Human Physiology - Maryville University
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Transcript Human Physiology - Maryville University
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Chapter 17
Physiology of the Kidneys
17-1
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Chapter 17 Outline
Overview
of Kidney Structure
Nephron
Glomerular
Filtration
Function of Nephron Segments
Renal Clearance
Hormonal Effects
Na+, K+, H+, & HC03- Relationships
Clinical Aspects
17-2
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Kidney Function
Is
to regulate plasma & interstitial fluid by formation of
urine
In process of urine formation, kidneys regulate:
Volume of blood plasma, which contributes to BP
Waste products in blood
Concentration of electrolytes
Including Na+, K+, HC03-, & others
Plasma pH
17-3
Overview of Kidney Structure
17-4
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Structure of Urinary System
Paired
kidneys are
on either side of
vertebral column
below diaphragm
About size of fist
Urine flows from
kidneys into ureters
which empty into
bladder
Fig 17.1
17-5
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Structure of Kidney
Cortex
contains many capillaries & outer parts of nephrons
Medulla consists of renal pyramids separated by renal columns
Pyramid contains minor calyces which unite to form a major
calyx
Fig 17.2
17-6
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Structure of Kidney continued
Fig 17.3
Major
calyces join
to form renal pelvis
which collects urine
Conducts urine
to ureters which
empty into
bladder
17-7
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Micturition Reflex (Urination)
Actions
of internal & external urethral sphincters are regulated
by reflex center located in sacral part of cord
Filling of bladder activates stretch receptors that send impulses
to micturition reflex center
This activates Parasymp neurons causing contraction of
detrusor muscle that relaxes internal urethral sphincter
creating sense of urgency
There is voluntary control over external urethral sphincter
When urination is consciously initiated, descending motor tracts
to micturition center inhibit somatic motor fibers of external
urethral sphincter & urine is expelled
17-8
Nephron
17-9
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Nephron
Is
functional unit of kidney responsible for forming urine
>1 million nephrons/kidney
Is a long tube & has associated blood vessels
Fig 17.2
17-10
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Renal Blood Vessels
Blood
enters kidney through renal artery
Which divides into interlobar arteries
That divide into arcuate arteries that give rise to
interlobular arteries
Fig 17.4
17-11
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Renal Blood Vessels
Interlobular
arteries give rise to afferent arterioles
which supply glomeruli
Glomeruli are mass of capillaries inside glomerular
capsule that gives rise to filtrate that enters nephron
tubule
Efferent arteriole drains glomerulus & delivers that
blood to peritubular capillaries (vasa recta)
Blood from peritubular capillaries enters veins
17-12
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Fig 17.5
17-13
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Nephron Tubules
Tubular
part of nephron begins with glomerular capsule which
transitions into proximal convoluted tubule (PCT), then to
descending & ascending limbs of Loop of Henle (LH), & distal
convoluted tubule (DCT)
Tubule ends where it empties into collecting duct (CD)
Fig 17.2
17-14
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Glomerular (Bowman's) Capsule
Surrounds
glomerulus
Together they form
renal corpuscle
Is where glomerular
filtration occurs
Filtrate passes into
PCT
PCT
Glomerular
capsule
Fig 17.6
17-15
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Proximal Convoluted Tubule
Walls
consist of single layer of cuboidal cells with
millions of microvilli
Which increase surface area for reabsorption
17-16
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Type of Nephrons
Cortical
nephrons
originate in outer 2/3
of cortex
Juxtamedullary
nephrons originate
in inner 1/3 cortex
Have long LHs
Important in
producing
concentrated
urine
Fig 17.6
17-17
Glomerular Filtration
17-18
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Glomerular Filtration
Glomerular
