Contrast-induced nephropathy

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Contrast-induced nephropathy
Specialty Nephrology, radiology

Contrast-induced nephropathy (CIN) is a purported form of kidney damage in which there has been recent exposure to medical imaging contrast material without another clear cause for the acute kidney injury.

Contents

Despite extensive speculation, the actual occurrence of contrast-induced nephropathy has not been demonstrated in the literature. [1] Analysis of observational studies has shown that radiocontrast use in CT scanning is not causally related to changes in kidney function. [2]

Terminology

Given the increasing doubts about the contribution of radiocontrast to acute kidney injury, the American College of Radiology has proposed the name contrast-associated acute kidney injury (CA-AKI) (formerly referred to as post-contrast acute kidney injury; PC-AKI) because it does not imply a causal role, with the name contrast-induced acute kidney injury (CI-AKI) (formerly referred to as contrast-induced nephropathy; CIN) reserved for the rare cases where radiocontrast is likely to be causally related. [3]

Risk factors

There are multiple risk factors of contrast-induced nephropathy, whereof a 2016 review emphasized chronic kidney disease, diabetes mellitus, high blood pressure, reduced intravascular volume, and old age. [4]

Decreased kidney function

European guidelines classify a pre-existing decreased kidney function to be a risk factor of contrast-induced nephropathy in the following cases: [5]

To calculate estimated GFR (a measure of kidney function) from creatinine, European guidelines use the CKD-EPI formula in adults ≥ 18 years, and the revised Schwartz formula in children. [5] Swedish guidelines recommends no specific formula in children because of lack of evidence, but on the other hand recommends GFR based on cystatin C rather than creatinine in those with abnormal muscle mass, liver failure, or cirrhosis. [5]

Mehran score

The Mehran score is a clinical prediction rule to estimate probability of CIN which includes the following risk factors: systolic blood pressure <80 mm Hg for at least one hour requiring inotropic support, intra-aortic balloon pump, congestive heart failure with New York Heart Association Functional Classification class III or worse, history of pulmonary edema, age >75 years, hematocrit level <39% for men and <35% for women, diabetes mellitus, contrast media volume, decreased kidney function (serum creatinine level >1.5 g/dL or decreased estimated glomerular filtration rate). [6] [7]

Other factors

European guidelines include the following procedure-related risk factors: [5]

Swedish guidelines list the following additional risk factors: [5]

Prevention

The main alternatives in people with a risk of contrast-induced nephropathy are:[ citation needed ]

Dose adjustment

According to European guidelines, the ratio of the contrast dose (in grams of iodine) divided by the absolute estimated glomerular filtration rate (GFR) should be less than 1.1 g/(ml/min) for intra-arterial contrast medium administration with first-pass renal exposure (not passing lungs or peripheral tissue before reaching the kidneys). [5] Swedish guidelines are more restrictive, recommending a ratio of less than 0.5 g/(ml/min) in patients with risk factors and irrespective of route of administration, and even more caution in first-pass renal exposure. [5]

Treating or mitigating risk factors

Hydration by drinking or intravenous volume expander, either before or after contrast administration, decreases the risk of contrast-induced nephropathy. [8] Evidence also supports the use of N-acetylcysteine with intravenous saline among those getting low molecular weight contrast. [9] [ dubious – discuss ] The use of statins with N-acetylcysteine and intravenous saline is also supported. [9]

Diagnosis

CIN is classically defined as a serum creatinine increase of at least 25% and/or an absolute increase in serum creatinine of 0.5 mg/dL [17] after using iodine contrast agent without another clear cause for acute kidney injury, [4] but other definitions have also been used. [2]

The American College of Radiology recommends the usage of the AKIN criteria for the diagnosis of CIN or PC-AKI. The AKIN criteria states that the diagnosis is made if within 48 hours from intravascular contrast medium exposure one of the following occurs: [18]

  1. Absolute serum creatinine increase of ≥0.3 mg/dl (>26.4 µmol/L) [18]
  2. Relative serum creatinine increase of ≥50 % (≥1.5-fold above baseline) [18]
  3. Urine output reduced to ≤0.5 mL/kg/hour for at least 6 hours [18]

Mechanism

The mechanism of contrast-induced nephropathy is not entirely understood, but is thought to include a combination of direct renal tubule damage from the contrast agent and reductions in blood flow to areas of the kidney. [19] The contrast agent directly damages renal tubule cells by a variety of mechanisms, one proposed mechanism is by causing changes in cell polarity. The sodium potassium pump (also known as the Na+/K+ ATPase) is redistributed from the basal surface to the luminal surface of renal tubule cells. [19] This causes sodium to be transported into the lumen where it is delivered to the distal renal tubule. This sodium load being delivered to the distal renal tubule leads to renal vasoconstriction via tubuloglomerular feedback, with the vasoconstriction and restriction of blood flow leading to injury of tubular cells. [19] Contrast agents cause damage to renal tubular cells in other ways specific to the type of contrast agent, leading to apoptosis and necrosis of the tubular cells. [19] The damaged renal tubular cells detach from the basement membrane and accumulate in the tubules which causes an increase in tubular pressure, reduced glomerular filtration rate and luminal blockage. [19] The viscosity of contrast filtered into the tubule may also contribute to increases in tubular pressure. [19]

