Renal blood flow factors altering

Column C represents a case in which sympathetically mediated renal vascular tone is assumed to be a significant factor in maintaining the elevated pressure, and column D depicts possible changes in the few cases of human essential hypertension in which a continued fall in pressure is noted for some time after sympathectomy, perhaps also on the basis of altered renal blood flow. Column E represents a common result of sympathectomy or adrenergic blockade in renal and essential hypertension this result may or may not be preceded by some early fall in pressure such as illustrated in column C. 

Both prerenal factors (dehydration, blood loss, altered vasomotor tone, age-related decreases in renal blood flow in rats) and postrenal factors (obstruction or extravasation of urine to the peritoneal cavity) may cause elevations of the commonly measured analytes that do not reflect primary kidney injury. Plasma analytes also cannot be used to determine the location of renal injury (glomerular versus tubular, or tubular segment affected) (Baum et al. 1975 Corman and Michel 1987 Finco 1997 Newman and Price 1999). 

Functional renal insufficiency is manifested as increases in serum creatinine and blood urea nitrogen. As cardiac output and renal blood flow decline, renal perfusion is maintained by the vasoconstrictor effect of angiotensin II on the efferent arteriole. Patients most dependent on this system for maintenance of renal perfusion (and therefore most likely to develop functional renal insufficiency with ACE inhibitors) are those with severe heart failure, hypotension, hyponatremia, volume depletion, and concomitant use of NSAIDs. - Sodium depletion (usually secondary to diuretic therapy) is the most important factor in the development of functional renal insufficiency with ACE inhibitor therapy. Renal insufficiency therefore can be minimized in many cases by reduction in diuretic dosage or liberalization of sodium intake. In some patients, the serum creatinine concentration will return to baseline levels without a reduction in ACE inhibitor dose. Since renal dysfunction with ACE inhibitors is secondary to alterations in renal hemodynamics, it is almost always reversible on discontinuation of the drug. ... 

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