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Abstract: PUB177

Lithium Induced Partial Nephrogenic Diabetes Insipidus: An Unusual Presentation

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical

Authors

  • Vega-Colon, Jesus Daniel, University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico
  • Rivera, Maria Eugenia, University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico
  • Rivera Gonzalez, Alexis, University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico
  • Rios Torres, Hillarie Ann, University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico
  • Casas Loyola, Cristina Marie, University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico
  • Rivera-Bermudez, Carlos G., University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico
  • Andujar-Rivera, Krystahl Z., University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico
  • Ocasio Melendez, Ileana E., University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico
Introduction

Nephrogenic Diabetes Insipidus (NDI) is described as a reduction in urinary concentrating ability caused by a resistance of vasopressin. It is characterized by hypotonic polyuria, polydipsia, and hypernatremia. Hereditary causes or acquisition from drugs like lithium and amphotericin B most be considered as potential triggers. Fluid deprivation with subsequent urine osmolality (Uosm) measurement can help us classify this disorder into partial (Uosm: 250-750 mOsm/Kg) or complete NDI (Uosm <250 mOsm/Kg). Few cases describe the occurrence of partial NDI in a Hispanic male with history of lithium use.

Case Description

We report a 47-year-old Puerto Rican male with Bipolar disorder and Epilepsy brought to our institution due to general weakness, lethargy and decrease appetite in the past 7 days. Caretaker reported use of lithium carbonate 300 mg twice a day for the past 12 years. During hospital stay nephrology service was consulted due to hypernatremia of 155 meq/L and lithium toxicity (1.97 mg/dl). Urine output showed evidence of persistent polyuria of 4.5 liters in 24 hours. Upon further evaluation urine osmolality was obtained showing results of 358 mOsm/Kg. Decision was made to stop lithium and perform fluid deprivation achieving minimal increase in urine osmolality to 391 mOsm/kg. As part of treatment, low dose thiazide diuretic was started with goal of impairing free water excretion. Resolution of hypernatremia to 143 meq/L and adequate uresis of 1.4 liters in 24 hrs was acquired following 72 hours. Based on the association of hypernatremia, polyuria with initial Uosm greater than 250 mOm/Kg, history of Lithium use and minimal increase in Uosm following fluid deprivation, the diagnosis of partial NDI was recognized.

Discussion

This case exemplifies an uncommon type of NDI that should be involved on the differential diagnosis. A thorough history is essential as it can help unravel the offending agent. Increased awareness of lithium toxicity side effects will help clinicians prevent life-threatening electrolyte disorders. The uniqueness of our case lies on the rarity of this type of NDI reported on literature. Our patient successfully responded to low dose thiazide diuretic correcting dysnatremia and archiving satisfactory uresis.