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PubMed2001

Downregulation of AQP1, -2, and -3 after ureteral obstruction is associated with a long-term urine-concentrating defect.

Previously, we demonstrated that 24 h of bilateral ureteral obstruction (BUO) and short-term release of BUO was associated with a decrease in the expression of aquaporin-2 (AQP2), polyuria, and a reduced urinary concentrating capacity (10). The purposes of the present study were to examine whether BUO and the long-term release of BUO (BUO-R) for 3, 14, and 30 days were associated with changes in the expression of renal AQP1, AQP2, and AQP3 and whether such changes were associated with parallel changes in urinary output and urinary concentrating capacity. Rats (n = 4-7 in each group) were kept in metabolic cages for measurements of urinary output. Kidneys were removed to determine the expression levels of AQP1, AQP2, and AQP3 by semiquantitative immunoblotting. AQP2 was downregulated after 24 h of BUO (42 +/- 3%). Downregulation of AQP2 persisted 3 (43 +/- 14%; P < 0.01) and 15 days after BUO-R (48 +/- 11%; P < 0.01) but was normalized 30 days after BUO-R. AQP3 showed a similar pattern. Moreover, AQP1 was downregulated in response to BUO (65 +/- 7%) and remained downregulated 3 days after BUO-R (41 +/- 5%), 14 days after BUO-R (57 +/- 8%), and 30 days after BUO-R (59 +/- 5%). BUO-R resulted in a significant polyuria that gradually decreased, although it remained significant at day 30. Urinary concentrating capacity remained significantly impaired when determined 3, 14, and 30 days after BUO-R in response to a 24-h period of thirst (1,712 +/- 270 vs. 2,880 +/- 91 mosmol/kgH2O at day 30, P < 0.05). In conclusion, the expression of AQP1, AQP2, and AQP3 were long-term downregulated after BUO-R, suggesting that dysregulation of aquaporins located at the proximal tubule, thin descending limb of the loop of Henle, and the collecting duct may contribute to the long-term polyuria and impairment of urinary concentrating capacity associated with obstructive nephropathy.

Animals↗
PubMed1976

Administration of lithium to rats by different routes.

Rats were given identical doses of lithium chloride, 4 mmol/kg body weight/day for 8 days, by different routes. Intraperitoneal administration led to a high serum lithium peak and the development of pronounced polyuria-polydipsia. Subcutaneous administration led to a lower serum peak and the development of less pronounced polyuria-polydipsia. Administration by gastric tube led to a nearly constant serum lithium concentration without any peak and the development of moderate polyuria-polydipsia. Our study shows that the route by which lithium is administered affects the lithium concentration pattern and may influence lithium effects.

Administration, Oral↗
PubMed1981

Glomerular filtration rate and calcium metabolism in long-term lithium treatment.

Does long-term lithium treatment induce an irreversible renal damage, and does polyuria or changes in the calcium metabolism indicate this? To elucidate these questions GFR, diuresis, S-Ca, S-Mg, S-PTH and bone mineral content (photonabsorptiometry) were determined in 29 consecutive patients on long-term lithium therapy for 2.5--12 years and in 4 patients, who had been admitted to the Renal Clinic with lithium-induced polyuria. Only 1 of the patients had had a known lithium intoxication (S-Li > 2 mmol/l). None had a history of renal disease or significant analgesic consumption. In the consecutive series the GFR was not significantly reduced and no correlations were found between this parameter and the duration of lithium therapy, average S-Li, highest S-Li noted, diuresis or any of the calcium parameters. The morning diuresis was significantly increased in comparison with a control group with normal kidney function. 2 of the 4 polyuric patients had a decreased GFR, but in 1 case it was normalized on desmopressin supplementation. Renal biopsy in the patient with one S-Li of 2.35 and a low GFR in the consecutive series, and in 3 of the polyuric patients, revealed focal interstitial fibrosis and nephron atrophy. The mean S-Ca, S-Mg, S-PTH and bone mineral content were increased, but no significant intercorrelations between these parameters were found. Neither were any intercorrelations found between the calcium parameters and time on lithium therapy, average S-Li, highest S-Li noted or morning diuresis. In conclusion a relatively well-managed lithium therapy for up to 12.5 years does not seem to influence the GFR, even if renal biopsy in 4 of our patients revealed interstitial nephritis and data in the literature indicate a progressive interstitial nephritis. The present study did not support the proposition that polyuria is an alarming sign of pronounced renal lesion. Calcium metabolism is influenced by lithium therapy but from the clinical point of view no negative effects could be found. S-Ca should probably be checked regularly in patients on long-term lithium therapy.

