A nephron is the tiny functional unit of the kidney, responsible for filtering blood, reclaiming useful substances, and producing urine. Each human kidney contains roughly 900,000 nephrons on average, though the range is enormous: autopsy studies have counted as few as 210,000 and as many as 2.7 million per kidney. Every drop of urine you produce is the end result of millions of nephrons working simultaneously, each one performing a precise sequence of filtration, reabsorption, and secretion.
How a Nephron Is Structured
A nephron has two main parts: a filtering component and a long tube that processes the filtered fluid. The filtering component is a tiny ball of capillaries called the glomerulus, wrapped inside a cup-shaped structure. The tube extends from that cup through several distinct segments, each with a different job. In order, these segments are the proximal tubule, the loop of Henle, the distal tubule, and the collecting duct (which is technically shared by multiple nephrons).
All nephron filters sit in the kidney’s outer layer, called the cortex. But not all nephrons are the same length. About 85% are cortical nephrons with short loops that stay near the outer kidney. The remaining 15% are juxtamedullary nephrons with long loops that plunge deep into the kidney’s inner tissue, the medulla. Those long-looped nephrons are especially important for concentrating urine, which is why they’re surrounded by specialized blood vessels called the vasa recta that help maintain the chemical gradients needed for that process.
Step 1: Filtering the Blood
The nephron’s first job is to push a large volume of fluid out of the blood and into the tubule. This happens at the glomerulus, where high blood pressure forces water and small dissolved molecules through a three-layered filter. The first layer is the wall of the capillary itself, which has tiny windows (fenestrations) in it. The second is a mesh-like basement membrane. The third and final barrier consists of specialized cells called podocytes, which wrap around the capillary and form narrow slits between their finger-like projections.
Together, these three layers act like a very selective sieve. Water, salts, glucose, amino acids, and waste products pass through easily. Large proteins and blood cells do not. When protein does show up in urine, it’s often a sign that this filtration barrier has been damaged. In a healthy adult, the combined filtering rate across all nephrons produces a glomerular filtration rate (GFR) of 90 or above, measured in milliliters per minute. That number is one of the most common benchmarks doctors use to assess kidney health.
Step 2: Reclaiming What the Body Needs
The raw filtrate that enters the tubule contains a lot of things the body can’t afford to lose. The proximal tubule, the first stretch of tubing after the filter, does the heaviest lifting: it reabsorbs 60% to 70% of all filtered salt and water. It also reclaims virtually all filtered glucose and amino acids under normal conditions. The cells lining this segment are packed with energy-burning transport proteins that actively pull these substances back into the blood.
This is why the proximal tubule is so vulnerable to toxins and low blood flow. It has one of the highest metabolic demands of any tissue in the body. When it’s overwhelmed, substances like glucose can spill into the urine, which is exactly what happens when blood sugar is very high in uncontrolled diabetes.
Step 3: Concentrating the Urine
After the proximal tubule, the filtrate enters the loop of Henle, a hairpin-shaped segment that dips down into the medulla and then climbs back up. This loop creates the conditions that allow the kidney to produce urine that’s either very dilute or very concentrated, depending on how much water the body needs to conserve.
The loop works through a countercurrent multiplier system. The ascending limb actively pumps chloride and sodium out of the tubule into the surrounding tissue, making the medulla increasingly salty. Meanwhile, the descending limb is permeable to water, so water flows out of the tubule passively, drawn by that surrounding saltiness. Urea, a waste product, also gets trapped in the medulla and adds to the concentration gradient. The net effect is a medulla that grows progressively saltier from the outer edge to the inner tip, creating the osmotic pull needed to concentrate urine in the final stages.
Step 4: Fine-Tuning Salt and Water Balance
The distal tubule and collecting duct are where hormones step in to make final adjustments. Aldosterone, a hormone released by the adrenal glands, acts on the late distal tubule and collecting duct to increase sodium reabsorption. When sodium is pulled back into the blood, potassium is pushed out in exchange. This linked mechanism is why aldosterone is central to controlling both sodium and potassium levels, and why drugs that block aldosterone can raise potassium.
Water balance is controlled separately by a hormone called vasopressin (also known as antidiuretic hormone, or ADH). When you’re dehydrated, vasopressin levels rise. The hormone triggers collecting duct cells to insert water channel proteins into their surfaces, making the duct walls permeable to water. Because the surrounding medulla is so salty from the work of the loop of Henle, water rushes out of the collecting duct and back into the blood. The result is small volumes of concentrated urine. When you’re well-hydrated, vasopressin drops, the water channels are pulled back inside the cells, and the collecting duct becomes waterproof. You produce large volumes of dilute urine instead. This process is entirely reversible and can shift within minutes.
Tubular Secretion: The Other Direction
Reabsorption moves substances from the tubule back into the blood, but the nephron also works in the opposite direction. Tubular secretion actively transports certain waste products and drugs from the blood into the tubule for elimination. This is especially important for substances that weren’t efficiently filtered at the glomerulus or that need to be cleared quickly.
The nephron has separate transport systems for positively and negatively charged molecules. Positively charged compounds like certain diabetes and antiviral medications are handled by one set of transporters. Negatively charged compounds, including many antibiotics, anti-inflammatory drugs, and diuretics, use another. This broad capacity for secretion is one reason the kidney is so susceptible to drug interactions: two medications competing for the same transporter can slow each other’s clearance and raise blood levels unexpectedly.
Nephron Loss Over a Lifetime
You’re born with all the nephrons you’ll ever have. Unlike liver cells or skin cells, nephrons do not regenerate once lost. And loss is inevitable. A study published in the Journal of the American Society of Nephrology found that healthy adults lose about 6,200 nephrons per year, amounting to a 7.3% decline per decade. Young adults aged 18 to 29 averaged about 991,000 functioning nephrons per kidney. By ages 70 to 75, that number had dropped to roughly 520,000, nearly half.
The remaining nephrons compensate by working harder, which is why kidney function can stay adequate for decades even as nephron numbers fall. But this compensation has limits. People who start with fewer nephrons (due to low birth weight, genetics, or other factors) have less reserve and may be more vulnerable to kidney disease later in life. Scarred nephrons don’t simply sit idle: they gradually shrink and get reabsorbed until they’re no longer detectable, which is why older estimates based on visible scarring underestimated the true extent of nephron loss by a wide margin.