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Document Details :

Title: Hoe nefroprotectief zijn de antihypertensiva?
Author(s): VERBEKE F
Journal: Tijdschrift voor Geneeskunde
Volume: 63    Issue: 6   Date: 2007   
Pages: 238-240
DOI: 10.2143/TVG.63.06.2000046

Abstract :
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Nephroprotective effects of antihypertensive drugs
Chronic kidney disease is the most common identifiable cause of hypertension but may be a consequence of essential hypertension as well. Both conditions result in a vicious circle, the residual renal function being further damaged by the increased blood pressure.
Activation of the renin-angiotensin-aldosteron system and the resulting fluid overload play a key role in causing systemic as well as intraglomerular hypertension, resulting in macrovascular complications, glomerular hyperfiltration, proteinuria and subsequent loss of renal function. Hyperfiltration induced glomerulosclerosis is thought to be the final common pathway of most renal diseases, including diabetic nephropathy, and is the principal target of pharmacological intervention intended to slow the progression to end-stage renal failure.
Angiotensin-converting enzyme inhibitors and/or angiotensin-receptor blockers are considered first-line agents in diabetic nephropathy and nondiabetic renal disease with proteinuria. The renoprotective effect is strongly related to the obtained reduction of the proteinuria. Non-dihydropiridine calcium channel blockers also reduce proteinuria, but less data on hard endpoints are currently available. For other antihypertensive agents and in case of non-proteinuric kidney disease, no additional renoprotection beyond the blood pressure lowering effect has been demonstrated.

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