EARLY EFFECTS OF CONTRAST-MEDIA ON RENAL HEMODYNAMICS AND TUBULAR FUNCTION IN CHRONIC-RENAL-FAILURE

The pathophysiology and prevention of contrast media (CM)-induced neph ropathy in chronic renal failure (CRF) are still ill defined. GFR, RPF , endothelin-1 (ET-1) levels, urinary sodium concentration, and fracti onal excretion of sodium were measured in CRF patients undergoing wate r diuresis in basal conditions and 20 to 120 min after an iv bolus of either the high-osmolar CM diatrizoate (D) or the low-osmolar CM iopam idol (I). The two CM induced an immediate and progressive decline of b oth GFR and RPF in the absence of hypovolemia, more pronounced in D (- 36% at 120 min) than after I (-19% at 120 min; P< 0.05 versus D). Both CM determined a marked and steady increase of the fractional excretio n of sodium. The natriuresis could not be totally ascribed to a CM-ind uced osmotic diuresis as because the urinary sodium concentration mark edly increased. In two further groups of patients receiving D, we stud ied the effects of pretreatment with a single dose of either captopril or nifedipine. Both drugs, although not preventing the increase of na triuresis, partially antagonized D-induced renal hypoperfusion: GFR an d RPF were equally reduced by 20% in D/captopril and D/nifedipine (P < 0.05 versus D). In unpretreated patients receiving either D or I, pla sma ET-1 did not change but urinary levels increased; these changes we re, however, dissociated from those observed in renal hemodynamics. Bo th plasma and urinary levels of ET-1 did not vary in pretreated groups . The 72-h follow-up evidenced a significant reduction of renal functi on only in the unpretreated D group. Therefore, the main findings afte r CM administration in CRF patients are: (1) an immediate GFR decline proportional to the osmolarity of CM and secondary to the renal hypope rfusion that is neither caused by hypovolemia nor mediated by ET-1, (2 ) an early tubular dysfunction at the level of the proximal nephron, a nd (3) a protective effect of single-dose pretreatment with either cap topril or nifedipine on D-induced acute and short-term GFR changes.