Acute Renal Failure
Prerrenal Intrinsic / Parenquimatous Postrenal / Obstructive
Definition Abrupt and sustained ↓ in renal function that results in ↑BUN & creatinine in a period of < 3 months. Renal damage persistent for >
RIFLE Classification CKD classification
GFR criteria Urine output criteria Stage GFR
Risk Serum creatinine ↑ by 50% (1.5x baseline) <0.5 ml/kg/h for 6 hours 1 >90 ml/mi
Injury Serum creatinine ↑ by 100% (2x baseline) <0.5 ml/kg/h for 12 hours 2 60-89 ml/m
Staging
Failure Serum creatinine ↑ by 200% (3x baseline) <0.3 ml/kg/h for 24 hours or anuria for 12 h 3 30-59 ml/m
Loss Persistent ARF; complete loss of kidney function > 4 weeks 4 15-29 ml/m
ESRD ESRD for > 3 months 5 <15 ml/mi
- Most common cause: D
Epidemiology - 60% of all ARF - 35% of all ARF - 5% of all ARF
- Other common causes
- Pre-existing renal impairment - DM - Peripheral vascular disease - HTN
Risk Factors - Hypertension - Jaundice - DM
- Heart disease - Advanced age → polypharmacy, ↓metabolism, systemic diseases - Vascular disease
Hypovolemia - Acute tubular necrosis (85%) - Congenital malformations Etiology→ Prolonged ARF for
- Hemorrhage ● Drugs:2 aminoglycosides, amphotericin B, - Acquired obstructions Renal functions impaired
- Diarrhea penicillins, vancomycin, chemotherapeutic ● Nephrolithiasis - Hydroelectrolytic balan
- Dehydration agents. ● Pelvic neoplasia - Waste excretion → firs
- Burns ● Contrast agents:2 i odinated, gadolinium ● Benign prostatic - Acid-base balance → n
↓ effective volume ● Endogenous toxins:2 myoglobin, hemoglobin, hyperplasia - Hormonal production →
- Distributive shock (also rhabdomyolysis) uric acid, myeloma light chains ● Aortic aneurysms - EPO after > 12
Etiology
- Congestive heart failure ● Ischemic injury1 ● Urethral stricture - Vit D
- Bilateral renal artery stenosis (or ● Sepsis-related ATN - Neurogenic bladder - Renin
unilateral in px w/ 1 kidney) - Glomerulonephritis → different lab values ● Multiple sclerosis Stages 1 and 2 → asymptoma
- Intrarenal vasoconstriction - Tubulointerstitial nephritis ● Peripheral neuropathy - Due to nephron adapta
● NSAID use - Vascular:1 malignant HTN, vasculitis, HUS ● Spinal cord lesions Stage 3
● ARBs & ACEi - Prolonged prerenal failure1 ● Post surgery - Anemia
● Cyclosporine & tacrolimus - Prolonged postrenal failure - Mild alterations in Ca a
- Hyperlipidemia
Secondary Ischemic Injury1 - Obstruction must be: - Hyperuricemia
- Appropriate response to hypoperfusion - PCT cells are more susceptible to ischemia due to ● Upper bilateral - Volume retention → H
→ kidney is STILL working ↑Na/K ATPase activity (↑ energy & O2 need) ● Lower (urethra) - Inability to concentrate
- Hypoperfusion of kidney → ↑ RAAS → ↑ - ↓ perfusion → cytoskeleton breakdown, loss of cell ● Upper unilateral in a pxs Stage 4
Na & H2O reabsorption → FeNa <1% polarity & cell junctions → apoptosis and necrosis → with 1 kidney - Intensification of previo
- Hypovolemia → ADH secretion → Toxic Injury2 - Prevention of urine outflow → - Metabolic acidosis & e
↑water reabsorption in collecting tubule → - Direct toxicity to cells → apoptosis and necrosis → ↓ pressure gradient from - Pruritus
Pathophysiology ↑ urea reabsorption Both ( → ) glomerulus to tubules → Stage 5 → start renal replacem
● Desquamation → tubular obstruction → ● ↑Reabsorption of BUN, Uremic Syndrome → malnutriti
backleak → ↓GFR Na, and fluid - Ca balance: ↓Vit D, ↓C
