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PubMed1986

Clinical features of hyperosmolar hyperglycemic nonketotic diabetic coma associated with cardiac operations.

Hyperosmolar hyperglycemic nonketotic diabetic coma after cardiac operations was reviewed in a total of 12 patients from the literature and from my experience in an attempt to determine the clinical features of this condition. Among the unique features of this disease were the following: The mortality is high (42%). The morbidity and mortality are higher in patients with no previous history of diabetes mellitus (67% and 50%) than in those with such a history (33% and 25%). Polyuria is usually a heralding symptom. There is an average time lag of 6 days between the onset of polyuria and the established diagnosis of hyperosmolar hyperglycemic nonketotic diabetic coma. The time lag in patients who died was 7.5 +/- 0.8 days (mean +/- standard error of the mean), significantly longer than in survivors (4.5 +/- 0.8 days). Polyuria usually emerges after the stormy immediate postoperative days have passed (on postoperative day 5.3 on the average). Polyuria is generally regarded as a favorable sign not suggestive of complicating hyperosmolar hyperglycemic nonketotic diabetic coma. Therapies known to precipitate this disorder are continued even after development of polyuria. Gastrointestinal bleeding can be a precipitating factor. Hyperalimentation or elemental diet may cause dehydration and trigger hyperosmolar hyperglycemic nonketotic diabetic coma. A high or rising serum sodium concentration and/or blood urea nitrogen level with polyuria may be a warning sign of this complication. Too hasty correction of the hyperosmolar state can be dangerous. Pulmonary dysfunction may be involved in the symptoms of hyperosmolar hyperglycemic nonketotic diabetic coma.

Adult↗

PubMed1999

Ureteral growth in animal models with increased renal excretion of urine.

The influence of increased functional load on the macroscopical and histological appearance of the ureter was investigated. Sixty rats were divided into five groups: (1) sucrose-fed rats with non-osmotic polyuria; (2) diabetic rats with osmotic polyuria; (3) uninephrectomized rats; (4) sham-operated control rats; and (5) control rats. The 24-hour urinary volume was measured on days 7, 14 and 21. Growth of the kidney, ureter and bladder was investigated and the histological appearance of the ureter was further evaluated. Diabetic and sucrose-fed rats had comparable polyuria with a seven-fold increase in urinary output. The urinary volume for the remaining kidney was doubled in uninephrectomized rats. After 3 weeks, diabetic rats had increased weight of the kidney, ureter and bladder, sucrose-fed rats had increased weight of the bladder, whereas uninephrectomized rats had increased weight of the kidney and ureter. The cross-sectional area (CSA) of the ureter wall from control rats increased from the proximal to the distal portion. The size of the whole ureter from diabetic rats was dramatically increased, the CSA of the wall of the distal ureter portion being four times that of the controls. The CSA of the ureter wall from sucrose-fed rats was increased only in the distal portion, whereas the ureter from uninephrectomized rats was increased only in the proximal portion. The results demonstrate the importance of differentiating between different portions of the rat ureter when examining histological sections of this organ. Moreover, polyuria per se is shown to induce growth of the bladder and of the adjacent distal part of the ureter, whereas uninephrectomy and diabetes caused growth of the kidney and the upper parts of the ureter, in addition to the growth induced by polyuria.

Administration, Oral↗

PubMed2000

Renal synthesis of prostacyclin and thromboxane in healthy women: differential effects of a short-term saline loading.

