Original Article
Aggravation of Subclinical Diabetes Insipidus during Pregnancy
N Engl J Med 1991; 324:522-526February 21, 1991
- Abstract
- Abstract
Background.
Transient polyuria and polydip-sia during pregnancy are rare, and their cause is not en-tirely clear. Possible explanations include the exacerba-tion of preexisting abnormalities in the secretion or action of vasopressin and abnormally large increases in plasma vasopressinase activity.
Methods.
We studied two women in whom overt poly-uria and polydipsia developed during the third trimester of pregnancy and disappeared after delivery. The secretion and action of vasopressin were studied both when the women had polyuria and polydipsia and later, when their water intake and urine volume were normal.
Results.
One patient had partial nephrogenic diabetes insipidus. She had little increase in urine osmolality in re-sponse to water deprivation, hypertonic-saline infusion, and vasopressin injection and no response to desmopres-sin acetate (1-deamino-8-D-arginine vasopressin) during the immediate postpartum period. Her basal and stimulat-ed plasma vasopressin concentrations were high (16.5 to 203.4 pmol per liter) before and during hypertonic-saline infusion 30 months post partum. The other patient had partial neurogenic diabetes insipidus. She had subnormal basal plasma vasopressin concentrations, a subnormal increase in the plasma vasopressin level and a subnormal decrease in urine flow in response to the administration of vasopressin, and a normal response to desmopressin. After pregnancy, when her urine volume was normal, she had no increase in plasma vasopressin in response to hypertonic-saline infusion, but she had a normal rise in the plasma vasopressin level and a normal renal response to vasopressin administration.
Conclusions.
Pregnancy may unmask subclinical forms of both nephrogenic and neurogenic diabetes insipidus. This exacerbation may result from both increased vasopressinase activity and diminished renal responsiveness to vasopressin. (N Engl J Med 1991; 324:522–6.)
Article Activity
- Article
TRANSIENT polyuria and polydipsia during pregnancy are infrequent but well recognized, 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 although the mechanisms responsible for their occurrence are not entirely clear. Possible explanations include abnormally increased vasopressinase activity10 , 18 or exacerbation of preexisting osmoregulatory defects during pregnancy.2 , 3 , 5 , 7 , 13 , 15 , 19
This report describes two women who had transient overt polyuria and polydipsia during late pregnancy, in whom we studied the osmoregulation of vasopressin secretion during both the polyuric and nonpolyuric periods. Each woman had a different underlying disorder — partial nephrogenic diabetes insipidus in one and partial neurogenic diabetes insipidus in the other. The results suggest that subclinical forms of these disorders of water metabolism become apparent during pregnancy because of an increased rate of hormonal disposal due to increased vasopressinase activity or an intrarenal mechanism that impairs the action of vasopressin.
Case Reports
Patient 1
A 23-year-old nulliparous woman was hospitalized during her 36th week of pregnancy because of severe polyuria and polydipsia that had developed during the third trimester. She had had mild polyuria and nocturia during both childhood and adulthood, but because these symptoms were minimal, she had not sought medical attention. Her paternal grandfather and older brother also had polyuria and polydipsia. Her mild polyuria and nocturia did not change during the first two trimesters of her pregnancy but then worsened to the point at which she drank 500 ml of tap water several times daily and had increased nocturia (urinating two to four times a night). Physical examination revealed a blood pressure of 110/76 mm Hg, uterine enlargement appropriate for the duration of gestation, and minimal pretibial edema. Her hemoglobin level was 119 g per liter, the serum concentration of sodium was 146 mmol per liter, urea nitrogen 2.9 mmol per liter, creatinine 44 μmol per liter, and uric acid 420 μmol per liter. The level of total serum protein, results of liver-function tests, and fasting plasma glucose levels were normal. Urinalysis revealed trace proteinuria.
