Effects of Dipyridamole on the Short-Term Evolution of Glomerulonephritis

Cámara, Sebastián Bruque; Cruz, J. P. De La; Frutos, M.Á.; Sánchez, Pedro; Novales, E. Lopez de; Sanchez, Eric; Cuesta, Felipe Sánchez de la

doi:10.1159/000186370

Cited by 24 publications

(7 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Anti-proliferative effects on rat mesangial cells have also been reported [8], and, over 15 years ago, Cattell and Mehotra [13] noted that matrix expansion in a rat model of mesangioproliferative glomerulonephritis was also decreased after DP treatment. In addition, several previous studies have shown that DP exerts an anti-proteinuric effect and can reduce the progression of glomerular disease, albeit in small numbers of subjects [14, 15]. …”

Section: Discussionmentioning

confidence: 99%

Dipyridamole Inhibits Human Mesangial Cell Proliferation

Hillis

Duthie²,

MacLeod³

1998

Nephron

View full text Add to dashboard Cite

Background: Many glomerular diseases are associated with mesangial cell proliferation and the accumulation of extracellular matrix. At present, there are, however, few treatments which can inhibit these processes. The current study assessed the effects of the anti-platelet and putative anti-proliferative drug dipyridamole (DP) on the growth of human mesangial cells in vitro and their production of the extracellular matrix protein, fibronectin. Methods: Human mesangial cell proliferation, both intrinsic and stimulated by platelet-derived growth factor, was assessed using ³H-thymidine incorporation and an MTT proliferation assay. A sandwich enzyme-linked immunosorbent assay was used to study the effects of DP on fibronectin synthesis, again in cells stimulated by transforming growth factor beta 1 and in unstimulated cells. Results: At concentrations compatible with the serum levels found in subjects consuming standard dosages, DP significantly inhibited the growth of human mesangial cells in vitro in a dose-dependent fashion. DP also abrogated the mitogenic effects of platelet-derived growth factor. It had no significant effects on the synthesis of fibronectin by these cells (either spontaneous or induced by transforming growth factor beta 1). There was no evidence of cytotoxicity. Conclusion: These data suggest that DP may have a therapeutic role in proliferative glomerulonephritis and possibly other diseases characterized by cell proliferation.

show abstract

Section: Discussionmentioning

confidence: 99%

Dipyridamole Inhibits Human Mesangial Cell Proliferation

Hillis

Duthie²,

MacLeod³

1998

Nephron

View full text Add to dashboard Cite

show abstract

“…Mea sures inhibiting mesangial proliferation at any stage of glomerular disease may have important clinical implica tions in delaying the progression of renal disease [1]. Dipyridamole has been reported to be beneficial for patients with glomerulonephritis [21,22], The mecha nism is often thought to be related to its antiplatelet action or hemodynamic effect [23,24]. Dipyridamole has also been shown to decrease mesangial proliferation in either experimental glomerulonephritic models or in human subjects [25,26], Our study may be the first to prove the effect of dipyridamole on mesangial cell proliferation in a cell culture system.…”

Section: Discussionmentioning

confidence: 99%

Vasodilator Agents Modulate Rat Glomerular Mesangial Cell Growth and Collagen Synthesis

Tsai¹,

Lin

Chang

et al. 1995

Nephron

View full text Add to dashboard Cite

Mesangial cell activation and extracellular matrix accumulation are hallmarks of many forms of glomerulonephropathy. We investigated the effect of several agents possessing vasodilating activities on rat mesangial cell growth and collagen synthesis. Using cell counting and a modified MTT assay, it was shown that dipyridamole, pentoxifylline, dicentrine, prazosin and doxazosin all caused a dose-dependent inhibition of serum-stimulated rat mesangial cell proliferation. Platelet-derived growth factor-induced cell proliferation was also inhibited by doxazosin and pentoxifylline. Dipyridamole and pentoxifylline inhibited collagen synthesis in confluent mesangial cells while dicentrine and doxazosin did not. The procollagen α1 (I) mRNA expression was also decreased by dipyridamole and pentoxifylline. These results suggested that, in addition to dipyridamole, pentoxifylline and α1-adrenoceptor blockers may have a potential to delay the progression of chronic glomerulopathy associated with mesangial proliferation.

show abstract

“…The importance of platelets in the development of renal injury can also be inferred by several studies demonstrating beneficial effects of antiplatelet therapy in glomerulonephritis. Treatment with antiplatelet agents reduced proteinuria in patients with IgAN [15, 16] or MGN [15]. Long-term administration of antiplatelet agents in combination with low dose warfarin retarded the deterioration of renal function in IgAN [17].…”

Section: Discussionmentioning

confidence: 99%

Influence of β3 Integrin Gene Leu33/Pro33 Polymorphism on Primary Glomerulonephritis

Bantis

Heering

Aker

et al. 2004

Nephron Exp Nephrol

View full text Add to dashboard Cite

Background: β₃ integrin subunit is expressed as α_IIbβ₃ integrin on platelets and as α_vβ₃ integrin on a variety of cells including renal endothelial, mesangial and tubular cells. Leu³³/Pro³³ polymorphism of β₃ integrin has been associated with altered platelet functions, cardiovascular complications and the incidence of acute rejection episodes in renal transplantation. We investigated its influence on IgA nephropathy (IgAN), focal segmental glomerulosclerosis (FSGS) and membranous glomerulonephritis (MGN). Methods: We studied 251 patients with biopsy-proven primary glomerulonephritis (IgAN n = 127, FSGS n = 71, MGN n = 53) followed up for 6.3 ± 5.3 years and 100 control subjects. Patients were classified according to the slope of reciprocal serum creatinine into slow (n = 162) and fast progressors (n = 89). Leu³³/Pro³³ polymorphism was determined by PCR amplification followed by restriction with the endonuclease Bcnl. Results: The genotype frequencies were similar in patients and controls (n.s.). Initial renal function, proteinuria and blood pressure did not differ significantly between patients with different genotypes (n.s.). The genotype frequencies were similar in slow and fast progressors (n.s.). Furthermore, Leu³³/Pro³³ polymorphism had no impact on renal survival in the Kaplan-Meier analysis (n.s.). Conclusion: Our results indicate that β₃ integrin Leu³³/Pro³³ polymorphism is not a risk factor or a marker of progression in primary glomerulonephritis.

show abstract

Effects of Dipyridamole on the Short-Term Evolution of Glomerulonephritis

Cited by 24 publications

References 12 publications

Dipyridamole Inhibits Human Mesangial Cell Proliferation

Dipyridamole Inhibits Human Mesangial Cell Proliferation

Vasodilator Agents Modulate Rat Glomerular Mesangial Cell Growth and Collagen Synthesis

Influence of β<sub>3</sub> Integrin Gene Leu<sup>33</sup>/Pro<sup>33</sup> Polymorphism on Primary Glomerulonephritis

Contact Info

Product

Resources

About