It is accepted that the urinary excretions of the stable metabolites of prostaglandin (PG)I2 and thromboxane(Tx) A2, 6-keto-PGF1alpha (6KPGF) and TxB2 respectively, provide an accurate estimate of both basal and stimulated renal synthesis of their precursors. The excretory profile of these metabolites has been evaluated in healthy women submitted to a short-term expansion in extracellular fluid volume. Salt retention (SR group, n=6) was induced by physiological saline (0.9% NaCl) i.v. infusions (2 L per day) over a period of 2 days. On the third day the increase in body weight was 0.92 +/- 0.27 kg (P<0.05). The results of the study have been compared to those previously obtained in normal balance of sodium and potassium (N group, n=20) and in induced salt depletion (SD group, n=14). A common study protocol was used. Basal values of plasma renin activity (PRA) and urinary aldosterone excretion were determined. Renal functional exploration [clearance (cl.) method] was performed during hypotonic polyuria (induced by oral water load) and subsequent moderate antidiuresis (induced by low-dose infusion of an antidiuretic hormone analogue). Urinary 6KPGF and TxB2 concentrations were estimated by RIA method and their urinary excretions were determined at both high and low urinary flow rates. The linear regressions of the urinary metabolite excretions vs. urinary flow rate were estimated by using the data obtained in both hypotonic polyuria and antidiuresis. Salt retention (SR vs. N group) was effective in decreasing the basal values of plasma renin activity and urinary aldosterone excretion. Moreover, during hypotonic polyuria it was effective in increasing the absolute and fractional excretions of sodium and chloride, in the absence of significant variations in mean arterial pressure and creatinine cl. Regarding urinary prostanoid excretions the following results were obtained. 1. Comparative data for hypotonic polyuria. In the SR vs. N group, the urinary excretion of 6KPGF was significantly higher, whereas that of TxB2 was not significantly different. In the SR vs. SD group, the urinary excretion of 6KPGF was not significantly different, whereas that of TxB2 was significantly lower. 2. Comparative data for the regression lines of the urinary prostanoid excretions vs. diuresis. In the SR vs. N group, the regression line slope for 6KPGF excretion was significantly higher, whereas that for TxB2 excretion was not significantly different. In the SR vs. SD group, the regression line slope for 6KPGF excretion was not significantly different, whereas that for TxB2 excretion was significantly lower. 3. Correlative data in the SR group during hypotonic polyuria. The plasma chloride concentration was positively correlated with urinary flow rate, absolute and fractional chloride excretions, and 6KPGF excretion but not with TxB2 excretion. In conclusion, functionally effective salt retention in healthy women induces a selective stimulation of renal synthesis of prostacyclin, unlike salt depletion, in which the synthesis of both PGI2 and TxA2 is upregulated.

6-Ketoprostaglandin F1 alpha↗

PubMed1987

Increased plasma levels of atrial natriuretic peptide (ANP) in patients with paroxysmal supraventricular tachyarrhythmias.

Atrial natriuretic peptide (ANP) is a cardiac hormone originating from atrial cardiocytes. It seems to be involved in the regulatory control of circulating volume and vascular tone. Plasma immunoreactive atrial natriuretic peptide (IrANP) was investigated in 22 patients with paroxysmal supraventricular tachyarrhythmia (16 with atrial fibrillation, 4 with atrial flutter, one with a Wolf-Parkinson-White syndrome (WPW) and one with atrial tachycardia). During the aute attack, IrANP was significantly increased (125.3 +/- 11.4 pmol/l) compared to samples obtained during convalescence (55.9 +/- 4.7 pmol/l). Heart rate (HR) was 144 +/- 4.3 beats/min during the arrhythmia and 75 +/- 2.6 during convalescence. The reduction of IrANP in plasma from the acute attack of tachycardia to follow-up was significantly related to the reduction of HR (p less than 0.05). Irrespective of type of paroxysmal supraventricular tachyarrhythmia, 50% of the patients experienced polyuria during the attack. This symptom was more frequent in younger patients with a shorter duration of tachycardia. Polyuria patients had a higher HR during the attack of supraventricular tachycardia. Even though polyuria was not always found in the patients with the highest IrANP values, the symptom was associated with significantly higher concentrations of IrANP in plasma compared to the non-polyuria group. We conclude that IrANP is increased in plasma during acute attacks of paroxysmal supraventricular tachycardia. Furthermore, the polyuria frequently associated with this condition may partly be due to excess release of ANP from cardiac myocytes.

Adult↗

PubMed1996

Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex.

