Abstract: SA-PO738
Use of Copeptin to Diagnose Nephrogenic Diabetes Insipidus Secondary to Hypercalcemia
Session Information
- Fluid, Electrolyte, Acid-Base Disorders: Clinical - II
November 04, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Drummond, Olivia Rae, Tulane University School of Medicine, New Orleans, Louisiana, United States
- Baudy, Adrian J., Tulane University School of Medicine, New Orleans, Louisiana, United States
Introduction
Diabetes insipidus (DI) is a condition characterized by polyuria caused by inadequate antidiuretic diuretic hormone (ADH) activity. Differentiating between central and nephrogenic DI is usually accomplished by an indirect water deprivation test, which is effective, however inconsistencies in sample collecting can confound results. An emerging method of determining the etiology of DI is through the measurement of Copeptin, a moiety which is cleaved off the pro-ADH molecule and is a surrogate marker for ADH levels. Here, we discuss a case of a nephrogenic DI, in which a Copeptin level was used to assist in diagnosis.
Case Description
A 23-year-old woman presented to the hospital with abdominal pain and vomiting. She was found to have necrotizing pancreatitis and a calcium of 16 mg/dL. She was treated with IV fluids, calcitonin and zoledronic acid. An ultrasound and sestamibi scan revealed a parathyroid adenoma. The patient then developed hypernatremia up to 167 mmol/L with urine osmolality of 130 mosmol/kg, despite daily fluid resuscitation. Workup for differentiating central from nephrogenic DI included TSH, cortisol, MRI brain which were unrevealing. The patient had no response to DDAVP 0.1 mcg or 2 mcg subcutaneously. However, with a higher dose of 4 mcg, the urine osmolality increased to 307mosmol/kg and sodium decreased by 2 mmol/L. Given the incomplete response to DDAVP, nephrogenic DI was diagnosed and treated with a thiazide diuretic and D5W until her sodium normalized. Copeptin levels returned at more than double the upper limit of normal, confirming the diagnosis of nephrogenic DI. This further confirmed hypercalcemia as the culprit and parathyroidectomy was planned after discharge.
Discussion
Copeptin can be a useful tool in differentiating nephrogenic DI from central DI. Response to DDAVP or water deprivation tests are widely used, however in our patient, as in many cases, the results were difficult to interpret as the lab collection times and urine output measurements were inconsistent. An elevated copeptin level provided a simplified way to assess the patient’s level of ADH and confirm the diagnosis of nephrogenic DI. ADH is an unstable molecule and degrades quickly, thus cannot easily be measured directly. However, copeptin is a stable, surrogate marker for ADH levels and can be measured alone or in combination with water deprivation.