When mice lose the KDM6A gene in their kidneys, certain salt-handling proteins increase, which makes it harder for their kidneys to get rid of salt.

Scientific Claim

Upregulation of NKCC2 and NCC transporters in mice with kidney-specific KDM6A deletion is associated with impaired sodium excretion.

Original Statement

“the expression of NKCC2 (Na-K-2Cl cotransporter 2) and NCC (Na-Cl cotransporters) was upregulated which contributes to impaired Na excretion in KDM6A-cKO mice.”

From study:KDM6A Demethylase Regulates Renal Sodium Excretion and Blood Pressure

Evidence Quality Assessment

Claim Status

overstated

Study Design Support

Design cannot support claim

Appropriate Language Strength

association

Can only show association/correlation

Assessment Explanation

Based on abstract only - full methodology not available to verify. The abstract uses causal language ('contributes to'), but the study is an animal model without explicit RCT design, so causation cannot be established.

Evidence from Studies

Supporting (1)

KDM6A Demethylase Regulates Renal Sodium Excretion and Blood Pressure

Cohort Study

Animal

2024 Mar

Contradicting (0)

No contradicting evidence found

Source Study

KDM6A Demethylase Regulates Renal Sodium Excretion and Blood Pressure

Score: 6

DOI: 10.1161/HYPERTENSIONAHA.123.22026

Similar Assertions

When mice lose the KDM6A gene in their kidney cells, their kidneys hold onto more salt and their blood pressure goes up, which might be linked to changes in a specific protein mark.

78%

Mice with extra kidney lymphatic vessels on a high-salt diet had lower levels of genes that control salt reabsorption in the kidneys.

76%