Polyuria

Polyuria is defined as the passage of large volumes of dilute urine, in excess of 2L/m2/day or approximately 40mL/kg/day in older children and adults.

From: Complications in Neuroanesthesia , 2016

Posterior Pituitary

Shlomo Melmed MB ChB, MACP , in Williams Textbook of Endocrinology , 2020

Approach to the Differential Diagnosis of Polyuric States

The first diagnostic step is to confirm polyuria, because up to 15% of patients referred for investigation of polyuria have urinary frequency due to bladder wall defects, infection, or prostate disease, with normal urine volume. A 24-hour urine volume greater than 50 mL/kg body weight is worthy of further investigation. Diabetes mellitus, hypercalcemia, hypokalemia, and chronic renal failure are excluded by biochemical tests. Urine osmolality should be low in all polyuric states; however, a random urine osmolality above 700 mOsm/kg excludes diabetes insipidus and makes the diagnosis of primary polydipsia certain. Presenting serum sodium concentration is almost always normal in diabetes insipidus, but results at the higher part of the reference range are more suggestive of DI than primary polydipsia. However, it is difficult to confidently distinguish between CDI, NDI, and thirst disorders solely on baseline laboratory measurements, so osmotic stimulation of the posterior pituitary is needed to secure a firm diagnosis.

The water deprivation test, which incorporates a dehydration step followed by a desmopressin challenge, is usually the first line of investigation. The interpretation of the initial period of water deprivation is based on the understanding that a functioning osmoregulatory system will respond to elevation of plasma osmolality with the secretion of vasopressin and subsequent concentration of the urine. As the test progresses, urine volume decreases and urine osmolality rises usually to over 750 mOsm/kg H2O. Importantly, an adequate osmotic stimulus to AVP secretion is necessary; a plasma osmolality of over 295 mOsm/kg H2O is needed to stimulate sufficient AVP to maximally concentrate the urine. In primary polydipsia urine should concentrate relatively normally, as AVP secretion is normal, whereas in patients with either CDI or NDI, urine remains dilute at the end of dehydration. The second part of the test, the administration of desmopressin, is designed to differentiate CDI from NDI. As patients withCDI are deficient in AVP, exogenous desmopressin concentrates urine osmolality, whereas patients with NDI do not respond to the antidiuretic effects of desmopressin and do not concentrate urine appropriately. The water deprivation test is best performed in a specialized center. Careful patient supervision to monitor for surreptitious drinking is important, and body weight is checked as patients with severe CDI can develop hypernatremia when fluid is withheld due to excess urination. In addition, there are subtleties of interpretation of results that must be considered. Although the water deprivation test differentiates between primary polydipsia, CDI, and NDI in classic and complete cases, published data have shown that accurate diagnosis was made in only 70% of polyuric patients, and the correct diagnosis in primary polydipsia was concluded in only 41% of cases. 161 A number of confounding factors can produce misleading or uninterpretable results:

1.

Patients with prolonged severe polyuria may not concentrate urine in response to endogenous or exogenous vasopressin. Chronic hypoosmolality suppresses AVP secretion, and in the absence of V2 receptor stimulation intracellular aquaporin 2 is not generated. Patients with thirst disorders may therefore be classified as partial DI on the basis of a subnormal rise in urine osmolality during the water deprivation step, despite normal AVP responses. For the same reason, receptor stimulation with desmopressin in step 2 might not stimulate increased urine concentration in patients with CDI, leading to an erroneous diagnosis of NDI.

2.

In patients with partial CDI, upregulation of V2 receptors can result in urine concentration with relatively low plasma AVP concentrations.

3.

High plasma AVP concentrations achieved by fluid deprivation in NDI can partially overcome renal resistance; urine osmolality can rise to over 300 mOsm/kg H2O, leading to diagnostic confusion with partial CDI. 162

The Paraclinic Examination

Dr. Manuela Stoicescu , in Medical Semiology Guide of the Renal System, 2020

5.1.1.1 Polyuria

Polyuria increases uresis to more than 2000 mL/24 h, which results in an increase in the glomerular filtration or decrease in the tubular reabsorption of water.

