Ks. Kamel et al., A patient with partial central diabetes insipidus: Clarifying pathophysiology and designing treatment, AM J KIDNEY, 37(6), 2001, pp. 1290-1293
Studies were undertaken in a 32-year-old man who developed polyuria (4 L/d)
a few days after a basal skull fracture; the condition persisted 1 year af
ter the accident, The other major features were thirst, a plasma sodium of
143 mmol/L, 24-hour urine osmolality of 221 mOsm/kg H2O1 and levels of vaso
pressin in plasma that were less than 0.5 pg/mL on 20 separate occasions. T
he 24-hour urine volume implied that the diagnosis was partial rather than
complete central diabetes insipidus; however, several random urine samples
had a much higher osmolality, An infusion of hypertonic saline led to the r
elease of vasopressin and the excretion of concentrated urine. We propose t
hat the basis for the lesion may be the transection of some, but not all, o
f the fibers connecting the osmostat and vasopressin release center. This p
artial transection could permit vasopressin to be secreted in response to a
larger rise in plasma sodium concentration. This pathophysiologic analysis
provided the basis for therapy to minimize the degree of polyuria, (C) 200
1 by the National Kidney Foundation, Inc.