Pathophysiology

ARF to CRF Overview

Predisposing Factors Precipitating Factors

- Age
- DM Prerenal causes (~55%)
- Heredity/Genes
- Primary Intrerenal causes (~40%)
hypertension
- Cardio and Postrenal causes (~5%)
peripheral vascular
diseases
- SLE
- AIDS Legend:
Phenomen
on
Manifestation/
s
Direction of Pathogenesis (P)
Abrupt
deterioration of
renal structural Possible Direction of P

Renal
function - Fluid and Electrolyte imbalances Stages
compromise - Impaired wound healing
- Increased susceptibility to
Major infections
- Acidosis
manifestations - Gastrointestinal complications
show: - Anemia
- Increased incidence of
pericarditis
Sustained - Uremic encephalopathy
renal damages - Platelet dysfunction
- Fluid and Electrolyte imbalances
or destruction - Metabolic changes
- Hematologic changes
End Stage Multisyste - Gastrointestinal changes
- Immunologic changes
Total GFR renal m - Changes in medication
decreased Disease involveme metabolism
- Cardiovascular changes
- Respiratory changes
Renal Serious inability of - Musculoskeletal changes
the kidneys to rid - Integumentary changes
Pathophysiology:
damage ARF Concentration - Neurologic changes
advances body of all waste - Reproductive chnges
- Endocrine changes
- Psychosocial changes
1st Precipitating Factors
Prerenal Causes:
All Known -Volume depletion (from hemorrhage,
Predisposing renal losses, GI losses)
Factors -Impaired cardiac efficiency resulting
from MI, heart failure, dysrhythmias,
cardiogenic shock
-vasodilation from sepsis
 Hypovole
mia
Falling O2 levels, Increased osmolality of
High CO2 and H exracecellular fluid
ions Reduced arterial
(e.g. carotid sinus) Excites osmoreceptors
Excites
and cardiac located @ anterior
vasomotor
baroreceptors hypothalamus
center
(Allows) vasomotor Intrinsic kidney Excites supraoptic
center to send secretions nuclei
causes:
vasoconstriction
Protein Causes posterior
signals
molecules to pituitary to release
split causing Vasopressin Arginine
1.Almost all arterioles to
Renin release Acts on the
constrict
into kidney basolateral
2.Small and large veins
and the membrane of
constrict
bloodstream
3. Heart stimulated to Activates the
Reacts with
Angiotensinog enzyme adenyl
en in liver cyclase
Causes formation of cyclic
Angiotensin 1 adenosine monophosphate
released (cyclic AMP) in cytoplasm

Continues to Causes mild Diffuses to the

persist in the vasoconstricti laminal side

Reacts with ACE Development of elongated

in the lungs vesicular structures

Becomes
Angiotensinogen
Fuses to the
2 laminal Thirst
membrane mechanism
Inactivated by activated
Angiotensinase
Laminal membrane General thirst
becomes highly sensation
permeable to H2O
General
constriction of H2O moves to the inside
arterioles of the cell

Causes adrenal Decreased kidney H2O proceeds to

glands to blood flow basolateral membrane
secrete
Aldonsterone
H2O proceeds to Drinking of H2O
Decreased
interstitial tissue
Increased blood flow in
tubular peritubular
reabsorption of capillaries
sodium
 Decreased fluid
Rapid osmotic filters from
reabsorption of glomeruli to
fluid from tubules
tubules

H2O
conservation

Increase
arterial
pressure

Adequate
Isovolemia or
mechanism
Homeostasis
Possibilities restored

Inadequate Decreased renal Decreased O2

Cycle
mechanism perfusion delivery to
repeats proximal tubules

Decreased
GFR
Decreased
Decreased cellular ATP
2nd Precipitating Factors
tubular flow
All Known Intrarenal Causes:
-Prolonged parenchymal ischemia from
Predisposing pigment nephropathy, myoglubinuria,
Factors hemoglobinuria
-nephrotoxic agents- aminoglycosides,
radiopaque contrast agents, heavy metals and
solvents, NSAIDs, ACE inhibitors, infectious
1st stage processes

Damaged
tubules
Inability to Renin-angiotensin-
conserve sodium aldosterone
reactivation
2nd
Some cell death
oliguric More
vasoconstriction
Some tubular
Less fluid necrosis Decreased
filtered renal
perfusion
Large numbers of
excretory substances in
tubules of functional
nephrons
 Throughout the
stages:
increased BUN
3rd diuretic and creatinine
Acts as osmotic
Rapid fluid
diuretic pulling
flushing
water with it
4th
recovery
Too rapid Gradual improvement
tubular fluid Possibilities in metabolic waste
removal

Disruption of
concentrating and
diluting mechanisms

3rd Precipitating Factors

All Known Postrenal Causes:
-Urinary tract obstruction
Predisposing -Calculi
Factors -tumors
-BPH
-Strictures
-Blood clots

Obstruction @ lower
urinary tract

Backing up of urine
to the kidneys

Overloading of urinary Increased

secretions pressure in
Tubular
collecting ducts damage
and tubules
 More nephrons are
destroyed
progressively

Pathophysiology: CRF Concentration

Precipitating Factor
All Known
Predisposing Untreated Acute Renal
Factors Failure

More nephrons are

destroyed
progressively

Decreased GFR

Hypertrophy of remaining Inability to reabsorb

nephrons electrolytes

Inadequate urine
Sodium
concentration
wasting

H2O wasting

Thickening or an
increase in the
amount of collagen in
basement membrane
of small
Sluggish/impaired blood
flow
Glomerulosclerosis

Decreased GFR

Stage I DIMINISHED Sodium and water Increased vascular

RENAL RESERVE balance disturbed volume
GFR 50%
Edema and
More than 75% hypertensi
damage of nephrons Potassium balance on
disturbed
Stage IIRenal Hyperkalmei
Insufficiency a
GFR 20-50% Pericarditis
Accumulation of
Uremia
BUN, creatinine levels nitrogenous wastes
continue to rise Skin disorders

Remaining nephrons undergo

changes to compensate for Gastrointestinal
those damaged nephrons Manifestations

Filtration of more concentrated

blood by the remaining nephrons Neurologic
Manifestations
Hypertrophy of
nephrons

Intolerance and exhaustion Sexual

of the remaining nephrons dysfunction
Erythropoeitin
production impaired Anemi
Further damage of
a
the nephrons

80-90% damage Skeletal Buffering

Acid-base imbalances
Acidos
Stage III RENAL FAILURE
is
GFR 10-20% Vitamin D activation
Osteodystrophies
impaired
Impaired kidney
function and
Vitamin D activation
Uremia
impaired
 Hyperparathyroidism

Stage IV End-Stage Renal

Phosphate
Disease
GFR 20% and below accumulation

Please note that due to the complexity of the disease process, I have deemed necessary not to include the management
both medical and nursing related in this diagram. Furthermore, only important manifestations were included also. Readers
are encouraged to continue reading instead for it is indicated below.