A 23-year-old male was admitted to medical ICU with high grade fever. On admission the BP was 100/60mm of Hg and Platelet count was 18000 with no active bleeding. The patient tested positive for Dengue NS1Ag and had mild transaminitis with Serum Creatinine of 1.0 on admission. Patient developed acute Upper Gl bleed and went into shock. He was treated with IV Fluids and platelet transfusion. After 72 hours, the patient was stable with BP of 106/74mm of Hg. However, repeat Serum Creatinine was 1.6. There was no hematuria or cast in the urine. Chart revealed a urine output of 2.6 L in the last 24 hours. What is diagnosis?
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dengue fever acute kidney injury raised creatinine polyuria diagnosis
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I now have sufficient information to provide a thorough, well-reasoned answer. Let me synthesize all the findings.
Diagnosis: Acute Tubular Necrosis (ATN) - Non-oliguric (Polyuric) Phase
Step-by-Step Clinical Reasoning
The Key Clue: Urine Output of 2.6 L/24 hours with rising creatinine
This is the pivotal finding. The patient is making good urine (polyuria/non-oliguria), yet the serum creatinine has risen from 1.0 to 1.6 mg/dL. This dissociation - high urine output + rising creatinine - is the hallmark of non-oliguric ATN (or the diuretic/recovery phase of ATN).
Putting the Case Together
| Finding | Significance |
|---|---|
| Dengue NS1Ag positive | Confirms dengue, a known cause of AKI via direct tubular injury |
| Platelets 18,000; hemorrhagic shock | Dengue hemorrhagic fever with dengue shock syndrome |
| BP 100/60 on admission → shock | Hemodynamic insult causing renal hypoperfusion |
| GI bleed + fluid resuscitation | Additional hemodynamic compromise |
| 72 hours later: BP 106/74, stable | Hemodynamic recovery; capillary leak phase resolving |
| Serum Cr: 1.0 → 1.6 mg/dL | Rising creatinine despite stability = intrinsic AKI |
| Urine output 2.6 L/24h (>1 mL/kg/hr) | Non-oliguric state |
| No hematuria, no casts | Argues against glomerulonephritis; tubular injury more likely |
Why ATN and Not Something Else?
1. Not pre-renal AKI:
- Patient is now hemodynamically stable (BP 106/74)
- Large urine output (2.6 L/day) means the kidney is not in a "conserving" pre-renal state
- Pre-renal AKI would show oliguria and concentrated urine, not polyuria
2. Not glomerulonephritis:
- No hematuria
- No casts in urine (red cell casts are expected in GN)
- No significant proteinuria mentioned
3. ATN - the mechanism in Dengue:
As confirmed by Brenner & Rector's The Kidney: "Proposed mechanisms for AKI [in dengue] are capillary leak, shock resulting in hypoperfusion, and acute tubular necrosis." The initial shock (from dengue hemorrhagic fever and GI bleed) caused ischemic tubular injury.
4. Why is creatinine still rising despite recovery?
In ATN, tubular cells are injured and lose their concentrating ability and ability to reclaim filtrate. As tubules begin to recover (polyuric phase), large volumes of urine are passed, but the creatinine clearance is still reduced because:
- Tubular cells are not yet fully functional
- GFR recovery lags behind tubular recovery
- The kidneys can make urine in volume but not in quality (poor concentration, poor waste clearance)
The Two Phases of ATN Relevant Here
| Phase | Urine Output | Creatinine |
|---|---|---|
| Oliguric phase | <400 mL/day | Rising |
| Diuretic/Recovery phase | >1-3 L/day (polyuria) | Still rising or plateauing |
| Late recovery | Normalizing | Falling toward baseline |
This patient is in the diuretic phase of ATN - the transition after the oliguric phase where tubular cells begin recovering but GFR and creatinine clearance are not yet restored. This is a recognized and important phase where, paradoxically, the patient may look clinically better but biochemically the creatinine can still rise or remain elevated for days.
Summary
Primary Diagnosis: Non-oliguric ATN / Diuretic phase of ATN complicating Dengue Shock Syndrome (Dengue Hemorrhagic Fever)
The underlying cause is ischemic ATN from the dengue shock episode compounded by the GI hemorrhage. The combination of:
- Dengue NS1Ag positivity
- Thrombocytopenia (18,000)
- Hemodynamic shock
- GI bleed
- Rising creatinine at 72 hours with preserved/high urine output and absent urinary sediment (no casts, no hematuria)
...points unequivocally to non-oliguric ATN in the recovery/diuretic phase as the diagnosis.
Source: Brenner and Rector's The Kidney, 2-Volume Set - Dengue Fever section (AKI mechanisms including ATN from hypoperfusion and shock); Dengue-associated AKI review (PMC4655808) confirming tubular pathology as a major mechanism.
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