capillaries & Bowman's capsule form a
filter for blood
Glomerular Caps are fenestrated--have large pores
between its endothelial cells
100-400 times more permeable than other Caps
Small enough to keep RBCs, platelets, & WBCs
from passing
Pores are lined with negative charges to keep
blood proteins from filtering
17-19
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Glomerular Filtration continued
To
enter tubule
filtrate must
pass through
narrow
filtration slits
formed
between
pedicels of
podycytes of
glomerular
capsule
Fig 17.8
17-20
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Fig 17.7
17-21
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Fig 17.9
17-22
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Glomerular Ultrafiltrate
Is
fluid that enters
glomerular
capsule, whose
filtration was driven
by blood pressure
Fig 17.10
17-23
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Glomerular Filtration Rate (GFR)
Is
volume of filtrate produced by both kidneys/min
Averages 115 ml/min in women; 125 ml/min in men
Totals about 180L/day (45 gallons)
So most filtered water must be reabsorbed or
death would ensue from water lost through
urination
17-24
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Regulation of GFR
Is
controlled by extrinsic & intrinsic (autoregulation)
mechanisms
Vasoconstriction or dilation of afferent arterioles affects
rate of blood flow to glomeruli & thus GFR
17-25
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Sympathetic Effects
Sympathetic
activity
constricts afferent
arteriole
Helps maintain
BP & shunts
blood to heart &
muscles
Fig 17.11
17-26
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Renal Autoregulation
Allows
kidney to maintain a constant GFR over wide
range of BPs
Achieved via effects of locally produced chemicals on
afferent arterioles
When average BP drops to 70 mm Hg afferent
arteriole dilates
When average BP increases, afferent arterioles
constrict
17-27
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17-28
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Renal Autoregulation
Is
also maintained by negative feedback between afferent
arteriole & volume of filtrate (tubuloglomerular feedback)
Increased flow of filtrate sensed by macula densa (part of
juxtaglomerular apparatus) in thick ascending LH
Signals afferent arterioles to constrict
17-29
Function of Nephron Segments
17-30
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Reabsorption of Salt & H20
In
PCT returns most molecules & H20 from filtrate back
to peritubular capillaries
About 180 L/day of ultrafiltrate produced; only 1–2 L
of urine excreted/24 hours
Urine volume varies according to needs of body
Minimum of 400 ml/day urine necessary to
excrete metabolic wastes (obligatory water loss)
17-31
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Reabsorption of Salt & H20 continued
Return
of filtered
molecules is called
reabsorption
Water is never
transported
Other molecules are
transported & water
follows by osmosis
Fig 17.13
17-32
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PCT
Filtrate
in PCT is
isosmotic to blood (300
mOsm/L)
Thus reabsorption of H20
by osmosis cannot occur
without active transport
(AT)
Is achieved by AT of
Na+ out of filtrate
Loss of + charges
causes Cl- to
passively follow
Na+
Water follows salt
by osmosis
Fig 17.14
17-33
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Insert fig. 17.14
Fig 17.15
17-34
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Significance of PCT Reabsorption
≈65%
Na+, Cl-, & H20 is reabsorbed in PCT & returned
to bloodstream
An additional 20% is reabsorbed in descending loop of
Henle
Thus 85% of filtered H20 & salt are reabsorbed early in
tubule
This is constant & independent of hydration levels
Energy cost is 6% of calories consumed at rest
The remaining 15% is reabsorbed variably,
depending on level of hydration
17-35
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Concentration Gradient in Kidney
In
order for H20 to be reabsorbed, interstitial fluid must
be hypertonic
Osmolality of medulla interstitial fluid (1200-1400
m O sm) is 4X that of cortex & plasma (300 m O sm)
This concentration gradient results largely from loop
of Henle which allows interaction between
descending & ascending limbs
17-36
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Descending Limb LH
Is
permeable to H20
