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American Journal of Kidney Diseases

Evaluation of Polyuria: The Roles of Solute Loading and Water Diuresis

  • Bhavna Bhasin
    Correspondence
    Address correspondence to Bhavna Bhasin, MD, 96 Jonathan Lucas St, Clinical Sciences Bldg, Rm 829 MSC 629, Charleston, SC 29425.
    Affiliations
    Division of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC
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  • Juan Carlos Q. Velez
    Affiliations
    Division of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC

    Section of Nephrology, Medical Service, Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC
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Published:December 10, 2015DOI:https://doi.org/10.1053/j.ajkd.2015.10.021
      Polyuria, defined as daily urine output in excess of 3.0 to 3.5 L/d, can occur due to solute or water diuresis. Solute-induced polyuria can be seen in hospitalized patients after a high solute load from exogenous protein administration or following relief of urinary obstruction. Similar clinical scenarios are rarely encountered in the outpatient setting. We describe a case of polyuria due to high solute ingestion and excessive water intake leading to a mixed picture of solute and water diuresis. Restriction of the daily solute load and water intake resulted in complete resolution of polyuria. Determination of the daily excreted urinary osmoles may yield important clues to the cause of polyuria and should be included in the routine workup of polyuria.

      Index Words

      Introduction

      Polyuria is an important clinical condition characterized by urine output in excess of 3.0 to 3.5 L/d and low urine osmolality of <300 mOsm/kg.
      • Makaryus A.N.
      • McFarlane S.I.
      Diabetes insipidus: diagnosis and treatment of a complex disease.
      • Singer I.
      • Oster J.R.
      • Fishman L.M.
      The management of diabetes insipidus in adults.
      Polyuria can be incapacitating for patients by disrupting their daily activities and sleep cycle. Polyuria can result in volume depletion, rapid fluctuations in serum sodium levels, and distension of the renal outflow tract due to high urinary output volume.
      • Oster J.R.
      • Singer I.
      • Thatte L.
      • Grant-Taylor I.
      • Diego J.M.
      The polyuria of solute diuresis.
      The differential diagnosis of polyuria includes central diabetes insipidus, congenital or acquired nephrogenic diabetes insipidus, psychogenic polydipsia, high protein or hyperglycemic osmotic diuresis, salt-wasting nephropathies, mixed polyuria due to excess solute and water intake, and postobstructive diuresis following recovery from urinary obstruction.
      • Oster J.R.
      • Singer I.
      • Thatte L.
      • Grant-Taylor I.
      • Diego J.M.
      The polyuria of solute diuresis.
      • Zerbe R.L.
      • Vinicor F.
      • Robertson G.L.
      Plasma vasopressin in uncontrolled diabetes mellitus.
      • Liamis G.
      • Liberopoulos E.
      • Barkas F.
      • Elisaf M.
      Diabetes mellitus and electrolyte disorders.
      • Popli S.
      • Tzamaloukas A.H.
      • Ing T.S.
      Osmotic diuresis-induced hypernatremia: better explained by solute-free water clearance or electrolyte-free water clearance?.
      • Visser L.
      • Devuyst O.
      Physiopathology of hypernatremia following relief of urinary tract obstruction.
      • Robertson G.L.
      Differential diagnosis of polyuria.
      • Goldman M.B.
      • Luchins D.J.
      • Robertson G.L.
      Mechanisms of altered water metabolism in psychotic patients with polydipsia and hyponatremia.
      • Bichet D.G.
      Nephrogenic diabetes insipidus.
      • Batlle D.C.
      • von Riotte A.B.
      • Gaviria M.
      • Grupp M.
      Amelioration of polyuria by amiloride in patients receiving long-term lithium therapy.
      • Qureshi S.
      • Galiveeti S.
      • Bichet D.G.
      • Roth J.
      Diabetes insipidus: celebrating a century of vasopressin therapy.
      • Michelis M.F.
      • Warms P.C.
      • Davis B.B.
      An approach to the diagnosis and therapy of hyponatremic states.
      • Uribarri J.
      • Oh M.S.
      • Carroll H.J.
      Salt-losing nephropathy. Clinical presentation and mechanisms.
      Osmotic diuresis, driven by high protein intake, is typically encountered in hospitalized patients fed with exogenous protein administered by the enteral or parenteral route.
      • Lindner G.
      • Schwarz C.
      • Funk G.C.
      Osmotic diuresis due to urea as the cause of hypernatraemia in critically ill patients.
      • Gault M.H.
      • Dixon M.E.
      • Doyle M.
      • Cohen W.M.
      Hypernatremia, azotemia, and dehydration ue to high-protein tube feeding.
      However, this phenomenon is not commonly observed outside the hospital setting. We describe a case of a woman who presented with concerns regarding polyuria and polydipsia of more than one year duration. The diagnostic principles used in this teaching case illustrate the approach to the evaluation of polyuria in an outpatient setting.

