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Tubular reabsorption article

What is tubular reabsorption?

The fluid that filters through the glomerulus and Bowman’s capsule (glomerular filtrate) is very similar to blood plasma without the proteins, and at this point not at all like urine. If this filtrate flowed straight to your bladder and then out your body, you would lose more than 10-times the entire volume of your extracellular body fluids (plasma and interstitial fluid) every day. Fortunately, tubular reabsorption mechanisms in the nephrons of your kidneys return the water and solutes that you need back into your extracellular fluid and circulatory system. In addition to reabsorbing the substances that you need, your nephrons are able to secrete unwanted substances from your bloodstream into the filtrate. Together these processes complete the transformation of the glomerular filtrate into urine.
  • Tubular reabsorption is the process that moves solutes and water out of the filtrate and back into your bloodstream. This process is known as reabsorption, because this is the second time they have been absorbed; the first time being when they were absorbed into the bloodstream from the digestive tract after a meal.

How does reabsorption in the nephrons work?

The nephrons in your kidneys are specifically designed to maintain body fluid homeostasis. This means keeping extracellular body fluid volumes stable, as well as maintaining the right levels of the salts and minerals that are essential for the normal function of your tissues and organs; regardless of how much you eat, or how active you are. Nephrons are divided into five segments, with different segments responsible for reabsorbing different substances.
Reabsorption is a two-step process:
  • The first step is the passive or active movement of water and dissolved substances from the fluid inside the tubule through the tubule wall into the space outside.
  • The second step is for water and these substances to move through the capillary walls back into your bloodstream, again, either by passive or active transport.
Nephrons are comprised of different segments that perform specific functions. The walls of the nephron are made of a single layer of cube-like cells, called cuboidal epithelial cells, and their ultrastructure changes depending on the function of the segment they are in. For example, the surface of the cells facing the lumen of the proximal convoluted tubule are covered in microvilli (tiny finger-like structures). This type of surface is called a brush border. The brush border and the extensive length of the proximal tubule dramatically increase the surface area available for reabsorption of substances into the blood enabling around 80% of the glomerular filtrate to be reabsorbed in this segment. Another notable feature of these cells is that they are densely packed with mitochondria (the cell’s energy generators). The mitochondria ensure a good supply of energy is available to fuel the active transport systems needed for efficient reabsorption.
Passive transport is when substances use specific transporters to move down their concentration gradient (from areas of high concentration to areas of low concentration) or in the case of charged ions, down their electrochemical gradient.
Active transport is when substances are moved up (or against) their concentration or electrochemical gradients (from low to high). In this case, the substances are transported back into the bloodstream via energy-dependent, or active transport proteins.

