Part of the TeachMe Series

Water Filtration and Reabsorption

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Original Author(s): Omar Haque
Last updated: 6th January 2022
Revisions: 20

Original Author(s): Omar Haque
Last updated: 6th January 2022
Revisions: 20

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Water is vital for maintaining homeostasis as it is the primary component of intra- and extracellular fluid and is needed to maintain intra- and extracellular volumes. In addition to this, it plays a vital role in maintaining electrolyte balance by regulating the concentration of different ions such as sodium (Na+), potassium (K+), magnesium (Mg2+) and calcium (Ca2+). This article will discuss water filtration and reabsorption in the urinary system and the clinical relevance of volume status.

Water Intake

There are two main sources of H2O in the body: the food/drink we take in and endogenous water created as a product of aerobic respiration – this endogenous water is so small it is negligible.

On average, 180L of water is filtered by the kidneys daily. However, only 1.5-2L actually ends up being excreted as urine. This means almost 99% of the water filtered is either reabsorbed into the circulation or enters the interstitium.

Water Filtration and Reabsorption in the Nephron

In the glomerulus, water is initially filtered out, along with the other solutes e.g. Na+, K+ and glucose. From here H2O needs to be reabsorbed into the tubule cells and then back into the interstitial space. From the interstitial space, H2O can move back into the vasa recta, the blood vessels running alongside the nephron.

There are 3 main places where H2O reabsorption occurs: the proximal convoluted tubule (PCT), the descending limb of the Loop of Henle and the collecting ducts.

It is also important to note that water reabsorption is heavily driven by the movement of Na+ – as a rule of thumb, water tends to follow the direction that sodium moves in.

Diagram showing water filtration and absorption in the nephron

Figure 1. Water filtration and absorption in the nephron.

Proximal Convoluted Tubule (PCT)

In the PCT, sodium is taken up from the filtrate back into the tubule by sodium-linked glucose transporters (SGLTs). Click here to read the article on ion reabsorption in the PCT, where this is discussed in more detail.

Na+ movement makes the tubule intracellular fluid more concentrated than the filtrate. This creates a concentration gradient to drive H2O movement into the tubule cell. This is known as transcellular movement and occurs when H2O molecules move across the cell membrane via aquaporin-1 (AQP-1) channels, driven by osmosis.

Once in the cell, H2O molecules then move out of the cell into the cortical interstitial space via another AQP-1 channel on the basolateral surface.

Paracellular movement of H2O occurs between tubule cells and is due to the higher hydrostatic pressure in the filtrate than in the interstitial space. This forces water between the tubule cells through leaky tight junctions. Transcellular movement of H2O effectively bypasses the tubule cell and moves it straight from the filtrate to the interstitial space directly.

By the end of the PCT, the concentration of water in the filtrate and interstitial space is almost the same. Overall, about 67% of the filtered water is reabsorbed in the PCT.

Loop of Henle

Water reabsorption occurs in the thin descending limb of the Loop of Henle. It is permeable to water, which means that H2O molecules are freely able to leave it. Similarly to in the PCT, water can leave the thin descending limb into the more concentrated medulla through transcellular and paracellular movement.

Because the thin descending limb is permeable to water, water can move out into the more concentrated medulla via osmosis. The driving force behind this is the movement of Na+, Cl and K+ from the tubule to the medulla, via NKCC symporters in the thick ascending limb. This makes the renal medulla more concentrated, providing an osmotic gradient.

To learn more about the specifics of the Loop of Henle, click here.

Collecting Duct

In the collecting duct, H2O reabsorption is driven by antidiuretic hormone (ADH). ADH is produced in the hypothalamus and is secreted from the posterior pituitary gland in response to low plasma volume or high osmolality.

ADH acts on the principal cells in the collecting duct by binding to receptors. This triggers an intracellular signalling pathway that causes increased aquaporin-2 (AQP-2) production for the apical surface of the principal cell. The water can then move through the tubule and back into the renal medulla. Similarly to in the Loop of Henle, the force driving this movement is the high concentration of Na+ in the renal medulla.

More information on ADH specifically can be found here.

Reabsorption Back into the Circulation

Blood moves from the interstitial space back into the circulation via the vasa recta, a network of capillaries that run alongside the nephron.

Because the vasa recta contains mostly large proteins and red blood cells (as the other contents have been filtered in the glomerulus), it is very concentrated and therefore water moves into it via osmosis.

Clinical Relevance- Hypervolemia 

Hypervolaemia and hypovolaemia are technically not the same as increased or decreased extracellular volume respectively – for example, if a patient has oedema, they may have a normal extracellular volume, but because fluid has moved from the blood vessels to the tissues, they will have a low plasma volume, therefore being hypovolaemic.

Hypervolaemia is when the circulating plasma volume is higher than normal. The main causes of hypervolaemia are:

  • Heart failure
  • Liver cirrhosis
  • Renal problems –  e.g. nephrotic syndrome

This can produce symptoms and signs such as:

  • Pedal oedema
  • Pleural effusions
  • Pericardial effusions
  • Shortness of breath – caused by pulmonary oedema
  • Fatigue
  • Abdominal distension – caused by ascites

Hypervolaemia is managed conservatively through fluid and sodium restriction. Diuretics are also used to increase the amount of water that is excreted, thus reducing the volume of water in the body. Potassium levels should also be monitored with particular diuretics such as furosemide. This is because they cause potassium to be excreted along with water, resulting in hypokalaemia (low serum potassium levels).

In order to prevent further hypervolaemia, the underlying cause should also be investigated and managed.

Clinical Relevance- Hypovolemia 

Hypovolaemia is reduced circulating plasma volume in the blood vessels. This can have various causes such as:

  • Shock
  • Haemorrhage
  • Dehydration
  • Sepsis
  • Diuretic usage

Symptoms and signs of hypovolaemia include:

  • Thirst – dry lips/mucous membranes
  • Loss of skin elasticity
  • Tachycardia – occurs in order to try and keep BP in the normal range
  • Hypotension – may present as postural hypotension
  • Confusion – caused by lack of cerebral perfusion

Treatment of hypovolaemia usually involves increasing the amount of fluid in the blood vessels. This can be done by encouraging fluid intake, or if fluid is needed quickly, intravenous fluid infusions/boluses of saline, dextrose or Hartmann’s solution can be used.

The underlying cause behind the hypovolaemia should also be treated where possible.