The urinary podocyte is postulated to be a marker for estimation of the severity of active glomerular injury and a predictor of
disease progression in children with
glomerulonephritis. Non-
dihydropyridine calcium antagonist, including
verapamil, reduce
proteinuria to an extent similar to that of the
angiotensin-converting enzyme inhibitor (ACEI), including
trandolapril, but to a greater extent than other
antihypertensives.
Angiotensin (Ang) II receptor antagonists, including
candesartan cilexetil, show potent and long-term preventive effects against the progression of renal injury. The aim of the present study is to assess whether
verapamil,
trandolapril and
candesartan cilexetil affect
proteinuria and urinary podocytes in patients with
IgA nephropathy. Thirty-two normotensive patients aged 18-54 years with biopsy-proven
IgA nephropathy, nonnephrotic
proteinuria (1-3 g/day), and normal renal function (
creatinine clearance >80 ml/min) were studied. Twenty patients with diffuse mesangial proliferative
glomerulonephritis (non-
IgA PGN) and 20 healthy controls were also included in this study. The number of urinary podocytes in patients with advanced
IgA nephropathy (n = 16) was significantly higher than that in patients with the disease in the mild stage (n = 16) (p < 0.01) or in patients with non-
IgA PGN (p < 0.01). Urinary podocytes were not detected in healthy controls. The 32 patients with
IgA nephropathy were randomly divided into four treatment groups: those treated with
verapamil (120 mg/day, n = 8); those treated with
trandolapril (2 mg/day, n = 8); those treated with
candesartan cilexetil (8 mg/day, n = 8), and those given a placebo (n = 8). Treatment continued for 3 months. Antiproteinuric response in the
trandolapril group was similar to that in the
candesartan cilexetil group (-38 vs. -40%). The action of
trandolapril or
candesartan cilexetil was greater than that of
verapamil (p < 0.01). Reduction in the number of urinary podocytes from baseline was significantly greater in patients treated with
trandolapril or
candesartan cilexetil than in patients treated with
verapamil (p < 0.01). However, there was no difference between patients treated with
trandolapril and those treated with
candesartan cilexetil.
Proteinuria and urinary podocytes were unaffected in the placebo group. These data suggest that urinary podocytes may be a marker of disease activity in adult patients with
IgA nephropathy and that
trandolapril and
candesartan cilexetil are more effective than
verapamil in reducing the number of podocytes.