ACUTE RENAL FAILURE

NON-MODIFIABLE RISK FACTORS:

Increased age (72y.o.)
Family History of kidney disease
Obesity
Smoking

MODIFIABLE RISK FACTORS:

Acute Gastroenteritis
Hospitalization: Intensive Care,
Major Surgery (TAHBSO)
Bleeding and blood transfusion
reaction
Medications (NSAIDS:Naproxen)
Use of ACE Inhibitors
Chronic disease: Diabetes
Mellitus, kidney disease, heart
disease, liver disease,
hypertension
Obstructive causes such
as benign prostatic
hypertrophy and bladder tumor

Inhibit COX-1 and

COX-2 production

Decrease renal
prostaglandin
production

Trauma/Injury in
Muscle

Dehydration

Rhabdomyolosis

Decreased BP

Release of
Myoglobin and
Hemoglobin

Kidney release
Renin
Angiotensinogen
from liver

Vasoconstriction
of renal afferent
arteriole

pH is <5.6
Angiotensin I
Becomes
ferrihemate
Free hydroxyl
radicals
production
Vasoconstriction

ACE from Pulmonary and

Renal Endothelium

Angiotensin II

Vasoconstriction
Hypertension
Na reabsorption

Ischemia

Acute Tubular
Necrosis

PRE-RENAL
FAILURE

Initiation
Phase

Additional Risk
Factors:
Hypotension
Blood transfusion
reactions
Severe Infection
(WBC:23.81)
Dye/Contrast use

Injured tubular
epithelial cells

Cell death and

detachment from
basement membrane

Oliguric Phase

Decrease renal
perfusion
Tubular necrosis
Decrease blood
volume
Low GFR
High Creatinine
High BUN

Aldosterone

Na reabsorption
K excretion
Water retention

Maintenance
Phase

Oliguric Phase

Renal Injury
Established

(10-20 days)
Endothelial cells
necrosis and
sloughing
Tubular destruction

MEDICAL MANAGEMENT:
Objectives:
Restore normal chemical balance
Prevent complications
Recognition and treatment of
underlying cause
BP monitoring
I and O monitoring, including
drainage
Monitoring of electrolyte levels
ECG
ABG and Serum bicarbonate level
monitoring
May have blood transfusion
May initiate dialysis
Pharmacologic Therapy:
Cation-exchange resins for
hyperkalemia
IV dextrose 50%
Insulin
Calcium replacement
Albuterol Sulfate nebule
Avoidance of nephrotoxic
agents: radiocontrast
agents, antibiotics with
nephrotoxic potential, heavy
metal preparations, cancer
chemotherapeutic agents,
nonsteroidal antiinflammatory drugs [NSAIDs]
Diuretic agents
Nutritional therapy:
Weigh patient daily
Dietary proteins
High carbohydrate diet
Low salt, potassium, low
phosphorus food
Restrict potassium intake
Follow up check up within 1-2
weeks

Increase tubular
permeability
Low GFR (5-10mL/m)
High Creatinine
High BUN
Oliguria

Decreased nephron
ability to
eliminate waste
Azotemia
Fluid retention
Electrolyte
imbalance
Metabolic
acidosis

If managed

Kidneys have a remarkable

ability to recover

Recovery
Phase

Diuretic Phase

Growth factors
released

Repair and
regeneration of
renal tissue
Recover tubular
function

Recover renal
function

If not managed

Prolonged damage
to kidney tubules

End-stage Renal
Disease

Increase Urine
output
Decreased urea
Decreased
Creatinine