describe the microscopic anatomy of the ureter, bladder, and urethra and how they differ
between males and females.
Renal Embryology (Dennis/Keim)
Dev. Human: Ch 12 – stop at ‘Dev of Genital System’
Larsen’s: Ch 15 – stop at ‘Genital System arises w/Urinary System’

1. Describe the origin and location of the intermediate mesoderm.

2. Explain the origin and development of the pronephros, mesonephros and metanephros.
3. Differentiate between the origin of the mesonephric duct and the mesonephric tubules.
4. Distinguish between the ureteric bud and the metanephric blastema.
5. Identify the derivatives of the ureteric bud.
6. Identify the derivatives of the metanephric blastema.
7. Describe the development of the excretory unit (nephron).
8. Relate the regions of the adult kidney (pyramid, pelvis etc.) to their embryonic
development.
9. Explain the development of the bladder.
10. Explain why the trigone of the bladder is derived from mesoderm.
11. Identify the derivatives of the vesicle part, pelvic part and phallic part of the urogenital
sinus.
12. Describe the development of the condition known as epispadias.
13. Identify the origin of the components of the suprarenal gland.
14. Analyze patient features, signs and symptoms to determine the congenital abnormalities.
15. Apply embryological mechanisms to explain the congenital abnormalities.
Renal 1 COM 2022

Monica N. Kinde, PhD: Division of Basic Sciences

Topic/Lecture Name: Nitrogen Metabolism

OBJECTIVES
After reviewing the relevant reading material and studying the lecture notes, students should
demonstrate knowledge of:

1. Describe general aspects of nitrogen excretion (pages 254-255; Fig. 15.1), particularly the following
correlation boxes: Hartnup disease (blue, p. 93) and cystinuria (blue, p. 93).

2. Summarize the significance of the urine-derived metabolites that are associated with errors in
phenylalanine metabolism (p. 262-267; Fig. 15.9, 15.10, 15.12), particularly the following correlation
boxes: Tetrahydrobiopterin/dihydrobiopterin (green, p. 268), Phenylketouria (blue, p. 268), Tyrosinemia
(blue, p. 268), Alkaptonuria (blue, p. 268).

3. Summarize the mechanism of toxicity of ammonia and uric acid (p. 270 and 278; Fig. 15.13 and 16.5A),
particularly the following correlation boxes: Ammonia toxicity (blue, p. 273), Gout (blue, p. 278), Uric
acid levels as a diagnostic marker for gout (orange, p. 278)

4. Recall the urine-derived metabolites associated with errors in urea cycle and pyrimidine metabolism (p.
270- 273; Fig. 15.14, 16.7 and Table 5), particularly the following correlation boxes: Hyperammonemia
(blue, p. 273), Carbamoyl phosphate synthetase II (cytosolic) (green, p. 273).

5. Recall the urine-derived metabolites associated with heme catabolism (p. 290-293; Fig. 16.13),
particularly the following correlation boxes: Direct and indirect bilirubin (blue, p. 292).

This resource is provided to assist you in addressing the learning objectives in preparation for lecture
presentation.

Page 1
Learning Objectives

Topic: Body Fluid Compartments: (PHYS: Dr. Walker)

