RENAL

PHYSIOLOGY
1
UNIT OUTLINE:
I. Introduction
i. General Functions of the Renal System
II. Levels of Organization
i. Path of Fluid Movement through the Kidney
III. Structure & Function
i. Filtration, Reabsorption & Secretion
ii. Urine Formation & Concentration
IV. Homeostasis
i. Autoregulation
ii. Neural
iii. Hormonal
V. Integration
i. Involvement in larger processes
ii. Clinical

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I. INTRODUCTION:

Functions of the Kidneys

Regulation of extracellular fluid volume and blood pressure
Regulation of osmolarity
Maintenance of ion balance
Homeostatic regulation of pH
Excretion of wastes
Production of hormones

3
I. INTRODUCTION:

URINARY SYSTEM
Waste products
• Produced from all cells of the body
• End up in the blood
• Filtered from the blood by the kidneys
• Form urine
• eliminated from the body by ureters, urinary bladder,
urethra
Urinary system
• The body’s“water treatment plant”
• Composed of kidneys, ureters, urinary bladder, urethra

4
I. INTRODUCTION:

Components of urinary system

• Kidney, filtering blood
• removes waste products and converts filtrate into
urine
• Ureters, transporting urine
• from kidneys to urinary bladder
• Bladder, expandable muscular sac
• stores as much as 1 L urine
• Urethra, eliminating urine from body

5
I. INTRODUCTION:

Other functions of the kidney

• Formation of calcitriol
• synthesizes final enzyme in calcitriol hormone formation
• Production and release of erythropoietin
• indirectly measures oxygen level of blood
• secretes erythropoietin (EPO) in response to low blood oxygen
• stimulates red bone marrow to increase rate of erythrocyte formation
• erythrocytes transporting additional oxygen from lungs
• Regulation of ion levels and acid-base balance
• helps control blood’s inorganic ion balance
• e.g., Na+, K+, Ca2+
• aids in maintaining acid-base balance
• alters levels of H+ and HCO3-
• Regulation of blood pressure
• alters amount of fluid lost in urine
• helps regulate blood volume
• releases renin enzyme
• required for production of angiotensin II
• hormone increasing blood pressure

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I. INTRODUCTION:

Other functions of the kidney (continued)

• Regulation of blood pressure
• alters amount of fluid lost in urine
• helps regulate blood volume
• releases renin enzyme
• required for production of angiotensin II
• hormone increasing blood pressure
• Potential to engage in gluconeogenesis
• during prolonged fasting or starvation
• produces glucose from noncarbohydrate sources
• helps maintain normal blood glucose levels

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II. LEVELS OF ORGANIZATION

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 II. LEVELS OF ORGANIZATION

Nephrons Arterioles

Cortex Nephrons
Cortex

Medulla

Renal pelvis Medulla

Ureter

Capsule
The kidney, in cross section.
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 II. LEVELS OF ORGANIZATION

Efferent arteriole
Peritubular Peritubular
Juxtaglomerular capillaries capillaries
apparatus Glomerulus

Afferent
arteriole
Glomerulus Vasa recta
(capillaries)

Collecting
duct
Loop of
Henle

One nephron has two arterioles Juxtamedullary nephron

and two sets of capillaries. with vasa recta
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II. LEVELS OF ORGANIZATION
Nephron

Renal corpuscle Renal tubule

Efferent
arteriole
Glomerulus Collecting
Proximal convoluted Nephron loop Distal convoluted
duct
tubule (PCT) tubule (DCT)

Tubular pole
Vascular
pole Visceral layer Collecting
Glomerular
Afferent Capsular Parietal layer capsule tubule
arteriole space
Thick
segment
Collecting
Cortex duct
Thick
segment
Medulla Descending Ascending
limb limb
Intercalated
NEPHRON STRUCTURE Thin
segment
cells
Thin
(NEPHRON STRETCHED OUT) segment Principal
cells

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III. STRUCTURE & FUNCTION

General Topics -
i. Filtration & Filtration Rate
ii. Reabsorption
iii. Secretion
iv. Excretion
v. Urine Formation
vi. Urine Concentration

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III. STRUCTURE & FUNCTION

Filtration, reabsorption, secretion, and excretion

Peritubular capillaries Distal tubule

Efferent
arteriole
Glomerulus

Afferent
arteriole
Bowman’s Proximal
capsule tubule

KEY
= Filtration: blood to lumen Loop Collecting To renal
of duct vein
= Reabsorption: lumen to blood
Henle
= Secretion: blood to lumen
= Excretion: lumen to external To bladder and
environment external environment

