Abstract
BackgroundThe role of T-regulatory cells (Tregs) in inflammatory renal disease is not yet established. We attempted to study peripherally circulating T-cells expressing RORγt+Foxp3+ dynamics in acute kidney injury (AKI) and chronic kidney disease (CKD).AimTo determine the role of T-regulatory cells in AKI and CKD.Research methodology This is a cross-sectional study conducted between January 2019 to January 2021 at a single tertiary care centre in Pune, India. Candidates enrolled in the study were either patients with CKD not on maintenance hemodialysis or newly diagnosed cases of AKI. Kidney transplant recipients, patients with autoimmune diseases like systemic lupus erythematosus (SLE), IgA nephropathy, or those receiving immuno-suppressants were excluded. T-lymphocytes were analyzed using a flow cytometer. ResultsWe studied 80 patients with kidney injury, 40 each belonging to the AKI and CKD study groups and 10 healthy volunteers as controls. The rationale behind having a small control group was to merely get an idea of T helper 17 (Th17):Treg ratio and different immune cell-phenotype profiles in healthy volunteers without kidney injury, diabetes, hypertension or any other risk factors. The ratio of RORγt:Foxp3 was ≤ 1 in these individuals (control group) while this ratio was significantly altered (MFI RORγt:Foxp3 ≥1) in the AKI/CKD study arm. We examined peripherally circulating T-lymphocytes in acute kidney injury and chronic kidney disease, comparing their activity to healthy volunteers. Biopsy-proven kidney injury patients (29/80) were also included in this study. We found that the ratio of RORγt:Foxp3 was altered in patients with kidney injury (acute and chronic) and was statistically significant compared to controls, indicating that injury may be attributed to T-cell dysfunction. ConclusionOur study provides some evidence of T-cell dysfunction in the pathology of kidney injury in acute and chronic kidney disease via activity of Foxp3 and RORγt. We found that there is evidence of altered Th17/Treg activity in kidney injury, more prevalent in acute than chronic, when compared to healthy volunteers.
Highlights
The kidney is a highly vascular organ, vital for maintaining internal homeostasis via removal of toxins from the blood
We studied 80 patients with kidney injury, 40 each belonging to the acute kidney injury (AKI) and chronic kidney disease (CKD) study groups and 10 healthy volunteers as controls
We found that the ratio of RORγt:Foxp3 was altered in patients with kidney injury and was statistically significant compared to controls, indicating that injury may be attributed to T-cell dysfunction
Summary
The kidney is a highly vascular organ, vital for maintaining internal homeostasis via removal of toxins from the blood. Its anatomical structure and function render it vulnerable to a variety of immune, and nonimmune mediated injury. Kidney disease is a heterogeneous group of disorders affecting its structure and/or function. Inflammation contributes to a myriad of acute and chronic diseases affecting the kidneys. There is a complex relationship between acute kidney injury (AKI) and chronic kidney disease (CKD); AKI can lead to CKD, and CKD increases the risk of AKI [1]. The role of T-regulatory cells (Tregs) in inflammatory renal disease is not yet established. We attempted to study peripherally circulating T-cells expressing RORγt+Foxp3+ dynamics in acute kidney injury (AKI) and chronic kidney disease (CKD)
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