1. To understand how fluid is normally distributed, you should be able to list the
body fluid compartments and their relative contribution to total body water (TBW).
2. To understand how normal body fluid compartments are maintained, you should
be able to state the contribution of the “third space” to alterations in body fluid
balance.
3. To understand how normal homeostasis in body fluid compartments are
maintained, you should be able to compare and contrast the ionic and
nonelectrolyte composition of the ECF, including plasma and interstitial fluid, to
the ICF.
4. Predict the body compartment a drug will distribute into based on its V D .
5. Predict the impact of altered Starling Forces on body fluid compartment
osmolarity and fluid distribution.
6. Describe the role of compartment osmolarity in fluid shifts and maintenance of
fluid balance, aka, osmotic equilibration.
7. Use plasma sodium concentration to estimate plasma osmolarity.
8. Describe the influence of the Gibbs-Donnan Effect on concentration of plasma
electrolytes.
9. Explain how permeability of cell membranes impacts water movement in the ECF
and ICF and generates osmotic pressure.
10. Given the composition and osmolality of a fluid, identify it as hyper-, iso-, or
hypotonic and predict the change in transmembrane fluid exchange that would
be caused by placing a red blood cell into solutions of varying tonicities.
11. Describe the effect of introduction into the ECF of iso-, hypo-, and hyperosmotic
solutions on ECF and ICF osmolarity and volume in words and via Darrow-
Yennet diagrams.
12. Describe the neurohumoral and effector mechanisms that maintain homeostasis
and osmolarity and volume in the ECF and ICF compartments.
13. Predict the changes in ECF and ICF volume and osmolality in words and via
Darrow-Yennet diagrams in conditions such as vomiting, diarrhea, hemorrhage,
dehydration, diabetes insipidus, diabetes mellitus, hypoaldosteronism, syndrome
of inappropriate anti-diuretic hormone (SIADH).
14. Apply this information to case studies and clinical vignettes.
Topic: Renal transport mechanisms (PHYS: Dr. Walker)
1. State the percentages of filtered Na+ and water reabsorbed in each nephron
segment along with the changes in luminal potential difference in each segment.
2. Describe the function and predominant localization of the following renal
transporters along the tubular system with regard to nephron segment and apical
versus basolateral membranes:
a. Transport ATPases: (Na-K ATPase, H-K ATPase, H-ATPase, Ca-
ATPase);
b. Ion and water channels: (K, Na, Cl, Ca, aquaporins);
c. Coupled transporters: (Na-glucose, Na-H antiporter, Na-K-2Cl
cotransporter, NaCl cotransporter, Na-HCO 3 cotransporter, Cl-HCO 3
antiporter).
3. State the percentages of filtered Na+ and water reabsorbed in each nephron
segment along with the changes in luminal potential difference in each segment.
4. Describe the role of the ascending limb of the loop of Henle in solute and water
reabsorption.
5. Describe the mechanisms of Cl- reabsorption in each of the nephron segments.
6. Identify the major hormones that regulate NaCl and water reabsorption by the
kidneys and the nephron site of action of each hormone. Describe the role of
these hormones in the kidney.
7. Describe the composition of normal urine and the processes involved in the
production of urine.

Topic: Regulation of Body Fluid Osmolality: Regulation of Water Balance (PHYS:

Dr. Walker)
1. Describe the role of the ascending limb of the loop of Henle in producing a high
renal interstitial fluid osmolality, and predict the consequence on urine
concentrating ability if the medullary osmotic gradient is disrupted.
2. State tubular fluid osmolalities during diuresis and antidiuresis at the distal end of
each of the following tubular segments of juxtamedullary nephrons: the proximal
convoluted tubule, descending limb of Henle's loop, thick ascending limb of
Henle's loop, distal convoluted tubule, cortical collecting duct, and inner
medullary collecting duct.
3. Identify the tubular segments and the cellular mechanism by which ADH
increases permeability to water and urea. Describe the role of these changes on
the ability of the kidney to produce either a dilute or concentrated urine.
4. List the two most powerful stimuli for ADH release and describe the negative
feedback control mechanisms for each.
 5. Distinguish between SIADH, and central and nephrogenic diabetes insipidus
based on plasma ADH levels and expected response to an injection of ADH.
6. Predict changes in body fluid volume and osmolality caused by a net water (or
NaCl) loss or gain in the body and how each of these disturbances would alter
the rate of urine production and osmotic composition of the urine.
7. Describe the actions of diuretics on the ability of the kidneys to maximally
concentrate and dilute urine.
8. Given urine and plasma osmolarities and urine volume, provide equations and be
able to calculate osmolar clearance and free water clearance. Identify expected
free water clearance for an individual producing either a dilute or concentrated
urine.
9. Apply this information to case studies and clinical vignettes.

