In an adult with stable vital signs who presents with dizziness and nausea, no vomiting, poor oral intake, a recent rise in serum creatinine indicating acute kidney injury, and improving iron‑deficiency anemia, what is the most likely contributing factor and how should it be managed?

Acute Kidney Injury with Uremia as the Primary Driver

The most likely contributing factor to this patient's dizziness and nausea is uremia from acute kidney injury, and management should focus on immediate nephrotoxin withdrawal, cautious isotonic fluid resuscitation guided by volume status, and close monitoring for progression requiring renal replacement therapy. 1, 2

Primary Pathophysiology

The uptrending creatinine indicates acute kidney injury (AKI), which is defined by KDIGO criteria as an increase in serum creatinine ≥0.3 mg/dL within 48 hours or ≥1.5 times baseline within 7 days 2. The constellation of dizziness, nausea, and poor oral intake in the setting of rising creatinine strongly suggests uremic symptoms from declining renal function 3.

Poor oral intake is both a consequence and contributor: uremia causes gastrointestinal symptoms (nausea) that perpetuate poor intake, which in turn worsens prerenal azotemia through volume depletion 1. This creates a vicious cycle that must be interrupted.

Immediate Management Algorithm

Step 1: Discontinue All Nephrotoxins Immediately

Stop all potentially nephrotoxic medications regardless of AKI etiology 2:

• NSAIDs
• ACE inhibitors and ARBs
• Diuretics (if being used)
• Any aminoglycosides or other nephrotoxic antibiotics
• Recent contrast agents 2

This is a KDIGO Grade 1B recommendation and takes priority over other interventions 2.

Step 2: Assess Volume Status and Initiate Isotonic Crystalloid Resuscitation

Use isotonic crystalloids (normal saline or lactated Ringer's) for volume expansion—NOT colloids or albumin 2. The American College of Physicians explicitly recommends crystalloids over colloids, as hydroxyethyl starch increases mortality and dialysis requirement in critically ill patients 2.

Volume resuscitation should be guided by careful clinical assessment to avoid fluid overload, particularly given the stable vital signs 2. The goal is to restore renal perfusion without causing congestion, as volume overload independently worsens outcomes 4.

Step 3: Determine AKI Etiology

Check urine sodium and fractional excretion of sodium (FENa) to differentiate prerenal from intrinsic AKI 1:

• FENa <1% or urine sodium <20 mEq/L suggests prerenal (hypovolemic) AKI
• Bland urinalysis without casts supports prerenal etiology 1

Given the poor oral intake and stable vitals, prerenal AKI from volume depletion is most likely 1, 5.

Step 4: Monitor Response to Therapy

Measure serum creatinine every 2-4 days during hospitalization to assess AKI progression 2. With adequate isotonic fluid replacement, serum creatinine should decrease to within 0.3 mg/dL of baseline in hypovolemic AKI 1.

If creatinine continues to rise despite volume optimization, consider:

• Intrinsic renal pathology (acute tubular necrosis)
• Urinary obstruction (obtain renal ultrasound)
• Progression to Stage 2 or 3 AKI requiring escalation of care 2

Management of Anemia in the Context of AKI

The improving iron-deficiency anemia is a secondary issue but requires specific consideration in AKI:

Functional iron deficiency is common in advanced chronic kidney disease and contributes to anemia 6. However, in the acute setting with uptrending creatinine, defer decisions about iron supplementation until AKI stabilizes 6.

If hemoglobin drops significantly during AKI management:

• Transfuse red blood cells to maintain hemoglobin 7-9 g/dL if there is significant blood loss 1
• Avoid aggressive transfusion that could worsen volume overload 1
• Intravenous iron in AKI has not been shown to cause adverse outcomes including worsening of AKI or mortality, even in septic patients 7, but should be coordinated with nephrology 6

Criteria for Nephrology Referral and RRT

Consider renal replacement therapy if any of the following develop 2:

• Oliguria persisting despite fluid optimization (<0.5 mL/kg/h for ≥6 hours)
• Severe hyperkalemia refractory to medical management
• Severe metabolic acidosis
• Uremic symptoms (pericarditis, encephalopathy, refractory nausea/vomiting)
• Refractory fluid overload 2

Refer to nephrology if:

• Creatinine fails to return to within 115% of baseline after 6 months 2
• AKI progresses to Stage 2 or 3 despite initial management 2
• Uncertainty about etiology or need for kidney biopsy 6

Common Pitfalls to Avoid

Do not use percentage changes in creatinine alone to assess AKI severity in patients with pre-existing CKD 8. A 50% rise in creatinine represents vastly different GFR changes depending on baseline function—from 4 hours to reach this threshold with normal baseline kidney function to 27 hours with Stage 4 CKD 8. Absolute changes (≥0.3 mg/dL) are more reliable across the spectrum of baseline function 8.

Do not assume all creatinine rises require aggressive intervention 4. In the context of decongestion therapy (e.g., heart failure), acute creatinine rises may not confer increased risk and should not prompt cessation of appropriate diuretics 4. However, in this case with poor oral intake and prerenal physiology, volume repletion is appropriate 1.

Do not delay nephrotoxin withdrawal while awaiting diagnostic workup 2. This is the single most evidence-based intervention and should occur immediately upon recognition of AKI 2.

Long-Term Follow-Up

Patients who experience AKI remain at significantly increased long-term risk of recurrent AKI, progression to CKD, cardiovascular events, and mortality 2. After discharge, check creatinine every 2-4 weeks for 6 months 2.