How should you treat a patient with acute kidney injury (AKI) and impaired renal function, with a rise in creatinine, with fluids or by obtaining a urinalysis (Ua)?

How to Treat AKI: Fluids First, Then Urinalysis

You should treat with fluids first while simultaneously obtaining a urinalysis—these are complementary, not mutually exclusive actions. The immediate priority is determining the cause of AKI through diagnostic workup (including urinalysis) while initiating appropriate fluid resuscitation if hypovolemia is suspected. 1, 2

Immediate Diagnostic Approach

Obtain urinalysis immediately as part of the initial workup—it is essential for determining AKI etiology, not something to delay. 1, 2 The diagnostic evaluation must include:

• Urinalysis with microscopy to identify muddy brown casts (suggesting acute tubular necrosis) versus normal sediment (suggesting prerenal azotemia) 2
• Urine chemistry including fractional excretion of sodium (FeNa) and urine sodium to differentiate prerenal (FeNa <1%) from intrinsic renal causes (FeNa >2%) 1, 2
• Blood work including BUN:creatinine ratio—a ratio >20:1 suggests prerenal azotemia from volume depletion, while <20:1 suggests intrinsic renal injury 2
• Renal ultrasound to rule out postrenal obstruction, particularly in older men with prostatic hypertrophy, history of nephrolithiasis, or pelvic malignancy 2

Fluid Management Algorithm

The decision to give fluids depends on clinical assessment of volume status and the suspected AKI etiology:

If Prerenal AKI is Suspected (Hypovolemia Present):

• Assess for clinical hypovolemia: poor skin turgor, dry mucous membranes, orthostatic hypotension, tachycardia, decreased jugular venous pressure 2
• Initiate isotonic crystalloids (not colloids or albumin) for volume expansion in non-cirrhotic patients 1
• Hold all diuretics immediately and discontinue nephrotoxic medications (NSAIDs, ACE inhibitors, ARBs) 1, 3
• In cirrhotic patients specifically: administer albumin 1 g/kg/day for 2 days if creatinine doubles from baseline 1
• Monitor response: Use urine output, vital signs, and when indicated, echocardiography or CVP to assess fluid status 1

If Intrinsic Renal AKI is Suspected (ATN):

• Avoid aggressive fluid resuscitation—the goal is euvolemia, not volume loading 2
• Do not give fluids to "reverse" AKI—this is a common pitfall. Overzealous fluid administration in ATN causes volume overload without improving renal function 1, 2
• Discontinue all nephrotoxic medications and adjust all drug doses for reduced GFR 2, 3

Critical Pitfalls to Avoid

• Never delay urinalysis—it provides essential diagnostic information that determines whether fluids are appropriate 1, 2
• Do not give fluids blindly without assessing volume status—fluid overload in ATN worsens outcomes and may precipitate pulmonary edema 1, 2
• Physical examination is mandatory before fluid administration—BUN:Cr ratio and FeNa are meaningless without clinical context 2
• In patients with cirrhosis, use albumin (not crystalloids alone) for volume resuscitation when creatinine doubles from baseline 1

Monitoring Requirements

• Check creatinine every 4-6 hours initially, then daily once stable 3
• Strict input/output monitoring—oliguria (<0.5 mL/kg/hour for >6 hours) is a diagnostic criterion for AKI and may indicate need for renal replacement therapy 1, 3
• Monitor for fluid overload complications: pulmonary edema, worsening hypoxemia, peripheral edema 1

When Diuretics May Be Appropriate

Diuretics do not reverse AKI but may facilitate volume management in oliguric patients already volume overloaded. 4

• Furosemide 1-1.5 mg/kg as initial bolus in oliguric AKI patients with volume overload 4
• Urine output ≥200 mL in first 6 hours after diuretic challenge predicts lower likelihood of progression to dialysis and lower mortality 4
• Never use diuretics as initial treatment in hypovolemic prerenal AKI—this worsens renal perfusion 1, 5