Abstract

CD4+CD25+ T cells are critical for maintenance of immunologic self-tolerance. We measured the number of CD4+CD25+ cells in the patients with primary malignant hypertension related kidney injury, to explore the molecular pathogenesis of this disease. We selected 30 patients with primary malignant hypertension related kidney injury and 30 healthy volunteers. Information on clinical characteristics and laboratory tests was obtained from each subject. The number of CD4+CD25+ cells and glomerular injury were assessed by flow cytometry and histopathology, respectively. Both serum IL-2, IL-4, and IL-6 and endothelial cell markers were analyzed by ELISA. ADAMTS13 antibody was detected by Western blotting. CD4+CD25+ cells were significantly reduced in patients with primary malignant hypertension related kidney injury compared to controls (P < 0.05). The number of CD4+CD25+ cells was negatively related to blood urea nitrogen, serum uric acid, proteinuria, and supernatant IL-4; whereas positively associated with estimated glomerular filtration rate in patients. Gradually decreasing CD4+CD25+ cells were also found as increasing renal injury. Additionally, patients exhibited increasing supernatant IL-4, serum IL-2 and IL-6, endothelial cell markers, and anti-ADAMTS13 antibody compared with controls (all P < 0.05). CD4+CD25+ cells may play a key role in the pathogenesis of primary malignant hypertension related kidney injury.

Highlights

  • Malignant hypertension (MHTN) is defined as severely elevated blood pressure (BP) with a Keith and Wagener stage III or IV retinopathy[1]

  • The results from flow cytometry analysis peripheral blood live-dead lymphocytes showed live lymphocytes accounted for 99% in both patients with MHTN related kidney injury and controls (CD3- FITC positive cells; PI negative cells); whereas the number of dead lymphocytes was less than 1% (Fig. 1)

  • The results exhibited that the number of CD4+CD25+ cells was significantly decreased in patients with primary MHTN related kidney injury compared to controls (P < 0.05) (Table 1)

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Summary

Introduction

Malignant hypertension (MHTN) is defined as severely elevated blood pressure (BP) (diastolic BP > 130 mm Hg) with a Keith and Wagener stage III or IV retinopathy[1]. Recent studies have shown that CD4+CD25+ cells display a crucial role in the immunological self-tolerance via inhibiting the proliferation and activation of autoreactive T cells[6]. Their depletion might result in the organ-specific autoimmunity developing and autoimmunity diseases, and these changes could be prevented by CD4+CD25+ cells in the animal models[7]. We investigated the association between the number change of CD4+CD25+ cells and the development of MHTN related kidney injury using a case-control study to test the hypothesis that a numerical or functional deficit of CD4+CD25+ cells might trigger the development of disease

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