Heat shock protein 70 and anti-heat shock protein 70 antibodies in patients with chronic glomerulonephritis

Abstract

We evaluated the heat shock system 70 (HSP70) in patients with chronic glomerulonephritis (CGN). Seventy-six patients with CGN patients were included in our study. Ten patients with mild proteinuria (median 0.48 [0.16–0.78] g/24 h) and ten healthy subjects served as positive and negative controls, respectively. Urinary levels of HSP70, interleukin-10, and serum levels of anti-HSP70 were measured by ELISA. The immunohistochemical peroxidase method was used to study the expression of HSP70 and Foxp3+ in kidney biopsies. Treg^FoxP3+ cells in the interstitium were determined morphometrically. Median urinary HSP70 levels in patients with nephrotic syndrome (NS) [6.57 (4.49–8.33) pg/mg] and subnephrotic range proteinuria [5.7 (4.12–6.9) pg/mg] were higher (p < 0.05) than in positive [3.7 (2.5–4.82) pg/mg] and negative [3.78 (2.89–4.84) pg/mg] controls. HSP70 expression index in tubular cells positively correlated with urinary HSP70 (Rs = 0.948, р < 0.05) and proteinuria (Rs = 0.362, p < 0.05). The number of Treg^Foxp3+ cells in the kidney interstitium and interleukin-10 excretion were lower in patients with NS. Anti-HSP70 antibody serum levels in patients with NS [21.1 (17.47–29.72) pg/ml] and subnephrotic range proteinuria [24.9 (18.86–30.92) pg/ml] were significantly higher than in positive [17.8 (12.95–23.03) pg/ml] and negative [18.9 (13.5–23.9) pg/ml] controls. In patients with CGN, increasing proteinuria was associated with higher HSP70 renal tissue and urinary levels. However, activation of HSP70 in patients with nephrotic syndrome did not lead to an increase in tissue levels of Treg^Foxp3+ cells or to the release of IL-10.