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PubMed1998

Hypercalcemia in an euthyroid patient with secondary hypoadrenalism and diabetes insipidus due to hypothalamic tumor.

A 20-year-old Japanese man with a hypothalamic tumor (most likely germ-cell tumor) which caused secondary hypoadrenalism, hypogonadism and diabetes insipidus developed hypercalcemia and acute renal failure. The serum levels of intact PTH (iPTH), PTH-related protein (PTH-rP), 1,25-dihydroxy vitamin D (1,25- (OH)2 D), ACTH, cortisol, gonadotropins and testosterone were decreased, but his serum levels of triiodothyronine (T3) and thyroxine (T4) were within the normal range at admission, with depressed TSH and slightly increased thyroglobulin. The hypercalcemia was refractory to extensive hydration and calcitonin, but was ameliorated by pamidronate. After irradiation of the hypothalamic tumor, panhypopituitarism gradually developed. The patient has been normocalcemic for the last 2 years and is doing well under replacement therapy with glucocorticoid, L-thyroxine, methyltestosterone and 1-desamino D arginine vasopressin (dDAVP). As to the mechanism of euthyroidism at admission, transient destructive thyroiditis associated with hypopituitarism or delayed development of hypothyroidism following the hypoadrenalism was suggested. This is the first reported case of hypercalcemia in secondary hypoadrenalism due to hypothalamic tumor. Hypercalcemia was most likely induced by increased bone resorption, which was probably elicited by the combined effects of deficient glucocorticoid and sufficient thyroid hormones in addition to hypovolemia and reduced renal calcium excretion. Furthermore, severe dehydration due to diabetes insipidus and disturbance of thirst sensation caused by the hypothalamic tumor aggravated the hypercalcemia, leading to acute renal failure.

Acute Kidney Injury↗
PubMed1982

[Lithium and diabetes insipidus. Theoretical and practical aspects. Therapeutic value of thiazide diuretics (author's transl)].

Lithium is increasingly prescribed by psychiatrists for manic-depressive psychosis and other affective disorders. Therefore, psychiatrists should be familiar with lithium-induced nephrogenic diabetes insipidus. Management of this condition is discussed. Thiazide diuretics have a paradoxical antidiuretic effect in lithium-induced diabetes insipidus. For this reason, it is no longer warranted to contraindicate concomitant use of lithium and thiazide diuretics.

Adult↗
PubMed1998

Central diabetes insipidus as a complication of neonatal pathology: report of three cases.

Three patients, 11, 17 and 41 days old with various degrees of central nervous system (CNS) lesions developed central diabetes insipidus as a complication of hypothalamic damage. Two of the children had congenital CNS malformations including meningomyelocele, hydrocephalus, and prosencephaly, while the third child presented Streptococcus agalactiae meningitis, complicated with CNS hemorrhage and hypertensive dilatation of the lateral ventricles. All of them fulfilled the criteria for central diabetes insipidus, reaching high levels of serum sodium and osmolality, along with hypotonic urine. The responses to intranasal arginine-vasopressin were prompt, normalizing the serum levels of sodium and increasing urinary osmolality, allowing a better metabolic balance, avoiding continuing damage to the already compromised CNS. The neonatologist must be aware of the possibility of this kind of complication even in a normal child with CNS infection. Imaging studies showing hemorrhage in the region of the posterior hypothalamus must be a sign that this type of complication is able to occur.

Adolescent↗
PubMed1985

Diabetes insipidus caused by extramedullary hematopoiesis.

Myeloid metaplasia involving the central nervous system is a rare occurrence most frequently found as an incidental finding at autopsy. A case is presented of a 56-year-old man with myeloid metaplasia and myelofibrosis, who developed diabetes insipidus. Postmortem examination revealed posterior pituitary involvement by extramedullary hematopoiesis with fibrosis and gliosis. Diabetes insipidus caused by extramedullary hematopoiesis is a rare event and is thus noteworthy.

Bone Marrow↗
PubMed1990

[Syndrome of optic nerve atrophy, diabetes mellitus and diabetes insipidus].

The paper is concerned with a case of a familial variant of the hereditary De Lawter syndrome, optic nerve atrophy coupled with diabetes mellitus and insipidus. Double diabetes was detected in two brothers. Their uncle suffered from deaf-mutism. Diabetes mellitus was insulin-dependent, diabetes insipidus responded well to adiurekrin, pituitrin, chloropropamide; optic nerve atrophy was characterized by white discs with clearly defined borders. Apparently, the syndrome is based on several mutant genes the action of which manifests as isolated and in different combinations as well.

