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PubMed2006

Pregnancy complicated by multiple pituitary hormone deficiencies.

We report a case of pituitary dwarfism and diabetes insipidus due to pituitary stalk transection in a pregnant Japanese woman, 138 cm in height, born by breech delivery with no evidence of ante- or intrapartum asphyxia. The patient had no central nervous disturbance, was diagnosed with pituitary dwarfism during childhood and was treated at another hospital with growth hormone supplement from 5 to 14 years of age. This patient was referred to our department at 17 weeks' gestation due to a change of residence. At 30 weeks' gestation, she was hospitalized for assessment of hydronephrosis and polyuria (15-20 L/day). Analysis of a 24-h urine sample showed creatinine clearance of 157 mL/min and urine osmolality of 38 mOsm/L. The patient's urine output decreased after receiving a test dose of 0.75 g of 1-desamino-8-D-arginine vasopressin (DDAVP). Cranial magnetic resonance imaging showed transection of the pituitary stalk. Subsequently, the patient's urine output was well controlled by a maintenance dose of 0.275 mL/day intranasal DDAVP. A cesarean section was performed at 37 weeks, as the patient height was 138 cm, and a pelvic X-ray showed cephalopelvic disproportion. She delivered a female baby weighing 2302 g, and both 1- and 5-min Apgar scores were 9. The patient was followed up after 4 months and showed no visual deterioration or polyuria while on DDAVP therapy, while the neonate grew favorably.

Adult↗
PubMed1988

Changes in renal function in cadmium-intoxicated rats.

Changes in renal function, Na+-K+-ATPase activity and PAH transport system in kidney cortex were studied in rats treated with cadmium. Subcutaneous injections of CdCl2 (2 mg Cd/kg.day) for 16 days induced a marked polyuria and a hyposthenuria. These changes were accompanied by increase in urinary protein, glucose, urea, calcium, phosphate, chloride and potassium excretions. The change in urine flow was proportional to the change in total osmotic solute excretion. Creatinine excretion and TcH2O remained unchanged. Na+ excretion was not increased, but the Na+-K+-ATPase of renal cortex was significantly inhibited. PAH uptake by renal cortical slices was markedly attenuated in Cd-treated rats. The Vmax for active PAH influx was drastically reduced, but the Km was not changed. The passive influx and efflux of PAH across the basolateral membrane and the renal tissue oxygen consumption were not apparently altered in Cd-treated animals. These results indicate that 1) the nature of Cd-induced polyuria and hyposthenuria is an osmotic diuresis induced by proximal tubular rejection of various substances, and 2) the mechanism of impaired renal PAH excretion in Cd-treated animals is a loss of organic anion carriers in proximal tubular basolateral membranes.

Animals↗
PubMed1979

Diabetes insipidus in children. I. Arginine-vasopressin determination in plasma during short dehydration test.

Plasma vasopressin as well as plasma and urinary osmolality are measured during an overnight dehydration test in vasopressin is undetectable. It is present in plasma from patients with partial diabetes insipidus but the level is not appropriate for plasma osmolality. In patients with polyuria of renal origin plasma vasopressin was significantly higher than in patients with neurogenic diabetes insipidus. Plasma vasopressin measurement is of diagnostic values in partial neurogenic diabetes insipidus and may be of considerable help to distinguish this group of patients from children with polyuria of renal origin.

Adolescent↗
PubMed1999

Transient diabetes insipidus in a dog with acromegaly.

A nine-year-old female beagle with acromegaly and extreme polyuria and polydipsia during dioestrus is described. It was demonstrated that polyuria was related to an inadequate rise of arginine-vasopressin (AVP) levels after water deprivation and stimulation with hypertonic saline. Administration of AVP did not lead to a significant increase in urine osmolality or reduction of urine volume. Clinical signs, except for bony changes, completely disappeared following ovariohysterectomy.

Acromegaly↗
PubMed1971

Intrarenal distribution of blood flow and cortico-medullary sodium gradient after unilateral splanchnicotomy in the dog.

1. Intrarenal distribution of blood flow and cortico-medullary sodium gradients have been studied in anaesthetized dogs, previously subjected to unilateral splanchnicotomy. Experiments were carried out on hydropoenic, normal, isotonic and hypotonic volume expanded animals.2. Polyuria and natriuresis were present under all experimental conditions after denervation.3. Denervation resulted in an increase in medullary blood flow, particularly in hydropoenic and normal dogs. In isotonic and hypotonic volume expansion, the increases in the medullary circulation were smaller despite a greater increase in urine flow and sodium excretion of the denervated side.4. Under no experimental condition did the cortico-medullary sodium gradient of denervated kidneys differ significantly from that of the intact kidneys.5. It is concluded that denervation polyuria might be attributed in part to an increase in medullary blood flow; the natriuresis, however, could not be accounted for by these circulatory changes. Other possibilities are discussed.

