USMLE® Step 1 style questions USMLE
There are many factors that influence sodium reabsorption and excretion in the kidneys. Which of the following causes increased excretion of sodium into the urine?
Content Reviewers:Viviana Popa, MD
Sodium is a positive ion or a cation noted with Na.
In the extracellular fluid, sodium has a concentration of about 135 milliequivalents (mEq) per liter.
Sodium is essential in maintaining water balance, as well as for nerve impulse conduction and muscle contraction.
Now, osmolality refers to the total solute concentration in a certain amount of solvent or water.
By affecting plasma osmolality, sodium determines plasma and blood volume.
So, at the end of the day, it’s important to maintain the sodium concentration in order to keep enough blood inside our arteries.
This blood is called the effective arterial blood volume or EABV, and it’s what ends up perfusing our various organs and tissues.
Okay, now, sodium comes from our diet.
The daily recommended sodium intake is about 2.3 grams per day which is the equivalent of a teaspoon of salt per day.
Once ingested, sodium is absorbed in the blood by the GI tract, and travels through the bloodstream unbound to plasma proteins.
At the other end, some sodium is eliminated from the body through sweat and through feces, but most of it comes out, along with water, as pee.
So the kidneys are the cornerstone of sodium homeostasis.
The renal corpuscle, in turn, is made up of the glomerulus, which is a tiny clump of capillaries, and Bowman’s capsule surrounding it.
So, blood gets to the glomerulus through the afferent arteriole, which is a branch of the renal artery, and leaves the glomerulus through the efferent arterioles.
These vessels act like a coffee filter, allowing everything but red blood cells and proteins to pass from the bloodstream into Bowman’s capsule - which is connected to the renal tubule.
And the resulting fluid is called filtrate.
Now, upon exiting the glomerulus, the efferent arterioles divide into capillaries a second time, forming the peritubular vessels, which wrap around the segments of the renal tubule: the proximal convoluted tubule, the U- shaped loop of Henle, which has a descending and ascending limb, the distal convoluted tubule, and the collecting duct.
As filtrate passes through the renal tubule, ions like sodium are filtered from the capillaries into the lumen of the tubule, and reabsorbed from the lumen into the capillaries, depending on the amount of sodium in the bloodstream.
So first, 67% of the sodium in the tubule lumen is reabsorbed in the proximal convoluted tubule or in the PCT.
This segment is also permeable to water, so whenever a sodium molecule is reabsorbed, water is reabsorbed along with it - which is called isosmotic reabsorption.
Now, in the early PCT, sodium is reabsorbed together with other molecules, through 3 different channels found on the surface of tubular cells.
Sodium and glucose are reabsorbed together through the sodium-glucose cotransporter, sodium and amino acids are also reabsorbed together through the sodium- amino acid cotransporter and finally, phosphate and sodium are reabsorbed together through the sodium-phosphate cotransporter.
PTH inhibits the sodium-phosphate cotransporter, so more sodium and phosphate are excreted.
Finally, in the early PCT there’s also a sodium-hydrogen exchanger, which is a cell membrane protein that reabsorbs sodium in exchange for hydrogen.
And this is mainly regulated by a molecule called angiotensin II, which is a product of the renin-angiotensin-aldosterone system.
Now, renin is an enzyme that’s released by the kidneys in response to hypotension.
In short, the way it goes is that renin stimulates angiotensinogen conversion into angiotensin I which is then converted into angiotensin II.
Angiotensin II has many functions, some of which include vasoconstriction of the efferent renal arteriole and stimulating the sodium-hydrogen exchanger.
In turn, this increases sodium reabsorption and water reabsorption, in order to bring up blood pressure.
Second, in the late PCT, sodium is still reabsorbed through the sodium-hydrogen exchanger, and also along with chloride, through the chloride-formate exchanger.
This transporter reabsorbs chloride and secretes formate, which is a negative ion derived from formic acid.
In the late PCT, sodium and chloride can also get reabsorbed through a paracellular way, meaning that they don’t use any channels, but rather they sneak between two epithelial cells and go back into the bloodstream.
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