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Contrast Media Induced Nephropathy: Causes, Pathogenesis, Risk Factors, and Treatment, Slides of Medicine

An in-depth analysis of contrast media induced nephropathy (cmin), the third leading cause of hospital-acquired acute renal failure. It covers the pathogenesis, risk factors, and treatment options for this condition. The document also discusses the role of radiocontrast agents in nephropathy and the preventive measures that can be taken.

Typology: Slides

2011/2012

Uploaded on 12/13/2012

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Download Contrast Media Induced Nephropathy: Causes, Pathogenesis, Risk Factors, and Treatment and more Slides Medicine in PDF only on Docsity!

Radiocontratst Nephropathy

  • Contrast media induced nephropathy (CMIN) is

the third highest cause of hospital-acquired

acute renal failure.

  • In nearly half of these patients, CMIN occurred

during cardiac diagnostic or interventional

procedures such as percutaneous coronary

intervention.

Risk

factors

Baseline renal insufficiency

DM

CHF

Large volume of contrast NSAIDs or ACEI

Volume depletion

ARF:increase in serum creat of>50 % above baseline or >1 mg/dl if baseline>2 mg/dl

  • Normal baseline creat negilgible risk
  • Mild to moderate CKD 5-10 % risk
  • Mild to moderate CKD + DM 10- 40 %
  • Advanced renal insufficiency >50 % risk
  • Endothelial dysfunction
  • Vasoactive mediators
  • Free radicals and reperfusion damage
  • Haemorheological factors
  • Tubular toxicity and immunological mechanisms

Treatment

  • The administration of Intravenous Saline.

Isotonic saline at a rate of 1 mL/kg per hour, begun at

least two and preferably 6 to 12 hours prior to the

procedure, and continuing for 6 to 12 hours after

contrast administration.

  • The administration of the antioxidant

Acetylcysteine.

Dose of 600 to 1200 mg orally twice daily,

administered the day before and the day of the

procedure, based upon its potential for benefit and

low toxicity and cost.

Treatment

  • Routine hemofiltration or hemodialysis for the

prevention of contrast nephropathy in patients

with stage 3 and 4 CKD is not recommended.

  • More data are needed in stage 5 CKD (Prophylactic

use of hemodialysis in patients with stage 5 CKD,

can be considered,provided that a functioning

access is already available)

Extracorporeal blood purification therapies for prevention of radiocontrast-induced nephropathy: a systematicreview. Am J Kidney Dis 2006; 48:361. Renal protection for coronary angiography in advanced renal failure patients by prophylactic hemodialysis. Arandomized controlled trial. J Am Coll Cardiol 2007; 50:1015.

Treatment

  • Therapies with Limited Evidence
  • Calcium Channel Blockers
  • Diuretics
  • Atrial Natriuretic Peptide (ANP)
  • Endothelin (ET) Antagonists
  • Prostaglandin E
  • ACE Inhibitors
  • The high-osmolal contrast media (osmolality 1500– 1800 mOsm/kg) are first generation agents.
  • Low-osmolal contrast media still have an increased osmolality compared with plasma (600– mOsm/kg),
  • The newest nonionic radiocontrast agents have a lower osmolality, 290 mOsm/kg, iso-osmolal to plasma
  • The volume of contrast administered to the patien also appears to correlate with the incidence of nephrotoxicity.
  • In patients who undergo only diagnostic coronary procedures, the volume of dye (approximately 100 mL) is considerably less than in patients who undergo interventional procedures (approximately 250-300 mL).

Heme pigment-induced acute tubular necrosis

  • Myoglobinuria: rhabdomyolysis.
  • Hemoglobinuria: intravascular hemolysis.

The majority of cases of rhabdomyolysis are nontraumatic

Alcohol abuse

Massive muscle compression from immobilization in drug induced coma

Drug-induced

Seizures

Occlusive peripheral vascular disease.

Combination therapy with itraconazole, simvastatin, and cyclosporine Conversion from one fibric acid to another, or from one statin-fibrate combination to another Detergent ingestion

Hemolysis

  • Transfusion reactions due to ABO incompatible blood are probably the most frequently encountered hemolytic processes that can lead to acute renal failure.
  • Severe acute hemolytic episodes in patients with glucose-6- phosphate dehydrogenase deficiency.