The patient had overt polyuria; her urine volume was 4.2 liters per day, and the specific gravity of the urine was 1.001. Two days after admission, she spontaneously delivered a 2430-g male infant. Uterine contractions were normal, as was lactation. After delivery, her urine volume was about 4 liters per day for several days, but then it gradually decreased and by the second postpartum week was 2.2 to 2.7 liters per day. The patient's basal plasma vasopressin concentrations on the 1st and 14th postpartum days were 1.4 and 4.6 pmol per liter, respectively. X-ray films and a computed tomographic scan of the head were normal. The hormonal responses of the anterior pituitary gland to insulin-induced hypoglycemia, gonadotropin-releasing hormone, and thyrotropin-releasing hormone were normal, except for an impaired response of serum follicle-stimulating hormone and luteinizing hormone that is characteristic of the postpartum period. Water-deprivation, hypertonic-saline-infusion, and vasopressin-injection tests were performed on the 4th, 7th, and 18th postpartum days, respectively. The patient received desmopressin acetate (l-deamino-8-D-arginine vasopressin, or DDAVP; 10 μg twice daily intranasally) from the 13th through the 15th days of the puerperium; this treatment had no effect on urine volume. A second hypertonic-saline-infusion test was performed 30 months after delivery.
Patient 2
A 29-year-old primiparous woman noted polyuria and polydipsia during the second trimester of her second pregnancy. Her history and that of her family were normal, except that the patient had had severe polyuria and polydipsia during the second and third trimesters of her first pregnancy, when she was 27 years old. That pregnancy had ended with the spontaneous delivery of a stillborn fetus during the last month of gestation, and the polyuria and polydipsia disappeared soon thereafter. She became pregnant again one year later. The pregnancy progressed normally until the fifth month, when polyuria and polydipsia reappeared. The patient was admitted to the hospital during the sixth month, at which time her physical examination was normal, except for a blood pressure of 132/98 mm Hg, and her uterine size was consistent with the date of conception. Her urine volume was 4.5 liters per day, and the specific gravity was 1.002. Her hemoglobin level was 114 g per liter, the serum sodium concentration was 150 mmol per liter, urea nitrogen 4.3 mmol per liter, creatinine 71 μmol per liter, and uric acid 510 μmol per liter. The level of total serum protein, results of liver-function tests, and fasting plasma glucose levels were normal, as was urinalysis. X-ray films and a computed tomographic scan of the head were normal.
The patient's diabetes insipidus was assessed during the 28th week of pregnancy by measurements of basal plasma osmolality and vasopressin after overnight dehydration for three consecutive days. No hypertonic-saline-infusion test was performed, because the basal plasma osmolality was high. Treatment with desmopressin (10 to 20 μg twice daily intranasally) was started one week later and resulted in a reduction in urine volume to under 2 liters per day. During the patient's 33rd and 34th weeks of gestation, a vasopressin-injection test and desmopressin-challenge test were performed after a discontinuation of desmopressin therapy for 24 hours. Spontaneous labor commenced during week 37, resulting in the vaginal delivery of a 2810-g normal male infant. Uterine contractions and lactation were normal. Desmopressin therapy was discontinued after the delivery, and the patient had urine volumes of more than 4 liters per day for several days post partum, but the volume gradually decreased to 1.4 to 2.0 liters per day two weeks after delivery. Hormone secretion from the anterior pituitary gland, tested in a manner similar to that used for Patient 1, was normal except for blunted serum gonadotropin responses to gonadotropin-releasing hormone. The vasopressin-injection test was repeated on the 22nd postpartum day, and a hypertonic-saline-infusion test was performed on the 24th day, at which time neither polyuria nor polydipsia was present.
The woman had a third pregnancy at the age of 30, and polyuria and polydipsia developed again. This time, the administration of desmopressin was begun during the early phase of pregnancy, and the gestation was completed successfully with the delivery of another normal infant.
Methods
Informed consent was obtained from both patients. Neither patient smoked or ingested alcohol throughout the study.
