In an ICU patient with normal blood pressure, oliguria (~100 mL/day), serum creatinine ~4 mg/dL, hyperkalaemia, and hyaline casts on urinalysis, what type of acute kidney injury is present?

Acute Tubular Necrosis (Intrinsic/Intrarenal AKI)

This patient has intrinsic acute kidney injury, specifically acute tubular necrosis (ATN), evidenced by the combination of oliguria (100 mL/day), elevated creatinine (4 mg/dL), hyperkalemia, and hyaline casts on urinalysis in the setting of normal blood pressure. 1, 2

Classification and Staging

• This represents KDIGO Stage 3 AKI based on the creatinine of 4 mg/dL (assuming baseline was normal) and severe oliguria of approximately 100 mL/day (roughly 0.06 mL/kg/hr in a 70 kg patient, well below the 0.3 mL/kg/hr threshold for Stage 3). 1

• The KDIGO criteria define Stage 3 as: creatinine ≥3.0 times baseline OR creatinine ≥4.0 mg/dL with an acute rise ≥0.3 mg/dL OR urine output <0.3 mL/kg/hr for ≥24 hours OR initiation of renal replacement therapy. 1

Diagnostic Reasoning: Why This is ATN (Intrinsic AKI)

Key Clinical Features Supporting ATN

• The presence of hyaline casts on urinalysis, while nonspecific, combined with severe oliguria and elevated creatinine in an ICU patient strongly suggests intrinsic renal injury rather than prerenal azotemia. 1, 2 Muddy brown granular casts would be more specific for ATN, but their absence does not exclude it. 3

• Normal blood pressure argues against prerenal AKI, which typically presents with hypotension or evidence of volume depletion. 2, 4 Prerenal AKI is characterized by renal hypoperfusion with intact tubular function. 5

• Severe oliguria (100 mL/day) with hyperkalemia indicates established tubular dysfunction, not simply reduced renal perfusion. 6 In prerenal states, the kidneys retain their concentrating ability and sodium-conserving mechanisms. 4

Differentiating from Other AKI Types

Prerenal AKI is excluded by:

• Normal blood pressure (prerenal typically shows hypotension or volume depletion signs) 2
• Severe oliguria with hyperkalemia suggests tubular damage rather than functional hypoperfusion 4
• In prerenal AKI, urine sodium is typically <20 mEq/L, fractional excretion of sodium (FENa) <1%, and urine specific gravity >1.020 due to preserved tubular function 4

Postrenal (obstructive) AKI is unlikely:

• Postrenal obstruction accounts for <3% of AKI cases 3
• The clinical presentation doesn't suggest obstruction, though renal ultrasound should still be performed to definitively exclude this 3, 2

Hepatorenal syndrome (HRS-AKI) is excluded:

• HRS-AKI requires cirrhosis with ascites and specific diagnostic criteria including lack of response to volume expansion 1
• No mention of liver disease in this case 1

Pathophysiology of ATN in ICU Patients

• ATN in critically ill patients is not simply renal ischemia with vasoconstriction and tubular necrosis. Recent evidence shows that in septic AKI, renal blood flow may actually be increased, with intrarenal vasodilation, microcirculatory changes, and blood flow redistribution leading to functional GFR decline. 7

• The spectrum of ATN ranges from mild injury to advanced disease requiring renal replacement therapy. 2, 5 This patient's severe oliguria and creatinine of 4 mg/dL places them in the advanced category. 1

Immediate Management Priorities

Critical Interventions Required Now

• Discontinue all nephrotoxic medications immediately including NSAIDs, ACE inhibitors, ARBs (especially in volume-depleted states), aminoglycosides, and any contrast agents. 3, 8

• Hold diuretics temporarily until volume status is clarified and optimized, as they can worsen prerenal components. 3

• Adjust all medication dosages based on current renal function (creatinine 4 mg/dL) rather than baseline values to prevent drug accumulation and toxicity. 3

Urgent Nephrology Consultation

• KDIGO guidelines mandate immediate nephrology consultation for Stage 3 AKI (creatinine ≥3× baseline or ≥4.0 mg/dL). 3, 9 This patient meets criteria with creatinine of 4 mg/dL.

• Refractory hyperkalemia alone is an indication for urgent nephrology evaluation, as it may require emergent renal replacement therapy. 3

Renal Replacement Therapy Considerations

Emergent dialysis indications include: 3, 8

• Refractory hyperkalemia unresponsive to medical management

• Severe metabolic acidosis (pH <7.1 or bicarbonate <12 mEq/L)

• Refractory volume overload causing pulmonary edema

• Uremic symptoms (encephalopathy, pericarditis, pleuritis)

• In hemodynamically unstable ICU patients, continuous renal replacement therapy (CRRT) is preferred over intermittent hemodialysis. 8

Diagnostic Workup to Complete

Essential Laboratory Tests

• Obtain comprehensive metabolic panel to assess for severe metabolic acidosis (pH <7.2 or bicarbonate <12 mEq/L), which would trigger urgent nephrology consultation. 3

• Measure serum creatinine daily to track trajectory and assess for progression or recovery. 3, 8

• Calculate fractional excretion of sodium (FENa) if not on diuretics: FENa >2% supports ATN, while FENa <1% suggests prerenal azotemia. 2, 4 However, loop diuretics invalidate this test. 4

• Urine sodium >40 mEq/L and renal failure index (RFI) >2 are highly specific for ATN and can be determined from spot urine. 4

Imaging

• Renal ultrasound should be performed to definitively exclude postrenal obstruction, particularly important in older patients. 3, 2

Critical Pitfalls to Avoid

• Do not use standard eGFR equations (MDRD, CKD-EPI) during rapidly changing creatinine levels in AKI, as they are unreliable and developed for stable chronic kidney disease. 1, 3

• Do not rely solely on urine output as the marker of kidney function; serum creatinine remains more reliable in acute settings, though oliguria of ≥4 hours has 86% specificity for predicting AKI. 1, 6

• Do not continue any nephrotoxic agents while attempting other interventions; immediate discontinuation is essential. 3, 8

• Do not delay nephrology consultation when Stage 2 or higher AKI develops; this increases risk of adverse outcomes. 3

Prognosis and Follow-Up

• This patient is in the acute kidney disease (AKD) period, defined as renal dysfunction persisting 7-90 days after the AKI-initiating event. 1 Close monitoring is required throughout this window.

• Arrange nephrology follow-up within 1-2 weeks for Stage 3 AKI given the high risk of progression to chronic kidney disease. 3

• Kidney function must be monitored for at least 90 days after the AKI event to assess for CKD development. 1, 3 Evaluation at 3 months is recommended by KDIGO guidelines. 1

• Even with complete recovery, this patient carries long-term increased risk of major adverse cardiac and kidney events, CKD progression, and mortality. 1, 9