Animals↗
PubMed2003

Downregulation of renal AQP2 water channel and NKCC2 in mice lacking the apical Na+-H+ exchanger NHE3.

The apical Na+-H+ exchanger NHE3 plays an important role in fluid reabsorption in the proximal tubule. However, whether its deletion alters the salt and water transport in the distal nephron remains unknown. To answer these questions, wild-type (Nhe3+/+) and NHE3 null mice (Nhe3-/-) were placed in metabolic cages and their water balance and urine osmolality were examined. Nhe3-/- mice demonstrated a significant polydipsia (P < 0.03) and polyuria (P < 0.04), with a lower urine osmolality (P < 0.003) as compared to Nhe3+/+ mice. Northern hybridization and immunoblotting studies indicated that the mRNA expression and protein abundance of the collecting duct (CD) water channel AQP2 decreased by 52 % (P < 0.0003) and 73 % (P < 0.003) in the cortex, and by 53 % and 54 % (P < 0.002) in the inner medulla (IM) of Nhe3-/- vs. Nhe3+/+ mice. The expression of AQP2 in the outer medulla (OM) remained unchanged. Further, the mRNA expression and protein abundance of the medullary thick ascending limb (mTAL) apical Na+-K+-2Cl- cotransporter (NKCC2) decreased by 52 % (P < 0.02) and 44 % (P < 0.01), respectively, in the OM of Nhe3-/- vs. Nhe3+/+ mice. The circulating plasma levels of vasopressin as well as the mRNA expression of vasopressin prohormone were significantly increased in Nhe3-/- vs. Nhe3+/+ mice (P < 0.05). Studies in mice treated with acetazolamide indicated that increased bicarbonate and fluid delivery to distal nephron did not alter the expression of NKCC2 in mTAL and decreased AQP2 protein only in OM but not in the cortex or IM. In conclusion, mice lacking the apical NHE3 have impairment in their water balance and urine osmolality, which correlates with the downregulation of AQP2 expression. These defects occur despite increased circulating levels of vasopressin. We propose that an ADH-independent mechanism is responsible for the downregulation of AQP2 and the resulting polyuria in NHE3 null mice.

Acetazolamide↗
PubMed2006

Angiotensin II mediates downregulation of aquaporin water channels and key renal sodium transporters in response to urinary tract obstruction.

The renin-angiotensin system is well known to be involved in the pathophysiological changes in renal function after obstruction of the ureter. Previously, we demonstrated that bilateral ureteral obstruction (BUO) is associated with dramatic changes in the expression of both renal sodium transporters and aquaporin water channels (AQPs). We now examined the effects of the AT(1)-receptor antagonist candesartan on the dysregulation of AQPs and key renal sodium transporters in rats subjected to 24-h BUO and followed 2 days after release of BUO (BUO-2R). Consistent with previous observations, BUO-2R resulted in a significantly decreased expression of AQP1, -2, and -3 compared with control rats. Concomitantly, the rats developed polyuria and reduced urine osmolality. Moreover, expression of the type 2 Na-phosphate cotransporter (NaPi-2) and type 1 bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2) was markedly reduced, consistent with postobstructive natriuresis. Candesartan treatment from the onset of obstruction attenuated the reduction in GFR (3.1 +/- 0.4 vs. 1.7 +/- 0.3 ml.min(-1).kg(-1)) and partially prevented the reduction in the expression of AQP2 (66 +/- 21 vs. 13 +/- 2%, n = 7; P < 0.05), NaPi-2 (84 +/- 6 vs. 57 +/- 10%, n = 7; P < 0.05), and NKCC2 (89 +/- 12 vs. 46% +/- 11, n = 7; P < 0.05). Consistent with this, candesartan treatment attenuated the increase in urine output (58 +/- 4 vs. 97 +/- 5 microl.min(-1).kg(-1), n = 7; P < 0.01) and the reduction in sodium reabsorption (433 +/- 62 vs. 233 +/- 45 micromol.min(-1).kg(-1), n = 7; P < 0.05) normally found in rats subjected to BUO. Moreover, candesartan treatment attenuated induction of cyclooxygenase 2 (COX-2) expression in the inner medulla, suggesting that COX-2 induction in response to obstruction is regulated by ANG II. In conclusion, candesartan prevents dysregulation of AQP2, sodium transporters, and development of polyuria seen in BUO. This strongly supports the view that candesartan protects kidney function in response to urinary tract obstruction.

