Early effects of contrast media on renal hemodynamics and tubular function in chronic renal failure.

The pathophysiology and prevention of contrast media (CM)-induced nephropathy in chronic renal failure (CRF) are still ill defined. GFR, RPF, endothelin-1 (ET-1) levels, urinary sodium concentration, and fractional excretion of sodium were measured in CRF patients undergoing water 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 iopamidol (I). The two CM induced an immediate and progressive decline of both 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 excretion of sodium. The natriuresis could not be totally ascribed to a CM-induced osmotic diuresis as because the urinary sodium concentration markedly increased. In two further groups of patients receiving D, we studied the effects of pretreatment with a single dose of either captopril or nifedipine. Both drugs, although not preventing the increase of natriuresis, partially antagonized D-induced renal hypoperfusion: GFR and 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, plasma ET-1 did not change but urinary levels increased; these changes were, however, dissociated from those observed in renal hemodynamics. Both plasma and urinary levels of ET-1 did not vary in pretreated groups. The 72-h follow-up evidenced a significant reduction of renal function only in the unpretreated D group. Therefore, the main findings after CM administration in CRF patients are: (1) an immediate GFR decline proportional to the osmolarity of CM and secondary to the renal hypoperfusion that is neither caused by hypovolemia nor mediated by ET-1, (2) an early tubular dysfunction at the level of the proximal nephron, and (3) a protective effect of single-dose pretreatment with either captopril or nifedipine on D-induced acute and short-term GFR changes.

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Inhibition of neutral endopeptidase stimulates renal sodium excretion in patients with chronic renal failure

Clinical Science ◽

10.1042/cs0840031 ◽

1993 ◽

Vol 84 (1) ◽

pp. 31-39 ◽

Cited By ~ 10

Author(s):

J. C. Dussaule ◽

C. Michel ◽

M. N. Peraldi ◽

J. M. Lecomte ◽

C. Gros ◽

...

Keyword(s):

Renal Failure ◽

Chronic Renal Failure ◽

Cyclic Gmp ◽

Atrial Natriuretic Factor ◽

Fractional Excretion ◽

Neutral Endopeptidase ◽

Factor Level ◽

Natriuretic Factor ◽

Fractional Excretion Of Sodium ◽

Atrial Natriuretic

1. The acute effects of a single oral dose of sinorphan (100 mg), an inhibitor of neutral endopeptidase, on the plasma atrial natriuretic factor level and the fractional excretion of sodium were examined in 12 patients with severe chronic renal failure who were not on maintenance haemodialysis and who ingested a normal sodium diet. The drug was administered against placebo by a double-blind cross-over protocol. 2. Basal plasma atrial natriuretic factor level and fractional excretion of sodium were high (23.2 ± 3.7 pmol/l and 2.64 ± 0.38%, respectively). Sinorphan inhibited plasma neutral endopeptidase activity by 68–75% 30 min after ingestion. This effect persisted for at least 4 h. There were simultaneously increases in plasma atrial natriuretic factor and cyclic GMP levels to 1.9 and 1.4 times the basal values, respectively. Fractional excretion of sodium increased during the second and third hour periods after ingestion of the drug with a peak of 1.9 times the basal value in the second period. Changes in fractional excretion of sodium were significantly correlated with those in plasma atrial natriuretic factor and cyclic GMP levels. Plasma aldosterone level, creatinine clearance and mean blood pressure were unchanged, whereas plasma renin activity increased slightly. An increase in urinary cyclic GMP excretion was observed in parallel with the increase in plasma cyclic GMP level. 3. The results of the present study indicate that (i) high basal values of plasma atrial natriuretic factor level and fractional excretion of sodium, as observed in patients with chronic renal failure, are associated with marked effects of neutral endopeptidase inhibition; (ii) fractional sodium excretion increases after protection of endogenous atrial natriuretic factor from degradation independently of any initial change in extracellular fluid volume or sodium intake, which suggests that this hormone may play a role in the control of sodium excretion in chronic renal failure.

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Low fractional excretion of sodium with contrast media-induced acute renal failure

Archives of Internal Medicine ◽

10.1001/archinte.140.4.531 ◽

1980 ◽

Vol 140 (4) ◽

pp. 531-533 ◽

Cited By ~ 9

Author(s):

L. S. Fang

Keyword(s):

Renal Failure ◽

Acute Renal Failure ◽

Contrast Media ◽

Fractional Excretion ◽

Fractional Excretion Of Sodium

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Low Fractional Excretion of Sodium With Contrast Media-Induced Acute Renal Failure

Archives of Internal Medicine ◽

10.1001/archinte.1980.00330160091033 ◽

1980 ◽

Vol 140 (4) ◽

pp. 531 ◽

Cited By ~ 91

Author(s):

Leslie S. T. Fang

Keyword(s):

Renal Failure ◽

Acute Renal Failure ◽

Contrast Media ◽

Fractional Excretion ◽

Fractional Excretion Of Sodium

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Uroangiographic Contrast Media-Induced Nephropathy: Correlations between Their Physicochemical Properties and Renal Damage

Urologia Journal ◽

10.1177/039156030507200405 ◽

2005 ◽

Vol 72 (4) ◽

pp. 446-456

Author(s):

C. Alberti ◽

M. Piovano ◽

A. Tizzani

Keyword(s):

Diabetes Mellitus ◽

Renal Failure ◽

Acute Renal Failure ◽

Chronic Renal Failure ◽

Contrast Media ◽

Renal Damage ◽

Contrast Material ◽

Vasoactive Mediators ◽

Adequate Hydration ◽

Hospital Acquired

Contrast media-induced nephropathy (CN) is an important cause of hospital-acquired acute renal failure. Patients with both diabetes mellitus and renal impairment are at high risk. CN pathophysiology involves activation of the tubulo-glomerular feedback and vasoactive mediators such as renin-angiotensin 2, endothelin, adenosine, ADH, etc. The risk of CN can be minimized by the use of non-ionic, low or isoosmolar, contrast material, adequate hydration and prophylactic pharmacological measures. In patients with chronic renal failure who are undergoing arteriography (e.g. coronary angiography and angioplasty), periprocedural hemofiltration appears effective in preventing further renal damage due to contrast agents.

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