Hypertonic-Saline-lnfusion Test
In Patient 1, a test involving the infusion of 2.5 percent hypertonic saline27 was performed on the seventh postpartum day, at which time the urine volume was 2.3 liters per day. The patient had a second test with 5 percent hypertonic saline 30 months post partum, as described below.28 In Patient 2, a test involving the infusion of 5 percent hypertonic saline was performed on the 24th postpartum day, when the urine volume was 1.4 liters per day. After overnight dehydration, the patient was given an infusion of a 5 percent saline solution for two hours at a rate of 0.05 ml per kilogram of body weight per minute, and serial blood samples were obtained for determinations of plasma vasopressin levels and plasma osmolality. The results were compared with those in 15 normal nonpregnant adults reported in an earlier study.29
Vasopressin-Injection Test
A vasopressin-injection test was performed in Patient 1 on postpartum day 18, when the patient's urine volume was 2.2 liters per day. In Patient 2, vasopressin-injection tests were performed during the 33rd week of gestation, when the patient had overt polyuria, and again 22 days post partum, when her urine volume was 1.6 liters per day. One hundred milliunits of synthetic aqueous vasopressin (Pitressin, Parke-Davis, Morris Plains, N.J.) was rapidly injected intravenously, and serial blood and urine samples were collected for determinations of plasma osmolality, urine volume, urine osmolality, and free-water clearance. The plasma vasopressin concentration was not determined in Patient 1. Urine samples were collected serially with an indwelling catheter to determine volume and osmolality.
Desmopressin-Challenge Test
A desmopressin-challenge test was performed in Patient 2 during her 34th week of gestation. Ten micrograms of desmopressin was given intranasally, and urine samples were collected hourly for eight hours for measurements of volume and osmolality.
Water-Deprivation Test
A water-deprivation test30 was performed in Patient 1 on postpartum day 4, when her urine volume was 4.1 liters per day. After fluids were kept from the patient overnight, an hourly urine collection was started at 8 a.m., followed by a subcutaneous injection of 5 U of synthetic aqueous vasopressin at noon. Serial blood and urine samples were obtained for determinations of plasma osmolality, urine volume, urine osmolality, and free-water clearance.
Laboratory Analysis
In these experiments, the blood samples used in the vasopressin determinations were drawn into chilled tubes containing edetate dipotassium, mixed thoroughly, put on ice, centrifuged immediately, and then extracted with Sep-Pak C18 columns (Waters Associates, Milford, Mass.). Plasma vasopressin levels were measured with a highly sensitive radioimmunoassay31 (Mitsubishi Petrochemical, Tokyo). The sensitivity of this radioimmunoassay was 0.06 fmol per tube, and the rate of recovery of vasopressin ranged from 71.1 to 85.5 percent.
Serum sodium levels were measured by flame photometry, and plasma glucose and serum urea nitrogen levels by Parallel Analyzer (American Monitor, Indianapolis). Plasma osmolality was calculated with the following formula (with all values expressed in millimoles per liter): Plasma osmolality = 2 × serum sodium + plasma glucose + serum urea nitrogen. The osmolality of the urine was measured with a freezing-point-depression osmometer (Knauer Type M, Adenauerallee, Germany).
