Absence of Diabetes Insipidus in Brain Dead patients secondary to renal insufficiency

Document Type

Conference Proceeding

Publication Date

8-9-2023

Publication Title

Neurocrit Care

Abstract

Background & Purpose Critics of brain death allege that up to 50% of brain dead (BD) patients have residual brain function based on the absence of central diabetes insipidus (Dl), which suggests remaining hypothalamic/pituitary function. We hypothesized that different degrees of renal dysfunction may impact the presence of Dl in BD patients. Methods All adult patients declared BD over 12 years at Henry Ford Hospital were evaluated. Dl was diagnosed by polyuria (>300 ml urine output for 2 or more consecutive hours), low urine specific gravity (< 1.005) and increasing serum sodium. Renal function was assessed by the estimated glomerular filtration rate (eGFR), calculated using the simplified Modification of Diet in Renal Disease (sMDRD) equation (validated for ages > 18). 192/266 BD patients were included in the analysis after excluding those with missing data, < 18-years-old or on vasopressin infusions (for hypotension). 122 (63.5%) developed Dl. The proportion with Dl decreased significantly with decreasing eGFR: for eGFR > 60ml/min, Dl was present in 77.2%; for eGFR 15-60ml/min in 54.5%, and for eGFR < 15ml/min in 32% (p < 0.001). There were 14 patients with eGFR <9.7 ml/min (all with serum creatinine > 7.1 mg/dL); none experienced Dl. Using logistic regression, for every 10 ml/min increase in eGFR the odds of Dl increased by 1.2 times (95% CI: 1.10 to 1.32, p < 0.001) Conclusion Presence of hypothalamic/pituitary function (based on the absence of Dl) is less common than previously thought in BD patients, as kidney dysfunction significantly impacts Dl development. Dl is observed less frequently in BD patients who have renal injury, and some patients with severe renal dysfunction never develop Dl. Renal dysfunction should be accounted for when considering the presence or absence of Dl in brain death.

PubMed ID

Not assigned.

Volume

39

Issue

1

First Page

S37

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