Adult↗
PubMed1979

[Desobstructive sodium and water diuresis: pathophysiologic and clinical aspects of bilateral obstructive nephropathy (author's transl)].

The measurement of sodium and water loss after relieve of the obstruction shows that the obstructive nephropathy originates in three pathogenetic mechanisms. (1) Acute complete bilateral ureteric obstruction causes tubular atrophy, prevents both resorption and glomerular filtration, reduces the renal blood flow and increases the extracellular space by retention of water and products subject to urinary excretion. (2) Relieve of obstruction results in excess polyuria as blood flow and glomerular filtration recover rapidly, the extracellular space gets rid of its osmotic load, and the tubular dysfunction of resorption continues for several days until the epithelium has recovered from its pressure atrophy. All this will result in a high loss of sodium and water which requires adequate substitution; otherwise, natriuretic shock will result. (3) The chronic (bilateral) obstruction behaves in a similar way, yet is less reversible. The tubular damage is the same. Moderate polyuria occurs already during the stage of obstruction. Hereby the extracellular space decreases. After relieve of the obstruction the polyuria increases significantly, yet less rapidly than after acute obstruction as the glomerular function does not recover completely. The renal blood flow remains diminished, the vascular calibers stay narrowed, and the kidney remains shrunken. Loss of sodium and water will endanger the patient with chronic obstruction. Furthermore, the patient will be at risk due to dehydration, acidosis, anemia and uremia. The infusion therapy of the desobstructive nephropathy syndrome is based upon the venous pressure and the serum electrolytes which are measured twice daily.

Adult↗
PubMed1986

Medroxyprogesterone acetate induces diabetes insipidus in Chinese hamsters.

Injection of a synthetic progesterone, medroxyprogesterone acetate (MPA or Depo-ProveraR), a widely used contraceptive, into Chinese hamsters (Cricetulus griseus) induced a profound polyuria with daily output of dilute urine equal to about 50% body weight of the hamster. However, relatively normal ability for renal urine concentration was demonstrated by administration of exogenous vasopressin. Body weight did not increase during onset of MPA-induced polyuria or during interval of vasopressin-induced oliguria, suggesting that primary polydipsia was not etiologic. Administration of this steroid to Chinese hamsters was nontoxic, although these polyuric animals were unusually sensitive to water deprivation. This polyuria was not observed when progesterone alone was injected into Chinese hamsters or when MPA was given to other related hamster species (Armenian, Syrian, Turkish or Djzungarian). The MPA-injected Chinese hamster represents a unique model of vasopressin sensitive diabetes insipidus induced by a steroid in a species-specific fashion.

Animals↗
PubMed2002

Toxicological study of a new maintenance fluid, Veen 3G, in rats.