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III. STRUCTURE & FUNCTION

The urinary excretion of substance depends on its

filtration, reabsorption, and secretion

Glomerulus
Efferent
Peritubular
arteriole To renal vein
capillaries

Tubule

Afferent Bowman’s To bladder and

arteriole capsule external environment
Amount Amount Amount amount of solute
filtered – reabsorbed + secreted = excreted

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 III. STRUCTURE & FUNCTION

THE FILTRATION FRACTION

4 >99% of plasma
entering kidney
Efferent arteriole Peritubular returns to systemic
circulation.
capillaries

80%
5 <1% of
2 20% of 3 >19% of fluid volume is
volume is reabsorbed. excreted to
Afferent filters. external
arteriole environment.
Bowman’s Remainder
1 Plasma volume
entering afferent
capsule of nephron
arteriole = 100% Glomerulus

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III. STRUCTURE & FUNCTION
THE RENAL CORPUSCLE (GLOMERULUS)

Thick Efferent Bowman’s Capsular

ascending arteriole capsule epithelium
limb of
loop of
Henle

Podocyte

Proximal
tubule

Glomerular
capillary
Afferent Lumen of
arteriole Bowman’s
capsule

The epithelium around glomerular

capillaries is modified into podocytes. 16
III. STRUCTURE & FUNCTION

THE RENAL CORPUSCLE (GLOMERULUS)

Podocyte Lumen of
Podocyte foot processes surround Bowman’s
each capillary, leaving slits capsule
through which filtration takes Glomerular
place. capillary
Podocyte
foot
processes

Capillary
endothelium
Mesangial
cell

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III. STRUCTURE & FUNCTION Filtration membrane
GLOMERULAR FILTRATION Endothelium (blocks formed elements)
Basement membrane (blocks large proteins)
Filtration slits of visceral layer (block
Small
small proteins)
protein

Leukocyte

Filtrate
includes water,
glucose, amino acids,
Large ions, urea, many
protein hormones, vitamins
Platelet B and C, ketones, and
very small amounts
of protein
Erythrocyte

Not filtered Filtered

Capillary Capsular space

Substances filtered by filtration membrane 18
III. STRUCTURE & FUNCTION Forces that Influence Filtration
GLOMERULAR FILTRATION Hydrostatic pressure (blood pressure)
Colloid osmotic pressure
Fluid pressure created by fluid in
Bowman’s capsule

Efferent Pfluid
arteriole
p Net filtration
pressure (NFP)
PH

Filtration pressure in Afferent Bowman’s

arteriole Glomerulus capsule
the renal corpuscle
depends on hydrostatic
pressure, and is
opposed by colloid KEY
osmotic pressure and PH = Hydrostatic pressure (blood pressure)

capsule fluid pressure p = Colloid osmotic pressure gradient due to proteins in plasma
but not in Bowman’s capsule
Pfluid = Fluid pressure created by fluid in Bowman’s capsule
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III. STRUCTURE & FUNCTION
GLOMERULAR FILTRATION

Glomerular filtration is a passive process in which hydrostatic pressures force the fluids and solute through a
membrane.

The glomeruli in the kidney are a much more efficient filter than other capillary beds in the body because:

1. Filtration membrane is a large surface area and very permeable to water and solutes.
2. Glomerular pressure is higher (~55 mm Hg), so they produce
180 L/day vs. 3-4 formed by other capillary beds.

During filtration it is important to keep the plasma proteins in the plasma to maintain osmotic (oncotic)
pressure.

If you see blood cells or protein in the urine (protinuria) then there is a problem with the filtration
membrane. This is a common finding during diabetes and hypertension that signals that kidney damage has
occurred. If untreated will progress to end stage renal disease and renal failure.

20
 III. STRUCTURE & FUNCTION

“DIVISION OF LABOR” IN THE TUBULES

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Most reabsorption in
PCT and loop of Henle

Fine tuning of the amount

reabsorbed & secreted,
depending upon hormone
levels.
Ensures that the masses of
solutes and the volume of
water entering the tubular
segments beyond Henle’s loop
are relatively small.

