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Human Physiology · Renal system

Water Balance and Urine Concentration

The kidney can make urine more dilute or four times more concentrated than plasma, keeping body water within narrow limits. This page explains how the loop of Henle and antidiuretic hormone do this, how thirst works, and how to advise patients and athletes on drinking.

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Part 5 · Renal System · Chapter 23 of 47

Learning objectives

By the end of this page you should be able to:

  • Describe daily water intake and output.
  • Explain how the loop of Henle creates the medullary concentration gradient.
  • Describe the actions and control of antidiuretic hormone.
  • Distinguish water balance from sodium balance.
  • Advise on fluid replacement during exercise.
  • Recognise and explain exercise-associated hyponatraemia.

Why it matters

Physiotherapists supervise exercise in heat, run sports events and treat older adults who drink too little. Dehydration lowers performance and raises the risk of heat illness and kidney injury.

Drinking too much is also dangerous. Low blood sodium after long events has killed marathon runners. Good advice depends on understanding how the body handles water.

Daily water balance

Figure 1 · Daily water balance

Daily water intake and output in a sedentary adult Two stacked bars of about 2.6 litres each. Intake: drinks 1.5, water in food 0.8 and water made by metabolism 0.3 litres. Output: urine 1.5, unnoticed loss from skin and lungs 0.9, and faeces with a little sweat 0.2. Drinks 1.5 LWater in food 0.8 LMade by metabolism 0.3 LIn: about 2.6 L/dayUrine 1.5 LSkin and lungs (unnoticed) 0.9 LFaeces and sweat 0.2 LOut: about 2.6 L/dayTypical temperate-climate day, sedentary adult
Urine is the adjustable part. Sweat can rise to more than a litre per hour in hard exercise in heat, so intake must then rise too. Typical values.

Body water is held remarkably constant. Unnoticed losses through skin and breathing continue regardless, so urine volume and thirst are the adjustable parts. The kidney must excrete a minimum volume of about half a litre a day to remove the day’s waste solutes.

Making concentrated urine

Figure 2 · Building and using the medullary gradient

Countercurrent multiplication in the loop of Henle and water reabsorption in the collecting duct The medulla becomes saltier with depth, from 300 to about 1200 milliosmoles per kilogram. Water leaves the descending limb; salt is pumped out of the water-tight ascending limb. In the collecting duct, water leaves into the salty medulla only when antidiuretic hormone opens water channels. 3006009001200mOsm/kgwater outNaCl pumped out;wall blocks waterdescendingascendingcollecting ductwater outonly with ADHconcentrated urine
The loop makes the gradient; ADH decides whether to use it. Without ADH, dilute urine flows out; with ADH, urine can reach about four times plasma concentration.

The thick ascending limb of the loop of Henle pumps sodium chloride into the surrounding tissue but does not let water follow. The descending limb lets water out but not much salt. Flowing in opposite directions, the two limbs multiply a small difference into a large gradient: the countercurrent multiplier.

Urea recycling adds to the gradient, and the slow blood flow in looping capillaries, the vasa recta, preserves it. Deep in the medulla, the tissue reaches about 1,200 mOsm/kg, four times plasma.

Urine typeOsmolalityADHSituation
Maximally diluteAbout 50 mOsm/kgAbsentAfter drinking a lot of water
Similar to plasmaAbout 300 mOsm/kgModerateNormal day
Maximally concentratedAbout 1,200 mOsm/kgHighDehydration, overnight

Antidiuretic hormone

Antidiuretic hormone (ADH, vasopressin) is made in the hypothalamus and released from the posterior pituitary. It inserts water channels, aquaporin-2, into the collecting duct, so water moves out into the salty medulla and urine becomes concentrated.

