The biomarker suPAR and nephrology

The suPAR level is associated with:

  • Chronic renal diseases3
  • Future incidence of chronic renal diseases4
  • Declining eGFR4,5

In the kidneys, suPAR plays a role in the regulation of the permeability of the glomerular filtration barrier, and suPAR may be involved in podocyte damage and development of focal segmental glomerulosclerosis and diabetic nephropathy1,2.

The suPAR level increases in patients with chronic renal diseases, and a high level is significantly associated with mortality and incidence of cardiovascular diseases in these patients3.

The association between suPAR and chronic renal diseases has been further studied in a large study4. It was found that the suPAR level was an independent predictor of declining eGFR. During the study follow-up period of 3.7 years, the decline in eGFR in subjects in the lower suPAR quartile was 0.9 mL/min/1.73 m2 and 4.2 mL/min/1.73 m2 in the upper quartile.

In 1335 individuals with an eGFR >60 mL/min/1.73 m2 at study start, a suPAR level in the upper quartile was associated with a significantly increased incidence of chronic renal diseases compared to those in the lower quartile; all in all, a 3-fold increased risk4.

In patients with primary and secondary glomerulonephritis, an elevated suPAR level is similarly associated with reduced eGFR and presence of proteinuria5.

Reduced renal function causes a significant increase in suPAR level, and in hemodialysis patients, the mean value is 14.8 ng/mL. In this group of patients, a high level is associated with increased mortality and increased risk of hospitalization6.

Another resent study further supports the strong link between suPAR and development of kidney disease. This study of patients with type 1 diabetes showed that elevated suPAR is associated with increased risk of fast eGFR decline and of end-stage renal disease7.

1. Wei c, El Hindi S, Li J et al. Nat Med 2011;17:952-60.
2. Yoo H, Pedigo CE, Guzman J. J AM Soc Nephrol 2015 jan;26(1):133-47
3. Meijers B, Poesen R, Claes K et al. Kidney Int 2015 Jan;87(1):210-216.
4. Hayek S, Sever S, Ko Y et al. N Engl J Med. 2015 Nov 12; 373(20):1916-25.
5. Musetti C, Quaglia M, Cena T et al. J Nephrol 2015 Jun;28(3):299-305.
6. Griveas I, Andpriopoulos C, Sitaras P et al. Dial. Transplant 2015;30(suppl 3)
7. Rotbain Curovic V et al, Diabetes Care. 2019. pii: dc181427.