A study of the different volume and infusion rates of a new maintenance fluid, Veen 3G, on the general conditions of rats was investigated during the 14 days after infusion. In Experiment I, 100 ml/kg and 200 ml/kg of Veen 3G were infused at a rate of 300 ml/kg/h in male and female rats. Results were compared with those for Gurunon Ringer solution (GRS) in male and female rats. We observed only transient polyuria in animals administered by each dose of Veen 3G and GRS for 0-15 min after infusion. Necropsy was not observed in any of the animals tested 14 days after infusion. In Experiment II, 200 ml/kg of Veen 3G was infused at rates of 200, 400, 800 and 1600 ml/kg/h in male rats. At 800 and 1600 ml/kg/h, irregular respiration and decrease in movement were observed concomitantly with polyuria. Three out of 4 rats died immediately after the infusion of Veen 3G at a rate of 1600 ml/kg/h, and one rat was still alive 14 days after the infusion. In this experiment, 200 ml/kg Veen 3G was safe when we infused at a rate of less than 400 ml/kg/h in male rats. Since this rate is about 27-80 times higher than that used clinically in maintenance treatment, Veen 3G is suggested to be safe, with the exception of polyuria, in clinical situations at the standard infusion rate (5-15 ml/kg/h).

Animals↗
PubMed1998

Decreased aquaporin-2 expression and apical plasma membrane delivery in kidney collecting ducts of polyuric hypercalcemic rats.

Hypercalcemia is frequently associated with a urinary concentrating defect and overt polyuria. The molecular mechanisms underlying this defect are poorly understood. Dysregulation of aquaporin-2 (AQP2), the predominant vasopressin-regulated water channel, is known to be associated with a range of congenital and acquired water balance disorders including nephrogenic diabetes insipidus and states of water retention. This study examines the effect of hypercalcemia on the expression of AQP2 in rat kidney. Rats were treated orally for 7 d with dihydrotachysterol, which produced significant hypercalcemia with a 15 +/- 2% increase in plasma calcium concentration. Immunoblotting and densitometry of membrane fractions revealed a significant decrease in AQP2 expression in kidney inner medulla of hypercalcemic rats to 45.7 +/- 6.8% (n = 11) of control levels (100 +/- 12%, n = 9). A similar reduction in AQP2 expression was seen in cortex (36.9 +/- 4.2% of control levels, n = 6). Urine production increased in parallel, from 11.3 +/- 1.4 to a maximum of 25.3 +/- 1.9 ml/d (P < 0.01), whereas urine osmolality decreased from 2007 +/- 186 mosmol/kg x H2O to 925 +/- 103 mosmol/kg x H2O (P < 0.01). Immunocytochemistry confirmed a decrease in total AQP2 labeling of collecting duct principal cells from kidneys of hypercalcemic rats, and reduced apical labeling. Immunoelectron microscopy demonstrated a significant reduction in AQP2 labeling of the apical plasma membrane, consistent with the development 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.

Animals↗
PubMedDate not supplied

Disturbed vasopressin release in 4 dogs with so-called primary polydipsia.

Primary polydipsia is characterized by a marked increase in water intake and secondary polyuria, and in dogs often is described as a behavioral problem or a psychological disorder. We describe 4 dogs with primary polydipsia, diagnosed on the basis of a modified water deprivation test, in which further examination included serial measurements of urine osmolality (UOsm) and plasma vasopressin (VP) measurements during water deprivation and hypertonic saline infusion. The dogs, ranging in age from 4 months to 4 years, all were presented for evaluation of polyuria and polydipsia. Physical examination, routine blood chemistry, and urinalysis disclosed no specific cause for the polyuria and polydipsia. During serial measurements UOsm spontaneously reached high concentrations in 2 dogs, whereas in the other 2 dogs UOsm also fluctuated but on no occasion exceeded 1,000 mosm/kg. Primary polydipsia was diagnosed when UOsm exceeded 1,000 mosm/kg at the end of the modified water deprivation test and plasma osmolality did not exceed the upper limit of the reference range during testing. During water deprivation, plasma VP concentrations remained relatively low. The VP response to hypertonic saline infusion was abnormal, with an increased threshold value in 3 dogs, an increased sensitivity in 2 dogs, and an exaggerated response in 1 dog. It is concluded that some dogs fulfilling current criteria for primary polydipsia produce concentrated urine spontaneously throughout the day in a pattern similar to what has been observed in healthy pet dogs. This finding can be regarded as diagnostic and precludes the need for a water deprivation test. During water deprivation testing, all 4 dogs produced highly concentrated urine in the face of low basal plasma VP concentrations. The observed abnormal VP release in response to hypertonic stimulation may be interpreted as a primary disturbance in the regulation of VP secretion, although it might also be the result of overhydration caused by a primary abnormality in drinking behavior.

