ACUTE RENAL FAILURE

NON-MODIFIABLE RISK FACTORS: MODIFIABLE RISK FACTORS:

 Increased age (72y.o.)
 Family History of kidney disease  Acute Gastroenteritis
 Obesity  Hospitalization: Intensive Care,
 Smoking 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

Trauma/Injury in Dehydration
Inhibit COX-1 and
COX-2 production Muscle

Rhabdomyolosis Decreased BP
Decrease renal
prostaglandin
production Release of Kidney release
Myoglobin and Renin
Hemoglobin
Angiotensinogen
Vasoconstriction from liver
of renal afferent pH is <5.6
arteriole
Angiotensin I
Becomes ACE from Pulmonary and
ferrihemate Renal Endothelium

Free hydroxyl Angiotensin II Aldosterone

radicals
production
 Vasoconstriction  Na reabsorption
Vasoconstriction  Hypertension  K excretion
 Na reabsorption  Water retention

Ischemia Additional Risk

Factors:
 Hypotension
Acute Tubular  Blood transfusion
PRE-RENAL reactions
Necrosis
FAILURE  Severe Infection
(WBC:23.81)
 Dye/Contrast use

Initiation Injured tubular

Phase epithelial cells

Cell death and

detachment from
basement membrane

Decrease renal
perfusion
Oliguric Phase
Tubular necrosis

Decrease blood
volume

 Low GFR
 High Creatinine
 High BUN
 Maintenance Renal Injury
Phase Established
Oliguric Phase
(10-20 days)
Endothelial cells
necrosis and
sloughing

Tubular destruction

MEDICAL MANAGEMENT:
Increase tubular
Objectives: permeability
 Restore normal chemical balance
 Prevent complications
Low GFR (5-10mL/m)
 Recognition and treatment of
underlying cause
 BP monitoring  High Creatinine
 High BUN
 I and O monitoring, including
drainage  Oliguria
 Monitoring of electrolyte levels
 ECG
Decreased nephron
 ABG and Serum bicarbonate level ability to
monitoring eliminate waste
 May have blood transfusion
 May initiate dialysis
 Pharmacologic Therapy:  Azotemia
 Cation-exchange resins for  Fluid retention
hyperkalemia  Electrolyte
imbalance
 IV dextrose 50%
 Metabolic
 Insulin acidosis
 Calcium replacement
 Albuterol Sulfate nebule
 Avoidance of nephrotoxic
agents: radiocontrast
agents, antibiotics with If managed Kidneys have a remarkable
nephrotoxic potential, heavy
metal preparations, cancer
ability to recover Diuretic Phase
chemotherapeutic agents,
nonsteroidal anti-
inflammatory drugs [NSAIDs]
 Diuretic agents Recovery Growth factors
 Nutritional therapy: Phase released
 Weigh patient daily
 Dietary proteins
Repair and
 High carbohydrate diet regeneration of
 Low salt, potassium, low renal tissue
phosphorus food
 Restrict potassium intake
Recover tubular
 Follow up check up within 1-2 function
weeks

Recover renal
function
If not managed
 Increase Urine
output
Prolonged damage  Decreased urea
to kidney tubules  Decreased
Creatinine

End-stage Renal
Disease