The thick ascending limb of the loop of Henle is impermeable to water, though sodium is actively transported out of this region. By pumping sodium out of the thick ascending limb, the urine becomes less concentrated that it was after the descending limb of the loop of Henle.

Antidiuretic hormone (vasopressin) is produced by the posterior pituitary, and is responsible for the increased rate of water reabsorption in the collecting duct of the kidney. The collecting duct serves as the last site of blood volume and blood pressure regulation before the urine flows down the kidney ureter into the bladder for excretion. The collecting duct is usually relatively impermeable to water. Action of antidiuretic hormone causes the insertion of aquaporins in the collecting duct, allowing water to exit the filtrate into the extracellular space.

Filtrate from Bowman's capsule enters the proximal tubule and flows down the descending loop of Henle, where water is reabsorbed from the tubule. Once through the descending limb of the loop, the filtrate enters the thin and thick ascending limbs of the loop of Henle, where sodium is reabsorbed, but water is not. Additional sodium can be reabsorbed in the collecting duct. Water could only be reabsorbed in the collecting duct if antidiuretic hormone were present.

We need to look for the point where sodium concentrations are the highest and water concentrations the lowest in the filtrate. This corresponds to the descending limb of the loop of Henle. At the bottom of the descending loop of Henle the filtrate is the most concentrated. Water is drawn out of the filtrate as it travels down the descending limb, but ions remain in the tubule, causing the osmolarity to increase. As the filtrate begins to ascend the loop, ions are pumped out of the filtrate, reducing the concentration again.

When antidiuretic hormone is present, higher osmolarity levels could be found in the collecting duct; however, we are told that antidiuretic hormone is not present, thus additional water will not be reabsorbed in the collecting duct.

Aldosterone acts in the distal tubule to increase the rate of sodium reabsorption by increasing the number of sodium-potassium pump proteins implanted in the cells of this region. To maintain electrical neutrality, when sodium is reabsorbed, potassium is secreted.

Too much aldosterone can thus make someone hypernatremic (high blood sodium) and hypokalemic (low blood potassium). High blood pressure results from the hypernatremia, and cardiac arrhythmias can result from the hypokalemia. 

The glomerulus is the capillary bed that feeds filtrate into the nephron via Bowman's capsule. Under normal circumstances, the glomerulus functions to create the urine filtrate. One of its main functions is to inhibit the filtration of red blood cells and large proteins. The glomerulus is the only part of the nephron that has any intimate contact with red blood cells. None of the other portions of the nephron will be in close proximity to red blood cells; thus, the glomerulus is the only nephron structure that could cause the lysis of red blood cells.

Diabetes mellitus is the product of decreased insulin effectiveness in the body. As a result, blood glucose levels are extremely high. When filtrate enters the nephron through Bowman's capsule, glucose is generally transported as well. In a healthy individual, this glucose is rapidly removed from the filtrate in the proximal convoluted tubule. In a diabetes patient, however, the level of glucose in the filtrate can overwhelm the reabsorption of the tubule, resulting in glucose in the urine. This increases urine osmolarity, causing the filtrate to retain water. The result is an increase in urine volume, resulting in more frequent urination.

The purpose of the proximal tubule is to reduce the amount of filtrate in the nephron. The proximal tubule does alter the solute concentrations in the filtrate, but it does not alter the osmolarity of the filtrate. This is because the proximal tubule is where reabsorption of solutes, proteins, and glucose takes place. Meanwhile, drugs and toxins are being secreted into the filtrate. Essentially, the volume of filtrate in the proximal tubule decreases, but the filtrate remains isotonic to the blood.

The descending loop of Henle is responsible for the first step in urine concentration. Due to the high concentration of salt in the space surrounding the descending limb of the loop of Henle, water flows out of the tubule, concentrating the filtrate. The descending limb is impermeable to sodium, potassium, and albumin (the principle protein component in blood).

The glomerulus is a capillary bed. Afferent arterioles carry blood to enter the glomerulus, and efferent arterioles carry blood away from the glomerulus after filtration. Both types of arteriole are able to tighten and relax to modulate pressure within the glomerulus, driving filtration. Though fenestrated capillaries form the glomerulus itself, these vessels cannot regulate flow and pressure because they have no smooth muscle.

The kidney is responsible for excreting nitrogenous waste produced by the urea cycle, maintaining water balance (and thus blood pressure), maintaining salt concentrations in the blood, and controlling blood pH by excreting or retaining protons. Blood flows into the nephrons through the glomerulus and is pushed into Bowman's capsule. The filtrate then flows through the proximal tubule, the main site for most reabsorption of glucose, proteins, and electrolytes. From the proximal tubule it enters the loop of Henle, where salt and water balance is regulated via the ion gradient in the extracellular space of the renal medulla. Finally, the filtrate enters the distal tubule and collecting duct, where salt, water, and proton balance is further regulates.

The liver is responsible for gluconeogenesis and glycogen storage.