Effect of Dipyridamole Treatment on Proteinuria in Pediatric Renal Disease

Abstract

The effect of dipyridamole on proteinuria was studied in 60 children with various renal diseases. A significant decrease in 24-hour urine protein excretion was observed within a few months after treatment in 32 (53%) of the patients with minimal or moderate mesangial proliferation. The effect was reproducible and parallelled by a reduction in plasma levels of β-thromboglobulin. Renal function in patients significantly improved with the therapeutical effect. The appropriate dosage was 4–10 mg/kg daily and no serious toxicity was seen despite large dosage and even in long-term application. The data suggest that dipyridamole treatment appears safe and has a beneficial effect on proteinuria dependent on its effect on platelets in renal disease.

Is the Antiproteinuric Effect of Dipyridamole Hemodynamically Mediated?

“…A more than 25% fall in proteinuria was observed in only 5 out of the 13 patients. In our hands, urinary protein excretion also decreases only in a minor ity of the patients by more than 25% during long-term oral dipyridamole therapy (150 mg in the retard formula three times a day), in contrast to the studies by Tojo et al [3] and Ueda et al [4], We conclude that the effect of dipyridamole in decreasing urinary protein excretion appears at least partly hemodynamically mediated in salt-depleted ne phrotic patients. An efferent vasodilation results in a fall in intraglomerular pressure with a concomitant, but li mited, fall in proteinuria.…”

“…Also in children with proteinuria of different etiology urinary protein loss significantly decreased in half of the patients [4].…”

Platelets mediate neutrophil-dependent immune complex nephritis in the rat.

“…The urine volume was actually higher in the platelet-depleted rats, which further suggests that the blood loss did not result in significant volume depletion. Anemia has also been reported to decrease glomerular pressures and reduce proteinuria (30 (35,36), as well as in membranoproliferative and mesangial proliferative GN in man (37,38). However, previous studies of selective platelet depletion in experimental models of glomerular disease have not consistently confirmed a role for the platelet in mediating immune renal injury.…”

Cells and Mediators in Glomerulonephritis

“…A role for anticoagulation in the treatment of prolifer ative nephritis has been under consideration for a long time [109], Indeed, the use of heparin followed by war farin and dipyridamole and a cytotoxic drug has become standard in some centres [100], There is good evidence that dipyridamole alone [110] or in combination with ticlopidine will reduce proteinuria in various types of nephritis [101]. We can now anticipate that modulation of IL-1 and/or TNF should have a good effect in stopping capillary coagulation [102].…”