      Case Report

      Clinical History and Initial Laboratory Data

      A 40-year-old woman with a history of migraines, depression, and anxiety disorder presented for evaluation of polyuria of 1.5 years’ duration. She had maintained a voiding diary that showed a daily urine output of 6.5 to 9.6 L/d. She also reported nocturia, with a night-time voiding frequency of 2 to 3 times per night and nocturnal urine volume of 2.0 L. Her average daily fluid intake was >7.5 L. There was no history of hematuria or symptoms suggestive of urinary tract infection. One week prior to evaluation, she was referred to an endocrinology clinic to undergo a water deprivation test (Fig 1). Based on the interpretation of the test results, treatment with oral desmopressin was prescribed. This was complicated by the onset of headache and nausea within 48 hours of starting treatment. Serum sodium levels were obtained and found to be low at 128 mEq/L, and desmopressin therapy was immediately stopped.
      Figure thumbnail gr1
      Figure 1(Top panel) Serum osmolality, serum sodium, and (bottom panel) urine osmolality values obtained in our patient during the course of evaluation and follow-up.
      Results of a prior urologic assessment had been unremarkable. The patient had no significant surgical, social, or family history. Home medications included a stable dose of extended-release bupropion, 150 mg, daily; buspirone, 15 mg, 3 times a day; and clonazepam, 1 mg, 3 times a day as needed.
      On physical examination, the patient was noted to be slightly anxious, well nourished, and in no acute distress. Vital signs showed blood pressure of 124/74 mm Hg and pulse rate of 63 beats/min. She was afebrile, weight was 65 kg, and body mass index was 19.95 kg/m2. Skin turgor was normal, oral mucosa was moist, and no edema was noted. Findings from the rest of the examination were unremarkable.
      At the time of the evaluation, the patient had been restricting her fluid intake to 5.7 L/d and reported feeling “dehydrated.” Laboratory data showed serum sodium level of 143 mEq/L, serum osmolality of 295 mOsm/kg, and daily urine output of 7.8 L (Table 1). At this time, a 24-hour urine specimen was obtained to measure daily sodium, potassium, urea nitrogen, and creatinine excretion (Table 2). Results revealed remarkably high daily urinary excretion of 1,630 osmoles, suggesting high dietary solute intake.
      Table 1Laboratory Data
      1 wk Prior to Clinic Visit
      Laboratory results prior to starting the water deprivation test.
      Day of Clinic Visit
      Sodium, mEq/L139143
      Potassium, mEq/L4.204.20
      Chloride, mEq/L101107
      Bicarbonate, mEq/L3031
      Anion gap, mEq/L85
      Glucose, mg/dL8870
      SUN, mg/dL1615
      Serum creatinine, mg/dL0.90.9
      eGFR,
      Calculated by the CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) equation.29
      mL/min/1.73 m2
      8080
      Calcium, mg/dL9.09.4
      Serum osmolality, mOsm/kg286295
      Urine osmolality, mOsm/kg169214
      Daily urine output, L/d6.5-9.6
      Urine volume recorded by the patient in a voiding diary.
      7.8
      Note: Conversion factors for units: glucose in mg/dL to mmol/L, ×0.05551; SUN in mg/dL to mmol/L, ×0.357; creatinine in mg/dL to μmol/L, ×88.4; calcium in mg/dL to mmol/L, ×0.2495.
      Abbreviations: eGFR, estimated glomerular filtration rate; SUN, serum urea nitrogen.
      a Laboratory results prior to starting the water deprivation test.
      b Calculated by the CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) equation.
      • Levey A.S.
      • Stevens L.A.
      • Schmid C.H.
      • et al.
      A new equation to estimate glomerular filtration rate.
      c Urine volume recorded by the patient in a voiding diary.
      Table 2Daily Urine Output, Urine Solute Excretion, and Concomitant Serum Sodium Values
      Clinic Visit Day2 wk After Clinic Visit3 wk After Clinic VisitReference Range
      Serum sodium, mEq/L143143141134-146
      Urine volume, mL7,8004,1003,550<3,500
      Urine creatinine, g0.781.921.290.8-2.8
      Expected urine creatinine is 0.9 to 1.3g and is based on urine creatinine excretion of 15 to 20mg/kg per 24 hours (for females).30
      UNa, mmol1721726040-220
      UK, mmol179986625-125
      UUN, g261510.012-20
      Calculated urine osmoles1,6301,077600600-800
      Uosm, mOsm/kg214300-900
      Measured urine osmoles
       Osmoles from urea nitrogen928537347600-1,330
       Osmoles from sodium34434412180-440
       Osmoles from potassium35819613250-250
      Unmeasured osmoles39
      Note: Calculations and formulas used in this table are shown using the example of Clinic Visit Day:
      • 1.
        Calculation of urine osmolality:
        • 2 [UNa (mmol/L) + UK (mmol/L)] + (UUN (mg/dL)/2.8) + (Urine glucose (mg/dL)/18)
        • 2 [(172/7.8) + (179/7.8)] + [(333/2.8) + (0/18)] = 209 mOsm/kg
      • 2.
        Daily excretion of urine osmoles (calculated, ie, urine osmoles from formula (1) × 24-h urine volume):
        • 209 mOsm/kg × 7.8 L = 1,630 osmoles
      • 3.
        Daily excretion of urine osmoles (measured):
        • Measured Uosm × 24-h urine volume
        • 214 mOsm/kg × 7.8 L = 1,669 osmoles
      • 4.
        Unmeasured osmoles:
        • Measured osmoles − calculated osmoles
        • 1,669 − 1,630 = 39 osmoles
      Abbreviations: UK, urine potassium; UNa, urine sodium; Uosm, urine osmolality; UUN, urine urea nitrogen.
      a Expected urine creatinine is 0.9 to 1.3 g and is based on urine creatinine excretion of 15 to 20 mg/kg per 24 hours (for females).
      • Levey A.S.
      Measurement of renal function in chronic renal disease.

