Obstructive Nephropathy as a Rare Cause of Nephrogenic Diabetes Insipidus

Introduction: Nephrogenic diabetes insipidus (NDI) is marked by large volumes of dilute urine. It may be hereditary or acquired from causes such as medications, electrolyte disturbances, or obstructive uropathy. Though rare, obstruction can cause tubular damage and AVP resistance, as shown by Hong et al. (2000) in prostate cancer cases. Diagnosis relies on clinical history, labs, imaging, and new markers like copeptin - stable AVP surrogate. Case Description: A 61-year-old man with hypertension, stage 2 CKD and BPH presented with polyuria (3.7 L/day), polydipsia, and headache for 4 days. Labs revealed hypernatremia (Na 152 mEq/L), creatinine 1.55 mg/dL, low urine osmolality (106 mOsm/kg), and urine sodium 24 mmol/L. Desmopressin failed to concentrate urine, indicating AVP resistance. Thiazides helped reduce volume. Lithium use and electrolyte imbalances were excluded. Renal ultrasound showed bilateral moderate hydronephrosis, bladder wall thickening, and prostatomegaly. Foley catheterization resolved hydronephrosis. Copeptin was elevated at 11.1 pmol/L, confirming nephrogenic DI with partial AVP resistance. TURP led to symptom relief and improved serum sodium and urine osmolality, confirming obstruction as the etiology. Discussion: Copeptin, co-secreted with AVP, reflects AVP release. Per Christ-Crain & Fenske (2016), copeptin >20 pmol/L suggests nephrogenic DI, while low levels point to central DI. This patient’s copeptin (11.1 pmol/L) indicated partial AVP resistance, consistent with acquired NDI due to chronic obstruction. It confirmed an appropriate AVP response to hypernatremia and avoided water deprivation testing. This diagnosis is not often thought as patient presented with polyuria but in turn was diagnosed with obstruction. Copeptin helped clarify the etiology. Relief of obstruction improved urine osmolality and symptoms, underscoring obstructive uropathy as a rare but reversible cause of NDI.