Prerrenal Intrinsic / Parenquimatous Postrenal / Obstructive
Definition Abrupt and sustained ↓ in renal function that results in ↑BUN & creatinine in a period of < 3 months. Renal damage persistent for >
RIFLE Classification CKD classification
GFR criteria Urine output criteria Stage GFR
Risk Serum creatinine ↑ by 50% (1.5x baseline) <0.5 ml/kg/h for 6 hours 1 >90 ml/mi
Injury Serum creatinine ↑ by 100% (2x baseline) <0.5 ml/kg/h for 12 hours 2 60-89 ml/m
Staging
Failure Serum creatinine ↑ by 200% (3x baseline) <0.3 ml/kg/h for 24 hours or anuria for 12 h 3 30-59 ml/m
Loss Persistent ARF; complete loss of kidney function > 4 weeks 4 15-29 ml/m
ESRD ESRD for > 3 months 5 <15 ml/mi
- Most common cause: D
Epidemiology - 60% of all ARF - 35% of all ARF - 5% of all ARF
- Other common causes
- Pre-existing renal impairment - DM - Peripheral vascular disease - HTN
Risk Factors - Hypertension - Jaundice - DM
- Heart disease - Advanced age → polypharmacy, ↓metabolism, systemic diseases - Vascular disease
Hypovolemia - Acute tubular necrosis (85%) - Congenital malformations Etiology→ Prolonged ARF for
- Hemorrhage ● Drugs:2 aminoglycosides, amphotericin B, - Acquired obstructions Renal functions impaired
- Diarrhea penicillins, vancomycin, chemotherapeutic ● Nephrolithiasis - Hydroelectrolytic balan
- Dehydration agents. ● Pelvic neoplasia - Waste excretion → firs
- Burns ● Contrast agents:2 i odinated, gadolinium ● Benign prostatic - Acid-base balance → n
↓ effective volume ● Endogenous toxins:2 myoglobin, hemoglobin, hyperplasia - Hormonal production →
- Distributive shock (also rhabdomyolysis) uric acid, myeloma light chains ● Aortic aneurysms - EPO after > 12
Etiology
- Congestive heart failure ● Ischemic injury1 ● Urethral stricture - Vit D
- Bilateral renal artery stenosis (or ● Sepsis-related ATN - Neurogenic bladder - Renin
unilateral in px w/ 1 kidney) - Glomerulonephritis → different lab values ● Multiple sclerosis Stages 1 and 2 → asymptoma
- Intrarenal vasoconstriction - Tubulointerstitial nephritis ● Peripheral neuropathy - Due to nephron adapta
● NSAID use - Vascular:1 malignant HTN, vasculitis, HUS ● Spinal cord lesions Stage 3
● ARBs & ACEi - Prolonged prerenal failure1 ● Post surgery - Anemia
● Cyclosporine & tacrolimus - Prolonged postrenal failure - Mild alterations in Ca a
- Hyperlipidemia
Secondary Ischemic Injury1 - Obstruction must be: - Hyperuricemia
- Appropriate response to hypoperfusion - PCT cells are more susceptible to ischemia due to ● Upper bilateral - Volume retention → H
→ kidney is STILL working ↑Na/K ATPase activity (↑ energy & O2 need) ● Lower (urethra) - Inability to concentrate
- Hypoperfusion of kidney → ↑ RAAS → ↑ - ↓ perfusion → cytoskeleton breakdown, loss of cell ● Upper unilateral in a pxs Stage 4
Na & H2O reabsorption → FeNa <1% polarity & cell junctions → apoptosis and necrosis → with 1 kidney - Intensification of previo
- Hypovolemia → ADH secretion → Toxic Injury2 - Prevention of urine outflow → - Metabolic acidosis & e
↑water reabsorption in collecting tubule → - Direct toxicity to cells → apoptosis and necrosis → ↓ pressure gradient from - Pruritus
Pathophysiology ↑ urea reabsorption Both ( → ) glomerulus to tubules → Stage 5 → start renal replacem
● Desquamation → tubular obstruction → ● ↑Reabsorption of BUN, Uremic Syndrome → malnutriti
backleak → ↓GFR Na, and fluid - Ca balance: ↓Vit D, ↓C