Animals↗
PubMed2003

Cryptococcal pyelonephritis in a dog.

A 5-year-old castrated male Golden Retriever was evaluated for polyuria, polydipsia, and progressive regurgitation thought to be a result of bacterial pyelonephritis and megaesophagus. Bacteriologic culture of urine failed to yield clinically relevant growth, and results of a urine sediment examination were normal. With time, intention tremors and progressive neurologic dysfunction were also observed. At necropsy, a diagnosis of cryptococcal disease was confirmed histologically and immunohistochemically. Findings in the dog of this report were indicative of nephrogenic diabetes insipidus with polyuria and polydipsia caused by cryptococcal pyelonephritis. Neurologic manifestations of systemic cryptococcus infection included megaesophagus, esophageal hypomotility, and regurgitation attributed to localization of cryptococcal organisms in the brain stem in the region of the dorsal motor nucleus of the vagus nerve. To the authors' knowledge, this is the first report of polyuria secondary to cryptococcal pyelonephritis.

Animals↗
PubMed1978

Water disturbances in patients treated with oral lithium carbonate.

Forty-eight patients treated with oral lithium carbonate and 20 control subjects were studied to define the causes of lithium-induced water disturbances. Measurement of plasma immunoreactive arginine vasopressin, plasma osmolality, and urine osmolality after a period of dehydration separated nephrogenic diabetes insipidus, cranial diabetes insipidus, and primary polydipsia, the three postulated mechanisms of lithium-induced polyuria. Seventeen patients had a urinary concentrating defect despite serum lithium concentrations in the therapeutic range. Ten of these patients had nephrogenic diabetes insipidus, one had results suggestive of cranial diabetes insipidus, but none had evidence of primary polydipsia. Symptoms of thirst and polyuria were poor indicators of the degree of hypo-osmolar urine. No patient had electrolyte abnormalities, and none had sufficiently severe polyuria to stop lithium treatment.

Adult↗
PubMed1976

The participation of the renal tubules to the metabolism of insulin.

The role of renal tubules was explored by two kinds of experiments: (1) inhibition of the tubular reabsorption of insulin by induced polyuria; (2) suppression of insulin filtration by ureter clamping; 1. Anaesthetized dogs maintained in normoglycaemia by glucose compensation were infused with crystalline and 125I-insulins. Polyuria was induced by: (1) saline-bicarbonate infusion; (2) furosemide with saline-bicarbonate infusion to replace urine losses; (3) massive infusion of mannitol. Inulin and paraminohippuric acid were used to estimate the glomerular filtration rate and the renal plasma flow. The permeability of the glomerular wall (pore radius and total area of the pores per unit of path length) was determined by measuring the sieving curve of 131I-polyvinyl-pyrrolidone fractions during basal and treatment periods. Mannitol infusion was able to bring the insulin/inulin clearance ratio up the values of the sieving coefficient of insulin (insulin filtration rate) without modifying the permeability of the glomerular wall; saline infusion displayed a similar effect; furosemide, only a minute one although it induced a more marked polyuria. 2. Clamping of the left ureter was performed on dogs with catheters inserted into the artery, the left renal vein, the pelvis and a renal lymphatic vessel. Almost complete suppression of the glomerular filtration was achieved. It slightly increased the high insulinic concentration of the renal lymph, entailed a 1/3 decrease in the extraction ratio of insulin and reduced by half its renal clearance. In conclusion, the tubules participate to the catabolism of insulin by two different mechanisms: (1) an uptake from the tubular fluid which can be inhibited by diuretics exerting their main action on the proximal tubules; (2) a direct catabolism from the interstitial fluid resulting from the large permeability of the peritubular capillaries to insulin.