Topic: Regulation of Extracellular Fluid Volume and NaCl Balance

1. Compare and contrast the body sensors that communicate effective circulating
volume (ECV) and Na+ and water balance with the signal that mediates this
communication.
2. Describe the regulation of Na+ reabsorption along the nephron, including the
effects of the sympathetic nerves, angiotensin II, aldosterone, and ANP.
3. Describe the role of the renin-angiotensin-aldosterone system (RAAS) in the
regulation of Na+ balance and arterial pressure in euvolemic and hypovolemic
states with emphasis on the actions of angiotensin II on renal hemodynamics and
tubular transport.
4. Describe the effects of ANP in the nephron and identify a pathophysiological
condition in which circulating ANP is elevated.
5. Describe relationships between blood volume, plasma osmolality, and plasma
ADH activity.
6. Diagram the neural reflex regulation and physiological responses of renal salt
and water handling by the receptors involved in the monitoring of ECF volume
(high pressure baroreceptors & low pressure cardiopulmonary stretch receptors).
7. Describe the renal mechanisms for retaining salt and water evoked in response
to severe hemorrhage.
8. Apply this information to case studies and clinical vignettes.
Topic: Micturition (Pierce/Wang)

1. Describe autonomic control of ureteral peristalsis.

2. Predict the impact a ureter obstruction has on retrograde nephron function.
3. Classify the innervation of the urinary tract according to modality, function, and
neurotransmitter involvement from the spinal cord to the end organ.
4. Describe the exponential correlation between intravesical pressure and afferent nerve
discharge on micturition reflex stimulation.
5. Compare and contrast the role of the sympathetic and parasympathetic nerve
innervation in micturition.
6. Explain the stress-relaxation properties of the bladder.
7. Compare and contrast the roles of the brainstem and cerebral cortex on controlling the
micturition reflex.
8. Describe the sequence of events to initiate micturition.
9. Compare and contrast the reflex voiding responses in an infant, adult, and paraplegic
patient.

Topic: Renal blood flow and glomerular filtration rate (Pierce)

LO 1 - 16 appear in the Introduction to RBF_GFR DSA material

1. Describe the 3-layered structure of the glomerular capillary filtration barrier.

2. Describe the contribution of the glycocalyx to the barrier function of the endothelial
surface layer.
3. Recognize whether a molecule will pass through the filtration slit based on its molecular
size and/or charge.
4. Define Tamm-Horsfall protein.
5. Identify the components of the filtration barrier whose damage would result in hematuria
and proteinuria and the physiological consequences a damaged filtration barrier would
have on body fluid oncotic and hydrostatic pressures.
6. Summarize how anatomical arrangement of the kidney microcirculation influences
nephron function.
7. Contrast the physiological significance of blood flow through the renal cortex versus the
medulla.
8. Use the plasma and urine concentrations along with the urine flow rate to calculate the
filtered load, excretion, reabsorption and clearance of a substance.
9. Use the clearance equation to calculate renal clearance of a substance to estimate
glomerular filtration rate (GFR) with accurate units when given values for all variables.
10. Define filtration fraction and predict the impact changing GFR or renal blood flow (RBF)
would have on the filtration fraction.
 11. Predict how changes in filtration, reabsorption, or secretion will affect renal excretion of
each compound.
12. Compare and contrast the use of inulin and creatinine clearances as measures of
glomerular filtration rate.
13. Describe the means by which sympathetic nervous system stimulation increases
systemic blood pressure through its actions on arterial resistance vessels,
juxtaglomerular granular cells, and tubular epithelial cells and the associated
adrenoceptor subtypes involved in each.
14. Predict the acute and chronic effects of sympathetic stimulation on renal blood flow,
GFR, renin secretion, and proximal tubular Na+ reabsorption.
15. Interpret graphs of A) GFR versus plasma concentration of blood urea nitrogen (BUN) or
creatinine; and, B) urinary excretion of BUN or creatinine versus their plasma
concentrations.
16. Use the BUN/Creatinine ratio to isolate the etiology of a pathology to a pre-, intra-, or
post-renal source.
17. Explain why para-aminohippuric acid (PAH) can be used to estimate renal plasma flow.
18. Given the capillary and Bowman’s space hydrostatic and oncotic pressures, calculate
the net filtration force at the glomerular capillaries and predict changes in glomerular
filtration by increases or decreases in any of these pressures.
19. Define the ultrafiltration coefficient at the glomerular capillary, describe the membrane
properties that contribute to it, and explain its role in determining GFR.
20. Predict the changes in net filtration force that occur as blood travels along the glomerular
capillary and hydrostatic pressure falls while colloid oncotic pressure increases.
21. Describe and explain the effects of increased systemic arterial pressure as well as
selective changes in the relative resistance of afferent and efferent arterioles on RBF,
GFR and peritubular capillary reabsorption.
22. Describe the regulation of proximal tubule reabsorption that underlies the phenomenon
of glomerulotubular balance and its importance in the process of autoregulation.
23. Describe myogenic and tubuloglomerular feedback mechanisms that mediate the
autoregulation of renal plasma flow and GFR.
24. Predict the acute and chronic changes in RBF and GFR caused by: a) increased
angiotensin II synthesis; b) increased release of atrial natriuretic peptide (ANP); c)
decreased prostaglandin formation.