Reabsorption of sodium, nutrients, water, and other ions

Sodium is the major positively charged electrolyte in extracellular body fluid. The amount of sodium in the fluid influences its volume, which in turn determines blood volume and blood pressure. Most of the solute reabsorbed in the proximal tubule is in the form of sodium bicarbonate and sodium chloride, and about 70% of the sodium reabsorption occurs here. Sodium reabsorption is tightly coupled to passive water reabsorption, meaning when sodium moves, water follows. The movement of water balances the osmotic pressure within or across the tubule walls, which maintains extracellular body fluid volume.
Reabsorption in the early proximal convoluted tubule: The most essential substances in the filtrate are reabsorbed in the first half of the proximal convoluted tubule (early proximal tubule). These include glucose, amino acids, phosphate, lactate and citrate, which “piggy-back” on sodium co-transporters (membrane proteins that link the movement of two or more specific solutes together) that move sodium down its electrochemical gradient into tubule epithelial cells. For this to continue, the sodium gradient must be maintained, which means sodium cannot be allowed to build up inside the epithelial cells of the proximal tubule wall. This is achieved using:
  • Sodium/potassium ATPase, a sodium pump (active transporter) located on the opposite side of the epithelial cell that takes care of this by moving three sodium ions out of the cell for reabsorption into the bloodstream, and pumping two potassium ions back into the cell (see diagram below).
  • Sodium/proton exchanger, which enables reabsorption of bicarbonate. Glucose, amino acids and other substances diffuse out of the epithelial cell down their concentration gradients on passive transporters and are then reabsorbed by the blood capillaries. By the time the filtrate has reached the mid part of the proximal tubule, 100% of the filtered glucose and amino acids have been reabsorbed, and large amounts of sodium, bicarbonate, phosphate, lactate, and citrate ions.
Reabsorption in the late proximal convoluted tubule: The fluid entering the late proximal tubule has been depleted of the essential substances. As bicarbonate was the negatively charged ion initially reabsorbed with sodium, chloride ions have been left behind in the tubule. Due to the extensive reabsorption of water in the early section of the tubule, chloride ions are highly concentrated, and it is now their turn for reabsorption. They are transported into the tubule epithelial cells through the following processes:
  • Chloride/formate anion exchangers driven by the high concentration of chloride in the filtrate. Chloride diffuses out of the cell through channels in the cell wall, and then on into the bloodstream.
  • Passive movement through the spaces between epithelial cells of the tubule wall, known as tight junctions, which contrary to their name are not so tight. This is another important route for reabsorption of small solutes such as sodium chloride, and of water. Sodium continues to be reabsorbed in this part of the tubule via sodium/proton exchangers and actively transported through the tubule wall to the bloodstream by the sodium/potassium ATPase. After leaving the proximal convoluted tubule, the tubular fluid enters the proximal straight tubule, where around 15% of the phosphate is reabsorbed.
Reabsorption in the loop of Henle: The filtrate then enters the loop of Henle (descending and ascending limbs), which is responsible for concentrating or diluting the tubular fluid using a process called countercurrent multiplication. The distal convoluted tubule and collecting ducts are then largely responsible for reabsorbing water as required to produce urine at a concentration that maintains body fluid homeostasis.
Reabsorption in the thick ascending limb: A further 25% of the sodium and potassium is reabsorbed through the walls of the thick ascending limb of the loop of Henle via:
  • Three-ion cotransporter (sodium/potassium/chloride) and the sodium/potassium ATPase, which as before maintains the sodium concentration gradient. Sodium is actively pumped out, while potassium and chloride diffuse down their electrochemical gradients through channels in the tubule wall and into the bloodstream. The walls of the thick ascending limb are impermeable to water, so in this section of the nephron water is not reabsorbed along with sodium.
Reabsorption in the distal tubule and collecting duct: The tubular fluid now enters the distal tubule and collecting duct, or terminal nephron. The early distal tubule reabsorbs a further 5% of the sodium, and the late distal tubule and collecting duct fine tune reabsorption of the last little bit (around 3%), determining exactly how much sodium will be excreted. These segments of the nephron have slightly different transporters, as well as the sodium/potassium ATPase that drives reabsorption of calcium and chloride. Sodium reabsorption in the late distal tubule and collecting duct is regulated by hormones, which stimulate or inhibit sodium reabsorption as necessary.
Other ions: Calcium reabsorption throughout the nephron is largely similar to sodium reabsorption with over 99% being reabsorbed, while phosphate reabsorption is similar to that of glucose in that it primarily occurs within the proximal tubule. Reabsorption of magnesium differs in that the majority of the reabsorption occurs in the ascending limb of the loop of Henle.

Consider the following:

  • Urine contains a diverse range of substances that are either waste products or substances ingested in excess. The importance of the kidneys in maintaining body fluid composition is clear when we look at what happens when we consider the impact on the body when our kidneys start to fail. Retention of waste products causes disturbances in multiple organ systems including cardiovascular, hematological, gastrointestinal, neurological, skeletal, hormonal, respiratory, skin and reproductive systems. Loss of water and electrolyte homeostasis lead to elevated extracellular body fluid volume, which may produce edema and hypertension, reduced phosphate excretion, loss of bone calcium, and symptoms of lethargy, nausea, diarrhoea and vomiting.
  • Diabetes insipidus is a rare disorder that causes you to feel very thirsty (despite drinking a lot), and to produce large amounts of urine. It is usually caused by a malfunction in the production of antidiuretic hormone (ADH), a hormone that prevents the production of dilute urine (i.e., retains water in the body). This can happen for a number of different reasons, including damage to the pituitary; e.g., caused by a tumour, surgery, or an infection, that disrupts the normal production, storage and release of ADH. However, it may also occur due to a defect in the tubules themselves that prevents them from responding to ADH, or during pregnancy, when a placental enzyme destroys ADH in the mother.

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