Results
Figure 1Figure 1
Results of a Water-Deprivation Test (Left Panel), a 2.5 Percent Hypertonic-Saline-Infusion Test (Center Panel), and a Vasopressin-injection Test (Right Panel) in Patient 1. shows the results of the water-deprivation, hypertonic-saline-infusion, and vasopressin-injection tests in Patient 1. On postpartum day 4, when the patient had polyuria, the urine osmolality after four hours of water deprivation following overnight dehydration was 190 mmol per kilogram. After the subcutaneous injection of a large dose of vasopressin (5 U), the urine osmolality did not increase, and the free-water clearance remained positive. The patient also responded poorly to the small dose (100 mU) of vasopressin given intravenously on postpartum day 18, although her urine volume did decrease slightly. The urine osmolality and free-water clearance did not change during the hypertonic-saline infusion and subsequent injection of vasopressin performed on postpartum day 7. Figure 2Figure 2
Relation of the Plasma Vasopressin Concentration to Plasma Osmolality before and during Infusion with 5 Percent Hypertonic Saline in Patient 1, 30 Months Post Partum. shows the relation between plasma osmolality and vasopressin concentration in Patient 1 during hypertonic-saline infusion 30 months after delivery. The basal and stimulated plasma vasopressin values were extremely high, suggesting marked resistance to vasopressin. The patient was already thirsty at the start of the test and became more so as it proceeded.The results in Patient 2 are shown in Figures 3Figure 3
Relation of the Plasma Vasopressin Concentration to Plasma Osmolality in Patient 2. and 4Figure 4
Results of Vasopressin-injection Tests in Patient 2 during the 33rd Week of Pregnancy, When She Had Polyuria (Left Panel), and 22 Days after Delivery, When Her Urine Volume Was Normal (Right Panel).. During pregnancy, when she had polyuria, the patient's basal plasma vasopressin values (0.20 to 0.41 pmol per liter) were barely detectable, despite concurrent high values for plasma osmolality, ranging from 309 to 322 mmol per kilogram (Fig. 3). After the injection of vasopressin in late pregnancy, the patient's urine volume decreased transiently, and the urine osmolality increased minimally, from 104 to 227 mmol per kilogram, in parallel with a blunted increase in plasma vasopressin levels (Fig. 4). In contrast, during the desmopressin-challenge test performed during the 34th week of gestation, her urine volume decreased continuously, and the urine osmolality increased from 110 to 786 mmol per kilogram. Although the patient's polyuria subsided after delivery, there was no increase in the plasma vasopressin level in response to hypertonic-saline infusion (Fig. 3), indicating a decreased capacity to secrete vasopressin, but the osmotic threshold for thirst appeared normal during the test. After the second vasopressin-injection test, 22 days post partum, the plasma vasopressin level increased promptly. This increase was accompanied by a prolonged period of antidiuresis, as well as a substantial increase in urine osmolality, from 166 to 589 mmol per kilogram. The results of this test as compared with those of the first vasopressin test suggest that the metabolic clearance of vasopressin was increased during pregnancy.Discussion
These two women had polyuria and polydipsia in late pregnancy that subsided post partum. The results of the studies of the secretion and action of vasopressin show that both women had subclinical diabetes insipidus as the underlying cause of these symptoms. In one woman the diabetes insipidus was nephrogenic, and in the other it was neurogenic. Thus, our results support the view that aggravation of subclinical diabetes insipidus can be one of the causes of transient diabetes insipidus of pregnancy.
Patient 1 had overt polyuria during late gestation and the early puerperal period of her first pregnancy. In the immediate postpartum period, her renal responses to water deprivation, hypertonic-saline infusion, and injection of exogenous vasopressin were markedly impaired, despite substantial plasma levels of vasopressin. Furthermore, her polyuria and urine osmolality were resistant to the intranasal administration of desmopressin, an analogue of vasopressin resistant to inactivation by vasopressinase.32 When studied 30 months post partum, the patient's basal and stimulated plasma vasopressin levels were markedly elevated, ranging from 16.5 to 203.4 pmol per liter —far above those in normal adults undergoing the same stimulation. These results suggest that the patient had partial renal resistance to endogenous vasopressin. The elevated basal plasma osmolality in the presence of normal thirst after overnight dehydration also suggests a renal defect in free-water conservation. The family history of polyuria and the patient's history of mild polyuria since childhood further suggest that she had hereditary partial nephrogenic diabetes insipidus. Although transient diabetes insipidus has been reported in women known to be heterozygous for hereditary nephrogenic diabetes insipidus, 3 little is known about the osmoregulation of the plasma vasopressin concentration in such patients.
