Contrast Medium Associated Nephrotoxicity

RISK FACTORS THAT PREDISPOSE TO CONTRAST ASSOCIATED NEPHROPATHY

Confirmed

Suspected

Disproved

Chronic renal failure

Hypertension

Myeloma

Diabetic nephropathy

Generalized atherosclerosis

Diabetes without

Severe congestive

Abnormal liver

nephropathy

heart failure

function tests

Amount and frequency

Hyperuricemia

of contrast media

Proteinuria

Volume depletion

or hypotension

Risk factors that predispose to contrast-associated nephropathy. In random populations undergoing radiocontrast imaging the incidence of contrasts associated nephropathy defined by a change in serum creatinine of more than 0.5 mg/dL or a greater than 50% increase over baseline, is between 2% and 7%. For confirmed high-risk patients (baseline serum creatinine values greater than 1.5 mg/dL) it rises to 10% to 35%. In addition, there are suspected risk factors that should be taken into consideration when considering the value of contrast-enhanced imaging.

Hypersomolar radiocontrast medium

tPGE2

tANF2

tEndothelin tVasopressin tAdenosine iPGL

Systemic hypoxemia t Blood viscosity tRBF ÜRBF

Calcrnm antagonists

Theophylline

^ATPase

Osmotic load to distal tubule

Net -IO2 delivery! I Net tO2 consumption

Cell injury

tTH protein

\

7

Tubular obstruction

\

7

IGFR

tIntrarenal number of macrophages, T cells Stimulation of mesangium

Superoxidgte dis mutas:

Reactive O2 species lipid peroxidase

"V

Contrast associated nephropathy

FIGURE 11-22

A proposed model of the mechanisms involved in radiocontrast medium-induced renal dysfunction. Based on experimental mod els, a consensus is developing to the effect that contrast-associated nephropathy involves combined toxic and hypoxic insults to the kidney [35]. The initial glomerular vasoconstriction that follows the injection of radiocontrast medium induces the liberation of both vasoconstrictor (endothelin, vasopressin) and vasodilator (prostaglandin E2 [PGE2], adenosine, atrionatiuretic factor {ANP}) substances. The net effect is reduced oxygen delivery to tubule cells, especially those in the thick ascending limb of Henle. Because of the systemic hypoxemia, raised blood viscosity, inhibition of sodium-potassium-activated ATPase and the increased osmotic load to the distal tubule at a time of reduced oxygen delivery, the demand for oxygen increases, resulting in cellular hypoxia and, eventually cell death. Additional factors that contribute to the acute renal dysfunction of contrast-associated nephropathy are the tubule obstruction that results from increased secretion of Tamm-Horsfall proteins and the liberation of reactive oxygen species and lipid peroxidation that accompany cell death. As noted in the figure, calcium antagonists and theophylline (adenosine receptor antagonist) are thought to act to diminish the degree of vasoconstriction induced by contrast medium.

The clinical presentation of contrast-associated nephropathy involves an asymptomatic increase in serum creatinine within 24 hours of a radiographic imaging study using contrast medium, with or without oliguria [36].

We have recently reviewed the clinical outcome of 281 patients with contrast-associated nephropathy according to the presence or absence of oliguric acute renal failure at the time of diagnosis. Of oliguric acute renal failure patients, 32% have persistent elevations of serum creatinine at recovery and half require permanent dialysis. In the absence of oliguric acute renal failure the serum creatinine value does not return to baseline in 24% of patients, approximately a third of whom require permanent dialysis. Thus, this is not a benign condition but rather one whose defined risks are not only permanent dialysis but also death. GFR—glomerular filtration rate; RBF—renal blood flow; TH—Tamm Horsfall protein.

PREVENTION OF CONTRAST ASSOCIATED NEPHROPATHY

Hydrate patient before the study (1.5 mL/kg/h) 12 h before and after Hemodynamically stabilize hemodynamics. Minimize amount of contrast medium administered.

Use nonionic, iso-osmolar contrast media for patients at high risk (see Figure 11-21).

FIGURE 11-23

Prevention of contrast-associated nephropathy. The goal of management is the prevention of contrast-associated nephropathy.

Thus it is important to select the least invasive diagnostic procedure that provides the most information, so that the patient can make an informed choice from the available clinical alternatives.

Since radiographic contrast imaging is frequently performed for diabetic nephropathy, congestive heart failure, or chronic renal failure, concurrent administration of renoprotective agents has become an important aspect of imaging. A list of maneuvers that minimize the risk of contrast-associated nephropathy is contained in this table. The correction of prestudy volume depletion and the use of active hydration before and during the procedure are crucial to minimizing the risk of contrast-associated nephropathy. Limiting the total volume of contrast medium and using nonionic, isoosmolar media have proven to be protective for high-risk patients. Pretreatment with calcium antagonists is an intriguing but unsubstantiated approach.

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