Urine synaptopodin excretion is an important marker of glomerular disease progression

Podocytes play an important role in maintaining the glomerular filtration barrier and in formation of the slit diaphragm. Podocyte loss is associated with chronic kidney disease progression, but it is not clear whether urinary podocyte proteins in urine reflect the clinical extent of glomerular damage. We investigated the correlation between the amounts of urinary podocyte proteins and renal function and albuminuria.

The study enrolled 33 patients with diabetic kidney disease or glomerular disease and measured urinary podocytes proteins using Western blotting. Urinary podocyte proteins were measured according to the density of the bands on Western blotting. We measured serum creatinine and the spot urine albumin/creatinine ratio as markers of renal damage, and compared the correlation of urinary podocyte protein in the glomerular disease patients.

The mean patient age was 49.3 ± 16.5 years, the mean serum creatinine level was 2.30 ± 1.76 mg/dL, and the mean albumin/creatinine ratio was 4.85 ± 3.52. Among the podocyte proteins, urine synaptopodin showed strong correlation with serum creatinine by multivariate regression analysis (p < 0.001) and showed linear correlation (r = 0.429, p < 0.01). Urine podocyte proteins were increased in patients with diabetes, and synaptopodin showed the greatest significant difference (7.68 ± 5.61 vs. 2.56 ± 3.11, p < 0.001), but this might be associated with renal impairment. The urine albumin excretion did not differ between the diabetics and non-diabetics (p = 0.73).

Urine synaptopodin is associated with serum creatinine elevation in the patients with glomerulonephritis including diabetic kidney disease regardless of urine albumin excretion. We suggest that the urine synaptopodin level can predict glomerular damage independently of the urine albumin excretion.