Water is reabsorbed at various times during the excretion process as it passes through the nephron, in order to maintain proper ion levels. It is not, however, reabsorbed as urine ascends through the thin and thick ascending limbs in the loop of Henle. Rather, this region only involves ion reabsorption and urea secretion.

Sodium is reclaimed through passive transport in the thin ascending limb and is reclaimed by active transport in the thick ascending limb, distal tubule, and collecting duct. Each location of sodium resorption uses a different transport protein and mechanism.

The filtrate and surrounding interstitial fluid are at their highest osmolarities at the bottom of the loop of Henle. As the filtrate continues on, it enters the thin ascending limb of the loop of Henle, which is impermeable to water. As the thin ascending limb moves up through the nephron into areas with a lower osmolarity, sodium flows down its concentration gradient to exit the filtrate. At this point, the filtrate is at a lower osmolarity than the surrounding interstitial fluid due to sodium flowing out and water being barred from flowing in.

As filtrate travels down the descending limb of the loop of Henle, water passively leaves the filtrate as the descending limb passes through portions of the nephron that contain a more concentrated interstitial fluid. Water always travels from places of high water concentration (low osmolarity) to low water concentration (high osmolarity); thus, the water will passively flow out of the filtrate and into the interstitium.

As the loop of Henle turns, the filtrate passes through the thin ascending limb, which is impermeable to water, but permeable to ions. As the limb passes through less concentrated areas of the nephron, sodium passively flows down its concentration gradient from the filtrate to the interstitial fluid. At no point during this process is water actively transported.

In the presence of antidiuretic hormone (ADH), water is reabsorbed and the urine is concentrated. Antidiuretic hormone plays the biggest role on the collecting duct and distal tubule, allowing water to diffuse into the medulla by increasing the production of aquaporin proteins. These proteins become embedded in the membranes of the nephron epithelium and allow water to pass through the usually impermeable cells.

The other important regulator of water balance is aldosterone, which works by a different mechanism. Aldosterone increases production of sodium channels, allowing sodium to exit the filtrate in the distal tubule. Water diffuses to follow the reabsorbed sodium ions.

There are two main systems designed to regulate water reabsorption in the kidney: antidiuretic hormone (vasopressin) and the renin-angiotensin-aldosterone system (RAAS). The RAAS system includes a combination of substances that raise blood pressure through arteriole constriction and sodium reabsorption. It employs a specialized tissue that supplies blood to the glomerulus, called the juxtaglomerular apparatus (JGA), which produces the enzyme renin when stimulated by a drop in blood pressure.

Renin secretion is the first step in a series of reactions that serve to lower blood pressure. Renin enters the bloodstream, where it interacts with angiotensinogen and produces angiotensin I. Angiotensin-converting enzyme in the lungs further converts angiotensin I into angiotensin II. Angiotensin II has two primary functions: it acts as vasoconstrictor and stimulates release of aldosterone from the adrenal cortex. Vasoconstriction helps to immediately increase local blood pressure. Aldosterone interacts with the distal tubule of the nephron to increase sodium reabsorption. The increase in interstitial osmolarity helps pull water out of the filtrate, concentrating the urine and enhancing water conservation, which can increase blood volume and pressure.

Atrial natriuretic hormone serves to inhibit the RAAS system when blood pressure is low.

Vasopressin, also called antidiuretic hormone (ADH), is part of the hormonal control of urine excretion and functions to enhance water reabsorption and limit the excretion of water in urine. Vasopressin is released when osmoreceptor cells in the hypothalamus detect a rise in the osmolarity or solute concentration of the blood above a threshold level.

Conversely, intake of a large quantity of water will lower blood osmolarity and signal that water conservation is not needed. When blood volume or pressure increases and blood osmolarity decreases, production of vasopressin is inhibited in order to promote water excretion.

Vasopressin, also called antidiuretic hormone (ADH), is part of the hormonal control of urine excretion and functions to enhance reabsorption of water, limiting the excretion of water in urine. Vasopressin is released when osmoreceptor cells in the hypothalamus detect a rise in the osmolarity (solute concentration) of the blood above a threshold level. Upon release, vasopressin reaches the kidney and binds to receptors on cells in the collecting duct, which stimulates release of aquaporin water channels from storage vesicles within the cells. Aquaporin channels are selectively permeable to water, and allow the flow of water out of the filtrate/urine. This water is then reclaimed by the body and used to increase blood volume, increase blood pressure, and reduce blood osmolarity.

One of the key adaptations of the mammalian kidney is the ability to conserve water through reabsorption and excretion of concentrated urine. This is accomplished by maintenance of an osmolarity gradient, suitable for extracting water from the filtrate. The two primary solutes are sodium, which is deposited in the renal medulla by the loop of Henle, and urea, which crosses the epithelium of the collecting duct in the inner medulla. The increased osmolarity of the interstitial fluid enables water to be extracted and conserved through aquaporin proteins in the collecting duct.

Antidiuretic hormone (ADH) is responsible for concentrating the urine. This is accomplished by making the collecting duct permeable to water, and allowing it to passively diffuse into the renal medulla. Alcohol will inhibit the function of ADH, which means that the urine will be less concentrated because water is unable to leave the collecting duct, thus also increasing the volume.

In diabetes insipidus, ADH is not available to reabsorb the water from the collecting tubule of the renal system. As a result, more fluid will be lost and frequent urination will occur. In diabetes mellitus the osmolarity of the blood is high due to a constant high concentration of glucose in the blood. Due to the increase in osmolarity, water will be drawn from the tissues and into the blood. When the blood reaches the kidneys, it will be filtered and result in more water in the urine. More water into the urine increases its volume and leads to frequent urination. Hyperglycemia and glucose in the urine only occurs in diabetes mellitus and not in diabetes insipidus. In diabetes insipidus, the problem is not the blood glucose level but the inability to secrete ADH. The term "diabetes" does not automatically mean a problem related to sugar.