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In people with reduced eGFR, adaptations occur to maintain potassium homeostasis: the kidney adaptively increases potassium secretion in the remaining functioning nephrons, and gastrointestinal potassium excretion increases to up to 25% to 30% of total excretion in the case of G5 chronic kidney disease.[9,11] Serum potassium follows a circadian rhythm whereby potassium levels peak in the early afternoon and reach a nadir at 9 p.m.[12] The diurnal variability of serum potassium is much greater in the setting of chronic kidney disease (the difference between minimum and maximum potassium levels in an individual is 0.72 0.45 mmol/L) compared with normal kidney function.[12] Patients with chronic kidney disease commonly exhibit postprandial hyperkalemia with serum potassium transiently rising following a mealthis is referred to as impaired potassium tolerance.[13] Medications and comorbidities Hyperkalemia has multifactorial causes [Figure 1] .[13] Patients with chronic kidney disease, heart failure, or diabetes are commonly prescribed medications that further reduce renal potassium excretion (e.g., RAASis, MRAs) or block intracellular uptake (e.g., beta blockers)

Avoiding extreme calorie restriction often leads to better, more sustainable results

Key cardiovascular and metabolic conditions include: Hypertension particularly nocturnal hypotension or poorly controlled blood pressure Diabetes mellitus both type 1 and type 2, with microvascular complications Hyperlipidemia contributing to atherosclerotic vascular disease Obstructive sleep apnea causing intermittent hypoxia and hemodynamic fluctuations Coronary artery disease reflecting systemic atherosclerosis Smoking promoting endothelial dysfunction and vascular disease Age represents an independent risk factor, with NAION incidence increasing significantly after 50 years

Instead, it may be the result of reduced body fat and changes in circulation

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