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Pathophysiology of Acute Renal Failure
Pathophysiology of Acute Renal Failure
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