The results in Patient 2 were quite different. In this woman, transient polyuria appeared during three successive gestations, but she had no polyuria or polydipsia when not pregnant. The vasopressin response to osmotic stimuli was markedly impaired, however, both when she had polyuria during gestation and when her urine volume was normal post partum. These results indicate that this woman had latent idiopathic neurogenic diabetes insipidus, 33 which was not clinically apparent when she was not pregnant. Her course was similar to those of several previously described patients with preexisting pituitary disease in whom polyuria developed during late pregnancy.2 , 5 , 7 , 13 , 15
The mechanisms responsible for the development of polyuria and polydipsia during pregnancy in these two patients are still unclear. In Patient 1, marked increases in vasopressin secretion probably compensated for the patient's partial refractoriness to vasopressin, but during gestation decompensation occurred because of increased disposal of vasopressin due to increased vasopressinase activity. This hypothesis is supported by the fact that her basal plasma vasopressin levels during the postpartum period were considerably lower than those 30 months after delivery. In Patient 2, the rise in plasma vasopressin levels after the administration of vasopressin was much less during pregnancy than afterward, suggesting increased disposal of vasopressin in this patient also. However, her plasma vasopressin levels during hypertonic-saline infusion 24 days post partum were comparable to those when she had polyuria during pregnancy, suggesting that her polyuria cannot entirely be explained by enhanced metabolic clearance of vasopressin during pregnancy. One possible mechanism is a resetting of the thirst threshold, 15 , 34 but that seems unlikely in this patient, because basal plasma osmolality was increased rather than decreased. Renal hemodynamic changes, such as increases in the glomerular filtration rate and renal plasma flow, 35 altered renal sensitivity to vasopressin during pregnancy, or both, are other possible explanations. Renal production of prostaglandins, known to increase during pregnancy, 36 , 37 may cause polyuria by decreasing renal sensitivity to low plasma levels of vasopressin, 38 although the therapeutic doses of desmopressin were enough to increase urine osmolality and reduce urine volume.
Vasopressinase is a cystine aminopeptidase elaborated by placental tissue, which inactivates vasopressin, oxytocin, and some other small peptides.39 In normal pregnant women, vasopressinase activity increases steadily throughout pregnancy and disappears gradually after delivery.39 40 41 The enzyme also inactivates vasopressin in vitro unless an appropriate inhibitor is added. In this study we used edetate, which is a fairly effective, if not complete, inhibitor of vasopressinase.39 , 42 Although a small degree of in vitro degradation after phlebotomy during pregnancy cannot entirely be ruled out, the blunted rise in the plasma vasopressin level in association with the small and short-lasting urinary response after the administration of vasopressin in Patient 2 during pregnancy is best explained by substantial in vivo degradation. The larger increase in the plasma vasopressin level and the sustained renal response after the administration of vasopressin 22 days post partum suggest that the level of circulating vasopressinase had decreased substantially.40 , 43
These studies indicate that pregnancy may be regarded as a stress test likely to uncover latent forms of both neurogenic and nephrogenic diabetes insipidus.19 Patients who have the onset of polyuria and polydipsia during pregnancy should be studied carefully post partum in order to detect these underlying disorders. Such evaluation may also provide valuable information for the early treatment of polyuria during a subsequent pregnancy.
From the First Department of Internal Medicine (Y.I., Y.O., K.K., S.T., K.T.), Nagoya University School of Medicine, Nagoya; the Departments of Internal Medicine (H.H.) and Obstetrics and Gynecology (K.I., Y.F., S.K.), the Japanese Red Cross Nagoya First Hospital, Nagoya; and the Central Laboratory for Clinical Investigation (A.T.), Aichi Medical University, Nagakute; all in Japan. Address reprint requests to Dr. Iwasaki at the First Department of Internal Medicine, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466, Japan.
Supported in part by a Research Grant for Intractable Disease from the Ministry of Health and Welfare, Japan.
We are indebted to Dr. Gary L. Robertson, Dr. Marshall D. Lindheimer, and Dr. William M. Barron for helpful discussion, and to Mitsubishi Petrochemical Co. for the arginine vasopressin radioimmunoassay kits.
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