Is impermeable to, &
does not AT, salt
Because deep regions
of medulla are 1400
m O sm, H20 diffuses
out of filtrate until it
equilibrates with
interstitial fluid
This H20 is
reabsorbed by
capillaries
Fig 17.17
17-37
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Ascending Limb LH
Has
a thin segment in
depths of medulla &
thick part toward
cortex
Impermeable to H20;
permeable to salt;
thick part ATs salt out
of filtrate
AT of salt causes
filtrate to become
dilute (100
m O sm) by end of
LH
Fig 17.17
17-38
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AT in Ascending Limb LH
NaCl
is actively
extruded from thick
ascending limb into
interstitial fluid
Na+ diffuses into
tubular cell with
secondary active
transport of K+ and
Cl Occurs at a ratio of 1
Na+ & 1 K+ to 2 Cl-
Insert fig. 17.15
Fig 17.16
17-39
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AT in Ascending Limb LH continued
Na+
is AT across
basolateral
membrane by Na+/ K+
pump
Cl- passively follows
Na+ down electrical
gradient
K+ passively diffuses
back into filtrate
Fig 17.16
17-40
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Countercurrent Multiplier System
Countercurrent
flow & proximity allow descending & ascending
limbs of LH to interact in way that causes osmolality to build in
medulla
Salt pumping in thick ascending part raises osmolality around
descending limb, causing more H20 to diffuse out of filtrate
This raises osmolality of filtrate in descending limb which
causes more concentrated filtrate to be delivered to
ascending limb
As this concentrated filtrate is subjected to AT of salts, it
causes even higher osmolality around descending limb
(positive feedback)
Process repeats until equilibrium is reached when osmolality
of medulla is 1400
17-41
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Vasa Recta
Fig 17.18
Is
important component of
countercurrent multiplier
Permeable to salt, H20 (via
aquaporins), & urea
Recirculates salt, trapping
some in medulla interstitial
fluid
Reabsorbs H20 coming out
of descending limb
Descending section has
urea transporters
Ascending section has
fenestrated capillaries
17-42
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Effects of Urea
Urea
contributes to
high osmolality in
medulla
Deep region of
collecting duct is
permeable to
urea & transports
it
Fig 17.19
17-43
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17-44
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Collecting Duct (CD)
Plays
important role in water conservation
Is impermeable to salt in medulla
Permeability to H20 depends on levels of ADH
17-45
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ADH
Fig 17.21
Is
secreted by post
pituitary in response to
dehydration
Stimulates insertion of
aquaporins (water
channels) into plasma
membrane of CD
When ADH is high, H20
is drawn out of CD by
high osmolality of
interstitial fluid
& reabsorbed by vasa
recta
17-46
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Osmolality of Different Regions of the Kidney
Fig 17.20
17-47
Renal Clearance
17-48
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Renal Clearance
Refers
to ability of kidney to remove substances from blood &
excrete them in urine
Occurs by filtration & by secretion
Secretion is opposite of reabsorption--substances from vasa
recta are transported into tubule & excreted
Reabsorption decreases renal clearance; secretion increases
clearance
Fig 17.22
17-49
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Secretion of Drugs
Many
drugs, toxins, & metabolites are secreted by
organic anion transporters of the PCT
Involved in determining half-life of many therapeutic
drugs
17-50
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Inulin Measurement of GFR
Inulin,
a fructose polymer, is useful for measuring GFR because
is neither reabsorbed or secreted
Rate at which a substance is filtered by the glomeruli can be
calculated:
Quantity filtered = GFR x P
P = inulin concentration in plasma
Quantity excreted (mg/min) = V x U
V = rate of urine formation; U = inulin concentration in urine
Amount filtered = amount excreted
GFR = V x U
P
17-51
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Renal Clearance of Inulin
Fig 17.23
17-52
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Renal Plasma Clearance (RPC)
Is
volume of plasma from which a substance is
completely removed/min by excretion in urine
