<p>Inflammation plays a crucial role in the progression of autosomal dominant polycystic kidney disease (ADPKD). While tolvaptan is primarily known for its vasopressin V2 receptor antagonism, its potential anti-inflammatory effects remain under investigation. This study aimed to evaluate the impact of tolvaptan on inflammatory markers and renal progression in ADPKD patients. This retrospective, two-center cohort study included 80 ADPKD patients, with 40 receiving tolvaptan and 40 serving as controls. Inflammatory markers, including C-reactive protein (CRP), systemic inflammatory index (SII), platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio (NLR), and renal function parameters such as glomerular filtration rate (GFR) and proteinuria, were analyzed over a 1-year follow-up period. In the tolvaptan group, CRP, SII, PLR, proteinuria, and uric acid levels significantly decreased, whereas these markers increased in the control group. GFR remained stable in the tolvaptan group but declined significantly in the control group (<i>p</i> &lt; 0.001). No significant correlation was found between GFR and inflammatory markers in either group. Our findings suggest that tolvaptan may contribute to reducing systemic inflammation in ADPKD patients while preserving renal function. These results align with previous studies indicating a link between inflammation and ADPKD progression.</p>

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The effect of tolvaptan on renal progression and systemic inflammation in ADPKD

  • Ahmet Ziya Şahin,
  • Orhan Özdemir

摘要

Inflammation plays a crucial role in the progression of autosomal dominant polycystic kidney disease (ADPKD). While tolvaptan is primarily known for its vasopressin V2 receptor antagonism, its potential anti-inflammatory effects remain under investigation. This study aimed to evaluate the impact of tolvaptan on inflammatory markers and renal progression in ADPKD patients. This retrospective, two-center cohort study included 80 ADPKD patients, with 40 receiving tolvaptan and 40 serving as controls. Inflammatory markers, including C-reactive protein (CRP), systemic inflammatory index (SII), platelet-to-lymphocyte ratio (PLR), neutrophil-to-lymphocyte ratio (NLR), and renal function parameters such as glomerular filtration rate (GFR) and proteinuria, were analyzed over a 1-year follow-up period. In the tolvaptan group, CRP, SII, PLR, proteinuria, and uric acid levels significantly decreased, whereas these markers increased in the control group. GFR remained stable in the tolvaptan group but declined significantly in the control group (p < 0.001). No significant correlation was found between GFR and inflammatory markers in either group. Our findings suggest that tolvaptan may contribute to reducing systemic inflammation in ADPKD patients while preserving renal function. These results align with previous studies indicating a link between inflammation and ADPKD progression.