AKI: Prerenal vs ATN — Workup, Fluids & Nephrotoxins

Acute kidney injury (AKI) is a syndrome—not a single disease. Start by confirming it meets KDIGO criteria, then separate prerenal (perfusion), intrinsic (ATN, AIN, GN), and postrenal (obstruction). Treat the cause while protecting the kidneys from further hits.

Definition (KDIGO)

• Serum creatinine ↑ by ≥0.3 mg/dL within 48 h, or
• Serum creatinine ↑ to ≥1.5× baseline within 7 days, or
• Urine output <0.5 mL/kg/h for ≥6 h.

Initial Priorities (first 10 minutes)

• Assess hemodynamics (MAP, signs of shock, JVP, edema), review meds (ACEi/ARB, NSAIDs, diuretics, PPIs, aminoglycosides, contrast, calcineurin inhibitors, TMP-SMX).
• Check POCUS bladder for retention; scan kidneys for hydronephrosis if concern.
• Send labs: BMP, CBC, urinalysis with microscopy, urine Na/creatinine (for FeNa) or urine urea (for FeUrea if on diuretics).

Sorting the Big Three

• Prerenal (perfusion problem): hypovolemia (bleeding, GI losses), low effective arterial volume (HF, cirrhosis), renal vasoconstriction (NSAIDs), efferent dilation block (ACEi/ARB in RAS).
• Intrinsic:
  • ATN (ischemic/septic, or toxic—contrast, aminoglycosides, myoglobin).
  • AIN (drug-induced—PPIs, beta-lactams; sterile pyuria, WBC casts, ± eosinophilia).
  • Glomerulonephritis (RBC casts, proteinuria, hypertension, edema).
• Postrenal: obstruction from prostate, stones, pelvic malignancy, neurogenic bladder—think bilateral hydronephrosis or solitary kidney.

Urine Clues (high-yield)

• Prerenal: bland sediment or hyaline casts; Uosm >500 mOsm/kg; FeNa <1% (if not on diuretics); FeUrea <35% (useful if on diuretics).
• ATN: muddy brown granular casts, tubular epithelial cells; Uosm <350; FeNa often >2% (but can vary in sepsis/contrast).
• AIN: WBC casts, sterile pyuria, ± eosinophils, rash/fever/arthralgias.
• GN: RBC casts, dysmorphic RBCs, proteinuria—get complements/ANCA/anti-GBM as indicated and involve nephrology early.

Imaging

• Renal ultrasound for hydronephrosis or chronic changes; low-risk and fast.
• Bladder scan for retention; catheterize if volume high and watch for post-obstructive diuresis.

Management Algorithms

Prerenal (restore perfusion)

• Fluids: start with balanced crystalloids (e.g., LR/Plasma-Lyte) unless contraindicated. Titrate to MAP/urine output, lung exam, and ultrasound IVC/venous congestion signs.
• Cardiorenal/cirrhosis: avoid over-resuscitation; guide by hemodynamics. Consider diuretics for congestion, albumin in SBP, and vasoconstrictors for HRS per protocol.
• Temporarily hold ACEi/ARB, NSAIDs, diuretics while unstable; restart thoughtfully once perfusion recovers.

ATN (tubular injury)

• Treat the cause (sepsis source control, stop toxins, manage shock). Fluids only if hypovolemic—avoid fluid overload.
• Optimize MAP (vasopressors if needed). Strict I/O, daily weights, avoid further nephrotoxins, dose meds to GFR.
• Expect creatinine to rise then plateau; recovery over days–weeks if insult removed.

AIN

• Stop the culprit drug. Consider steroids early in biopsy-proven, severe cases after excluding infection—specialist input advised.

Glomerulonephritis

• Urgent nephrology; serologies and often biopsy. Control BP, edema; immunosuppression per etiology.

Postrenal (obstruction)

• Relieve obstruction: Foley for retention, urology for stones/strictures; nephrostomy if upper tract obstruction and septic/unstable.
• Monitor for post-obstructive diuresis (massive urine output); replace fluids/electrolytes carefully.

Nephrotoxin Stewardship

• Avoid/limit: NSAIDs, IV contrast (if unavoidable, give isotonic fluids; avoid simultaneous nephrotoxins), aminoglycosides, amphotericin B (use liposomal when possible).
• Review over-the-counter supplements and herbal products; monitor calcineurin inhibitor levels if applicable.

Rhabdomyolysis & Pigment Nephropathy (special case)

• Check CK, potassium, calcium, phosphate. Treat hyperkalemia aggressively.
• Early isotonic fluids to maintain urine output (e.g., 200–300 mL/h goal) if not volume overloaded.
• Alkalinization/diuretics are not routine; reserve for select scenarios with specialist input.

When to Dialyze (AEIOU)

• Acidosis refractory (pH ≤7.1).
• Electrolytes—severe/refractory hyperkalemia or other life-threatening derangements.
• Ingestions (dialyzable toxins: lithium, salicylates, etc.).
• Overload refractory to diuretics with hypoxia.
• Uremic complications (encephalopathy, pericarditis, bleeding).

Monitoring & Follow-up

• Trend creatinine, urine output, weights, electrolytes daily; adjust all renally-cleared meds.
• Plan outpatient BMP within 1–2 weeks post-discharge for recovering AKI.
• Address vaccine status, BP control, and CKD risk modification if recovery incomplete.

Patient FAQs

“Should I stop my blood pressure pills forever?” No—many are only held temporarily during AKI. Your team will restart once you’re stable.

“Will my kidneys recover?” Often yes if the cause is reversed early. Some patients transition to CKD—monitoring is key.

References & Notes

Practical AKI playbook: confirm KDIGO AKI, use urine microscopy + physiology (FeNa/FeUrea) thoughtfully, restore perfusion, avoid toxins, relieve obstruction, and use AEIOU for dialysis triggers. Local protocols vary—follow institutional guidance. Educational only.