Effect of dilazep dihydrochloride on urinary albumin excretion in patients with autosomal dominant polycystic kidney disease.

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Abstract

Proteinuria and microalbuminuria occur with a highly variable severity and are associated with progression of autosomal dominant polycystic kidney disease (ADPKD). Dilazep dihydrochloride, an antiplatelet drug, is effective in patients with immunoglobulin A nephropathy or diabetic nephropathy. We studied whether dilazep dihydrochloride affects the urinary albumin excretion (UAE) in normotensive and hypertensive patients with ADPKD. Twelve normotensive ADPKD patients with microalbuminuria were randomly assigned to two groups: a dilazep (300 mg/day) treatment group (n = 6, group A) and a placebo group (n = 6, group B). In addition, 10 hypertensive ADPKD patients with microalbuminuria were randomly assigned to two groups: a dilazep (300 mg/day) treatment group (n = 5, group C) and a placebo group (n = 5, group D). Treatment with dilazep was continued for a period of 6 months, at the end of which the UAE was reduced form 130 +/- 52 to 46 +/- 26 microg/min (p < 0.01) in group A. There was no reduction in group C. There were no changes in UAE in placebo groups B and D. These results suggest that dilazep dihydrochloride may be effective in reducing UAE in normotensive ADPKD patients with microalbuminuria.

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Proteinuria as a Mediator of Tubulointerstitial Injury

Mauro Abbate, Giuseppe Remuzzi (1999)

Proteinuria is one of the most potent risk factors for renal disease progression in patients with glomerular diseases. Studies in disease models have helped to delineate mechanisms leading to renal structural damage due to persistent dysfunction of the glomerular barrier to proteins, even when the primary immune or nonimmune insult to the kidney has ceased. The main focus of this review is the role of the tubular epithelial cell in the induction of interstitial inflammatory and fibrogenic reactions to ultrafiltered proteins. Antiproteinuric drugs (angiotensin–converting enzyme inhibitors, ACEi) while preserving the integrity of the glomerular permselective barrier limit both proteinuria and protein–dependent processes which contribute to tubulointerstitial injury, and in so doing ACEi halt the progression of proteinuric nephropathies toward terminal renal failure.