Figure 3 · Antidiuretic hormone responds to concentration

Plasma antidiuretic hormone against plasma osmolality ADH stays low until plasma osmolality reaches about 280 to 285 milliosmoles per kilogram, then rises steeply. Thirst begins at a slightly higher osmolality. A list notes that low volume, low pressure, nausea, pain, some drugs and exercise also raise ADH. ADH starts to riseabout 280–285thirst beginsa little higher270280290300310Plasma osmolality (mOsm/kg)Plasma ADHAlso raised by:low blood volumelow blood pressurenausea, pain, stresssome drugsexercise
A sensitive switch. A 1% rise in osmolality is enough to raise ADH. Non-osmotic triggers can keep ADH high even when the body is diluted, which matters in exercise-associated hyponatraemia [3]. Schematic.

Osmoreceptors in the hypothalamus detect plasma osmolality. A rise of about 1% raises ADH, and slightly larger rises cause thirst. Large falls in blood volume or pressure also release ADH, overriding osmolality.

Pain, nausea, stress, some drugs and prolonged exercise can stimulate ADH even when the body has plenty of water. This non-osmotic release is central to exercise-associated hyponatraemia [3].

DisorderProblemResult
Diabetes insipidusToo little ADH or kidney unresponsiveLarge volumes of dilute urine; thirst
Inappropriate ADH secretionADH released without osmotic needWater retention; low sodium
DehydrationWater loss exceeds intakeHigh ADH, concentrated urine, thirst

Water versus sodium

Two systems run in parallel. Water balance, controlled by ADH and thirst, sets the concentration of sodium in plasma. Sodium balance, controlled by aldosterone, the renin–angiotensin system and natriuretic peptides, sets the volume of extracellular fluid.

So a low blood sodium usually means too much water, not too little salt. That distinction is the key to exercise-associated hyponatraemia.

Fluid during exercise

The American College of Sports Medicine recommends starting exercise well hydrated and drinking enough to prevent a water deficit of more than about 2% of body weight [1]. Sweat rates vary widely between people, so drinking plans should be individual [1].

Figure 4 · Drinking too little and too much

Body mass change during exercise and associated risks A scale of body mass change from minus 5 to plus 3 per cent. Losses greater than 2 per cent are marked as dehydration that impairs performance. Small losses up to 2 per cent are the target zone. Any gain in weight suggests overdrinking with a risk of hyponatraemia. -5%-4%-3%-2%-1%0+1%+2%+3%Dehydrationmore than 2% loss impairs performance [1]Target zoneWeight gainoverdrinking: hyponatraemia risk [2]Change in body mass from before to after exerciseWeigh before and after: each kilogram lost is about one litre of sweat not replaced [1]
Both extremes are harmful. Customise drinking to sweat rate [1]; gaining weight during exercise is a warning sign [2, 3].

Practical skill · measuring sweat rate

Weigh the athlete in minimal clothing before and after a typical session, and record what they drank. Sweat loss in litres is roughly weight lost in kilograms plus fluid drunk [1]. Use this to plan intake for similar sessions.

Exercise-associated hyponatraemia

Almond and colleagues tested 488 finishers of the Boston Marathon. Thirteen per cent had a sodium of 135 mmol/L or less, and 0.6% had critically low values of 120 or less [2].

Figure 5 · Hyponatraemia in marathon runners

Frequency and risk factors of low blood sodium after the Boston Marathon Left: 13 per cent of runners had sodium of 135 or less and 0.6 per cent had critical levels of 120 or less. Right: independent risk factors were weight gain during the race, odds ratio 4.2, race time over four hours, odds ratio 7.4, and extremes of body mass index. Serum sodium at the finish [2]13.0%135 mmol/L or less0.6%120 or less (critical)488 runners with finish-line blood samplesIndependent risk factors (odds ratio) [2]Weight gain during race4.2Race time over 4 hours7.4Very low or high BMIraisedNot independently linked: sex, drink type, NSAID use
Overdrinking, not sweating, is the main problem. Slower runners who drink at every station and gain weight are most at risk [2].

Weight gain during the race and a finishing time over four hours were the strongest risk factors [2]. Female sex, the type of drink and anti-inflammatory use were not independent risk factors [2].

The international consensus explains the mechanism: drinking more than is lost, while ADH is not fully suppressed, dilutes body sodium [3]. Its key preventive advice is to drink according to thirst [3].