Prolonged hypokalemia causes vasopressin-resistant polyuria. 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). Consequently, we studied the effect in rats of 11 days' potassium deprivation on urine production and AQP2 expression and distribution. Membrane fractions were prepared from one kidney, while the contralateral kidney was perfusion-fixed for immunocytochemistry. Immunoblotting and densitometry revealed a decrease in AQP2 levels to 27+/-3.4% of control levels (n=11, P<0.001) in inner medulla, and 34+/-15% of controls (n=5, P<0.05) in cortex. Urine production increased in parallel, from 11+/-1.4 to 30+/-4.4 ml/day (n=11, P<0.01). After return to a potassium-containing diet both urine output and AQP2 labels normalized within 7 d. Immunocytochemistry confirmed decreased AQP2 labeling in principal cells of both inner medullary and cortical collecting ducts. AQP2 labeling was predominantly associated with the apical plasma membrane and intracellular vesicles. Lithium treatment for 24 d caused a more extensive reduction of AQP2 levels, to 4+/-1% of control levels in the inner medulla and 4+/-2% in cortex, in association with severe polyuria. The similar degree of downregulation in medulla and cortex suggests that interstitial tonicity is not the major factor in the regulation of AQP2 expression. Consistent with this furosemide treatment did not alter AQP2 levels. In summary,hypokalemia, like lithium treatment, results in a decrease in AQP2 expression in rat collecting ducts, in parallel with the development of polyuria, and the degree of downregulation is consistent with the level of polyuria induced, supporting the view that there is a causative link.

Animals↗

PubMed1990

[An interesting case of pituitary apoplexy showing abnormality in water-electrolyte before and after surgery].

Cases which present abnormality in water-electrolyte before and after operation of pituitary adenoma are occasionally reported. The authors have encountered a case in which neurological symptoms became aggravated abruptly with pituitary apoplexy after admission, hyponatremia was noted before operation and polyuria, not hypotonic urine was observed after operation. As a result of an endocrinological examination which may have an influence on water-electrolyte (ADH, aldosterone, ANP, etc.) the ADH level in hyponatremia before operation was high at 6.8 pg/ml; so, it was taken as SIADH. According to a study at the time of polyuria after operation, the ADH level was normal at 2.4 pg/ml, the ANP level was abnormally high at 140 pg/ml and the specific gravity of the urine was kept at 1.010 or more. So, polyuria was considered due to abnormally increased content of serum ANP. In polyuria due to abnormally increased content of serum ANP, the osmotic pressure of the urine is maintained relatively well, which is a clinical feature evidently different from diabetes insipidus. After operation for pituitary adenoma, water-electrolyte should be controlled with polyuria due to abnormally increased content of serum ANP in addition to diabetes insipidus taken into consideration.

Atrial Natriuretic Factor↗

PubMed1976

Obstructive polyuric renal failure following renal transplantation.

In a previously nephrectomized patient with a well functioning renal allograft, acute renal failure with massive polyuria and hypertension developed. Relief of a periureteric obstruction resulted in rapid correction of all three. Pathogenesis of hypotonic polyuria is thought to be a defect in the collecting duct permeability to water, stimulating nephrogenic diabetes insipidus. Normal urinary dilution and acidification suggest intact function of the ascending loop of Henle and distal convoluted tubules. The quick reversal of polyuria and renal failure after obtaining relief of the obstruction suggest that both the decrease in the glomerular filtration rate and tubular dysfunctions are due to functional changes in the nephron rather than to organic damage, a possibility also borne out by the findings in a renal biopsy specimen showing normal glomeruli and intact tubular epithelial cells. Ureteric obstruction should be considered in any patient with renal failure and polyuria; it may be a correctable cause of hypertension.

Acute Kidney Injury↗

PubMed1981

Lithium prophylaxis and the kidney.

We reviewed the records of 44 patients under age 55 with bipolar affective disorder, who were without known systemic illness and receiving lithium prophylactically for a minimum of 6 months. We systematically collected all demographic, family history, and clinical side-effect data. In addition, laboratory results of renal function were compiled. Polyuria was the earliest and most frequent side effect of lithium therapy. Patients receiving other psychotropic medication, plus lithium, showed a significant increased prevalence of polyuria particularly after 3 months of exposure to medication, as compared to patients receiving lithium alone. The onset of polyuria was correlated with duration of lithium treatment and patient's age at initiation of therapy. Our data suggest that polypharmacy, duration of exposure to lithium ion and patient age each predict the development of delayed polyuria, a symptom consistent with interstitial nephritis.