Topic: Regulation of K+ balance (Pierce)

1. State the normal ranges of plasma K+ concentration.
2. Describe K+ distribution in the body.
3. Define hypokalemia, hyperkalemia, and pseudohyperkalemia and identify the most
common cause of each.
4. Identify the major routes of K+ loss from the body.
5. Define the role of extracellular K+ in maintaining normal nerve and muscle function.
 6. Describe the role of epinephrine, insulin, and aldosterone in the extrarenal regulation of
plasma K+.
7. Describe the role of acid-base balance, plasma osmolality, cell lysis and exercise has on
the distribution of K+ across cell membranes.
8. Calculate the normal filtered load of K+.
9. Identify the tubular sites of K+ reabsorption and secretion.
10. Understand the cellular mechanisms of K+ transport by principal cells and intercalated
cells in the distal tubule and collecting duct.
11. Describe the factors that regulate K+ handling in the collecting duct (aldosterone, ADH,
plasma K+) and distinguish these from factors that alter K+ secretion at this site (luminal
flow rate, acid-base disturbances, glucocorticoids, and anion delivery).

Topic: Regulation of Ca2+, phosphate and Mg2+ balance (Pierce)

Calcium
1. Identify the normal range of dietary Ca2+ intake.
2. Describe the major storage pools of Ca2+ in the body.
3. Identify the major routes of Ca2+ loss from the body.
4. Define hypocalcemia and hypercalcemia and the impact of each condition on nerve and
muscle cell excitability.
5. Describe the ionized, complexed, and protein-bound distribution of Ca2+ in the plasma.
6. Explain the effect of plasma pH, hypoalbuminemia and hyperalbuminemia on ionized
Ca2+ concentration.
7. Describe the regulation of plasma Ca2+ and phosphate by calcitriol, calcitonin and
parathyroid hormone (PTH) and the role of the calcium-sensing receptor (CaSR) in
monitoring plasma Ca2+ concentration.
8. Calculate the normal filtered load of Ca2+.
9. Identify the tubular sites of and cellular mechanisms of Ca2+ reabsorption.
Phosphate
10. Identify the normal range of dietary phosphate intake.
11. Describe the major storage pools of phosphate in the body.
12. Identify the major routes of phosphate loss from the body.
13. Calculate the normal filtered load of phosphate.
14. Identify the tubular sites of and cellular mechanisms of phosphate reabsorption.
15. Describe the role of the kidney in the production of 1,25‑dihydroxy vitamin D (calcitriol).
16. Describe the renal regulation of Ca2+ and phosphate transport by PTH, calcitonin, and
1,25-dihydroxycholecalciferol (calcitriol) and distinguish from other factors that alter their
transport (ECF volume, acid-base disorders).
Magnesium
17. Describe the major storage pools of Mg2+ in the body.
18. Identify the major routes of Mg2+ absorption and excretion from the body.
19. Identify the tubular sites of and cellular mechanisms of Mg2+ reabsorption, including the
role of TRPM6 in this process.
20. Describe the renal regulation of Mg2+ transport as influenced by dietary depletion, PTH,
acid-base balance, and effective circulating volume.
Topic: Renal control of acid-base balance
Lecturer: Wolff
1. Identify the normal range of pH values.
2. Compare and contrast acidemia, alkalemia, acidosis, and alkalosis.
3. List the major chemical buffer systems of the extracellular and intracellular fluids.
4. State the Henderson-Hasselbalch equation and apply it to the CO 2 :HCO 3 - buffer system.
