Disease relevance of Polyuria

• Further, the apparent hypoaldosteronism of DI Brattleboro rats reflects differences in both tissue usage of the steroid and adrenocortical sensitivities associated with polyuria, hyperosmolarity and possibly potassium wasting [1].
• Prolonged hypokalemia causes vasopressin-resistant polyuria [2].
• Administration of 25 mg/kg uranyl nitrate (UN) to rats leads to a brief period of polyuria followed by progressive oliguria with death at 5 days [3].
• Use of vasopressin analogues to induce water retention in elderly patients with nocturnal polyuria is illogical and potentially hazardous; nocturia can be more safely alleviated by diuretic therapy [4].
• High plasma ANP levels were also found in 2 patients with paroxysmal supraventricular tachycardia and associated transient polyuria [5].

Psychiatry related information on Polyuria

• Two adolescent boys with Kearns-Sayre syndrome (progressive external ophthalmoplegia, heart block, elevated CSF protein, and ragged-red muscle fibers) developed lethargy, increasing somnolence, polydipsia, polyphagia, and polyuria after a brief course of steroid therapy [6].
• AQP1 null mice are polyuria and unable to generate a concentrated urine after water deprivation [7].
• PURPOSE: Desmopressin may not be effective for nocturnal enuresis associated with polyuria and hypercalciuria [8].
• Lithium, a drug frequently used for treatment of affective disorders, is known to cause a vasopressin-resistant state, leading to polyuria and polydipsia [9].
• 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 [10].

High impact information on Polyuria

• 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 [11].
• Thus, amiloride may provide a specific therapy for polyuria in lithium-treated patients while obviating the need for potassium supplementation in the treatment of this kind of polyuria [12].
• We also find drug-induced polyuria in mrp1(-/-) mice, which correlates with the presence of mrp1 protein in the urinary collecting tubules, the major site of kidney water reabsorption [13].
• In contrast, heterozygous mice expressing a mutation that truncates the AVP precursor (C67X) exhibited polyuria and polydipsia by 2 months of age and these features of DI progressively worsened with age [14].
• We have recently shown that another cause of severe polyuria, chronic lithium therapy, is associated with decreased aquaporin-2 (AQP2) water channel expression (Marples, D., S. Christensen, E.I. Christensen, P.D. Ottosen, and S. Nielsen, 1995. J. Clin. Invest., 95: 1838-1845) [2].

Chemical compound and disease context of Polyuria

• Amelioration of polyuria by amiloride in patients receiving long-term lithium therapy [12].
• The effect was not caused by angiotensin inhibiting antidiuretic hormone release since the polyuria occurred in hypophysectomized animals receiving a constant infusion of 10 muU/kg per min of aqueous Pitressin [15].
• Dopamine and polyuria [16].
• Thus absence of NKCC2 in the mouse causes polyuria that is not compensated elsewhere in the nephron [17].
• Two parameters were linked to the duration of remissions: the mean circulating level of cyclosporin during the first 3 mo and the duration of prediagnostic polyuria [18].

Biological context of Polyuria

• In summary, the results strongly suggest that AQP2 downregulation and reduced apical plasma membrane delivery of AQP2 play important roles in the development of polyuria in association with hypercalcemia [19].
• Two patients developed polyuria with natriuresis while receiving intravenous dopamine hydrochloride for the treatment of hypotension [20].
• These results indicate that the polyuria observed in Clcnk1-/- mice was water diuresis and not osmotic diuresis [21].
• Here we report that intravenous injections of 4.92 mmol of Na2SO4/kg body wt. to rats induced marked hepatic glycogenolysis in vivo, accompanied by polyuria, glycosuria and a mild hyperglycaemia [22].
• Lithium adversely affects renal tubular function, causing polyuria secondary to a deficit in urine concentrating ability [23].

Anatomical context of Polyuria

• A brain computerized tomographic scan taken soon after the onset of polyuria disclosed an enlarged pituitary gland that completely returned to its normal size after 5 months of cyclophosphamide therapy [24].
• Lithium intoxication causes polyuria, central nervous system manifestations, and ultimately stupor progressing to coma [25].
• Nocturnal polyuria and antidiuretic hormone levels in spinal cord injury [26].
• 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 [27].
• The adrenocortical nodule had the histological characteristics of an aldosteronoma, with the non-affected zona glomerulosa being atrophic.In this dog with primary hyperaldosteronism the polyuria was characterized by vasopressin resistance and increased osmotic threshold of vasopressin release, similar to the polyuria of glucocorticoid excess [28].

Gene context of Polyuria

• 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 [29].
• The present studies examined whether induction of the COX2 isoform contributes to LiCl-induced polyuria [30].
• Lithium-associated polyuria was also seen in COX1-/- mice and was associated with increased urinary PGE(2) [30].
• NPH3 shares with juvenile nephronophthisis (NPH1) the same disease manifestations such as polyuria, polydipsia, and secondary enuresis [31].
• For example, in kidney, deletion of AQP1 or AQP3 produced marked polyuria whereas AQP4 deletion produced only a mild concentrating defect [32].

Analytical, diagnostic and therapeutic context of Polyuria

• A comparison of plasma vasopressin measurements with a standard indirect test in the differential diagnosis of polyuria [33].
• Immunoblotting revealed that lithium treatment reduced AQP2 expression dramatically, to 31 +/- 8% after 10 d and to 4 +/- 1% after 25 d, coincident with development of severe polyuria [34].
• The expression of the neuronal nitric oxide synthase (nNOS) gene in the paraventricular (PVN) and supraoptic nuclei (SON) in rats with lithium (Li)-induced polyuria was examined by using in situ hybridization histochemistry [35].
• Subcutaneous injections of CdCl2 at a dose of 2 mg Cd/kg body wt per day for 2 weeks induced marked polyuria, glycosuria, proteinuria, and phosphaturia, which are characteristics of chronic cadmium intoxication [36].
• 2. Intraperitoneal injection of succinylacetone for 3 consecutive days into adult male Sprague-Dawley rats resulted in succinylacetone plasma concentration of 3 mmol/l. This concentration was associated with glucosuria, aminoaciduria, polyuria, reduced renal phosphate reabsorption and normal creatinine clearance [37].

References