Clinical StudiesHyperuricemia as a Clue for Central Diabetes Insipidus (Lack of V1 Effect) in the Differential Diagnosis of Polydipsia☆
Section snippets
Patients and Methods
We retrospectively analyzed the hospital records of all patients with severe chronic polyuria (>4 L/day) observed in our department over the last 10 years. Patients with a history of gout or alcohol abuse, or taking a medication known to interfere with uric acid metabolism were excluded.
In 13 patients with a diagnosis of central diabetes insipidus (CDI, group I) serum uric acid concentration was available in normonatremia (Na ≤ 145 mEq/L; while the patients were spontaneously taking a high
Results
All but 1 of the 13 patients with CDI (group I), presented a uric acid concentration higher than 5 mg/dL when normonatremic (see Fig. 1), whereas all the normonatremic PP patients presented a value lower than 5 mg/dL (mean value for CDI: 7.1 ± 2.2 mg/dL and 3 ± 0.75 mg/dL for the PP group; P <0.001) (see Table 1). Both groups presented lower blood urea concentration than controls (21 ± 7 mg/dl for CDI, P <0.01 and 22 ± 6 mg/dl for PP, P <0.05) and both presented high urea clearances. In the
Discussion
When intravenous fluid administration and osmotic diuresis, or different renal diseases (including potassium depletion or hypercalcemia) are excluded, the differential diagnosis of polyuria polydipsia must be made between primary polydipsia and diabetes insipidus either central (CDI) or nephrogenic (NDI). Our results suggest that hyperuricemia in a normonatremic polydipsic polyuric patient is highly suggestive of CDI.
In all our patients with PP and normonatremia, serum uric acid concentration
Acknowledgements
We are indebted to Dr G. Matte and Dr J. Unger for refering some of the patients.
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This work was supported by a grant from the Fonds National de la Recherche Scientifique (FNRS) (1-5.193.96F)/(1-5.198.97F).