ACUTE RENAL FAILURE

NON-MODIFIABLE RISK FACTORS: MODIFIABLE RISK FACTORS:

 IncreasedOliguric
age (72y.o.)
Phase
 Family History of kidney disease  Acute
Maintenance
Renal Injury
Gastroenteritis
Established
 Obesity Phase
 Hospitalization: Intensive
 Smoking Care, Major Surgery (TAHBSO)
Endothelial cells
 Bleeding and blood
necrosis andtransfusion
reaction sloughing

 Medications (NSAIDS:Naproxen)
Tubular destruction
 Use of ACE Inhibitors
MEDICAL MANAGEMENT:
Objectives:  Chronic Increase
disease: tubular
Diabetes
permeability
 Restore normal chemical Mellitus, kidney disease, heart
balance disease, liver disease,
 Prevent complications hypertension
Low GFR (5-10mL/m)
as benign prostatic
 Recognition and treatment of
 High Creatinine
hypertrophy and bladder tumor
underlying cause
 High BUN
 BP monitoring
 I and O monitoring, including  Oliguria
drainage
 Monitoring of electrolyte Decreased nephron
levels ability to
 ECG Trauma/Injury in Dehydration
Inhibit COX-1 and eliminate waste
 ABG and Serum bicarbonate levelMuscle
COX-2 production
monitoring
 May have blood transfusion  Azotemia
Decreased BP
Rhabdomyolosis
 Fluid retention
Decrease
May initiate
renaldialysis  Electrolyte
prostaglandin
Pharmacologic Therapy:
imbalance
 Cation-exchange resins Release
production for of Kidney release
hyperkalemia Myoglobin and Renin  Metabolic
Hemoglobin acidosis
 IV dextrose 50%
 Insulin Angiotensinogen
Vasoconstriction from liver
 Calcium
of renal replacement
afferent
arteriole
Albuterol Sulfate nebule pH is <5.6
Diuretic Phase
 Avoidance of nephrotoxic If managed Angiotensin
Kidneys I
have a remarkable
agents: radiocontrast ability to recover
Becomes ACE from Pulmonary and
agents, antibiotics with
ferrihemate Renal Endothelium
nephrotoxic potential, heavy
metal preparations, cancer
chemotherapeutic agents,
Free hydroxyl Angiotensin II Aldosterone
nonsteroidal anti- Growth factors
radicals Recovery
inflammatory drugs [NSAIDs] released
production Phase
 Diuretic agents
 Nutritional therapy:  Vasoconstriction  Na reabsorption
Repair and
 Weigh patient daily Vasoconstriction  Hypertension  K of
excretion
regeneration
 Dietary proteins  Na reabsorption  Water retention
renal tissue
 High carbohydrate diet
 Low salt, potassium, low
Recover tubular
phosphorus food function
 Restrict potassium intake Ischemia Additional Risk
Factors:
 Hypotension Recover renal
 Blood transfusion function
Acute Tubular
IfPRE-RENAL
not managed Necrosis
reactions
FAILURE  Severe Infection
(WBC:23.81)  Increase Urine
output
 Dye/Contrast use Decreased urea
Prolonged damage
to kidney tubules  Decreased
Injured tubular Creatinine
Initiation epithelial cells
Phase
End-stage Renal
Disease Cell death and
detachment from
basement membrane

Decrease renal
perfusion
Oliguric Phase
Tubular necrosis

Decrease blood
volume

 Low GFR
 High Creatinine
 High BUN