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III. STRUCTURE & FUNCTION

Principles governing the tubular reabsorption of solutes and water

Filtrate is similar to
interstitial fluid.

1 Na+ 1 Na+ is reabsorbed by active transport.

2 Anions 2 Electrochemical gradient drives anion

reabsorption.

3 HO 3 Water moves by osmosis, following

2
solute reabsorption.

4 K+, Ca2+, 4 Concentrations of other solutes

urea increase as fluid volume in lumen
Tubular decreases. Permeable solutes are
Tubule lumen epithelium Extracellular fluid
reabsorbed by diffusion.

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III. STRUCTURE & FUNCTION
Sodium reabsorption in the proximal tubule

Filtrate is similar to
interstitial fluid.
Na+ reabsorbed 1 Na+ enters cell through membrane proteins,
moving down its electrochemical gradient.

2 Na+ is pumped out the basolateral side

of cell by the Na+-K+-ATPase.
[Na+] high [Na+] low [Na+] high
1 2
Na+
Na+ ATP
K+

Tubule Interstitial KEY

lumen Proximal tubule cell fluid = Membrane protein ATP = Active transporter

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III. STRUCTURE & FUNCTION

Sodium-linked glucose reabsorption in the proximal tubule

Filtrate is similar to
interstitial fluid.
1 Na+ moving down its electrochemical gradient
Glc & Na+ using the SGLT protein pulls glucose into the
[Na+] high [Na+] low reabsorbed cell against its concentration gradient.
[glu] low [glu] high 2
[glu] low 2
Glucose diffuses out the basolateral side of
glu
1 glu the cell using the GLUT protein.
Na+ Na+ 3 3
[Na+] high Na+ is pumped out by Na+-K+-ATPase.
ATP
K+
KEY
ATP = Active transporter
= SGLT secondary active transporter
Tubule lumen Proximal tubule cell Interstitial fluid
= GLUT facilitated diffusion carrier

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III. STRUCTURE & FUNCTION

Saturation of mediated transport

Transport rate of substrate

Transport maximum (Tm) is transport
rate at saturation.

(mg/min)
Saturation occurs.

Renal threshold is
plasma concentration
at which saturation
occurs.

Plasma [substrate] (mg/mL)

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III. STRUCTURE & FUNCTION
SECRETION

Transfer of molecules from plasma/extracellular fluid into

lumen of the nephron
• Active process
Important in homeostatic regulation
• K+ and H+
Removal of metabolites/drugs
Increasing secretion enhances nephron excretion
A competitive process
• Penicillin and probenecid

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III. STRUCTURE & FUNCTION

Glucose handling by the nephron

Glucose Rate of Movement

Filtration Rate

(mg/min) Tm

300 Reabsorption Rate

Renal Threshold
Excretion Rate

Plasma Glucose Concentration (mg/100 mL)

[Glc]p
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III. STRUCTURE & FUNCTION

EXCRETION
Excretion = filtration – reabsorption + secretion
Clearance
• Rate at which a solute disappears from the body by
excretion or by metabolism
• Non-invasive way to measure GFR
• Inulin and creatinine used to measure GFR

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III. STRUCTURE & FUNCTION

INULIN CLEARANCE

Efferent Filtration
arteriole (100 mL/min)
Peritubular
capillaries
Glomerulus 2
Afferent
arteriole
1 Nephron
Inulin
molecules
KEY
= 100 mL of plasma or filtrate

1 Inulin concentration is 4/100 mL. 3 100 mL fluid,

0% inulin
2 GFR = 100 mL /min reabsorbed
3 100 mL plasma is reabsorbed.
No inulin is reabsorbed.
4 Inulin clearance
4 100% of inulin is excreted so 100% inulin = 100 mL/min
inulin clearance = 100 mL/min. excreted

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III. STRUCTURE & FUNCTION
EXCRETION EXAMPLES
The relationship between clearance and excretion
KEY
Filtration
(100 mL/min) = 100 mL of plasma or filtrate

1 Plasma concentration is 4/100 mL.

2
2 GFR = 100 mL /min
1
Glucose 3 100 mL plasma is reabsorbed.
molecules
4 Clearance depends on renal handling
of solute.
3 100 mL,
100% Glc
reabsorbed

4 Glucose
No glucose clearance
excreted = 0 mL/min

(a) Glucose clearance

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III. STRUCTURE & FUNCTION
EXCRETION EXAMPLES
The relationship between clearance and excretion
KEY
Filtration
(100 mL/min) = 100 mL of plasma or filtrate

