From the Research
In hydronephrosis due to an enlarged prostate, the expected arterial blood gas (ABG) changes would typically reflect a normal anion gap metabolic acidosis, as evidenced by a study on acute kidney injury caused by obstructive nephropathy 1. This occurs because kidney obstruction impairs the kidney's ability to excrete acid and reabsorb bicarbonate. The ABG would likely show:
- Decreased pH (below 7.35)
- Decreased bicarbonate (HCO3- below 22 mEq/L)
- A compensatory decrease in PaCO2 due to respiratory compensation
- A normal anion gap (8-12 mEq/L) As the condition progresses, you might see potassium retention leading to hyperkalemia. These changes develop because the obstructed urinary flow from prostatic enlargement causes back pressure on the kidneys, impairing tubular function responsible for acid-base regulation. The severity of these ABG abnormalities correlates with the degree and duration of obstruction, with more pronounced acidosis in bilateral or severe unilateral hydronephrosis, as discussed in a review on hydronephrosis diagnosis, grading, and treatment 2. Prompt urological intervention to relieve the obstruction, such as catheterization or prostate surgery, is essential to prevent permanent renal damage and normalize acid-base status, as supported by a study on the progression and medical management of symptomatic benign prostatic hyperplasia 3.