Acute Kidney Injury

Question 1

What are the main causes of acute tubular necrosis?

Answer 1

1. Ischemia (hypovolemia, post-op)

2. Toxins: exogenous (dyes) and endogenous (pigments)

Question 2

What is the pathophysiology of ATN?

Answer 2

1. Tubular back leak of filtrate into blood
2. Abnormal ultrafiltrate (Na+ increased, shuts down nephron)
3. Lumin obstruction (from cells and pigments)

Question 3

What are the clinical signs of ATN?

Answer 3

1. Decreased urine output

2. Increased serum creatinine

Question 4

What will investigations show for ATN?

Answer 4

1. Urinalysis: dysmorphic blood, heme granular casts, epithelial casts
2. Lytes: >40, FeNa> 2%, may have hyperkalemia

Question 5

How can we differentiate ATN from pre-renal causes of AKI?

Answer 5

1. ATN: slowly reversible, urine not bland, Uosm=Posm, FENa>2%, urine Na>40. INTRINSICALLY DAMAGED
2. Pre-renal: quickly reversible, urine bland, increase Uosm, FENa

Question 6

How is AKI treated?

Answer 6

1. Stop any nephrotoxic drugs (metformin, fibrates, LMW heparin)
2. Decrease salt intake
3. Maintain eletrolytes (watch for hyper K)
4. Treat uremia if present (hemodialysis)
5. IV saline prior to any IV contrast

Question 7

What causes acute interstitial nephritis?

Answer 7

1. Drugs* (beta lactams, abx, NSAIDS)
2. Infections
3. Autoimmune
4. Tubular obstruction causing inflammation (multiple myeloma, calcium oxalate, uric acid)

Question 8

How does acute interstitial nephritis present?

Answer 8

1. May be delayed from first exposure to drug (shorter latency with second exposure)
2. Triad: fever, rash, eosinphilia

Question 9

What do investigations show in IN?

Answer 9

1. Urinalysis: pyuria/eosinophils, hematuria, WBC casts
2. FENa>1%
3. Biopsy would show lymphocytic infiltrate

Question 10

How do we treat IN?

Answer 10

1. Stop causal drug
2. Course of prednisone
   usually kidneys recover

Question 11

What would investigations show in glomerulonephritis?

Answer 11

1. Urinalysis: RBC casts, proteinuria, eosinphilia, dysmorphic RBCs
2. Serological analysis: ANCA , anti-GBM ab, immune complexes

Question 12

What causes pre-renal AKI?

Answer 12

1. Cardiac: MI/CHF/valves/shock
2. Decreased SVR: sepsis/cirrhosis
3. Volume depletion
4. Decreased autoregulation: NSAIDS, ACEi

Question 13

What do investigations show in pre-renal AKI?

Answer 13

1. Urinalysis: bland, hyaline casts,

2. FENa

Question 14

What are the causes of a rapidly progressive glomerulonephritis?

Answer 14

1. Wegener’s
2. Goodpasture’s
3. Post-strep
4. Anti-GBM nephritis
5. IgA nephropathy
6. Lupus

Question 15

What urinalysis findings indicate glomerulonephritis?

Answer 15

1. RBC casts
2. proteinuria
3. Dysmorphic RBCs

Question 16

Active urine

Answer 16

1. Dysmorphic RBC and or casts +/- proteinuria

2. Means glomerulonephritis

Question 17

Diamond/rhomboid crystals

Answer 17

Uric Acid

Question 18

Envelope shaped crystals

Answer 18

Calcium oxalate* common!

Question 19

Needle shaped crystals

Answer 19

Calcium oxalate formed in ethylene glycol overdose

Question 20

Coffin shaped crystals

Answer 20

Struvite (from chronic bacterial infections). May form staghorn calculi

Question 21

How do we differentiate causes of glomerulonephritis based on serology?

Answer 21

1. ANCA ab= polyarteritis nodosa, granulomatosis with polyangitis
2. Anti-GBM= goodpastures, anti GBM nephritis
3. Low C3= lupus nephritis, anti-strep, cryoglobulinemia
4. Normal C3= IgA nephropathy