Question:
A child was operated on for a Posterior urethral Valve abnormality. What will be the electrolyte abnormality?
A child was operated on for a Posterior urethral Valve abnormality. What will be the electrolyte abnormality?
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Post-obstructive diuresis after PUV fulguration causes severe water loss due to medullary washout and tubular ADH resistance, making hypernatremic dehydration a critical postoperative risk.
Updated On: Sep 3, 2026
- Hyperkalemia
- Hypokalemia
- Hyponatremia
- Hypernatremia
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The Correct Option is D
Solution and Explanation
Concept:
Posterior urethral valves (PUV) cause severe congenital lower urinary tract obstruction in male infants, leading to secondary obstructive uropathy and renal dysplasia.
Surgical valve ablation relieves the anatomical obstruction but frequently triggers a profound, life-threatening post-obstructive diuresis (POD) accompanied by severe fluid and electrolyte disturbances.
Explanation:
• Relief of severe bilateral urinary tract obstruction precipitates post-obstructive diuresis due to accumulated urea excretion, fluid retention, and transient or permanent tubular dysfunction.
• Chronic elevated backpressure disrupts the renal medullary architecture and induces medullary insensitivity of the collecting ducts to antidiuretic hormone (acquired nephrogenic diabetes insipidus).
• Impaired collecting duct responsiveness to vasopressin leads to massive excretion of hyposthenuric, dilute urine containing excessive free water relative to solutes.
• If free water losses are not aggressively and accurately replaced milliliter-for-milliliter, the rapid unreplaced excretion of hypotonic urine results in severe dehydration and hypovolemic hypernatremia.
• In addition, impaired distal tubular hydrogen and potassium secretion during obstructive uropathy may cause type 4 renal tubular acidosis, but marked free water wasting following surgical relief primarily manifests as hypernatremia.
Final Answer:
Following relief of posterior urethral valves, acquired nephrogenic diabetes insipidus and profound post-obstructive free water loss characteristically lead to hypernatremia.
Posterior urethral valves (PUV) cause severe congenital lower urinary tract obstruction in male infants, leading to secondary obstructive uropathy and renal dysplasia.
Surgical valve ablation relieves the anatomical obstruction but frequently triggers a profound, life-threatening post-obstructive diuresis (POD) accompanied by severe fluid and electrolyte disturbances.
Explanation:
• Relief of severe bilateral urinary tract obstruction precipitates post-obstructive diuresis due to accumulated urea excretion, fluid retention, and transient or permanent tubular dysfunction.
• Chronic elevated backpressure disrupts the renal medullary architecture and induces medullary insensitivity of the collecting ducts to antidiuretic hormone (acquired nephrogenic diabetes insipidus).
• Impaired collecting duct responsiveness to vasopressin leads to massive excretion of hyposthenuric, dilute urine containing excessive free water relative to solutes.
• If free water losses are not aggressively and accurately replaced milliliter-for-milliliter, the rapid unreplaced excretion of hypotonic urine results in severe dehydration and hypovolemic hypernatremia.
• In addition, impaired distal tubular hydrogen and potassium secretion during obstructive uropathy may cause type 4 renal tubular acidosis, but marked free water wasting following surgical relief primarily manifests as hypernatremia.
Final Answer:
Following relief of posterior urethral valves, acquired nephrogenic diabetes insipidus and profound post-obstructive free water loss characteristically lead to hypernatremia.
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