Angiotensin II↗
PubMed2006

Hypokalemia in a mouse model of Gitelman's syndrome.

Hypokalemia is a prominent feature of Gitelman syndrome and a common side effect of thiazide use in the treatment of hypertension. It is widely recognized that genetic or pharmacological inhibition of the renal thiazide-sensitive sodium-chloride cotransporter (NCC) initiates the potentially severe renal potassium loss observed in these settings. Surprisingly, hypokalemia has not been detected in NCC (-/-) mice maintained on normal rodent diets (Schultheis PJ, Lorenz JN, Meneton P, Nieman ML, Riddle TM, Flagella M, Duffy JJ, Doetschman T, Miller ML, and Shull GE. J Biol Chem 273: 29150-29155, 1998). We show that modest reduction of dietary potassium induced a marked reduction in plasma potassium and elevated renal potassium excretion in NCC (-/-) mice that was associated with a pronounced polydipsia and polyuria of central origin. These findings are consistent with the development of potassium depletion in NCC (-/-) mice and were not seen in wild-type mice maintained on the same low-potassium diet. In addition, plasma aldosterone levels were significantly elevated in NCC (-/-) mice even in the presence of a low-potassium diet. Collectively, these findings suggest an early central component to the polyuria of Gitelman syndrome and show that both elevated aldosterone and dietary potassium content contribute to the development of hypokalemia in Gitelman syndrome. Therefore, NCC (-/-) mice are more sensitive to reductions in dietary potassium than wild-type mice and become hypokalemic, thus more faithfully representing the Gitelman phenotype seen in humans.

Aldosterone↗
PubMed1982

Water metabolism after cisplatin in the rat.

A polyuric state is often observed after cis-dichlorodiammine platinum (cisplatin). To study the mechanism of this polyuria we gave 5-6 mg/kg cisplatin to conscious rats and observed polydipsia and a polyuric form of mild acute renal failure. A defect in renal concentrating ability was observed 1 and 8 days after cisplatin. Animals demonstrated diminished postdehydration plasma vasopressin at 1 but not at 8 days after cisplatin, and exogenous vasopressin corrected the renal concentration defect at 1 but not at 8 days after cisplatin. To assess the role of polydipsia in the concentration defect, water intake in cisplatin-treated animals was matched to pair-fed controls. Prevention of polydipsia improved the polyuria but not the concentration defect seen 8 days after cisplatin. To assess intrarenal factors in the renal concentration defect, postdehydration interstitial solute was measured and was significantly lower in cisplatin-treated than in control animals. To determine whether the diminished interstitial solute was due to vascular mechanisms, inner medullary plasma flow was measured and was identical in cisplatin-treated and control rats. Treatment with cisplatin also resulted in decreased excretion of a water load. We conclude that either impaired synthesis or release of vasopressin is the cause of the impaired renal concentration seen 1 day after cisplatin. Eight days after cisplatin, the renal concentration defect is due in part to decreased interstitial tonicity.

Animals↗
PubMed2000

Downregulation of aquaporin-2 and -3 in aging kidney is independent of V(2) vasopressin receptor.

The mechanisms underlying age-related polyuria were investigated in 10- and 30-mo-old female WAG/Rij rats. Urinary volume and osmolality were 3.9 +/- 0.3 ml/24 h and 2,511 +/- 54 mosmol/kgH(2)O in adult rats and 12.8 +/- 0.8 ml/24 h and 1,042 +/- 44 mosmol/kgH(2)O in senescent animals. Vasopressin V(2) receptor mRNA did not significantly differ between 10 and 30 mo, and [(3)H]vasopressin binding sites in membrane papilla were reduced by 30%. The cAMP content of the papilla was unchanged with age, whereas papillary osmolality was significantly lowered in senescent animals. The expression of aquaporin-1 (AQP1) and -4 was mostly unaltered from 10 to 30 mo. In contrast, aquaporin-2 (AQP2) and -3 (AQP3) expression was downregulated by 80 and 50%, respectively, and AQP2 was markedly redistributed into the intracellular compartment, in inner medulla of senescent animals, but not in renal cortex. These results indicate that age-related polyuria is associated with a downregulation of AQP2 and AQP3 expression in the medullary collecting duct, which is independent of vasopressin-mediated cAMP accumulation.