1 Plasma concentration is 4/100 mL.

2 2 GFR = 100 mL /min
1
Urea 3 100 mL plasma is reabsorbed.
molecules
4 Clearance depends on renal handling
of solute.
3
100 mL,
50% Urea
reabsorbed
4 Urea
50% of Urea clearance
excreted = 50 mL/min
(b) Urea clearance

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III. STRUCTURE & FUNCTION
EXCRETION EXAMPLES
The relationship between clearance and excretion
KEY
Filtration
(100 mL/min) = 100 mL of plasma or filtrate

1 Plasma concentration is 4/100 mL.

2 2 GFR = 100 mL /min
Additional
1
Penicillin
penicillin 3 100 mL plasma is reabsorbed.
secreted
molecules
4 Clearance depends on renal handling
of solute.
3 100 mL,
No penicillin
reabsorbed

More penicillin
4 Penicillin
excreted than clearance
filtered = 150 mL/min
(c) Penicillin clearance

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III. STRUCTURE & FUNCTION

EXCRETION

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III. STRUCTURE & FUNCTION
COUNTERCURRENT MULTIPLIER
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Less Establishing the concentration gradient
concentrated
Most Descending Ascending
concentrated limb limb
300 mOsm 100 mOsm
Interstitial
Cortex fluid Tubular fluid
Medulla Blood

Descending limb Ascending limb

loses water and the loses salts and the
tubular fluid becomes interstitial fluid becomes
more concentrated. Salts Salts more concentrated.

Salts
Salts Water
Nephron
Vasa recta lose loop Vasa recta gain
salts, gain water. Water salts, lose water.

1200 mOsm

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 III. STRUCTURE & FUNCTION
COUNTERCURRENT MULTIPLIER

“Countercurrent” means
that fluid in one tube
flows the opposite way in
the adjoining tube. This
greatly increases the
opportunity for exchange
by increasing the amount
of surface area.

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 III. STRUCTURE & FUNCTION
COUNTERCURRENT MULTIPLIER

The descending The ascending limb is

loop of Henle is permeable to solutes,
relatively but not water.
impermeable to
solutes and freely
permeable to
water.
Urea recycling
contributes to the
medullary osmotic
gradient.
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 IV. HOMEOSTASIS
Regulation of GFR - Urine composition/concentration-
• Myogenic response • Hormones
• Similar to autoregulation in other • Aldosterone
systemic arterioles • Atrial Natriuretic Peptide
• Tubuloglomerular feedback • Antidiuretic Hormone
• Paracrine control
• Hormones and autonomic neurons
• By changing resistance in arterioles
• By altering the filtration coefficient

37
IV. HOMEOSTASIS

Autoregulation

Lower volume of urine

excess
urine

38
IV. HOMEOSTASIS

Myogenic Response -
Resistance changes in renal arterioles alter renal blood flow and GFR

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IV. HOMEOSTASIS
TUBULOGLOMERULAR FEEDBACK
JUXTAGLOMERULAR APPARATUS
Macula densa
group of modified epithelial cells in wall of distal convoluted tubule
located on tubule side next to afferent arteriole
detect changes in NaCl concentration of fluid in lumen of DCT
signal granular cells to release renin through paracrine stimulation

Bowman’s capsule
Efferent arteriole

Ascending Glomerulus
limb of loop
of Henle

Macula densa cells Proximal tubule

Granular cells
Afferent arteriole Endothelium
(a) (b) Granular cells
modified smooth muscle cells of afferent arteriole
located near entrance to renal corpuscle
contract when stimulated by stretch or sympathetic stimulation
synthesize, store and release renin 40
IV. HOMEOSTASIS

Tubuloglomerular Feedback
1 Glomerulus Distal tubule
GFR increases.
Efferent arteriole
2
Flow through tubule increases.
Bowman’s capsule
3 4
Flow past macula densa increases. Macula densa 1
5
Granular cells
4 Paracrine signal (adenosine) from Afferent arteriole
macula densa to afferent arteriole 2
3
Proximal
5
Afferent arteriole constricts. tubule

Resistance in afferent
arteriole increases.
Collecting
duct
Hydrostatic pressure
in glomerulus decreases.
Loop
of
GFR decreases. Henle