Polyuria could be occasional or permanent. Permanent or occasional polyuria can appear in a few special situations such as the following:

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Increased consumption of liquids

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Eating diuretic foods—watermelon, alcohol, coffee

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Very stressful or emotional situations because of increased levels of catecholamines in the circulation

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Exposure to cold because of vasoconstriction

In all these occasional physiological situations, polyuria could appear, but this is for a short period of time, only when these conditions exist, and after that the polyuria disappears and the volume of urine becomes normal.

There also exist a few pathologic situations in which polyuria could appear occasionally:

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Paroxysmal arrhythmias

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Crisis of chest pain like pectoral angina or acute myocardial infarction

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Gallbladder colic, renourethral colic

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Epilepsy

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In patients with edema in the context of cardiac failure disease, after diuretic therapy

These are a few examples of pathologic situations during conditions of stress and increased catecholamine levels, which can induce an occasional polyuria, and at the end of crisis, the urine volume becomes normal.

In persistent polyuria, the phenomenon is permanent and could be classified depending on the density of the urine in two important categories:

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Hypotonic polyuria

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Isotonic polyuria

The difference between hypotonic and isotonic polyuria depends on the urine osmolality and the plasma osmolality, and these depend on the concentration of sodium in the plasma and urine as well.

The definition of hypotonic polyuria states that the level of urine osmolality is decreased more than 200 mOsm/100 mL compared with the plasma osmolality.

Hypotonic polyuria appears in the following diseases:

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Kidney insipid diabetes mellitus

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Kidney failure developing polycystic kidney disease, chronic pyelonephritis

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Metabolic imbalance—hypokalemia, hypercalcemia

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Intoxication with antibiotics like aminoglycosides or others

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Disorders of Water Balance

Alan S.L. Yu MB, BChir , in Brenner and Rector's The Kidney , 2020

Differential Diagnosis of Polyuria

Before beginning involved diagnostic testing to differentiate among the various forms of DI and primary polydipsia, the presence of true hypotonic polyuria should be established by measurement of a 24-hour urine for volume and osmolality. Generally accepted standards are that the 24-hour urine volume should exceed 50 mL/kg BW, with an osmolality lower than 300 mOsm/kg H 2O. 219 Simultaneously, there should be a determination of whether the polyuria is due to an osmotic agent such as glucose or intrinsic renal disease. Routine laboratory studies and the clinical setting will usually distinguish these disorders; diabetes mellitus and other forms of solute diuresis usually can be excluded by the history, routine urinalysis for glucose, and/or measurement of the solute excretion rate (urine osmolality × 24-hour urine volume [in liters] > 15 mOsm/kg BW/day). There is general agreement that the diagnosis of DI requires stimulating AVP secretion osmotically and then measuring the adequacy of the secretion by direct measurement of plasma AVP levels or indirect assessment by urine osmolality.

In a patient who is already hyperosmolar, with submaximally concentrated urine (i.e., urine osmolality < 800 mOsm/kg H2O), the diagnosis is straightforward and simple; primary polydipsia is ruled out by the presence of hyperosmolality, 219 confirming a diagnosis of DI. CDI can then be distinguished from NDI by evaluating the response to the administration of AVP (5 units subcutaneously) or, preferably, of the AVP V2 receptor agonist desmopressin (1-deamino-8-d-arginine vasopressin [DDAVP], 1−2 µg subcutaneously or intravenously). A significant increase in urine osmolality within 1 to 2 hours after injection indicates insufficient endogenous AVP secretion, and therefore CDI, whereas an absent response indicates renal resistance to AVP effects, and therefore NDI. Although conceptually simple, interpretational difficulties can arise because the water diuresis produced by AVP deficiency in CDI produces a washout of the renal medullary concentrating gradient and downregulation of the kidney AQP2 water channels (see earlier), so that initial increases in urine osmolality in response to administered AVP or desmopressin are not as great as would be expected. Generally, increases of urine osmolality of more than 50% reliably indicate CDI, and responses of less than 10% indicate NDI, but responses between 10% and 50% are indeterminate. 147 Therefore, plasma AVP levels should be measured to aid in this distinction; hyperosmolar patients with NDI will have clearly elevated plasma AVP levels, whereas those with CDI will have absent (complete) or blunted (partial) AVP responses relative to their plasma osmolality (seeFig. 15.11). Because it will not be known beforehand which patients will have diagnostic versus indeterminate responses to AVP or desmopressin, a plasma AVP level should be determined prior to AVP or desmopressin administration in patients with hyperosmolality and inadequately concentrated urine without a solute diuresis.

