ArticleWorld journal of nephrology2026
Effect of pentoxifylline on inflammatory markers in non-diabetic chronic kidney disease patients: A prospective, interventional, open label.
Article in World journal of nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPentoxifylline (PTX), a methylxanthine derivative, has been shown to exert notable anti-inflammatory and antiproteinuric actions in diabetic kidney disease, contributing to improved sodium handling, attenuation of renal hypertrophy, and reductions in tumour necrosis factor-alpha (TNF-α), interleukin-6 levels, and albuminuria.
aimTo determine the impact of PTX on inflammatory biomarkers and the progression of chronic kidney disease (CKD) in non-diabetic patients.
methodsThis prospective, interventional, open label, randomized controlled clinical study was conducted on 42 participants aged 18 years or older, of both genders, with CKD stages 3 or 4 and proteinuria < 1 g/24 hours. Participants were placed into two equal groups. Group 1 had standard therapy, including angiotensin-converting enzyme inhibitors (ACEIs; ramipril 1.25 mg), calcium acetate (700 mg), alfacalcidol (0.25 µg), antihypertensives, and diuretics. Group 2 had the same standard therapy plus PTX 400 mg (Trental
resultsThere was no significant relationship between TNF-α and high-sensitivity C-reactive protein (hs-CRP) and participants' gender in both groups. An essential direct correlation was observed between TNF-α and creatinine in both groups. A critical direct correlation was observed between hs-CRP and calcium in group B. There was a significant inverse correlation between the change in TNF-α and estimated glomerular filtration rate, as well as between the change in TNF-α and the urinary protein-to-creatinine ratio. The change in protein creatinine ratio noted in group 2 was mainly due to changes in mean arterial pressure, followed by changes in TNF-α.
conclusionIn non-diabetic CKD patients, adjunctive treatment with PTX was associated with significant decreases in C-reactive protein levels and proteinuria. The reduction in proteinuria was mainly explained by changes in mean arterial pressure, followed by changes in TNF-α, indicating that hemodynamic factors may play a more prominent role than inflammatory modulation in mediating this effect.
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