If substance is filtered but not reabsorbed then all
filtered will be excreted RPC = GFR
If substance is filtered & reabsorbed then RPC < GFR
If substance is filtered but also secreted & excreted
then RPC will be > GFR (=120 ml/ min)
RPC = V x U
P
17-53
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Clearance of Urea
Urea
is freely filtered into glomerular capsule
Urea clearance calculations demonstrate how kidney handles a
substance: RPC = V X U/P
V = 2ml/min; U = 7.5 mg/ml of urea; P = 0.2 mg/ml of urea
RPC = (2ml/min)(7.5mg/ml)/(0.2mg/ml) = 75ml/min
Urea clearance is 75 ml/min, compared to clearance of inulin
(120 ml/min)
Thus 40-60% of filtered urea is always reabsorbed
Is passive process because of presence of carriers for
facilitative diffusion of urea
17-54
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Measurement of Renal Blood Flow
Not
all blood delivered to glomerulus is filtered into
glomerular capsule
20% is filtered; rest passes into efferent arteriole &
back into circulation
Substances that aren't filtered can still be cleared by
active transport (secretion) into tubules
17-55
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Total Renal Blood Flow Using PAH
PAH
clearance is used to measure total renal blood flow
Normally averages 625 ml/min
It is totally cleared by a single pass through a nephron
So it must be both filtered & secreted
Filtration & secretion clear only molecules dissolved in
plasma
To get total renal blood flow, amount of blood occupied by
erythrocytes must be taken into account
45% blood is RBCs; 55% is plasma
total renal blood flow = PAH clearance
= 625/0.55 = 1.1L/min
0.55
17-56
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Total Renal Blood Flow Using PAH continued
Fig 17.24
17-57
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Glucose & Amino Acid Reabsorption
Filtered
glucose & amino acids are normally 100%
reabsorbed from filtrate
Occurs in PCT by carrier-mediated cotransport with
Na+
Transporter displays saturation if ligand
concentration in filtrate is too high
Level needed to saturate carriers & achieve
maximum transport rate is transport maximum
(Tm)
Glucose & amino acid transporters don't saturate
under normal conditions
17-58
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Glycosuria
Is
presence of glucose in urine
Occurs when glucose > 180-200mg/100ml plasma
(= renal plasma threshold)
Glucose is normally absent because plasma levels
stay below this value
Hyperglycemia has to exceed renal plasma
threshold
Diabetes mellitus occurs when hyperglycemia
results in glycosuria
17-59
Hormonal Effects
17-60
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Electrolyte Balance
regulate levels of Na+, K+, H+, HC03-, Cl-, &
PO4-3 by matching excretion to ingestion
Control of plasma Na+ is important in regulation of
blood volume & pressure
Control of plasma of K+ important in proper function of
cardiac & skeletal muscles
Kidneys
17-61
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Role of Aldosterone in Na+/K+ Balance
filtered Na+ & K+ reabsorbed before DCT
Remaining is variably reabsorbed in DCT & cortical
CD according to bodily needs
Regulated by aldosterone (controls K+ secretion
& Na+ reabsorption)
In the absence of aldosterone, 80% of remaining
Na+ is reabsorbed in DCT & cortical CD
When aldosterone is high all remaining Na+ is
reabsorbed
90%
17-62
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K+ Secretion
only way K+ ends
up in urine
Is directed by
aldosterone &
occurs in DCT &
cortical CD
High K+ or Na+
will increase
aldosterone & K+
secretion
Is
Fig 17.25
17-63
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Juxtaglomerular Apparatus (JGA)
Is
specialized region in each nephron where afferent arteriole
comes in contact with thick ascending limb LH
Fig 17.26
17-64
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Renin-Angiotensin-Aldosterone System
Is
activated by release of renin from granular cells
within afferent arteriole
Renin converts angiotensinogen to angiotensin I
Which is converted to Angio II by angiotensinconverting enzyme (ACE) in lungs
Angio II stimulates release of aldosterone
17-65
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Regulation of Renin Secretion
Inadequate
intake of NaCl always causes decreased
blood volume
Because lower osmolality inhibits ADH, causing less
