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ACUTE KIDNEY INJURY (AKI)

  • Definition:

    • - Serum Cr increase ≥ 0.3 mg/dL within 48 hours

    • - Serum Cr increased to ≥ 1.5× baseline within the prior 7 days

    • - Urine volume <0.5 mL/kg/h for 6 hours

Pre-renal (decreased renal perfusion)

  • Etiologies: Hypovolemia (poor PO intake, diuresis, hemorrhage), vasodilation (sepsis, anaphylaxis), poor effective circulating volume (heart failure, cirrhosis, nephrotic syndrome), contrast, medications (ACE inhibitors, ARBs, NSAIDs), abdominal compartment syndrome

  • Clinical features: BUN/Cr >20:1, fractional excretion of sodium (FENa) <1%, urine osmolality >500 mOsm/kg H2O, urine Na+ <20 mEq/L, benign sediment, few hyaline casts, no cellular casts

Intra-renal (direct injury to renal tissue)

Acute tubular necrosis (ATN)

  • Etiologies:

    • - Ischemia: Prolonged or severe hypoperfusion (e.g., from hemorrhage or sepsis)

    • - Toxic: Pigment (rhabdomyolysis, hemolysis), paraproteins (multiple myeloma), medications (aminoglycosides, cisplatin, foscarnet, pentamidine, tenofovir), IV contrast

  • Clinical features: “Muddy brown” granular casts; usually FENa >2%

  • Pearl: Ischemic ATN lies on a spectrum of decreased renal perfusion along with “pre-renal” AKI; a single patient (or even a single kidney) may exhibit both pre-renal and ATN pathophysiology in tandem

Acute interstitial nephritis (AIN)

  • Etiologies:

    • - Medications: Antibiotics, especially beta-lactams, NSAIDs, and PPIs

    • - Infection: Streptococcal infection, diphtheria, CMV, EBV, tuberculosis, hantavirus, leptospirosis

    • - Systemic autoimmune disease: Sjögren’s, sarcoidosis, SLE, IgG4 disease

  • Clinical features:

    • - Rash, eosinophilia, WBC casts

    • - Eosinophils in the urine are not specific or sensitive (low diagnostic value); instead of ordering urine eos, if high suspicion for AIN, stop the culprit medication and consider a kidney biopsy

Acute Glomerulonephritis

  • Etiologies: Several causes listed under “Nephrotic Syndrome” and “Nephritic Syndrome”

  • Clinical features: Proteinuria, hypertension, hematuria, RBC casts

Post-renal (obstruction of urinary tract)

  • Etiology: Benign prostatic hyperplasia (BPH), malignancy, strictures, stones, functional urinary retention, congenital abnormalities. Typically, AKI is caused by obstruction of bilateral kidneys.

  • Clinical features: Increased PVR by ultrasound or Foley, hydronephrosis on ultrasound or CT

General Approach to the Diagnosis and Management of AKI

  • Step 1: Address any urgent management needs (e.g., treat severe hyperkalemia, hypoxemia due to pulmonary edema)

  • Step 2: Confirm baseline Cr and diagnose the etiology. See differential diagnosis above and in Figure 6.3. Volume exam suggesting hypovolemia may suggest a pre-renal cause. Obtain a bladder scan to rule out postrenal causes. Get a UA with microscopy. Consider checking the fractional excretion of sodium (FENa), which can help differentiate pre-renal AKI from ATN.

    • - Pearl: Most AKI in the hospital will be pre-renal due to hypovolemia, intra-renal due to ATN, or postrenal due to obstruction. Thus, a majority of inpatient AKI can be resolved with fluids and/or a Foley catheter.

  • Step 3: Treat the underlying cause (e.g., give fluids if pre-renal, place Foley if post-renal)

  • Step 4: Monitor for ...

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