Table 3.

Associations between normal anion gap (hyperchloremic) acidosis and cardiovascular outcomes in marginal structural models

	Outcome
	Cardiovascular events			Cardiovascular events and all-cause death
	HR	95% CI	P-value	HR	95% CI	P-value
Without normal anion gap acidosis	Ref.	–	–	Ref.	–	–
Normal anion gap acidosis	0.74	0.47‒1.17	0.2	1.11	0.80‒1.54	0.5

Normal anion gap acidosis is defined as an adjusted bicarbonate level ≤22.8 mEq/L.

Models were adjusted for (i) baseline covariates including age, sex, body mass index, smoking history, systolic blood pressure, diabetes mellitus, cardiovascular comorbidities, cardiothoracic ratio, albumin, eGFR, hemoglobin, sodium, potassium, calcium, phosphate, uric acid, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, UPCR, C-reactive protein, loop diuretics, thiazide diuretics, spironolactone, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, beta-blockers, statins and sodium bicarbonate, and (ii) time-dependent covariates including albumin, eGFR, hemoglobin, sodium, potassium, calcium, phosphate, uric acid, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, UPCR, C-reactive protein, loop diuretics, thiazide diuretics, spironolactone, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, beta-blockers, statins and sodium bicarbonate.

Ref., reference.