Table 3.

Results of multivariable Cox regression analyses assessing the associations between baseline serum suPAR concentration and CKD progression, ESKD, worsening proteinuria, and all-cause mortality, after stratification by APOL1 risk status in the African-American Study of Kidney Disease and Hypertension

APOL1 Risk Status	Outcome	No. of events	HRa (95% CI)	P Value
High risk: two risk alleles; n=143	CKD progression	81	1.25 (0.93 to 1.68)	0.15
	ESKD	69	1.32 (0.94 to 1.84)	0.10
	Doubling of UPCR to ≥220 mg/g	85	1.46 (1.08 to 1.99)	0.02
	All-cause mortality	20	1.37 (0.61 to 3.06)	0.44
Low risk: zero or one risk allele; n=464	CKD progression	168	1.42 (1.17 to 1.73)	<0.001
	ESKD	106	1.56 (1.20 to 2.04)	0.001
	Doubling of UPCR to ≥220 mg/g	235	1.12 (0.97 to 1.31)	0.13
	All-cause mortality	71	1.53 (1.19 to 1.97)	0.001
Not genotyped; n=348	CKD progression	114	1.15 (0.91 to 1.45)	0.24
	ESKD	96	1.35 (1.04 to 1.76)	0.03
	Doubling of UPCR to ≥220 mg/g	128	0.87 (0.71 to 1.05)	0.15
	All-cause mortality	127	1.17 (0.96 to 1.41)	0.12

Results were adjusted for demographics (age and sex), the African American Study of Kidney Disease and Hypertension trial arm (BP control goal and trial medication), kidney measures (UPCR and measured GFR), and clinical risk factors (history of heart disease, history of smoking, and C-reactive protein) at baseline. CKD progression was defined as doubling of serum creatinine from baseline or ESKD (requiring dialysis or kidney transplantation). Worsening proteinuria was defined as pre-ESKD doubling of 24-hour UPCR to ≥220 mg/g. suPAR, soluble urokinase-type plasminogen activator receptor; HR, hazard ratio; 95% CI, 95% confidence interval; UPCR, 24-hour urine protein-to-creatinine ratio.

^aHR per SD higher log-transformed baseline suPAR.