Adult↗

PubMed1985

Increased urine volume in chronic schizophrenic patients.

Polydipsia and polyuria have a long association with schizophrenia. To assess the prevalence of polydipsia and polyuria in schizophrenia, urine volume was examined in medication-free chronic schizophrenic patients, normal controls, and nonschizophrenic patients. Mean urine volume was significantly higher in the schizophrenic patients (2319 +/- SD 2052 ml/24 hours) than in the other two groups (1054 +/- SD 471 ml/24 hours for nonschizophrenic patients and 1265 +/- SD 613 ml/24 hours for normals). Seven of 35 patients with schizophrenia but 0/7 nonschizophrenics had urine volumes greater than any normal control. Polyuria was associated with a good premorbid history and a positive neuroleptic response. Among polyuric patients, those with hyponatremia may represent a different, distinct subgroup. Neuroleptic treatment was associated with a further, significant increase in urine volume. Hence, polydipsia and polyuria appear to be relatively common in schizophrenia.

Adult↗

PubMed1989

Polyuric states in man.

This chapter reviews the pathophysiological basis for the mechanisms of polyuria and discusses the causes in detail. A small proportion of patients with CDI are of the idiopathic type, with the majority of causes due to trans-spenoidal surgery, head injury following road traffic accidents, and an autoimmune variant. Indirect methods of investigating polyuria are inaccurate in a significant proportion of cases, and the incorporation of measurements of plasma AVP into a water-deprivation test or hypertonic saline infusion can improve diagnostic accuracy. Non-osmotic tests of AVP secretion are of no value in the differential diagnosis of polyuria. Most patients with CDI can maintain water homeostasis with adequate fluid intake, but desmopressin is a convenient, effective and safe therapy which is recommended on both social and medical grounds. Treatment of NDI remains problematic, as neither thiazide diuretics or indomethacin can completely abolish polyuria, and fluid intake remains of primary importance.

Diabetes Insipidus↗

PubMed2002

AQP3, p-AQP2, and AQP2 expression is reduced in polyuric rats with hypercalcemia: prevention by cAMP-PDE inhibitors.

The purpose of this study was to evaluate whether hypercalcemia is associated with downregulation of renal aquaporins (AQPs), including AQP1, AQP2, phosphorylated AQP2 (p-AQP2), AQP3, and AQP4, and if this is the case, to test whether cAMP-phosphodiesterase (PDE) inhibitor treatment can prevent AQP downregulation and prevent the development of polyuria. Vitamin D-induced hypercalcemia in rats was associated with increased urine output and reduced urine osmolality, consistent with previous findings (Levi M, Peterson L, and Berl T. Kidney Int 23: 489-497, 1983). Semiquantitative immunoblotting revealed a significant reduction in the abundance of inner medullary AQP2 (52 +/- 6% of control levels), consistent with previous studies, and of AQP2, which is phosphorylated at the PKA phosphorylation consensus site serine 256 (p-AQP2; 36 +/- 8%). Moreover, AQP3 abundance was also significantly decreased (45 +/- 7 and 61 +/- 6% of control levels in inner medulla and whole kidney, respectively). Consistent with this, immunohistochemistry demonstrated reduced AQP3 immunolabeling along the entire collecting duct. AQP4 expression was not reduced. Surprisingly, total kidney AQP1 abundance was also reduced (60 +/- 6%). AQP1 expression was reduced in the cortex and outer stripe of the outer medulla (48 +/- 7%; i.e., in proximal tubules). In contrast, AQP1 levels were not changed in the inner stripe of the outer medulla or in the inner medulla (i.e., descending thin limbs and vasa recta). Treatment with the cAMP-PDE inhibitors rolipram and milrinone in combination (inhibiting PDE IV and PDE III isoenzymes) at day 2 and onward completely prevented the hypercalcemia-induced downregulation of AQP2 and AQP3 (but not AQP1) and completely prevented the development of polyuria. In conclusion, AQP3, AQP2, and p-AQP2 are downregulated and are likely to play critical roles in the development of polyuria associated with vitamin D-induced hypercalcemia. Moreover, PDE inhibitor treatment significantly prevented the reduced expression of collecting duct AQPs and prevented the development of polyuria.