41
IV. HOMEOSTASIS
COORDINATED NEURAL
CONTROL OF GFR

42
IV. HOMEOSTASIS STIMULUS
1 Low BP, Low Na+ in
RENIN-ANGIOTENSIN tubule, Sympathetic
division stimulation

(ALDOSTERONE) SYSTEM RECEPTOR CONTROL CENTER

Juxtaglomerular
2 The juxtaglomerular 3 The JG apparatus
apparatus
NET EFFECT (JG) apparatus releases renin enzyme
responds to stimuli. into the blood.
6 Blood pressure increases.
Renin activates angiotensinogen to angiotensin I,
4 and angiotensin converting enzyme (ACE) converts
Kidney
angiotensin I to angiotensin II.
Renin

Blood
4 Angiotensinogen Renin Angiotensin I ACE
ACE Angiotensin II
(inactive hormone) (inactive)
(active)

Angiotensin II

5 EFFECTORS:
Angiotensin II binds to effectors to cause:
Systemic blood vessels Kidneys Hypothalamus Adrenal cortex

Aldosterone
ADH
Vasoconstriction; Decreased glomerular filtration rate Activation of thirst Release of ADH Release of aldosterone
increased peripheral (GFR); decreases urine output to center; increased fluid from hypothalamus; from adrenal cortex;
resistance and increased maintain blood volume and blood intake; increases blood maintains blood volume maintains blood volume
blood pressure pressure volume and blood with decreased urine with decreased urine
pressure output output

43
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IV. HOMEOSTASIS Aldosterone (ALDO)

Aldosterone STIMULUS
1 Angiotensin II
êNa+ blood plasma levels
é K+ blood plasma levels

Adrenal
cortex RECEPTOR CONTROL CENTER
2 3 The adrenal cortex
NET EFFECT The adrenal cortex
releases aldosterone
responds to stimuli. into the blood.
5 Plasma Na+ maintained; but
plasma K+ decreases.

BP & volume maintained (by ê urine ALDO

output). ALDO

AL
O
D

D
AL

O
DO
ALDO AL ALDO
Blood
Unbound
aldosterone
4
EFFECTORS: Aldosterone binds to effector to cause:
Kidney

Tubular Increases Na+ /H2 O

fluid reabsorption into
Na+ blood
H2 O
Blood
K+ (or H+,
Decreases Na+ /H2 O
if low pH)
Increases K+ secretion into tubular fluid and increases K+

44
(H+ can be substituted for K+ in conditions of low pH) lost in urine
IV. HOMEOSTASIS
Aldosterone

45
IV. HOMEOSTASIS
STIMULUS
ANTIDIURETIC HORMONE 1
Angiotensin II
ê blood volume
é blood osmolarity
RECEPTOR CONTROL CENTER
2 3 The hypothalamus
stimulates the posterior
NET EFFECT Hypothalamu The hypothalamus
responds to
pituitary to release ADH
s into the blood.
5 é BP (with fluid intake);
Posterior stimuli.
é blood volume (with fluid
intake); blood osmolarity pituitary
decreases. ADH
ADH

AD
H

H
AD
ADH H
AD
Blood

4 EFFECTORS: ADH

ADH binds to effectors to cause:

Kidneys

Hypothalamus Blood vessels

ADH (high doses of ADH)
binds

H2O

Activation of thirst
center; increased fluid
intake, which increases
blood volume and blood
pressure
Vasoconstriction;
Increased water reabsorption; Blood increases peripheral
decreases water lost in kidneys to resistance and blood
maintain blood volume and decreases pressure
blood osmolarity

46
IV. HOMEOSTASIS

ADH & AQUAPORINS

47
IV. HOMEOSTASIS

SUMMARY EXAMPLE

48
48
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IV. HOMEOSTASIS
Sodium (Na+) balance
135–145 mEq/L
Total K+
3.5–5.0 mEq/L

Urine
Feces
Diet
Sweat
Urine
Feces Na+ intake Na+ output
Diet
Sweat
K+ intake K+ output Hormones regulating Na+ concentration
by altering loss of both Na+ and H2O in urine
Aldosterone ADH ANP
Hormone regulating K+ blood plasma
concentration by altering loss of K+ in the urine Retains Na+ Retains water Increases
Aldosterone and water excretion of
Na+ and H2O
Causes K+ secretion by kidneys (and Maintains Na+ Decreases Na+ Decreases
excretion in urine) blood plasma blood plasma [Na+]
Decreases K+ blood plasma concentration concentration concentration Plasma

49
IV. HOMEOSTASIS
DIURETICS
• Diuretics are substances that promote the loss of Na+ and water.

• Alcohol acts like a diuretic by inhibiting the release of Vasopressin from

the pituitary gland.