Child↗
PubMed1989

Treatment of the young child with postoperative central diabetes insipidus.

A continuous intravenous infusion of aqueous vasopressin (dosage range, 1.0 to 3.0 mU/kg/h) was administered to two patients (respective ages, 2 weeks and 3 years 1 month) who had postoperative central diabetes insipidus to determine if this mode of therapy is helpful in the very young patient. In both patients the polyuria and serum hyperosmolality were corrected. These findings suggest that an intravenous infusion of aqueous vasopressin can provide satisfactory control of the polyuria and electrolyte disturbances found in young children with acute postoperative central diabetes insipidus.

Brain↗
PubMed1984

Renal effect of clonidine during acute hypobaric pressure breathing in normal and diabetes insipidus rats.

The renal effects of clonidine (100 and 500 micrograms/kg s.c.) during acute hypobaric pressure breathing (i.e. a protocol which induces an increase in intrathoracic blood volume) were studied in normal and diabetes insipidus rats. In normal rats, clonidine enhanced the increase in urine flow and urea concentration elicited by hypobaric breathing without change in urinary creatinine level. By contrast, in Brattleboro diabetes insipidus rats, clonidine reinforced the hypoxia-induced mechanisms: oliguria, decrease in both urinary urea and creatinine excretions. During normobaric and hypobaric conditions in normal rats administration of clonidine induced an increase in electrolytes (Na+, K+, Cl-) excretion. In Brattleboro rats, clonidine potentiated the decrease in electrolytes excretion elicited by the hypobaric pressure breathing. Since the diuretic reflex elicited by the hypobaric pressure breathing is due to an inhibition of vasopressin release, the present data show that clonidine induces an inhibition of vasopressin release. However, it is suggested that beside this property clonidine also possesses direct vasoconstrictor actions during hypobaric pressure breathing.

Animals↗
PubMed1986

Renal effect of acute hypobaric pressure breathing in normal and diabetes insipidus rats.

The role of blood volume regulatory mechanisms located in the low pressure system in the control of urinary excretion was studied using hypobaric pressure breathing in normal and diabetes insipidus (Brattleboro strain with a congenital lack of vasopressin) rats. Rats were placed in an altitude simulator chamber for 4 h. A pump maintained pressure reduced to 701, 577 and 472 mbar simulating respectively altitude of 3,000, 4,500 and 6,000 m. In normal rats, hypobaric breathing induced an increase in urine flow, urinary urea and K+ excretion and urinary pH but did not significantly modify creatinine and Na+ excretion. In diabetes insipidus rats, hypobaric breathing produced oliguria and an decrease in urea, creatinine, Na+, K+, Cl- urinary excretions. Since acute hypobaric pressure breathing induced opposed effects in normal and Brattleboro rats, it is suggested that this kind of experimental procedure which increases intrathoracic blood volume elicits a diuretic response through an inhibition of vasopressin release. These experiments confirm the main role of vasopressin in the control of central blood volume.

Air Pressure↗
PubMed2001

Diabetes insipidus revealing acute myelogenous leukaemia with a high platelet count, monosomy 7 and abnormalities of chromosome 3: a new entity?

We describe three cases of acute myeloid leukaemia revealed by diabetes insipidus. The patients were 42, 38 and 39 yr old and they had marked hyperleukocytosis, circulating immature granular cells and a normal or elevated platelet count. The leukaemia was type AML-M2 according to the FAB classification. Cytogenetic studies showed inversion of chromosome 3 (q21;q26) in 2 cases and a translocation (3;3)(q21;q29?) in the remaining case, both associated with monosomy 7. All the cerebral CT scans were normal. Complete remission was never achieved, and all three patients survived less than 14 months. Desmopressin therapy was active but treatment could not be reduced. The association of dysmegakaryopoiesis with a chromosome 3 abnormality and diabetes insipidus is probably not fortuitous and could represent a new entity.

Adult↗
PubMed2002

Postpartum hemorrhage complicated with irreversible renal failure and central diabetes insipidus.

Sheehan's syndrome is a rare complication of pregnancy with multiple hormone deficiency. The exact pathogenetic mechanism is not well understood, because such endocrine abnormalities are not obvious in most women with severe hemorrhage. Central diabetes insipidus with fluid and sodium disturbances occurred in about 5% of the patients. [1,2] There are very few existing literature discussing concomitant Sheehan's syndrome and acute renal failure. The following case reports a patient showing Sheehan's syndrome, irreversible acute renal failure and central diabetes insipidus concurrently.

Acute Kidney Injury↗