Browse evidence-based analysis of health-related claims and assertions
The levels of various blood chemicals like electrolytes, hormones, and kidney markers don't change based on how much sodium someone excretes in their urine.
Correlational
Sodium excretion levels don't affect blood pressure, heart rate, or how much blood the heart pumps when lying down.
People who excrete more sodium in their urine tend to have more fluid outside their cells.
After starting dapagliflozin, the kidneys produced more aldosterone hormone for a few days, which might help the body retain salt, but this effect didn't last after two weeks.
People with type 2 diabetes and healthy kidneys lost about 0.8 kg after a few days and 1.8 kg after two weeks of taking dapagliflozin, likely due to water loss.
Dapagliflozin made the kidneys less able to reabsorb sodium in the first part of the nephron, which is why more lithium was excreted, showing the drug's effect on kidney function.
As expected, dapagliflozin caused people with type 2 diabetes to excrete much more sugar in their urine, which is how the drug works to lower blood sugar.
Dapagliflozin didn't significantly change the amount of fluid in the bloodstream of people with type 2 diabetes and healthy kidneys, even after two weeks of treatment.
Dapagliflozin caused a temporary decrease in body fluid volume outside cells after 4 days, but this effect went away after two weeks in people with type 2 diabetes and healthy kidneys.
Even though dapagliflozin lowered blood pressure, it didn't cause people with type 2 diabetes and healthy kidneys to excrete more salt in their urine when they ate a controlled amount of salt.
Taking dapagliflozin for two weeks lowered blood pressure by about 6-7 points in people with type 2 diabetes and healthy kidneys, even when they ate a controlled amount of salt.
Mice with kidney-specific PER1 removal have higher levels of a kidney signaling molecule called endothelin-1. This finding is from the abstract summary - full study details were not available
Descriptive
Removing PER1 from mouse kidneys changes how genes related to body clock and stress hormones work in the adrenal glands. This finding is from the abstract summary - full study details were not available
Mice with kidney-specific PER1 removal show higher levels of a hormone that regulates salt and blood pressure. This finding is from the abstract summary - full study details were not available
When mice have the PER1 protein removed from their kidneys, their daily salt excretion rhythm stays normal even with a high-salt diet and hormone treatment. This finding is from the abstract summary - full study details were not available
When mice have the PER1 protein removed specifically from their kidneys, they retain more salt when given a high-salt diet and a hormone treatment, which could affect blood pressure regulation. This finding is from the abstract summary - full study details were not available
Mice with extra kidney lymphatic vessels on a hypertension-inducing drug had lower blood pressure compared to normal mice.
Quantitative
Mice with extra kidney lymphatic vessels on a high-salt diet had lower levels of genes that control salt reabsorption in the kidneys.
When mice got a quick salt injection, extra kidney lymphatic vessels didn't change how much salt they excreted right away.
When mice ate a normal diet, growing more lymphatic vessels in their kidneys didn't change how they handled salt or water.
Mice with extra kidney lymphatic vessels had less of two key proteins that reabsorb salt in the kidneys, helping them excrete more salt.
Mice with extra kidney lymphatic vessels on a high-salt diet had more of a hormone that helps the body get rid of salt and water.
Mice with extra kidney lymphatic vessels on a hypertension-inducing drug excreted more sodium relative to their kidney function compared to normal mice.
Growing more lymphatic vessels in mouse kidneys during high-salt intake doubled the amount of fluid in the kidney tissue, acting like a sponge to hold extra fluid.