Aging↗
PubMed1981

Attenuation of the lithium-induced diabetes-insipidus-like syndrome by amiloride in rats.

The effect of amiloride on lithium-induced polydipsia and polyuria and on the lithium concentration in the plasma, brain, kidney, thyroid and red blood cells was investigated in rats, chronically treated with LiCl. Amiloride reduced the drinking and urine volume of rats in an acute (6 or 12 h) and a subacute (3 days) experiment. 6 h after the administration of amiloride, a reduction was observed in the lithium content of the renal medulla but not in the other organs studied. At 12 h, all the tissues showed a slight increase in lithium levels. After 3 days of combined treatment, a marked elevation in plasma and tissue lithium levels accompanied a reduction in water intake. In all the experiments, the attenuation of the lithium-induced diabetes-insipidus-like syndrome by amiloride was accompanied by a reduction of the ratio between the lithium concentration in the renal medulla and its levels in the blood and an elevation in the plasma potassium level. It is concluded that acute amiloride administration to lithium-treated patients suffering from polydipsia and polyuria might relieve these patients but prolonged amiloride supplementation would result in elevated lithium levels and might be hazardous.

Amiloride↗
PubMed1994

Nephrogenic diabetes insipidus presenting after head trauma.

Water diuresis after head trauma is most often due to central diabetes insipidus (DI). We report a patient with a history of a bipolar disorder and past lithium use who was noted to have polyuria and hypernatremia after head trauma. Inappropriate high sodium and volume replacement resulted in an increase in the polyuria. A lack of response to antidiuretic hormone/antidiuretic-hormone-like preparations led to the diagnosis of nephrogenic DI. The case illustrates the importance of calculating electrolyte-free osmolar clearance in the correction of hypernatremia. Persistence of the DI and mild renal impairment probably due to past lithium use are discussed.

Adult↗
PubMedDate not supplied

Metastatic adenocarcinoma presenting with central diabetes insipidus.

The case of a previously healthy 63-year-old female with metastatic adenocarcinoma to the hypothalamus presenting with central diabetes insipidus is presented. The patient was found to have metastatic disease isolated to her hypothalamus on brain magnetic resonance imaging as well as a water deprivation test consistent with central diabetes insipidus. The patient had a decrease in symptoms of polyuria and polydypsia as well as a decrease in urine volumes after treatment with intranasal vasopressin. Even though a rare occurrence, physicians should consider metastatic adenocarcinoma in patients with recent-onset polyuria and polydypsia.

Adenocarcinoma↗
PubMed1993

Familial neurohypophyseal diabetes insipidus associated with a signal peptide mutation.

We studied the pathophysiology, natural history, and genetic basis of familial neurohypophyseal diabetes insipidus (FNDI) in a caucasian kindred. Twelve members had polyuria and a deficiency of plasma vasopressin (AVP), which progressed in severity over time. Another had normal urine volumes and plasma AVP when first tested at age 3 yr, but developed severe FNDI a year later. For unknown reasons, one man had a normal urine volume despite severe AVP deficiency and a history of polyuria in the past. When the AVP-neurophysin-II gene was amplified and sequenced, exon 2/3 was normal, but 7 of 12 clones of exon 1 contained a base substitution (G-->A) predicting a substitution of threonine for alanine at the -1 position of the signal peptide. Restriction analysis found the mutation in all 14 affected members, but in none of the 41 controls or 19 adult members with normal urine volumes and plasma or urinary AVP (lod score = 5.7). The mutation was also found in 2 infants in whom AVP was normal when tested at 6 and 9 months of age. We hypothesize that a mutation in exon 1 of the AVP-neurophysin-II gene causes FNDI in this kindred by making an abnormally processed precursor that gradually destroys vasopressinergic neurons.

Adolescent↗
PubMed2002

[Effects of Byakko-ka-ninjin-to, Bofu-tsusho-san and Gorei-san on blood glucose level, water intake and urine volume in KKAy mice].

