Definition:
Rapid decline in kidney function + increase in serum creatinine (50%, or 0.5-1.0 mg\dL increase)
Classification:
Presentation:
Oliguric (<400 mL\day) \anuric\non-oliguric (>400 mL\day), wt gain, edema, azotemia
Categories:
1. Prerenal: most common
- Pathophysiology: decrease in renal blood flow
- True volume depletion: lack of oral intake, vomiting, diarrhea, GI bleeding, diuretics, hyperglycemia, DI
- Reduction in effective circulating volume: CHF, cirrhosis, hepatorenal syndrome, Nephrotic syndrome, sepsis\shock,
- Medications: diuretics, ACEI\ARBs (dilate efferent), NSAIDs (constrict afferents)
- Reversible (unless persistent hypoperfusion -> ischemia -> ATN)
- Investigation:
- Oliguria (<400 mL\day)
- Increased BUN\Cr ratio (>20:1), due to increased water and urea reabsorption
- Increased urine osmolality (>500 mOsml\kg)
- Low urine sodium (<20 mEq\L)
- Low urine fractional excretion of sodium (FENa <1%)
- Treatment:
- Treat underlying cause, eliminate offending agent
- NS to restore blood volume and pressure (don’t give if edema)
2. Renal: 2nd most common
- Pathophysiology: damage to renal parenchyma
- Tubular ds (ATN): can be due to ischemia (shock, sepsis, hemorrhage, HF) and nephrotoxins (Meds: antibiotics ‘aminoglycosides and vancomysin’, NSAIDs, radiocontrast, myoglobinuria ‘muscle damage, strenuous exercise, rhabdomyolysis’, hemoglobinuria ‘hemolysis’, chemo ‘cisplastin’)
- Glomerular ds (GN)
- Vascular ds: renal artery occlusion, TTP, HUS
- Interstitial ds: allergic interstitial nephritis (due to hypersensitivity to meds)
- Investigations:
- Decreased BUN\Cr ratio (<20:1), bc urea is less absorbed here compared w\ prerenal
- Decreased urine osmolality (<350 mOsm\kg), bc impaired renal water reabsorption
- High urine sodium (>40 mEq\L)
- High urine fractional excretion of sodium (FENa >2-3%)
- Treatment:
- Supportive, eliminate offending agent
- If oligouric -> furosemid
3. Postrenal: least common
- Pathophysiology: urinary tract obstruction -> increase tubular pressure -> ↓GFR
- Reversible if obstruction is relieved. If not -> ATN
- MCC: BPH -> urethral obstruction
- Obstructing nephrolithiasis
- Obstructing neoplasm
- Retroperitoneal fibrosis
- Renal vein thrombosis
- Investigations:
- Ultrasound: test of choice
- Treatment:
- Bladder cath -> decompress compression
Diagnosis of acute kidney injury in general:
- Blood work: high BUN and Cr, electrolyte (K, Ca, PO), CBC
- Urine volume, urinalysis, urine sediment, urine chemistry
- Foley cath (rule out bladder outlet obstruction)
- Fluid challenge (rule out prerenal)
- Imaging: US (post renal obstruction and hydronephrosis)
- Renal biopsy (if sus GN or acute allergic interstitial nephritis)
- Renal arteriography
Complications:
- Volume overload -> pulmn edema -> give furosemide
- High anion gap metabolic acidosis w\ hyperkalemia
- Can’t form active vit D + PTH resistance -> Hypocalcemia
- Water intake is more than output or volume depleted patients consuming hypotonic solutions -> Hyponatremia
- Uremia
- Infection (multifactorial\uremia impairing immunity): pneumonia, UTI, wound infec, sepsis
Random notes:
- Most common cause of AKI in hospital setting is? Acute tubular necrosis, followed by prerenal causes
- Rhabdomyolysis: muscle breakdown (e.g. trauma, seizures, snake bites) -> release of muscle fiber content into blood stream (myoglobin) -> nephrotoxicity and AKI. High CPK and K. Treat with IV fluid, mannitol (osmotic diuretic), and bicarbonate (drives K back into cells)
- Course of ATN: oliguric phase -> diuretic phase -> recovery phase
Download the PDF version: here
References:
- Step up to medicine
- Master the boards
- Kaplan step 2 videos and lecture notes
- Toronto notes
- Step up to USMLE step 2