Animals↗

PubMed1996

Bilateral ureteral obstruction downregulates expression of vasopressin-sensitive AQP-2 water channel in rat kidney.

Polyuria after release of bilateral ureteral obstruction (BUO) is frequently seen in patients with urological disorders. In this study, we examined the effect of BUO and release of BUO on the expression of the vasopressin-regulated water channel aquaporin-2 (AQP-2) in rat kidney. Ureters were obstructed for 24 h in all experiments, and BUO was either not released or released for 24 or 48 h or 7 days. Each group of experimental rats were matched with sham-operated controls. One kidney was used for membrane fractionation and immunoblotting, whereas the contralateral was fixed for immunocytochemistry. Immunoblotting demonstrated a significant reduction in AQP-2 expression in inner medullar during 24 h of BUO to 26 +/- 8% (P < 0.001). Release of BUO was associated with immediate onset of a predominant osmotic-dependent polyuria. Forty-eight hours after release of BUO, the reduction in AQP-2 expression persisted (19 +/- 8%, P < 0.001), concurrent with a marked nonosmotic postobstructive polyuria, as determined by a significant reduction in free-water clearance (-50 +/- 7 vs. -85 +/- 10 microliters.min-1.kg-1, P < 0.05). Immunofluorescence and immunoelectron microscopy confirmed the reduced levels of AQP-2 in collecting duct principal cells. Seven days after release, the renal excretion of water and electrolytes had almost normalized. However, the downregulation of AQP-2 was not partly reversed (49 +/- 14%, P < 0.001), and, consistent with this, the urinary concentrating capacity was significantly reduced 7 days after release to a 18-h period of thirst. This strongly suggests that the persistent downregulation of AQP-2 is the cause of the slow recovery in concentration capacity. In conclusion, BUO and release of BUO were associated with a marked reduction in expression of AQP-2, coincident with the development and maintenance of postobstructive polyuria. Thus reduced AQP-2 levels may represent an important factor in the slow recovery from postobstructive diuresis.

Animals↗

PubMed2002

Impaired urinary concentrating ability in genetically polyuric mice.

Newly recognized strain of mice with hereditary polyuria (PUS mice) was characterized. Polyuria was inherited as a single autosomal-recessive trait. At 15 weeks, PUS mice excreted hypotonic (urine osmolality: PUS;270.8 +/- 15.5 vs. cont.; 3,228.6 +/- 163.6 mosm/kg) polyuria (urine volume: PUS; 25.0 +/- 1.5 vs. cont.; 1.1 +/- 0.1 ml/day). In PUS mice, plasma osmolality was slightly elevated as well as urinary excretion of vasopressin (AVP). Although PUS mice could concentrate urine after 24 h water deprivation, urine osmolality remained low. Blunted response to continuous infusion of dDAVP, a synthetic V2 agonist, was also observed. These in vivo studies indicated renal resistance to AVP contributed to the polyuria in this strain of mice. Microanalysis of isolated tubular segments revealed that AVP-induced cAMP accumulation in cortical collecting ducts (CCD) of PUS mice was significantly lower (60%) with or without a phosphodiesterase inhibitor, IBMX. Vasopressin induced similar cAMP accumulation in medullary ascending limbs of Henle (MAL), and medullary collecting ducts (MCD) between PUS and control mice. In CCDs, PUS mice had low basal adenylate cyclase (AdC) activity and responded less to AVP and forskolin stimulation than control mice. No difference in cyclic AMP phosphodiesterase activity was detected between control and PUS mice. These results indicate that impaired cAMP accumulation due to low AdC activity may be related to the impaired renal concentrating ability observed in this new strain of mice.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1987

Diabetes insipidus with renal resistance to vasopressin in the desoxycorticosterone-treated dog: a possible role for prostaglandins.

