Nyrefibrose

Nyrefibrose, or kidney fibrosis, is a pathological process characterized by scarring of renal parenchyma due to persistent injury. It involves excessive accumulation of extracellular matrix, loss of functional nephrons, and structural remodeling, ultimately leading to chronic kidney disease.

In pathophysiology, fibrosis develops as tubulointerstitial injury activates fibroblasts into myofibroblasts, which secrete matrix proteins, causing tubular atrophy and capillary rarefaction. Inflammation and hypoxia contribute. It is a common final pathway for many kidney diseases regardless of initial cause. Key mediators include transforming growth factor-beta (TGF-β) and other profibrotic cytokines.

Causes and risk factors include long-standing hypertension, diabetes mellitus, chronic glomerulonephritis, polycystic kidney disease, nephrotoxins, obstructive nephropathy, and aging. The condition may be present alongside proteinuria and progressive chronic kidney disease.

Clinical presentation and diagnosis: patients typically present with gradual decline in kidney function (reduced eGFR), possibly accompanied by proteinuria and hypertension. Diagnostics include measurements of renal function, urinalysis, imaging such as ultrasound showing small, echogenic kidneys, and, when indicated, kidney biopsy demonstrating interstitial fibrosis and tubular atrophy. The extent of fibrosis often correlates with prognosis, though management focuses on preserving remaining renal function.

Treatment and prognosis: no cure exists; treatment aims to slow progression and manage complications. Key strategies include blood pressure control with renin–angiotensin system inhibitors, glycemic control in diabetes, lipid management, smoking cessation, and avoidance of nephrotoxins. Emerging antifibrotic therapies are under investigation. Prognosis depends on the underlying cause and the extent of fibrosis, ranging from stabilization to progression to end-stage kidney disease.