Polyuria

Mitchell L. Halperin MD, FRCPC , ... Marc B. Goldstein MD, FRCPC , in Fluid, Electrolyte and Acid-Base Physiology (Fourth Edition), 2010

Introduction

Polyuria is due to either a water or an osmotic diuresis. Many patients who present with polyuria also have hypernatremia because they excrete a large volume of urine with a low concentration of Na + plus K+ (e.g., patients with diabetes insipidus or a urea-induced osmotic diuresis). Hence, there are areas of overlap between this chapter and the previous one on hypernatremia. Nevertheless, there are a number of issues that are pertinent to polyuria, and they are the focus of this chapter.

OBJECTIVES

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To illustrate that polyuria should be defined based on principles of physiology that determine the urine volume in a certain setting rather than be defined by a larger than usual urine volume.

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To illustrate that a large water diuresis can occur only if the distal nephron is virtually impermeable to water (lacks actions of vasopressin). In this setting, the magnitude of the water diuresis depends on the volume of hypotonic fluid delivered to the distal nephron and how much water is reabsorbed via residual water permeability in the inner medullary collecting duct.

▪

To emphasize that because actions of vasopressin must be present during an osmotic diuresis, the urine flow rate depends directly on the number of effective osmoles excreted and inversely on the medullary interstitial effective osmolality.

Case 12-1: Oliguria with a Urine Volume of 4 Liters per Day

(Case discussed on page 410)

A 22-year-old woman lives in a hot climate and runs each day to keep fit. She is very careful not to eat "unhealthy" foods, and she restricts her salt intake. She typically drinks a large volume of water. Her daily urine volume is 4 L. On repeated measurements done on visits to the office of her physician, her PNa was close to 130 mmol/L and her UOsm was close to 80 mOsm/kg H2O.

Questions

Does this patient have polyuria?

What dangers related to Na+ and water may develop in this patient?

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Nocturia

Alan W. Partin MD, PhD , in Campbell-Walsh-Wein Urology , 2021

Mixed Nocturnal Polyuria and Diminished Global and Nocturnal Bladder Capacity

In a review of 194 consecutive patients with nocturia, 13 (7%) had nocturnal polyuria (NPi >0.35), 111 (57%) had decreased nocturnal bladder capacity, and 70 (36%) had a "mixed" cause. Forty-five (23%) also had polyuria (defined as 24-hour urine output >2500 mL). Nocturnal polyuria was a significant component of nocturia in 43% of the patients. Thus the cause of nocturia was found to be multifactorial and often unrelated to an underlying urologic condition ( Weiss et al., 1998). In a US veteran population of men 50 years of age and older, Vaughan et al. demonstrated a significant improvement in ANV (P < .001), bother (P < .001), time to initiating sleep (P = .003), time to return to sleep (P = .03), and quality of sleep (P < .001) after single or combined pharmacotherapy and/or behavioral modification to address the mixed etiologic category of nocturia (Vaughan et al., 2009). Behavior modification included reduced caffeine and alcohol intake, limited nighttime fluid intake, and improved sleep hygiene through moderate exercise and attention to room temperature, noise, and lighting. Additional interventions included early evening leg elevation and compression stockings if patients had bilateral lower extremity edema. Also, if patients had BPH-related symptoms (American Urological Association symptom score ≥8, maximum uroflow [Qmax] 4 to 15 mL/sec), terazosin was titrated as tolerated/needed to 10 mg daily. If patients reported eight or more voids in 24 hours, Tolt ER 2 to 4 mg daily was initiated. If return to sleep required 30 minutes or more after an awakening, zaleplon 5 mg nightly after the first nocturia episode between 11:00 PM and 3:00 AM was recommended. This proved to be a structured, multimodal approach with little risk (one trip to an emergency room for hypotension after taking terazosin) (Vaughan et al., 2009). Multicomponent treatment was further found to be an effective strategy to treat nocturia in a study byJohnson et al. (2013) in which men on α-blockers received individually titrated drug therapy (extended-release oxybutynin) or multicomponent behavioral treatment (pelvic floor muscle training, delayed voiding, and urge-suppression techniques). Participants with two or more episodes of nocturia at baseline showed larger changes with behavioral treatment compared with antimuscarinic therapy (mean reduction = 1.26 vs. 0.61, respectively;P = .008).

