Tubular reabsorption article
What is tubular reabsorption?
- 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 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.
Reabsorption of sodium, nutrients, water, and other ions
- 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.
- 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.
- 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.
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.