Explain how this ‘open’ buffer system with a pKa of 6.1 is physiologically important in the
maintenance of the normal plasma pH of 7.4.
5. Compare and contrast the sources of volatile (CO 2 -derived) and nonvolatile acids and
the mechanisms for eliminating these acids from the body.
6. Describe the role of RAAS and other factors that control renal tubular secretion of H+.
7. Diagram the tubular epithelial mechanisms of HCO 3 - reabsorption and secretion, H+
secretion as a titratable acid, and H+ secretion as ammonium.
8. Discuss the role of urinary buffers (titratable acid, ammonium excretion) in determining
net acid excretion normally and during conditions of altered acid-base balance.
9. Describe mechanisms of H+ secretion in different nephron segments and its importance
in HCO 3 - reabsorption.
10. Describe adjustments in filtered load and reabsorption of HCO 3 - (H+ secretion) by altered
system acid-base balance.
11. Distinguish between the reclamation of filtered bicarbonate and formation of new
bicarbonate.
12. Given a sudden increase or decrease in pH, identify the magnitude and time course of
compensations that act to minimize a change in pH of the body fluids, including: a)
buffers; b) respiratory adjustments; and, c) renal adjustments.
13. Given laboratory values, be able to: a) identify simple metabolic and respiratory acid-
base disturbances, and b) distinguish between acute and chronic respiratory
disturbances.
14. Describe the appropriate renal responses to acidemia and alkalemia.
15. Using Davenport diagrams, describe changes in plasma pCO 2 , pH, and HCO 3 - that
occur in each of the four primary acid-base disorders.
16. Explain the changes in extracellular pH observed in Conn’s disease, Addison’s disease,
ECF volume changes and diuretic abuse.
17. Define and given appropriate data, calculate anion gap and distinguish between
increased and normal anion gap in the differential diagnosis of metabolic acidosis.
18. Identify processes or causes that lead to acid-base disturbances and apply this
information to case studies and clinical vignettes.
Learning Objectives

Lecture: Immunological Aspects of the Renal System

Dr. A. Shnyra

• Define important role of immune mechanisms in Acute Kidney Injury (AKI).

• Describe the pathogenesis of Ischemic AKI
• Explain the role of Damage-Associated Molecular Patterns (DAMPs) in sterile renal
inflammation.
• Define the role of complement activation in renal injury and inflammation.
• Explain the role of M1 macrophages and M2 macrophages in acute and chronic renal disease.
• Describe the pathogenic role of Th17 cells and IL-17 in adaptive immune responses occurring
renal tissue.
• Define Treg cells as the key regulators of immunological reactions in renal tissue.
• Describe major types of organ transplant.
• Define the role of tissue typing in transplantation.
• Describe techniques and procedures for matching donor and recipient (Blood group antigens,
class I HLA, and class II HLA).
• Explain the immune mechanisms of various types of allograft rejection (host-versus-graft
disease).
• Describe the immune mechanisms involved in graft-versus-host disease.

Primary References: Abbas AK, Lichtman AH. Basic Immunology. Second Edition, Saunders Elsevier, pp.
185-191.

Reading assignment (provided):

The immune system and kidney disease: basic concepts and clinical implications. 2013. Nature
Reviews in Immunology vol. 13, p.738