Animals↗
PubMed1999

Disturbances in plasma sodium in patients with war head injuries.

Polyuria with marked plasma sodium disturbance was present in 39 of 224 patients with isolated craniocerebral war injuries. Twenty-one of these 39 patients had hyponatremia (sodium level < 130 mmol/l) and polyuria. Eight of them (38%) died within 30 days after trauma. The remaining 18 patients developed classic diabetes insipidus syndrome, and 6 of them (33%) died of hypernatremia within 30 days after trauma. The mortality in both patients with hyponatremia and patients with diabetes insipidus was higher in those with greater disturbances of plasma sodium concentration with polyuria and those with lower Glasgow Coma Scale scores.

Craniocerebral Trauma↗
PubMed2003

[Prenatal Bartter's syndrome. Report of two cases].

Antenatal Bartter Syndrome (ABS) is a rare autosomic recessive tubulopathy characterized by idiopathic hydramnios, fetal polyuria and elevated levels of amniotic chloride. It is related to mutations affecting several transporters in the loop of Henle e.g. the Na-K-2Cl cotransporter, the chloride channel CLC-NKB and the potassium channel ROMK. We report two cases of ABS in siblings born to consanguineous parents (first cousins). The first pregnancy showed hydramnios of unknown etiology at week 23. Two amnio drains were performed at weeks 26 and 27. The baby was born in week 29 and developed polyuria with hyponatremia, hypokalemia and hyperaldosteronism. After eliminating diabetes insipidus and adrenal insufficiency, ABS was diagnosed. The baby was treated with 0.5 mg/kg/d indomethacine, which controlled the polyuria and the hydroelectrolytic disorder. The second pregnancy showed idiopathic hydramnios at week 24. The elevated amniotic chloride level (above 112 mmole/l) led to the antenatal diagnosis of ABS. The mother was treated with 1 mg/kg/d indomethacine until week 31 in order to stabilize the hydramnios. Two amnio drains at weeks 31 and 33 allowed the pregnancy to be prolonged until week 34. A genetic study of the family showed homozygosity of the NKCC2 gene marker suggesting its implication in the disease.

Adult↗
PubMed1975

[Physiological basis of homeostasis of the extracellular fluid volume].

Renal, glomerular and tubular, factors responsible for the volume control of extracellular liquid were examined. The part played by angiotensin II in mediating the compensation of this liquid losses was studied in patients with spontaneous polyuria due to diencephalo-posthypophyseal diabetes insipidus or psychogenic polydipsia and healthy subjects with induced hypotonic polyuria. It was noted that: 1) acute expansion elicited a natriuretic response and increased distal sodium load, due to an increase in filtrate and relative inhibition of proximal reabsorption, or proximal inhibition if the filtrate was unchanged. The efficiency of distal sodium transport was often unchanged. 2) Return to sodium balance parity during prolonged expansion of volume, was accomplished by varying renal means, in accordance with the experimental model employed. Distal reabsorption was essentially depressed during prolonged saline load (secondary hypoaldosteronism). When protracted mineralcorticoid treatment was used, however, distal reabsorption was high, even in the escape stage, and its saturation required marked augmentation of the sodium load reaching the distal tubules. 3) Depletion of volume caused by protracted natriuretic treatment in spontaneous polyuria reduced both diuresis and sodium excretion. This resistance to the natriuretic effect of the drug followed intrarenal compensation that reduced the distal sodium load and encouraged reabsorption in some distal sites (secondary hyperaldosteronism). 4) Infusion of angiotensin II in sub- or pauci-pressor doses causes an isosmotic sodium saving, since it reduced the glomerular filtrate and increases the fraction of filtrate reabsorbed by the proximal tubules; the tubular effect is likely secondary to increased vascular, especially postglomerular resistance. In the healthy subject, angiotensin II leads to antidiuresis referable, on account of its intensity and longer time cycle, to ADH release angiotensin-dependent.