      Additional Investigations

      On obtaining additional dietary history, the patient reported consuming a high-protein diet that included 4 oz of meat at each meal and a protein shake (Premier Protein, Premier Nutrition Corporation, St. Louis, MO) with 30 g of protein and a protein bar (Pure Protein, United States Nutrition, Inc., Bohemia, NY) with 20 g of protein. Her daily protein intake amounted to 133 g (2.0 g/kg/d). She also reported eating spinach (two 5-oz servings per day), broccoli, and cantaloupe daily, explaining her high potassium intake of 179 mEq/d. At the same time, she was not restricting sodium intake in her diet.
      Therefore, the patient was advised to make dietary changes in order to restrict daily intake of sodium to <120 mEq/d, potassium to <100 mEq/d, and protein to 1.0 g/kg.

      Diagnosis

      Polyuria due to solute and water diuresis.

      Clinical Follow-up

      The patient successfully followed these recommendations. Three weeks later, a new 24-hour urine specimen was collected to re-examine her daily solute excretion and urine volume. Results showed a significant reduction in daily solute excretion (Table 2). She reported feeling less thirsty as these dietary changes took effect. Concomitantly, her nocturia and polyuria improved and urine volume returned closer to a normal range of 3.5 L/d. She did not require additional therapy and continues to do well at the present time.

