Iatrogenic perpetuation of postobstructive diuresis

AKImedium

A 73-year-old man is admitted to the hospital after routine outpatient laboratory testing revealed AKI with a serum creatinine level of 3.8 mg/dL (reference, 0.7–1.3; baseline 1.0). He reports generalized fatigue, urinary hesitancy, and nocturia. He continues to produce urine but reports a decreased volume. On initial examination, BP is 148/88 mm Hg and moderate peripheral edema is present. Initial evaluation included a renal ultrasound that demonstrated bilateral moderate hydronephrosis, an enlarged prostate, and a distended bladder. Initial UA was bland. An indwelling urinary catheter was inserted, which immediately drained 1.2 L of straw-colored urine. Normal saline IV was initiated at 250 mL/h. After 48 hours, his daily urine output has remained >6 L/d, and he is eating and drinking normally. Examination reveals BP 144/82 mm Hg with persistent peripheral edema. Laboratory data (admission, current; reference): sodium 144, 148 mEq/L (136–145); potassium 5.1, 3.7 mEq/L (3.5–5.0); chloride 118, 120 mEq/L (98–106); total CO₂ 18, 19 mEq/L (23–28); BUN 95, 38 mg/dL (8–20); creatinine 3.8, 1.3 mg/dL (0.7–1.3). Which ONE of the following is the next BEST step in management?

  1. A.Prescribe sodium bicarbonate PO
  2. B.Change normal saline to 5% dextrose IV
  3. C.Prescribe desmopressin
  4. D.Discontinue normal salineCorrect

Explanation

This best option for this patient with improving AKI and postobstructive diuresis is to discontinue normal saline IV. This patient developed postobstructive diuresis following AKI due to bladder outlet obstruction that resolved after placement of an indwelling urinary catheter. The mechanism is multifactorial, including an osmotic diuresis from retained solute, impaired concentrating ability due to loss of inner medullary osmotic gradient (medullary washout), and a partial nephrogenic diabetes insipidus from downregulation of aquaporins. The diuresis is usually self-limited but can be sustained by continued administration of excess IV fluids, as in this case. Because this patient is hemodynamically stable, eating and drinking normally, and does not have evidence of volume depletion, the best next step is discontinuation of normal saline, which is likely contributing to the persistent high urine output. Changing IV fluids to 5% dextrose in water is not necessary at this time. The mild hypernatremia is expected with solute-driven diuresis and can be managed with oral water intake. Sodium bicarbonate is not needed. The hyperchloremic metabolic acidosis of obstruction reflects impaired hydrogen secretion and diminished ammoniagenesis, and typically resolves with recovery of renal function. The large amount of normal saline (6 L/d) is also likely contributing to this patient’s hyperchloremic metabolic acidosis, and discontinuing fluids may help correct this issue. Desmopressin is used for the treatment of polyuria secondary to central diabetes insipidus, but the lack of antidiuretic hormone is not the mechanism of polyuria in postobstructive diuresis. Rather, the persistent diuresis reflects solute washout, reduced concentrating capacity, and, in this case, ongoing delivery of isotonic fluid that the recovering kidney is excreting.

Why each option

A.
The hyperchloremic acidosis reflects obstruction-related impaired acid excretion plus saline loading and should resolve with recovery and stopping saline, without bicarbonate.
B.
Switching to dextrose in water still drives the diuresis with intravenous volume; mild hypernatremia in a patient drinking normally can be corrected with oral water.
C.
Postobstructive diuresis reflects solute load, medullary washout, and aquaporin downregulation, not vasopressin deficiency, so desmopressin is ineffective and potentially harmful.
D.
Correct. A recovering, edematous patient eating and drinking normally is excreting the 6 L/day of saline infused, so stopping it ends the iatrogenic diuresis.

Reference: Halbgewachs C, Can Fam Physician 2015 (postobstructive diuresis); KDIGO 2012 Clinical Practice Guideline for Acute Kidney Injury

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