Urol. praxi. 2025;26(3):165-168 | DOI: 10.36290/uro.2025.074
Tubulointerstitial nephritis (TIN) represents a broad group of relatively heterogeneous diseases, characterized by predominant involvement of the tubules and interstitium. The pathophysiological process involves immune-mediated infiltration by inflammatory cells. When kidney cells are damaged, local antigens are expressed, leading to infiltration by inflammatory cells and activation of cytokines, which act both proinflammatory and as chemoattractant. Cytokine production by inflammatory cells (macrophages, lymphocytes) is also mediated by kidney cells (proximal tubular cells, vascular endothelial cells, interstitial cells, and fibroblasts), resulting in interstitial scarring, fibrosis, and tubular atrophy, ultimately leading to progressive chronic kidney disease. Chronic TIN can be etiologically divided into infectious, typically chronic bacterial pyelonephritis, and non-infectious, where the inflammatory process is triggered by medications, metabolic disorders, cystic diseases, autoimmune diseases or vesicoureteral reflux in childhood. Secondary involvement of the tubulointerstitium may also occur, for example, in vascular or ischemic kidney injury. The clinical presentation of chronic TIN is often nonspecific and rather oligosymptomatic, with milder manifestations than in acute forms. It may present as various tubular dysfunctions or as progressive renal insufficiency. Treatment is targeted according to the primary cause.
Accepted: September 29, 2025; Published: October 17, 2025 Show citation