Polyuria

Kamel S. Kamel MD, FRCPC , Mitchell L. Halperin MD, FRCPC , in Fluid, Electrolyte and Acid-Base Physiology (Fifth Edition), 2017

Introduction

Polyuria is caused by either a water diuresis or an osmotic diuresis. Many patients who present with polyuria also have hypernatremia because they excrete a large volume of urine with a low concentration of sodium (Na +) plus potassium (K+) ions (e.g., patients with diabetes insipidus [DI] or patients with a urea-induced osmotic diuresis). Therefore, there are areas of overlap between this chapter and the previous one on hypernatremia. Nevertheless, there are a number of issues that are pertinent to polyuria, which are the focus of this chapter.

Abbreviations

DI, diabetes insipidus

RWP, residual water permeability

MCD, medullary collecting duct

PNa, concentration of sodium (Na+) ions in plasma

UOsm, urine osmolality

POsm, plasma osmolality

AQP, aquaporin water channel

PCT, proximal convoluted tubule

DCT, distal convoluted tubule

DtL, descending thin limb

TAL, thick ascending limb

MCD, medullary collecting duct

EABV, effective arterial blood volume

V2R, vasopressin receptor 2

PGlucose, concentration of glucose in plasma

PUrea, concentration of urea in plasma

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Renal Toxicology

E. Ulozas , in Comprehensive Toxicology, 2010

7.14.2.2.4 Urinary concentrating defect

Polyuria and decreased urinary concentrating ability are common in patients receiving AmB ( Bendz and Aurell 1999; Sawaya et al. 1995). Patients with AmB-induced polyuria are unable to maximally concentrate their urine in response to water deprivation or after exogenous vasopressin administration (Barbour et al. 1979). Polyuria and impaired renal concentrating ability, unresponsive to desmopressin administration, have also been demonstrated in a rat model of AmB nephrotoxicity (Mayer et al. 2002). As mentioned previously, hypokalemia is a common consequence of AmB administration and it is also a known cause of diabetes insipidus (Nielsen 2002; Rubini 1961). In vitro experiments showed that AmB inhibited vasopressin-stimulated water and urea permeability in rat inner medullary collecting ducts (Yano et al. 1994). Decreased aquaporin-2 expression in the inner and outer medulla was demonstrated in rats with AmB-induced renal failure and diabetes insipidus (Kim et al. 2001). Possible nephrogenic diabetes insipidus has also been reported in a patient receiving liposomal AmB formulation (Canada et al. 2003).

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Diabetes Insipidus

Detlef Böckenhauer , in Comprehensive Pediatric Nephrology, 2008

Obstructive Uropathy

Polyuria after the release of urinary tract obstruction is a well-recognized phenomenon (postobstructive diuresis). However, if obstruction is incomplete, it is often associated with polyuria as well. Animal studies show a decreased level of AQP2 expression with bilateral ureteric obstruction. 54 Experiments with unilateral obstruction show a marked decrease in AQP2 in the obstructed kidney, which is consistent with the view that local factors, such as increased pressure, affect AQP2 expression. 55 Supporting this view is also the fact that other signs of distal tubular dysfunction are usually present in obstructive uropathies, like hyperkalemia and acidosis. The downregulation of AQP2 persists for up to 30 days after the release of the obstruction, thus explaining the postobstructive diuresis. 30

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WATER BALANCE AND REGULATION OF OSMOLALITY

Michael J. Field MD, BS, BSc(Hons), FRACP , ... Carol A. Pollock MB, BS, PhD, FRACP , in The Renal System (Second Edition), 2010

Causes and assessment of polyuria

In principle, a high urine flow rate may be produced either by a primary increase in solute excretion or by a primary increase in water excretion.