Angiotensin II↗
PubMed1987

The use of arginine vasopressin measurements in the polyuric dog.

The direct measurements of AVP during water deprivation and salt loading demonstrate the inability of the direct water deprivation test to distinguish accurately between several forms of polyuria. Polyuria and polydipsia are commonly formed disorders in the dog and can be caused by osmotic diuresis; deficient release of anti-diuretic hormone-arginine vasopressin (AVP); a decreased renal response to AVP; excessive water intake. The differentiation between these forms often requires a water deprivation test followed by administration of vasopressin. The latter test is an indirect one and relies upon changes in urinary concentration as index of vasopressin function. With this it is usually possible to differentiate total neurogenic diabetes insipidus and total nephrogenic diabetes insipidus. However, several dipsogenic forms and partial diabetes insipidus forms are still very difficult to distinguish from each other and only the direct measurement of plasma AVP (PAVP) can give conclusive information. The role of AVP in osmoregulation was investigated by measuring plasma osmolality (Posm) and PAVP during; hypertonic saline infusions; water deprivation in both healthy experimental dogs and in dogs with polyuria.

Animals↗
PubMed1971

Renal effects of long term administration of triamcinolone acetonide in normal dogs.

Triamcinolone acetonide was administered in excessive dosage to dogs to study the renal mechanism responsible for polyuria which is a clinically undesirable side effect of long term glucocorticoid therapy.Polyuria occurred coincident with a significant increase in urinary solute output. Although continuous administration of triamcinolone acetonide at 0.1 or 0.2 mg/lb/day caused a small but significant increase in creatinine output, the primary mechanism for the polyuria was increased solute excretion. Associated with the polyuria was pronounced hyperphagia and polydipsia. The cause of the hyperphagia was not established. The increase in electrolyte excretion caused by this synthetic steroid was probably compensated for by the hyperphagia. Because all the dogs showed muscle weakness and loss of body condition, it is likely that alteration in protein and amino acid metabolism was responsible for the hyperphagia.

Animals↗
PubMed1977

Partial deficiency of antidiuretic hormone in a cat.

Marked polydipsia and polyuria developed subsequent to trauma in a 1 1/2-year-old male Abyssinian cat. Diabetes insipidus was suspected, inasmuch as intramuscualr vasopressin administration resulted in amelioration of polydipsia and polyuria. However, hypertonic (3%) saline solution given intravneously resulted in anuria, an indication of antidiuretic hormone activity. Polyuria and polydipsia were abolished by oral chlorpropamide therapy, which was indirect evidence for partial deficiency of antidiuretic hormone.

Animals↗
PubMed1978

[A case of cerebral polyuric hyponatremia (author's transl)].

A case of cerebral polyuric hyponatremia was reported. A 64-year-old lady had complained of visual disturbance for 4 years. She was operated upon under the diagnosis of tuberculum sellae meningioma. Sever days following operation tremendous polyuria was senn, i. e. polyuria over 40 l/day, massive sodium wasting in the urine, hyponatremia and severe thirst feeling. These situations could not easily controlled by pitressin, and 2 days after the onset of polyuria the level of sodium in the serum decreased up to 112 mEq/l, the amount of excretion of sodium into urine increased up to 186 mEq/l, and the patient had finally a convulsive seizure followed by loss of consciousness. This hyponatremia was easily controlled by infusion of hypertonic NaCl. The pathogenesis of this condition could not be explained by applying the classical concept of "Diabetes Insipidus" nor "SIADH". This hyponatremia might be the result of massive sodium wasting in the urine. And from the results obtained in our patient, these conditions should be classified in the syndrome of "Cerebral Polyuric Hyponatremia" as reported by Oi et al. It should be emphasized that the measurement of osmorality and level of electrolytes in the serum and urine had to be performed frequently when the postoperative polyuric situation was found, so that the clinical diagnosis could be established in the earlier stage. The clinical diagnosis and differentiation of postoperative disorders in water and electrolytes of central origin were discussed.

Female↗