      Discussion

      We present an interesting case of polyuria secondary to mixed water and solute diuresis with near-normal serum sodium levels. Polyuria may be seen in the inpatient setting due to administration of high protein feeds, uncontrolled hyperglycemia, and renal salt wasting due to cisplatin or cerebral salt wasting,
      • Lindner G.
      • Schwarz C.
      • Funk G.C.
      Osmotic diuresis due to urea as the cause of hypernatraemia in critically ill patients.
      • Gault M.H.
      • Dixon M.E.
      • Doyle M.
      • Cohen W.M.
      Hypernatremia, azotemia, and dehydration ue to high-protein tube feeding.
      • Cerda-Esteve M.
      • Cuadrado-Godia E.
      • Chillaron J.J.
      • et al.
      Cerebral salt wasting syndrome: review.
      • Sterns R.H.
      • Silver S.M.
      Cerebral salt wasting versus SIADH: what difference?.
      • Hamdi T.
      • Latta S.
      • Jallad B.
      • Kheir F.
      • Alhosaini M.N.
      • Patel A.
      Cisplatin-induced renal salt wasting syndrome.
      among other causes. However, solute diuresis leading to polyuria is rarely seen in the outpatient setting and may be easily confused with psychogenic polydipsia or diabetes insipidus. This interesting case highlights the importance of estimating daily solute excretion in the routine workup of polyuria. This essential step may often be overlooked but could be the answer to a perplexing clinical presentation, as seen in this patient (Fig 2).
      Figure thumbnail gr2
      Figure 2Proposed algorithm for the diagnostic approach to polyuria. Observed in cases of obstructive uropathy or unspecified acute kidney injury and chronic kidney disease (CKD). Abbreviations: DI, diabetes insipidus; Uosm, urine osmolality.
      Polyuria can be secondary to water or solute diuresis. Urine volume is in direct relation to the total number of osmoles excreted per day. Solutes responsible for driving water excretion could be electrolytes, such as sodium and potassium, or urea, glucose, and mannitol.
      • Levin A.
      • Klassen J.
      • Halperin M.L.
      Challenging consults: application of principles of physiology and biochemistry to the bedside. Osmotic diuresis: the importance of counting the number of osmoles excreted.
      The daily osmole excretion is estimated to be ∼10 mOsm/kg, or 500 to 750 mOsm/d, leading to obligate water losses with the solutes. When solute intake is >900 mOsm/d, a noticeable increase in urinary volume is seen.
      • Popli S.
      • Tzamaloukas A.H.
      • Ing T.S.
      Osmotic diuresis-induced hypernatremia: better explained by solute-free water clearance or electrolyte-free water clearance?.
      However, low solute intake leads to decreased free water excretion. This is often seen in patients with excessive consumption of beer and poor solute intake leading to hyponatremia.
      • Thaler S.M.
      • Teitelbaum I.
      • Berl T.
      “Beer potomania” in non-beer drinkers: effect of low dietary solute intake.
      • Srisung W.
      • Mankongpaisarnrung C.
      • Anaele C.
      • Dumrongmongcolgul N.
      • Ahmed V.
      A rare case of low-solute hyponatremia in a nonalcoholic person.
      The evaluation of polyuria includes performing a water deprivation test,
      • Sands J.M.
      • Bichet D.G.
      American College of Physicians, American Physiological Society
      Nephrogenic diabetes insipidus.
      which was done one week prior to the patient’s evaluation. The patient was able to achieve high urine osmolality of 650 mOsm/kg after 12 hours of water deprivation. Despite achieving high urine osmolality, the patient inappropriately received desmopressin at that point, which did not result in a further increase in urine osmolality (Fig 1). Subsequently, results of the test were mistakenly interpreted as partial central diabetes insipidus, which led the treating physician to prescribe oral desmopressin. As a result, the patient developed iatrogenic hyponatremia, reflecting her habitual excessive water intake. Psychogenic polydipsia remained in the differential diagnosis. However, this clinical entity often results in suppression of vasopressin and urine osmolality < 100 mOsm/kg at presentation,
      • Thompson C.
      • Berl T.
      • Tejedor A.
      • Johannsson G.
      Differential diagnosis of hyponatraemia.
      which was not the case in this patient. In search for other causes to explain the polyuria, we obtained a 24-hour urine collection for electrolytes, glucose, creatinine, and urea nitrogen. Her daily osmole excretion was calculated at 1,630 osmoles (Table 2), which is considerably higher than the expected average solute excretion based on a standard Western diet. We also performed a calculation for electrolyte free water excretion using the formula:
      Electrolytefreewaterexcretion=24-hurinevolume[1(UNa+UK)/SNa]


