hyperKalemia = too much potasium (K)
Typical sources of K = oranges, bananas, beans, etc
K is intracellular while sodium is extracellular

[www.ncbi.nlm.nih.gov]

We survive the banana smoothie because of a rapid response that shifts potassium into cells and into the urine. Thus the large intracellular potassium store constitutes a potential threat but is also a lifesaving buffer.

Hyperkalemia is associated with an increased risk of death, and this is only in part explicable by hyperkalemia-induced cardiac arrhythmia. In addition to its well-established effects on cardiac excitability, hyperkalemia could also contribute to peripheral neuropathy and cause renal tubular acidosis.

When the same potassium load was administered as part of a complex meal, there was no change in plasma [K+], probably reflecting insulin-mediated transcellular potassium shifts (Prong 2). Despite there being no change in venous plasma [K+], there was an increase in renal potassium excretion

Plasma [K+] is controlled by aldosterone in a negative feedback loop. Aldosterone is synthesized by aldosterone synthase (AS) in the adrenal cortex in response to high [K+]e and angiotensin II.

Ninety percent of excreted potassium exits via the kidneys and the kidneys have a remarkable capacity to increase potassium excretion in the face of potassium excess [16].

Diabetes mellitus is a risk factor for hyperkalemia (independent of RAS blockade) because of its association with hyporeninemic hypoaldosteronism.

The most notorious consequence of hyperkalemia is that of potentially fatal cardiac dysrhythmia.

Large observational studies demonstrate an association between hyperkalemia and an increased risk of death [39, 58, 59].

hyperkalemia may manifest as any of various ECG abnormalities: P, QRS, ST or T wave changes, resolution of conduction blocks, new conduction blocks, asystole, atrial fibrillation, ventricular fibrillation or ventricular tachycardia.

there is emerging evidence that hyperkalemia may also exert clinically important effects on neuronal excitability.

They speculate that chronic hyperkalemia could contribute to the pathogenesis of uremic neuropathy and myopathy. In support of this, dietary potassium restriction improved peripheral nerve function in patients with CKD in a single-blind RCT [71].



Edited 2 time(s). Last edit at 05/07/2022 10:28PM by Panchito.