Hypernatremia in Prerenal AKI: Mechanism
In a patient with prerenal acute kidney injury induced by profuse diarrhea and vomiting, the hypernatremia is caused by both increased gastrointestinal water loss and decreased water intake (Answer: A and B only).
Pathophysiologic Mechanism
The hypernatremia in this clinical scenario results from a net free-water deficit rather than primary renal dysfunction 1:
- Increased GI water loss occurs because diarrhea and vomiting remove hypotonic fluid relative to plasma, leaving behind a higher serum sodium concentration 1
- Decreased water intake compounds the problem, as the patient cannot adequately replace ongoing fluid losses 1
- The kidneys are appropriately conserving water in response to volume depletion—this is evidenced by urine osmolality >500 mOsm/kg and urinary sodium <20 mEq/L, which are hallmarks of prerenal azotemia 1
Why NOT Increased Renal Water Loss
The renal response in prerenal AKI is to maximize water conservation, not increase water loss 1. In this setting:
- ADH secretion is appropriately elevated due to hypovolemia 1
- The kidneys produce concentrated urine (>500 mOsm/kg) to retain as much water as possible 1
- Fractional excretion of sodium (FENa) is <1%, confirming the kidneys are avidly retaining both sodium and water 1
Why NOT Increased Renal Sodium Retention
While the kidneys do retain sodium in prerenal states, sodium retention does not cause hypernatremia—it causes volume expansion and potentially hyponatremia 1. The elevated serum sodium reflects water deficit, not sodium excess 2, 3.
Diagnostic Confirmation
Physical examination findings that support this mechanism include 1:
- Orthostatic hypotension
- Dry mucous membranes
- Reduced skin turgor
- Tachycardia
- BUN-to-creatinine ratio >20:1
Management Implications
Understanding this mechanism guides treatment 1:
- Initial resuscitation requires isotonic saline (0.9% NaCl) to restore intravascular volume
- After achieving euvolemia, switch to hypotonic fluids (0.45% NaCl or D5W) to replace the free-water deficit
- Correction rate must not exceed 10-15 mmol/L per 24 hours for chronic hypernatremia (>48 hours) to prevent cerebral edema 1, 2
- Avoid attributing the hypernatremia to renal water wasting—the kidneys are functioning appropriately 1
Common Pitfall
Do not use hypotonic fluids for initial resuscitation in severely hypovolemic patients; isotonic saline is required first to restore hemodynamic stability 1.