      where UNa is urine sodium, UK is urine potassium, and SNa is serum sodium. The calculation was noted to be high at 5.5 L.
      • Wesson Jr., L.G.
      • Anslow Jr., W.P.
      Effect of osmotic and mercurial diuresis on simultaneous water diuresis.
      • Goldberg M.
      Hyponatremia.
      • Nguyen M.K.
      • Kurtz I.
      Derivation of a new formula for calculating urinary electrolyte-free water clearance based on the Edelman equation.
      This can be attributed to osmotic diuresis from the high daily solute intake. Another important diagnostic indicator was the measured urine osmolality of 214 mOsm/kg, which is suggestive of a mixed polyuria rather than a pure solute or water diuresis
      • Oster J.R.
      • Singer I.
      • Thatte L.
      • Grant-Taylor I.
      • Diego J.M.
      The polyuria of solute diuresis.
      • Zerbe R.L.
      • Vinicor F.
      • Robertson G.L.
      Plasma vasopressin in uncontrolled diabetes mellitus.
      (Fig 1).
      Consequently, institution of dietary changes to decrease total protein and electrolyte intake was recommended to the patient, and she was able to successfully reduce her daily solute intake. With this intervention, urine volume decreased significantly from 7.8 to 3.5 L/d, thus confirming the role of solute loading and excessive water intake in causing her polyuria.
      The key difference in this case compared to intubated mechanically ventilated patients receiving total parenteral nutrition is that this patient drank water to match the urine losses and avoided significant hypernatremia. In contrast, intubated critically sick patients receiving total parenteral nutrition develop hypernatremia because they are unable to drink a copious amount of water to match the water losses. Polyuria persists as long as high solute intake does. If solute excretion diminishes, water loss diminishes and a decrease in thirst and water intake ensues.
      Serum sodium level was 143 mEq/L on initial evaluation. Although this value is close to normal, it is reflective of a mild degree of hypernatremia. The patient had attempted to restrict her water intake for 3 days preceding the evaluation. However, despite this restriction, she was still drinking a large amount of water and arrived mildly hypernatremic. Thus, this finding highlights the pivotal role of solute loading in inducing polyuria in this patient despite excessive water intake. If present alone, this would have otherwise led to hyponatremia. Subsequently, serum sodium levels normalized after the dietary modifications took place.
      In this age of health awareness, nutritional and protein supplements are abundantly available over the counter and heavily advertised to the general public or at athletic clubs and gymnasiums. Inadvertent increased solute intake through various dietary sources, including high-protein shakes, powders, and bars, can often be overlooked, leading to high solute excretion and polyuria. In parallel, the desire to stay well hydrated may result in excessive fluid intake and the ensuing phenomenon of habitual polydipsia.
      • Fenske W.
      • Allolio B.
      Clinical review: current state and future perspectives in the diagnosis of diabetes insipidus: a clinical review.
      As a result, an additive scenario of increased solute load and water diuresis can occur and mimic the clinical presentation of other more traditional forms of polyuria, such as diabetes insipidus or psychogenic polydipsia.
      In conclusion, accurate estimation of daily urinary osmole excretion, as well as the nature of the osmoles, are of paramount importance and should be included in the routine evaluation of polyuria (Box 1; Fig 2).
      Teaching Points
      • Polyuria is defined as urinary volume in excess of 3.0-3.5 L/d
      • Polyuria can be due to water diuresis or solute diuresis
      • Solute load is an important determinant of urinary volume
      • Solute diuresis may be seen in hospitalized patients who are given high protein feeds and following relief of urinary obstruction
      • High dietary solute intake can cause polyuria in the outpatient setting, particularly with unusually large ingestion of protein and fruits
      • Mixed polyuria due to solute loading and habitual excessive water intake can be seen in athletic individuals
      • Calculation of urinary osmoles and the nature of the osmoles is helpful in the diagnosis of solute diuresis
      • Estimation of daily osmole excretion should be included as a part of the routine workup for polyuria

      Acknowledgements

      Support: None.
      Financial Disclosure: The authors declare that they have no relevant financial interests.
      Peer Review: Evaluated by 2 external peer reviewers, the Feature Editor, the Education Editor, and the Editor-in-Chief.

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