• Osmotic diuretics; carbohydrates that are filtered but not reabsorbed (ex.
Mannitol).

• Loop diuretics (lasix, furosemide) are the most powerful diuretics because
they inhibit the formation of the medullar gradient by inhibiting Na+
reabsorption.

• Spironolactone is an aldosterone receptor antagonist. This is known as a K+

sparing diuretic. It acts because the K+ in the urine is from aldosterone-
driven active tubular secretion into the late DCT and collecting ducts.

50
V. INTEGRATION
General Topics -
i. Blood pressure
ii. Acid/Base balance
iii. Clinical Relationship

51
V. INTEGRATION
VOLUME & PRESSURE
é é
é

é GFR é
é

é
é

52
V. INTEGRATION

ACID/BASE BALANCE: BUFFERING OF HYDROGEN IONS IN THE BODY

The major extracellular buffer is the
CO2/HCO3- system.
The major intracellular buffers are
phosphate and proteins.

The kidneys and the respiratory system

work together to regulate hydrogen ion
concentrations.

The kidneys eliminate or replenish

hydrogen ions from the body by altering
plasma bicarbonate concentration.

53
 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
V. INTEGRATION +
Increased blood H concentration (decreased pH)
Contributing
factors GI tract
Cell

Loss
Acid is added to of HCO3–
the blood from the
GI tract and cell Various Lactic acid Ketoacids
metabolic waste. acids in Phosphoric Diarrhea
food acid

H+ increases.
Blood
HCO3–

Balance H+
Kidney
mechanism Input
Output
Excess H+ is excreted in
the urine and HCO3– is
added to the blood
through type A
intercalated cells of the Type A
kidney to maintain a intercalated
normal blood pH. cells –
function HCO 3
Urine
in acidic H+ H+
state.
Tubular fluid Blood

(a) 54
 Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.
V. INTEGRATION Decreased blood H+ concentration (increased pH)
Contributing
factors GI tract

Base is added Loss of H+

to the blood
from the GI tract. Vegetarian diet
and/or antacids
Vomiting

H+ decreases.
Blood
H+

Balance HCO3–
Kidney
mechanism Input
Output
Excess HCO3– is
excreted in the urine,
and H+ is added to the
blood through type B
intercalated cells of
the kidney to maintain Type B intercalated
a normal blood pH. cells function in
–
alkaline state. HCO 3 H+ Urine
HCO3–

Tubular fluid Blood

(b) 55
V. INTEGRATION

56
V. INTEGRATION

CLINICAL ISSUES

KIDNEY DISEASE
Many diseases affect the kidneys including:
• Bacterial infections
• Hypertension
• Diabetes

End stage renal disease is one of the leading causes of death in

the world and the leading cause of renal transplants.

57
V. INTEGRATION

CLINICAL ISSUES
• Abnormally low urine output (less the 50 mL/day) is called
anuria. This may indicate that glomerular blood pressure is too
low to cause filtration.

• Renal failure and anuria can result from any situation where the
nephrons cease to function, including acute nephritis, transfusion
reactions, and crush injuries.

58
V. INTEGRATION

HEMODIALYSIS, PERITONEAL DIALYSIS, AND TRANSPLANTATION

59
V. INTEGRATION
CLINICAL ISSUES - HORMONES
Aldosterone – Antidiuretic Hormone –

Hyperaldosteronism Diabetes Insipidus

Excess aldosterone production due
to a problem with the adrenal gland
(primary defect) or due to a problem
elsewhere that stimulates excess
aldosterone production (secondary
defect).
Lack of ADH signaling due to a lack
of production (central) or a resistance
to its functioning in the kidney
(nephrogenic).

Hypoaldosteronism Syndrome of inappropriate

An aldosterone deficiency due to antidiuretic hormone secretion
defect in the adrenal gland (Addison’s Excess production of ADH by the
disease), a defect in an enzyme
posterior pituitary (or another site).
involved in its production (CAH) or an
absence of the signal that stimulates
aldosterone production.

60