Polyuria caused by solute diuresis results from the delivery of a high load of solute through the nephron, either as a result of filtration of a poorly reabsorbed solute, or of blunted reabsorption of a solute normally transported out of the tubular fluid. (Note that increased glomerular filtration rate (GFR) per se is not a common cause of polyuria, largely because of glomerulotubular balance; see Chapter 2). The first mechanism applies to the osmotic diuresis produced by infusions of mannitol, which cannot be reabsorbed from the nephron and hence traps water osmotically within the tubular lumen, resulting in a high urine flow rate. Osmotic diuresis can also occur during disease states, notably in uncontrolled diabetes mellitus. In this case, increased plasma glucose concentrations result in the filtration of a glucose load greater than that which can be reabsorbed by the proximal tubule glucose reabsorption mechanism (saturation of the sodium–glucose cotransport carrier), leading to glycosuria accompanied by increased water flow because of the osmotic effect of the glucose trapped in the lumen. This mechanism accounts for the polyuria and dehydration encountered in newly presenting or uncontrolled insulin-dependent diabetes. A broadly similar mechanism is occasionally seen during the development of chronic kidney disease, where high levels of urea have a diuretic effect.

The second mechanism for solute diuresis is that produced by the commonly used diuretic drugs, which act to block the specific mechanisms for sodium reabsorption in discrete segments of the nephron (see Chapter 2). Polyuria of this cause is most prominent soon after commencement of the diuretic drug.

Water-based or dilute polyuria has a quite different mechanism, and can arise in one of two ways. First, a high intake of water will lead directly to a high output of dilute urine, through mechanisms to be described in this chapter. While a history of excessive water drinking might be expected in this situation, covert overdrinking is sometimes encountered in patients with psychiatric disturbances (psychogenic polydipsia). An alternative mechanism for polyuria associated with dilute urine is when the primary disorder involves the kidney's inability to concentrate the urine normally. The physiological defects giving rise to this condition, known as diabetes insipidus, will be detailed further below.

Table 3.1 illustrates some differential features in the diagnostic approach to polyuria. Of particular interest in this case and for the subject matter of this chapter, is the differentiation between the two forms of water diuresis. While in both forms the urine is dilute with low osmolality, in the case where the diuresis is being driven by high water intake the plasma would be expected to have a low osmolality, resulting directly from excessive water reabsorption from the gut. In the case of impaired urinary concentration mechanisms, the plasma osmolality would be high since the primary problem is excessive loss of water from the ECF into the urine.

By reference to Table 3.1, Mr Underwood's polyuria cannot be attributed to glucose or sodium as solutes, but is a water diuresis. Since the plasma sodium and osmolality are above the normal range, we can deduce that his problem arises from impaired urine concentration mechanisms rather than forced water drinking.

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Volume 1

Daniel G. Bichet , in Seldin and Giebisch's The Kidney (Fifth Edition), 2013

Polyuria and Nocturia in Diabetes Insipidus, Nocturnal Polyuria in Enuretic Children

Polyuria could be constant during the day but also present at night: the urine is normally most concentrated in the morning due to lack of fluid ingestion overnight and increased vasopressin secretion during the late sleep period. 209 Neurons in the suprachiasmatic nucleus, the brain biological clock, send axonal projections toward the supraoptic nucleus, one of the hypothalamic nuclei producing vasopressin, 5 providing a possible anatomical substrate for the circadian modulation, an osmoregulatory gain during the late sleep period. 209 As a result, the first manifestation of a mild-to-moderate loss of concentrating ability is often nocturia. However, nocturia is not diagnostic of a defect in concentrating ability, since it can also be caused by other factors such as drinking before going to bed or, in men, by prostatic hypertrophy, which is characterized by urinary frequency rather than polyuria. Psychogenic polydipsic patients tend to ingest large amounts of fluid during the day but not at night, therefore nocturia is rarely seen in primary polydipsic patients. 199 The pattern of nocturnal polyuria in enuretic children is similar to that observed in acute sleep deprivation, and enuresis in children might be related to the failure of sleep to cause a reflex reduction in arterial pressure and urine production. 210,211

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