We examined the release of vasopressin and the renal response to exogenous vasopressin before and during desoxycorticosterone acetate (DOCA) administration in the dog. As treatment with DOCA produced potassium loss, urine volume increased, urinary osmolality decreased, and urinary PGE2 tended to increase. The increase in urine volume was accompanied by increases in serum sodium, in plasma osmolality and in plasma arginine vasopressin. The threshold for vasopressin release measured during polyuria was higher than control but the rate of vasopressin release was unchanged. The DOCA-induced polyuria was not affected by treatment with vasopressin which further increased plasma vasopressin. Treatment with indomethacin which corrected the increase in urinary PGE2 excretion but not the hypokalemia, restored the renal responsiveness to vasopressin, decreased the secretion of vasopressin, and corrected the polyuria and the hypernatremia. These findings suggest that DOCA-induced polyuria is attributable to a decrease in renal responsiveness to vasopressin which may be mediated in part by an increase in the renal synthesis of prostaglandins.

Animals↗

PubMed1982

The role of prostaglandins in diabetes insipidus produced by desoxycorticosterone in the dog.

To determine the role of renal prostaglandins (PGs) in the renal response to desoxycorticosterone acetate (DOCA), dogs were studied on a constant diet in which sodium intake was restricted (2.5 meq/day) or high (115 meq/day). On the restricted sodium intake, DOCA (25 mg/day im for 6 days) did not affect urinary volume, sodium, potassium, PGE2, or PGF2 alpha. On the high sodium intake, DOCA produced sodium retention for 1 day and a sustained increase in urinary potassium with a fall in serum potassium to 3.1 meq/liter. Urine volume increased from 574 +/- 50 to 1726 +/- 177 ml/day (P less than 0.001) with a fall in urinary osmolality from 1545 +/- 122 to 495 +/- 55 mosmol/ liter (P less than 0.001) as serum sodium increased from 149.0 +/- 1.0 to 152.5 +/- 0.3 meq/liter (P less than 0.025) by the sixth day of DOCA. Urinary PGE2 and PGF2 alpha were unchanged during the first 2 days of DOCA, then increased progressively from control values of 261 +/- 60 and 1143 +/- 144 ng/day ng/day, respectively, to 730 +/- 62 (P less than 0.005) and 3013 +/- 479 ng/day (P less than 0.01), respectively. Potassium repletion during continued DOCA treatment restored urinary volume, osmolality, PGE2 and PGF2 alpha, and serum sodium to control values. Treatment with indomethacin during DOCA-induced hypokalemia, polyuria, hypernatremia, and increased urinary PG, restored urinary PGs to control values, and corrected the polyuria and hypernatremia without a change in serum potassium. Thus, DOCA produced potassium depletion, polyuria, increased urinary PGs, and hypernatremia in dogs on a high sodium intake but not in those on a restricted sodium intake. As polyuria and hypernatremia were corrected either by potassium repletion, which corrected the supranormal renal synthesis of PGs, or by indomethacin, which inhibited their synthesis, renal water loss was presumably the result of an increase in renal PG synthesis, probably stimulated by potassium depletion.

Animals↗

PubMed2004

Nocturnal enuresis in older adults.

BACKGROUND: Nocturnal enuresis is uncommon in older adults. The paucity of literature about this problem prompts us to review our cases to determine the management strategy. METHODS: Six older adults, including 2 females and 4 males, were evaluated for refractory nocturnal enuresis. Only 2 of them had minor daytime urge symptom. Most of them had failed in the treatment using anticholinergics and/or alpha-adrenergic blocker. Evaluation consisted of detailed medical history, voiding diary, and urodynamic studies. Clinical follow-up persisted for 12 months. We define nocturnal polyuria as nighttime urine amount being more than 35% of total daily urine amount. Bladder outlet obstruction in men was diagnosed based on the definition described by International Continence Society. RESULTS: The average age was 71 years (range 61-84). The average duration of the symptom was 3.1 months (range 0.5-6). Two patients had bladder outlet obstruction. Four patients used hypnotics for insomnia, which might result in difficult awakening on bladder distension. Nocturnal polyuria was found in 3 patients. Most patients had multiple factors contributing to their nocturnal enuresis except 1, who was found to have an enlarged prostate with chronic bladder distension. Specific treatments were given based on the causes for each patient. Hypnotics were discontinued for a certain meanwhile in some patients. Nocturnal polyuria was managed with afternoon diuretic or bedtime desmopressin. Bedtime anticholinergic agent was used in patients with detrusor overactivity. The patient with enlarged prostate and urinary retention was managed with indwelling catheter followed by elective transurethral prostatectomy. All patients were dry in the night following the treatment. CONCLUSIONS: Nocturnal enuresis in older adult is usually multi-factorial. Hypnotic usage and nocturnal polyuria are frequently overlooked. Detailed investigation is necessary to identify the causes. Tailored treatment may achieve satisfactory results.

