Central diabetes insipidus (CDI) is a rare endocrine disorder characterized by deficient secretion or action of arginine vasopressin (AVP), leading to hypotonic polyuria and compensatory polydipsia. Coexisting anterior pituitary dysfunction, such as hypogonadism, may suggest underlying hypothalamic-pituitary pathology.

We present a 27-year-old obese male (BMI 35.9) with a six-year history of progressive polydipsia (12–15 L/day) and polyuria, worsened by fluid restriction and accompanied by fatigue, tremors, irritability, hot flushes, weight loss (10 kg), and decreased libido. He reported one prior syncopal episode during prolonged fasting. No history of trauma, neurosurgery, or steroid use was elicited. Initial endocrine evaluation showed serum sodium: 151 mmol/L, 24-hour urine output: 11,350 mL, 24-hour urine osmolality: 80 mOsm/kg, Random urine specific gravity: 1.010, Serum osmolality: 297–302 mOsm/kg, Random urine osmolality: 74–81 mOsm/kg pre-desmopressin, Post-desmopressin urine osmolality: 242 mOsm/kg. Water deprivation testing confirmed the diagnosis of central diabetes insipidus based on failure to concentrate urine and an appropriate response to desmopressin. Pituitary MRI revealed a non-enlarged gland (5 mm height) with absence of the posterior pituitary bright spot, no infundibular thickening, and preserved midline position—suggestive but not definitive for idiopathic CDI. No mass lesions or inflammatory changes were noted. Comprehensive pituitary profiling revealed secondary hypogonadism: Total testosterone: 24.01 ng/dL, Repeat testosterone: 0.22 ng/mL (ref: 0.31–3.78), LH: 0.87 mIU/mL (inappropriately normal), FSH: 1.39 mIU/mL. Prolactin, TSH, FT4, FT3, cortisol, ACTH, IGF-1: All within normal range. Additional studies including prostate and inguinoscrotal ultrasound were unremarkable aside from small prostate volume (9g) and non-specific right testicular calcifications. No evidence of diabetes mellitus, thyroid dysfunction, dyslipidemia, or renal insufficiency was found.

The patient was initiated on oral desmopressin 0.05 mg once daily at bedtime, resulting in improved symptoms and significant reduction in urine output (from >5000 mL overnight to <1100 mL post-treatment). Further endocrine work-up was arranged for evaluation of hypogonadism including Inhibin B and semen analysis. Autoimmune hypophysitis remains an important consideration.

This case highlights the diagnostic complexity of central diabetes insipidus, particularly in young males presenting with chronic symptoms and coexisting secondary hypogonadism. Comprehensive endocrine testing, dynamic function testing, and targeted imaging are critical for diagnosis and guiding management. The absence of a pituitary bright spot on MRI supports idiopathic CDI, though continued monitoring for evolving pituitary pathology is warranted.