الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Chronic kidney disease (CKD) is a significant global health concern, affecting over 800 million individuals worldwide. In Egypt, CKD ranks as the 5th leading cause of death, contributing to the increasing burden of the disease.
Inflammation plays a crucial role in the progression of CKD, and various inflammatory markers have been implicated in the pathogenesis of the disease. inflammatory macrophages infiltrate the kidneys, leading to the release of proinflammatory cytokines such as IL-1β, TNF-α, IL-6, and IL-23. While these cytokines may have acute beneficial effects, chronic inflammation is known to have adverse consequences.
Pentoxifylline (PTX), a methylxanthine derivative, has shown promising effects in reducing proteinuria and inflammation in diabetic kidney disease (DKD) patients. Studies on diabetic kidney disease (DKD) models have shown that PTX can improve sodium retention, renal hypertrophy, and reduce renal TNF production. PTX also decreases albuminuria and reduces the expression of TNF-α and IL-6, indicating its anti-inflammatory and antioxidant properties. However, its efficacy and impact on inflammatory markers and proteinuria in non-diabetic CKD patients remain unclear
This study aimed to assess the effect of PTX on inflammatory markers, proteinuria, and CKD progression in non-diabetic CKD patients. The current study design was a prospective, interventional, open-label, randomized controlled clinical trial conducted on adult patients with chronic Kidney Disease at the outpatient clinics of Ain Shams University hospital, Cairo, Egypt, from the start of February (2023) to the end of July (2023).
A total of 42 non-diabetic CKD patients with stage 3-4 CKD and a protein/creatinine ratio < 1 gm were enrolled in this 6-month study. The patients were divided into two groups: group I (n=21) received standard therapy according to the KDIGO guidelines, while group II (n=21) received the standard therapy plus PTX. Baseline assessments were conducted, including measurements of blood urea nitrogen (BUN), creatinine, sodium, potassium, calcium, phosphate, complete blood count (CBC), and parathyroid hormone (PTH) levels. Additionally, C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), and urinary protein-to-creatinine ratio were measured at baseline and after 6 months.
Both group I and group II demonstrated a significant decrease in proteinuria, as indicated by the protein/creatinine ratio. However, group II exhibited a more pronounced reduction in proteinuria compared to group I. Similarly, both groups showed a significant decrease in TNF-α levels, but the reduction was greater in group II. group II also exhibited a significant decrease in CRP levels. Regarding estimated glomerular filtration rate (eGFR) levels, no statistical significance was observed; however, group II experienced a greater decline compared to group I. Correlation analysis revealed a highly positive correlation between TNF-α and creatinine in both groups, TNF-α and white blood cell count in group I, TNF-α and eGFR in group II, and CRP and calcium in group II.
This study demonstrated that the addition of PTX to standard therapy in non-diabetic CKD patients resulted in a significant reduction in proteinuria and inflammatory markers. group II, receiving PTX along with standard therapy, exhibited a more significant decrease in proteinuria compared to group I. Additionally, group II showed greater reductions in TNF-α levels and CRP levels. These findings suggest that PTX may have a beneficial effect on inflammation and proteinuria in non-diabetic CKD patients, potentially contributing to the attenuation of CKD progression. Further studies are needed to explore the long-term effects of PTX and its potential as an adjunctive therapy in this patient population