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Reviewed by:
Former Admissions Committee Member, Hofstra-Northwell School of Medicine
Reviewed: 2/14/25
We’re going to talk about one of the most important organs on the MCAT: the kidney. First, we want to understand the physiology of the nephron. The point of it is to make sure we keep important things like water and some salts, while getting rid of toxic or excess substances.
So, where does the nephron get all this fluid and solute to begin with? The blood, of course—specifically, the afferent arteriole.
The afferent arteriole brings bodily fluid to the nephron at Bowman’s capsule.
The bundle of arterioles inside Bowman’s capsule is called the glomerulus. The glomerulus filters out large proteins and only allows water or other small solutes through, like sodium and potassium. At Bowman’s capsule, this blood is filtered into the nephron. That’s the key word we use to describe when we move fluid from the blood into the nephron: filtration.
Now, the fluid is called filtrate.
The filtrate then moves to the proximal convoluted tubule, or PCT, where some solutes and water are reabsorbed. “Reabsorbed” means we’re going from the kidney to the blood again.
The efferent arteriole covers the whole kidney, and these water and salts are all directly going into this efferent arteriole through a process called reabsorption.
It’s called reabsorption because the first absorption happens when you ingest a substance, and it goes from the digestive system into the bloodstream. So now, it’s being reabsorbed into the bloodstream.
The filtrate will then move from the PCT to the next part of the kidneys: the loops of Henle. So we need to draw these in.
The filtrate will start moving down the descending loop of Henle. At the descending loop of Henle, this is where water is reabsorbed into the surrounding tissues. So how does this water move out here? Well, I’ll give you a hint: it doesn’t take any ATP. Since it takes no ATP, this means it must be going down its concentration gradient. As we see, the deeper we get, we see the higher the salt concentration. This allows for “free” energy to just let water move through, but as we’ll see in a second, this isn’t free at all.
Let’s continue following the path of our filtrate. It’s coming down; we just lost some water, so now the filtrate is saltier as it starts going up the ascending loop of Henle. At the ascending loop of Henle, here’s where we come full circle with the salt story. The ascending loop is only permeable to sodium.
But this does take ATP. So here’s where the energy is coming in: it takes ATP to pump out the sodium, and that makes sense because the sodium is going against its concentration gradient. We’re making it a saltier environment all because of the ascending loop of Henle.
The filtrate will now be much more concentrated as we head up to the distal convoluted tubule. Here at the distal convoluted tubule, we reabsorb more water, as well as some salts.
But now, something new happens: certain molecules the body wants to excrete in the urine are secreted from the blood into the distal convoluted tubule. So, let’s say we’ve got some blood over here. Well, what are these toxins?
A helpful mnemonic is “Dump the HUNK”:
All of these are going to move into the distal convoluted tubule to soon be excreted.
Finally, the filtrate with all of these toxins is going to move into the collecting duct, where a little bit of water is still reabsorbed before finally the fluid is secreted into the bladder.
Understanding how hormones regulate the nephron is crucial for success on the MCAT. This article breaks down the major hormones that influence kidney function, including aldosterone, antidiuretic hormone (ADH), and atrial natriuretic peptide (ANP). It also covers essential physiological concepts such as the renin-angiotensin-aldosterone system (RAAS), osmolarity, countercurrent multiplication, and glomerular filtration rate (GFR)—all of which play a vital role in homeostasis and are frequently tested on the MCAT.
Aldosterone is a steroid hormone secreted by the adrenal cortex that increases sodium reabsorption in the distal convoluted tubule (DCT) and collecting duct. Since water follows sodium via osmosis, this process leads to increased blood volume and blood pressure without altering osmolarity.
Aldosterone is a key component of the RAAS, which is activated in response to low blood pressure. When blood pressure drops:
This feedback loop ensures the body maintains adequate circulation and perfusion, a key concept for MCAT physiology questions.
Unlike aldosterone, which influences sodium movement, ADH (vasopressin) regulates water reabsorption. Secreted by the posterior pituitary, ADH increases aquaporin insertion in the collecting duct, enhancing water reabsorption and concentrating urine.
Water reabsorption via ADH depends on the osmotic gradient in the renal medulla, established by the countercurrent multiplication system:
This gradient enables water to leave the collecting duct when ADH is present, concentrating the urine.
MCAT Tip: ADH reduces blood osmolarity by diluting plasma, whereas aldosterone maintains osmolarity by reabsorbing both sodium and water.
ANP serves as a counterbalance to aldosterone, reducing sodium reabsorption and lowering blood pressure. Secreted by the heart’s atria in response to high blood volume, ANP promotes sodium excretion (natriuresis), which prevents excessive fluid retention.
Since ANP reduces sodium retention, less water is reabsorbed, leading to lower blood pressure—a mechanism frequently tested in MCAT renal physiology questions.
Glomerular Filtration Rate (GFR) is a measure of how much plasma is filtered per minute by the glomeruli. It is regulated by Starling forces, which determine fluid movement across capillaries:
MCAT questions often test how changes in vascular resistance affect GFR, so understanding these dynamics is essential.
Now, let’s apply your new knowledge to a real MCAT question:
In diabetes insipidus, ADH secretion is inhibited. What happens to thirst and urine output?
Normally, ADH increases water reabsorption, reducing thirst and urine production.
Without ADH:
Answer: Inhibiting ADH leads to increased thirst and urine output (Answer Choice A).
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