KKAy mouse, a genetic animal model of diabetes mellitus, is characterized by not only hyperglycemia, but also polydipsia and polyuria like human diabetes mellitus. In this study, we investigated the effects of Byakko-ka-ninjin-to (BKN), Bofu-tsusho-san (BOF) and Gorei-san (GRE) on blood glucose level, water intake and urine volume in KKAy mice. All these Kampo medicines were administered to the mice as the food admixture containing 1.5% or 4.5% of weight of food for 4 weeks. BKN at 1.5% and 4.5% decreased water intake without affecting blood glucose level. BOF at 1.5% showed the same effects as BKN did, but it decreased both water intake and blood glucose level at 4.5%. Furthermore, BOF at 4.5% obviously, but BKN at 4.5% slightly, decreased urine volume. However, GRE at 4.5% did not show any effects on blood glucose level, water intake and urine volume. From these results, BKN is confirmed to be effective against the polydipsia accompanied by diabetes mellitus, while BOF is suggested to be effective against not only polydipsia, but also polyuria and hyperglycemia in diabetes mellitus.

Animals↗
PubMed1997

A control of a golden retriever with renal dysplasia.

A six-month-old male Golden Retriever with a three-month history of polyuria and polydipsia was examined. Hematological examinations revealed nonregenerative anemia, azotemia, high serum creatinine level, hypercalcemia, hyperphosphatemia, hypercholesterolemia, hyperamylasemia, and low level of total serum protein. Urinalysis indicated mild proteinuria, and low specific gravity. Radiographic and ultrasonographic examinations revealed bilateral small sized kidneys. Histological examination by renal biopsy confirmed the diagnosis of renal dysplasia. Treatment with a dietary protein restriction, oral adsorbents, and dried aluminum hydroxide gel have been performed in this dog, and then, azotemia, high serum creatinine level, hypercalcemia, and hyperphosphatemia were improved. During 10 months after the initiation of treatments, no significant clinical change except polydipsia and polyuria has been observed.

Animals↗
PubMed2004

Novel mutant vasopressin-neurophysin II gene associated with familial neurohypophyseal diabetes insipidus.

We describe a novel missense mutant of arginine vasopressin (AVP)-dependent neurohypophyseal diabetes insipidus in an autosomal dominant family. A 54-year-old woman was admitted to our hospital because of thyroidectomy for thyroid cancer. After thyroidectomy she was found to have hypernatremia and polyuria and polydipsia both of which had been present from childhood. She had no obstructive hydronephrosis. Her father, father's younger sister and her third son also had polyuria and polydipsia. Basal plasma AVP concentration at normal plasma osmolality was normal but did not respond to increased plasma osmolality despite hyperosmolality during infusion of hypertonic saline infusion, indicating that plasma AVP secretion was impaired. Sodium concentration in urine and urine osmolality were low and increased after nasal administration of DDAVP. There was a diminished but bright signal of pituitary posterior gland on magnetic resonance T1 weighted image. Molecular genetic analysis demonstrated that the patient and her son had a single heterozygous missense mutation (G-->A) at nucleotide 1829 in 1 AVP allele, yielding an abnormal AVP precursor with lacking Glu-47 in its neurophysin II moiety. The abnormal AVP precursor may be related to the impaired AVP secretion.

Adult↗
PubMed1991

Cyclical edema in a patient with hypothalamic disorders and chronic glomerulonephritis: arginine vasopressin-dependent atrial natriuretic hormone release.

A 28-year-old woman had hypothalamic disorders (amenorrhea, obesity, psychiatric abnormalities, polydipsia and fever) and chronic glomerulonephritis. She also suffered from general edema associated with cyclical oliguria and polyuria. Her body weight and plasma osmolality increased during the oliguria phase lasting 2 to 8 days and decreased after paroxysmal polyuria accompanied by the natriuresis. These episodes occurred repeatedly, regardless of the treatment with or without diuretics. The release of arginine vasopressin in response to increased plasma osmolality was exaggerated, but changes in plasma volume did not affect arginine vasopressin release. Plasma atrial natriuretic hormone increased in response to a rise in plasma arginine vasopressin and plasma volume during the oliguria phase, thereby resulting in the diuresis and natriuresis. The renin-angiotensin-aldosterone system was secondarily activated by body fluid depletion and diuretics, and this might play an additive role in general swelling. Plasma gonadal hormones did not change to explain the edema. The mechanism of this cyclical edema remains unknown, but it is likely that hypothalamic dysfunction related to psychiatric abnormalities may exaggerate arginine vasopressin release, and enhanced renal sympathetic activity may cause retention of Na and water, and the increase in atrial natriuretic hormone release responding to the plasma volume expansion may bring about the diuresis and natriuresis.

Adult↗