FeatureDehydrationExercise-associated hyponatraemia
Body weightFallenUnchanged or increased
SymptomsThirst, fatigue, dizzinessNausea, headache, confusion, seizures
Typical runnerFast, hot day, little drinkingSlow, drinking at every station [2]
TreatmentFluidsRestrict fluids; hypertonic saline if severe [3]

Red flags at events

A confused or vomiting runner who has gained weight must not be given more water. Arrange urgent medical assessment and sodium measurement [3].

Clinical relevance for the physiotherapist

  • Exercise in heat. Plan fluids from measured sweat rates; aim to limit losses to about 2% [1].
  • Endurance events. Advise drinking to thirst and warn against drinking at every station [2, 3].
  • Older adults. Thirst is blunted with age; prompt regular drinking, especially in hot weather.
  • Medications. Diuretics and some antidepressants affect water and sodium; watch for confusion and falls.
  • Neurological patients. Head injury and some brain conditions can disturb ADH.

Assessment and application

SituationInterpretationAction
Athlete loses 3% body weight in a hot sessionExcess dehydration [1]Increase planned intake; rehydrate
Slow marathon runner confused at finish; weighs more than at startPossible hyponatraemia [2, 3]No more water; urgent medical care
Older patient with dark urine, dizziness, dry mouthDehydrationEncourage fluids; inform team
Patient passing large volumes of dilute urine after head injuryPossible diabetes insipidusReport to medical team

Common mistakes

  • Telling everyone to drink as much as possible during exercise [3].
  • Assuming hyponatraemia is caused by salt loss in sweat [2, 3].
  • Using a single drinking plan for all athletes [1].
  • Confusing water balance with sodium balance.
  • Giving water to a confused runner without checking sodium.

Exam preparation

Long answer

Describe the mechanism by which the kidney concentrates urine.

  • Medullary gradient and countercurrent multiplication (Figure 2).
  • Urea recycling and vasa recta.
  • ADH: secretion, control and action (Figure 3).
  • Dilute and concentrated urine (table).
  • Clinical: diabetes insipidus, inappropriate ADH, exercise hyponatraemia [3].

Short notes

  • Countercurrent multiplier.
  • Antidiuretic hormone.
  • Fluid replacement in exercise [1].
  • Exercise-associated hyponatraemia [2, 3].

Viva and practical

  • “Where does ADH act?” — the collecting duct.
  • “What is the main cause of low sodium in marathon runners?” — overdrinking [2, 3].
  • “How much weight loss impairs performance?” — more than about 2% [1].
  • OSCE: calculate sweat rate from pre- and post-exercise weight [1].

Current evidence

Exam and traditional teaching

Athletes are told to drink as much as possible and to stay ahead of thirst.

What the evidence adds

Fluid plans should be individual, preventing losses over about 2% [1].

Hyponatraemia is common in slower runners who gain weight [2]; drinking to thirst is advised [3].

What the student should understand

The kidney defends water balance well. The commonest error at events is drinking too much, not too little.

Check yourself

10 questions on this page. Tap one to see the answer and the reasoning.

Q1. The ACSM position stand aims to prevent body water loss during exercise of more than about:
  1. (A) 0.5% of body weight
  2. (B) 2% of body weight
  3. (C) 10% of body weight
  4. (D) 20% of body weight

Answer: (B) Drinking aims to prevent losses greater than 2% of body weight, which compromise performance [1].

Q2. The simplest way to estimate an individual’s sweat rate is to:
  1. (A) Measure heart rate
  2. (B) Weigh before and after exercise
  3. (C) Count breaths
  4. (D) Measure blood glucose

Answer: (B) Body weight change before and after exercise estimates sweat loss [1].

Q3. In the Boston Marathon study, what proportion of runners had hyponatraemia at the finish?
  1. (A) 0.1%
  2. (B) 13%
  3. (C) 50%
  4. (D) 90%

Answer: (B) Thirteen per cent had sodium of 135 mmol/L or less [2].