H2O reabsorption
Low blood volume & renal blood flow stimulate renin
release
Via direct effects of BP on granular cells & by
Symp activity initiated by arterial baroreceptor
reflex (see Fig 14.26)
17-66
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Fig 17.27
17-67
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Macula Densa
Is
region of
ascending limb in
contact with afferent
arteriole
Cells respond to
levels of Na+ in
filtrate
Inhibit renin
secretion when
Na+ levels are
high
Causing less
aldosterone
secretion, more
Na+ excretion
Fig 17.26
17-68
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17-69
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Atrial Natriuretic Peptide (ANP)
Is
produced by atria due to stretching of walls
Acts opposite to aldosterone
Stimulates salt & H20 excretion
Acts as an endogenous diuretic
17-70
Na+, K+, H+, & HC03- Relationships
17-71
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Na+, K+, & H+ Relationship
Na+
reabsorption in
DCT & CD creates
electrical gradient for
H+ & K+ secretion
When extracellular H+
increases, H+ moves
into cells causing K+ to
diffuse out & vice versa
Hyperkalemia can
cause acidosis
In severe acidosis, H+ is
secreted at expense of
K+
Insert fig. 17.27
Fig 17.28
17-72
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Renal Acid-Base Regulation
help regulate blood pH by excreting H+ &/or
reabsorbing HC03Most H+ secretion occurs across walls of PCT in
exchange for Na+ (Na+/H+ antiporter)
Normal urine is slightly acidic (pH = 5-7) because
kidneys reabsorb almost all HC03- & excrete H+
Kidneys
17-73
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Reabsorption of HCO3- in PCT
Is
indirect because apical membranes of PCT cells are
impermeable to HCO3-
17-74
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Reabsorption of HCO3- in PCT continued
urine is acidic, HCO3- combines with H+ to form H2C03
(catalyzed by CA on apical membrane of PCT cells)
H2C03 dissociates into C02 + H2O
C02 diffuses into PCT cell & forms H2C03 (catalyzed by CA)
H2C03 splits into HCO3- & H+ ; HCO3- diffuses into blood
When
Fig 17.29
17-75
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Urinary Buffers
Nephron
cannot produce urine with pH < 4.5
Excretes more H+ by buffering H+s with HPO4-2 or NH3
before excretion
Phosphate enters tubule during filtration
Ammonia produced in tubule by deaminating amino
acids
Buffering reactions
HPO4-2 + H+ H2PO4 NH3 + H+ NH4+ (ammonium ion)
17-76
Clinical Aspects
17-77
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Diuretics
Are
used to lower blood volume because of hypertension,
congestive heart failure, or edema
Increase volume of urine by increasing proportion of glomerular
filtrate that is excreted
Loop diuretics are most powerful; inhibit AT salt in thick
ascending limb of LH
Thiazide diuretics inhibit NaCl reabsorption in 1st part of DCT
Carbonic anhydrase inhibitors prevent H20 reabsorption in PCT
when HC0s- is reabsorbed
Osmotic diuretics increase osmotic pressure of filtrate
17-78
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Sites of Action of Clinical Diuretics
Fig 17.30
17-79
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Kidney Diseases
In
acute renal failure, ability of kidneys to excrete
wastes & regulate blood volume, pH, & electrolytes is
impaired
Rise in blood creatinine & decrease in renal plasma
clearance of creatinine
Can result from atherosclerosis, inflammation of
tubules, kidney ischemia, or overuse of NSAIDs
17-80
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Kidney Diseases continued
Glomerulonephritis
is inflammation of glomeruli
Autoimmune attack against glomerular capillary
basement membranes
Causes leakage of protein into urine resulting in
decreased colloid osmotic pressure & resulting
edema
17-81
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Kidney Diseases continued
In
renal insufficiency, nephrons have been destroyed as a result
of a disease
Clinical manifestations include salt & H20 retention & uremia
(high plasma urea levels)
Uremia is accompanied by high plasma H+ & K+ which
can cause uremic coma
Treatment includes hemodialysis
Patient's blood is passed through a dialysis machine
which separates molecules on basis of ability to diffuse
through selectively permeable membrane
Urea & other wastes are removed
17-82