The reasons for the different rates of progression to renal failure seen in individual patients exhibiting similar nosologic forms of glomerulopathies and equivalent levels of hypertension and for the lack of a uniform beneficial effect of antihypertensive therapy are disconcerting. Recent experimental data have offered several attractive hypotheses to explain the variable relationship between glomerular injury and hypertension. First, glomerular injury may depend on whether or not systemic hypertension is transmitted to the glomerular capillaries. For instance, immune-mediated glomerulonephritis in spontaneously hypertensive rats (SHR) leads to mild glomerular damage because an effective increment in preglomerular resistance prevents transmission of systemic pressure to the glomerular capillaries. Conversely, hypertensive Dahl salt-sensitive rats develop severe glomerular damage because deficient preglomerular vasoconstriction results in transmission of systemic pressure to the glomerular capillaries. Second, not all antihypertensive regimens have similar salutary effects on the kidney. Indeed, reduction in systemic blood pressure by certain antihypertensive agents may fail to reduce or may, in fact, increase glomerular injury if the agent reduces renal vasodilatation accompanied by glomerular hypertension. Finally, dietary variations in protein, lipid, and electrolyte content may modify the relationship between hypertension and glomerular injury. It is suggested that the variable rates of progression to renal failure observed in hypertensive humans with glomerulonephritis may be dependent on mechanisms similar to those found in experimental animals.
|Original language||English (US)|
|Issue number||4 II MONOGR. 121|
|State||Published - Jan 1 1986|
ASJC Scopus subject areas
- Internal Medicine