Q4. Which factor was most strongly associated with hyponatraemia in that study?
  1. (A) Female sex
  2. (B) Weight gain during the race and long race time
  3. (C) Drinking sports drinks rather than water
  4. (D) Taking NSAIDs

Answer: (B) Weight gain (OR 4.2) and race time over 4 hours (OR 7.4) were independent risk factors [2].

Q5. Exercise-associated hyponatraemia is mainly caused by:
  1. (A) Excess sweating alone
  2. (B) Drinking more fluid than is lost, with ADH not fully suppressed
  3. (C) Eating too much salt
  4. (D) Low blood glucose

Answer: (B) The consensus identifies overdrinking and non-osmotic ADH secretion as key mechanisms [3].

Q6. The consensus advice to reduce the risk of exercise-associated hyponatraemia is to:
  1. (A) Drink as much as possible
  2. (B) Drink according to thirst
  3. (C) Avoid all fluids
  4. (D) Drink only salt tablets

Answer: (B) Drinking to thirst is recommended to avoid overdrinking [3].

Q7. Antidiuretic hormone increases water reabsorption in the:
  1. (A) Proximal tubule
  2. (B) Collecting duct
  3. (C) Glomerulus
  4. (D) Bladder

Answer: (B) ADH inserts water channels in the collecting duct; non-osmotic ADH release contributes to hyponatraemia [3].

Q8. Sports drinks containing electrolytes and carbohydrate:
  1. (A) Are always harmful
  2. (B) Can offer benefits over water in some circumstances
  3. (C) Prevent all hyponatraemia
  4. (D) Should replace meals

Answer: (B) The position stand notes benefits over water alone under certain circumstances [1].

Q9. In the Boston Marathon study, fluid type and NSAID use were:
  1. (A) Strong risk factors
  2. (B) Not independently associated with hyponatraemia
  3. (C) Protective
  4. (D) Not measured

Answer: (B) Composition of fluids and NSAID use were not associated on multivariate analysis [2].

Q10. Severe exercise-associated hyponatraemia with confusion or seizures is treated urgently with:
  1. (A) Large volumes of water
  2. (B) Hypertonic saline under medical supervision
  3. (C) Rest only
  4. (D) Diuretic tablets by mouth

Answer: (B) The consensus recommends hypertonic saline for severe cases [3].

Quick review

Key takeaways

  • Intake about 2.6 L/day; urine is the adjustable output.
  • Loop of Henle builds a medullary gradient up to about 1,200 mOsm/kg.
  • ADH inserts aquaporins in the collecting duct; it rises with a 1% rise in osmolality.
  • Water balance sets sodium concentration; sodium balance sets volume.
  • Limit exercise losses to about 2% body weight [1].
  • Overdrinking causes hyponatraemia; drink to thirst [2, 3].

Further reading

SourceWhy it earns its place
ACSM; Sawka MN et al. — Med Sci Sports Exerc, 2007Fluid replacement guidance [1]
Almond CSD et al. — NEJM, 2005Hyponatraemia in marathon runners [2]
Hew-Butler T et al. — Clin J Sport Med, 2015Consensus on exercise hyponatraemia [3]

References

  1. American College of Sports Medicine; Sawka MN, Burke LM, Eichner ER, Maughan RJ, Montain SJ, Stachenfeld NS. American College of Sports Medicine position stand. Exercise and fluid replacement. Medicine and Science in Sports and Exercise. 2007;39(2):377–390. doi:10.1249/mss.0b013e31802ca597 PMID 17277604 Position stand
  2. Almond CSD, Shin AY, Fortescue EB, et al. Hyponatremia among runners in the Boston Marathon. New England Journal of Medicine. 2005;352(15):1550–1556. doi:10.1056/NEJMoa043901 PMID 15829535 Cohort study
  3. Hew-Butler T, Rosner MH, Fowkes-Godek S, et al. Statement of the Third International Exercise-Associated Hyponatremia Consensus Development Conference, Carlsbad, California, 2015. Clinical Journal of Sport Medicine. 2015;25(4):303–320. doi:10.1097/JSM.0000000000000221 PMID 26102445 Consensus statement

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