Expansion of extracellular fluid volume is central to the pathophysiology of heart failure.
Increased extracellular fluid leads to elevated intracardiac filling pressures, resulting in a …

Diuretic Treatment in Heart Failure | New England Journal of Medicine Skip to main content The
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Consumption of low dietary potassium, common with ultraprocessed foods, activates the
thiazide-sensitive sodium chloride cotransporter (NCC) via the w ith no (K) lysine …

Daily dietary potassium (K+) intake may be as large as the extracellular K+ pool. To avoid
acute hyperkalemia, rapid removal of K+ from the extracellular space is essential. This is …

Dietary potassium deficiency activates thiazide-sensitive sodium chloride cotransport along
the distal nephron. This may explain, in part, the hypertension and cardiovascular mortality …

WNK kinases, along with their upstream regulators (CUL3/KLHL3) and downstream targets
(the SPAK/OSR1 kinases and the cation-Cl− cotransporters [CCCs]), comprise a signaling …

The discovery of four genes responsible for pseudohypoaldosteronism type II, or familial
hyperkalemic hypertension, which features arterial hypertension with hyperkalemia and …

Aberrant activation of with no lysine (WNK) kinases causes familial hyperkalemic
hypertension (FHHt). Thiazide diuretics treat the disease, fostering the view that …

Potassium often has a negative connotation in Nephrology as patients with chronic kidney
disease (CKD) are prone to develop hyperkalaemia. Approaches to the management of …

Key points High dietary potassium (K+) intake dephosphorylates and inactivates the NaCl
cotransporter (NCC) in the renal distal convoluted tubule (DCT). Using several ex vivo …