ACUTE & CHRONIC RENAL

FAILURE

RONI YULIWAR
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Objectives

Upon completion of this

lesson, the student will be
able to

differentiate between acute

and chronic renal failure.

BUN & Creatinine

Evaluation of Renal Function

BUN: Blood Urea Nitrogen ( 10 mg/dL )

Reflects excretion of UREA

Urea is an end product of protein
metabolism
Is affected by volume status & protein intake
Rises when GFR decreases below 40-60%

Creatinine: ( 1 mg/ dL )

Product of muscle metabolism

Not affected by fluid status or diet
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Renal Failure

Renal failure results when the

kidneys cannot remove the bodys
metabolic wastes (urea) or perform
their regulatory functions.
The wastes accumulate in the body
fluids, leading to a disruption in
endocrine and metabolic functions
as well as fluid, electrolyte, and
acidbase disturbances.
Renal failure is a systemic disease
and is a final common pathway of
many different kidney and urinary
tract diseases.
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Acute Renal Failure (ARF)

Sudden interruption of renal function

Caused by: obstruction, poor circulation,
kidney disease or medications
Kidneys are unable to clear fluids &
nitrogen waste products
Classified as:

Prerenal

Intrarenal

Postrenal

Ethiology ARF:Pre Renal

Prerenal conditions occur as a
result of impaired blood flow that
leads to hypoperfusion of the
kidney and a drop in the GFR.
The causes could be
hemorrhage, myocardial
infarction, heart failure, or
cardiogenic shock, sepsis or
anaphylaxis.

Pre-renal
55- 60%

Any condition that reduces blood flow

to the kidneys ( upstream )

Cardiac failure

Hypovolemia

Burns, dehydration, trauma, shock, diuretic

overuse

Peripheral vasodilation

Decreased cardiac output

Antihypertensive medications

Renal artery stenosis or embolism

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ARF
Clinical Manifestations

Prerenal:
oliguria
tachycardia
hypotension
dry mucous membranes
lethargy progressing to coma

Ethiology ARF:Intra Renal

Intrarenal causes of ARF are the result of

actual parenchymal damage to the
glomeruli.
Conditions such as burns, crush injuries, and
infections, nephrotoxic agents (nonsteroidal
anti-inflammatory drugs (NSAIDs);
angiotensin-converting enzyme (ACE)
inhibitors), may lead to acute tubular
necrosis and cessation of renal function.
With burns and crush injuries, myoglobin (a
protein released from muscle when injury
occurs) and hemoglobin are liberated,
causing renal toxicity, ischemia, or both.

Intrarenal
35 - 40%

Filtering structures of the kidneys are damaged

Usually from acute tubular necrosis

Ischemic damage to tubular cells

Nephrotoxic substances
Gentamycin, NSAID, Lead, Analgesics, Diuretics
Rhabdomyolysis: breakdown of muscle
myoglobin
Caused by major trauma or systemic infections
Acute glomerularnephritis: inflammation of the
nephrons

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Ethiology ARF: Post Renal

Postrenal causes of ARF are usually

the result of an obstruction
somewhere distal to the kidney.
Pressure rises in the kidney tubules;
eventually, the GFR decreases.
Common causes include calculi
(stones), tumors, benign prostatic
hyperplasia, strictures, and blood
clots.
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ARF
Clinical Manifestations

Intrarenal:
Uremia: build up of urea (nitrogenous
wastes)

confusion

altered peripheral sensation

fluid shift to lungs

infection due to decreased cell mediated

immunity

electrolyte imbalances
acidosis ( H+ ions are not secreted )
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Post-renal
<5%

Results from obstructed outflow

Bladder obstruction

Infection, tumor, obstructed Foley catheter (FC)

Ureteral obstruction

Urolithiasis

Blood clots, calculi, accidental ligation, edema

Urethral obstruction

Prostatic hyperplasia or tumor

Strictures of the urethra
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Pathophysiology:Acute Renal Failure (ARF)

Acute renal failure (ARF) is a sudden and

almost complete loss of kidney function over
a period of hours to days.
ARF manifests with
oliguria (less than 400 mL/day of urine),
anuria (less than 50 mL/day of urine), or
normal urine volume.
The patient has high serum creatinine and
BUN levels (azotemia) and
retention of other metabolic waste
products normally excreted by the
kidneys.
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ARF
Pathophysiology

Oliguric Phase: less than 400mL / 24

hours

At risk for fluid volume excess

Azotemia: elevated BUN, Creatinine

and Uric Acid
decreased level of consciousness

Electrolyte imbalance: hyperkalemia

Renal cells can regenerate if
etiology is treated
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ARF
Pathophysiology

Diuretic Phase: those who recover renal

function
gradual increase in urine output
tubular transport is still hindered
urine is dilute
high urinary outputs places pt at risk
for dehydration
Recovery Phase: gradual return to normal
function
3 to 12 months or longer for recovery
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Comparing Types of Acute Renal Failure

TYPES
Characteristi
cs

Prerenal

Intrarenal

Postrenal

Etiology
BUN value

Hypoperfusio
n
Increased

Parenchymal
damage
Increased

Obstruction
Increased

Creatinine

Increased

Increased

Increased

Urine output

Decreased

Varies, often
decreased

Varies, may be
decreased, or
sudden anuria

Urine sodium Decreased to

<20 mEq/L

Increased to >40
mEq/L

Varies, often
decreased to
mEq/L or less 20

Urine specific Increased

gravity

Low normal, 1.010 Varies

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CHRONIC RENAL FAILURE

(CRF)

Progressive & irreversible loss of nephrons

24 hour creatinine clearance:

Changes in erythropoetin production

10-15% renal function

most accurate measurement of GFR

serum creatinine is compared to urine creatinine
may have very high creatinine levels d/t ability to
compensate initially

requires dialysis graft or shunt

Anuria: <100 ml urine/ 24 hours

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CLINICAL MANIFESTATIONS

Almost every system of the body is

affected when there is failure of the normal
renal regulatory mechanisms.
The patient may appear critically ill and
lethargic with persistent nausea, vomiting
and diarrhea.
The skin and mucous membranes are dry
from dehydration, and the breath may
have the odor of urine.
Central nervous system signs and
symptoms include drowsiness, headache,
muscle twitching, and seizures..
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References

Hansen, M. (1998). Pathophysiology:

Foundations of disease and clinical
intervention. Philadelphia: Saunders.
Huether, S. E., & McCance, K. L. (2002).
Pathophysiology. St. Louis: Mosby.
http://www.pathoplus.com

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