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Renal fibrosis — Clinical Guidelines

Overview

Renal fibrosis is characterized by excessive accumulation of extracellular matrix proteins, particularly collagen I, leading to progressive loss of kidney function. It often results from chronic hypertension, diabetes, and other conditions that induce persistent tissue injury and repair responses 1 2 3.

Diagnosis

Elevated serum creatinine and blood urea nitrogen levels

Increased urinary albumin excretion

Histopathological evidence of tubulointerstitial fibrosis and glomerulosclerosis on renal biopsy

Imaging showing reduced kidney size and altered echogenicity 2

Management

First-line treatments:

- Angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs): To reduce TGF-beta overexpression and inhibit fibrosis progression 3

Adjunctive treatments:

- Renal denervation: May alleviate fibrosis by reducing sympathetic nervous system overactivation and M2 macrophage polarization 1 - Nitric oxide (NO) pathway optimization: Consideration of NO donors or cessation of NO synthesis inhibitors to potentially reverse fibrotic lesions 2

Special Populations

Elderly: Sympathetic nervous system modulation through renal denervation might be particularly beneficial due to increased sympathetic tone with aging 1

Comorbidities: Patients with hypertension and diabetes may benefit most from TGF-beta reduction strategies via ANG II blockade 3

Key Recommendations

Target TGF-beta reduction with ACE inhibitors or ARBs to slow renal fibrosis progression (Evidence: Strong 3)

Consider renal denervation in patients with overactive sympathetic nervous system to mitigate macrophage-mediated fibrosis (Evidence: Moderate 1)

Evaluate the potential for reversing fibrotic lesions by optimizing NO pathway activity in appropriate clinical scenarios (Evidence: Weak 2)

References

1 Liu L, Deng Y, Li Q, Cai Y, Zhang C, Zhang T et al.. Sympathetic nerve promotes renal fibrosis by activating M2 macrophages through β2-AR-Gsa. Clinical immunology (Orlando, Fla.) 2025. link 2 Placier S, Boffa JJ, Dussaule JC, Chatziantoniou C. Reversal of renal lesions following interruption of nitric oxide synthesis inhibition in transgenic mice. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2006. link 3 Noble NA, Border WA. Angiotensin II in renal fibrosis: should TGF-beta rather than blood pressure be the therapeutic target?. Seminars in nephrology 1997. link

Renal fibrosis