Aged↗

PubMed1995

Challenging consults: application of principles of physiology and biochemistry to the bedside. Osmotic diuresis: the importance of counting the number of osmoles excreted.

Polyuria is usually the result of a water diuresis or an osmotic diuresis. Traditionally, the assessment of the extracellular fluid (ECF) volume and the concentration of Na+ in plasma is sufficient to differentiate between the two. We present a case and our approach, which is based on calculations and quantitation of osmoles, to demonstrate the utility of this approach. A patient with diabetes mellitus, human T-cell lymphocyte virus, type 1 (HTLV-1) associated lymphoma, and hypercalcemia presented with marked ECF volume contraction and polyuria. A spot urine osmolality was 567 mOsm/kg H2O in the face of urine output of approximately 6 L/d. The initial diagnosis was an osmotic diuresis. However, a quantitative analysis revealed the enormous number of osmoles could not be accounted for physiologically. Hence, we postulated a water diuresis to be the cause of the polyuria. To confirm this hypothesis, we found that at different times during his hospitalization, the urine specific gravity ranged from 1.005 to 1.022, and urine output varied markedly over 8-h periods. Despite a plasma sodium of 147 mmol/L, the patient did not complain of thirst. Taken together, this suggested the presence of a hypothalamic lesion which caused central diabetes insipidus with variable output of antidiuretic hormone together with a blunted thirst response. Illustration of the utility of a quantitative approach to polyuria is the focus of the discussion.

Chlorides↗

PubMed2004

Prevalence, impact on the quality of life and pathophysiological determinants of nocturia in urinary incontinent women.

The objective of this study was to estimate the prevalence of nocturia in incontinent women in a urogynaecologic practice and its association with the quality of life and to estimate the prevalences of the pathophysiological categories among nocturics. From 1 January 2002, all patients with complaints of urinary incontinence were analysed according to a specific protocol: multichannel urodynamic testing, a 1-h International Incontinence Society (ICS) pad test and a 3-day frequency-volume (FV) chart. From 1 June 2002, subjects had to fill in a standardised quality of life questionnaire as well. Nocturia was defined as two or more micturitions per night calculated from the FV chart. Evaluable FV charts were received from 111 patients, and 72 patients completed the questionnaires correctly. The overall prevalence of nocturia was 48.6% (confidence interval: 43.9-53.3%). Nocturia had a negative impact on several aspects of the quality of life. The maximum voided volume was significantly (p=0.005) less in nocturics. The 24-h frequency was higher in nocturics (p=0.001). Nocturics lost more urine during the pad test (p=0.039). The multivariate logistic regression analysis showed that the greater the proportion of 24-h urine excreted at night, the greater the odds of having nocturia and that the lesser the maximum voided volume, the greater the odds of having nocturia. The majority (92.7%) of the nocturics can be classified into one of the responsible pathophysiologic categories: nocturnal polyuria in 51.2%, a low functional bladder capacity in 14.6%, a combination of both in 9.8%, polyuria in 4.9% and a combination of polyuria and nocturnal polyuria in 12.2% of the cases. Nocturia is a frequent symptom among urinary incontinent patients, with a negative impact on several aspects of the quality of life. With a FV chart, nocturics can be classified into one of the responsible pathophysiologic categories in the majority (92.7%) of the cases.

Adolescent↗