Contrast agents may also cause renal tubular injury by causing renal vasoconstriction mediated by inhibition of vasodilators such as nitric oxide and prostaglandins and activation of endothelin. This renal vasoconstriction, along with increases in blood viscosity caused by the contrast agents themselves, leads to renal vasoconstriction and reduced blood flow to metabolically active areas of the kidneys thus causing kidney damage. [19] Changes in blood osmolality due to the contrast agents may lead to reduced red blood cell elasticity, thus leading to microthrombi development in the small blood vessels of the kidney thus further reducing glomerular blood flow. [19]

Prognosis

It is unclear if CIN causes persisting decline in renal function since few studies has followed patients for more than 72 hours. [18] In one meta-analysis the decline in renal function was shown to persist in 1.1 % of the patients with CIN. [20]

Clinical relevance

Doubts regarding the significance of the phenomenon appeared in the scientific literature. Several studies have shown that intravenous contrast material administration was not associated with excess risk of acute kidney injury, dialysis, or death, even among patients with comorbidities reported to predispose them to nephrotoxicity. [1] Moreover, hydration, the most established prevention measure to prevent contrast-induced nephropathy was shown to be ineffective in the POSEIDON trial, [21] raising further doubts regarding the significance of this disease state. [22] A meta-analysis of 28 studies of AKI after CT with radiocontrast showed no causal relationship between the use of radiocontrast and AKI. [2]

Related Research Articles

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<span class="mw-page-title-main">Creatinine</span> Breakdown product of creatine phosphate

Creatinine is a breakdown product of creatine phosphate from muscle and protein metabolism. It is released at a constant rate by the body.

<span class="mw-page-title-main">Kidney failure</span> Disease where the kidneys fail to adequately filter waste products from the blood

Kidney failure, also known as end-stage kidney disease, is a medical condition in which the kidneys can no longer adequately filter waste products from the blood, functioning at less than 15% of normal levels. Kidney failure is classified as either acute kidney failure, which develops rapidly and may resolve; and chronic kidney failure, which develops slowly and can often be irreversible. Symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications of acute and chronic failure include uremia, hyperkalaemia, and volume overload. Complications of chronic failure also include heart disease, high blood pressure, and anaemia.

<span class="mw-page-title-main">Glomerular filtration rate</span> Renal function test

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<span class="mw-page-title-main">Kidney disease</span> Damage to or disease of a kidney

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<span class="mw-page-title-main">Contrast CT</span> Medical imaging technique

Contrast CT, or contrast enhanced computed tomography (CECT), is X-ray computed tomography (CT) using radiocontrast. Radiocontrasts for X-ray CT are generally iodine-based types. This is useful to highlight structures such as blood vessels that otherwise would be difficult to delineate from their surroundings. Using contrast material can also help to obtain functional information about tissues. Often, images are taken both with and without radiocontrast. CT images are called precontrast or native-phase images before any radiocontrast has been administered, and postcontrast after radiocontrast administration.

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References

  1. 1 2 McDonald, Robert; McDonald, Jennifer S.; Carter, Rickey E.; Hartman, Robert P.; Katzberg, Richard W.; Kallmes, David F.; Williamson, Eric E. (December 2014). "Intravenous Contrast Material Exposure Is Not an Independent Risk Factor for Dialysis or Mortality". Radiology. 273 (3): 714–725. doi:10.1148/radiol.14132418. PMID   25203000.
  2. 1 2 3 Aycock, Ryan D.; Westafer, Lauren M.; Boxen, Jennifer L.; Majlesi, Nima; Schoenfeld, Elizabeth M.; Bannuru, Raveendhara R. (August 2017). "Acute Kidney Injury After Computed Tomography: A Meta-analysis". Annals of Emergency Medicine. 71 (1): 44–53.e4. doi:10.1016/j.annemergmed.2017.06.041. PMID   28811122. S2CID   27167779.
  3. ↑ "10. Post-Contrast Acute Kidney Injury and Contrast-Induced Nephropathy in Adults". ACR Manual on Contrast Media. American College of Radiology. 2022. pp. 40–50. ISBN   978-1-55903-012-0 . Retrieved 2022-08-02.
  4. 1 2 Subramaniam, RM; Suarez-Cuervo, C; Wilson, RF; Turban, S; Zhang, A; Sherrod, C; Aboagye, J; Eng, J; Choi, MJ; Hutfless, S; Bass, EB (February 2016). "Effectiveness of Prevention Strategies for Contrast-Induced Nephropathy: A Systematic Review and Meta-analysis". Annals of Internal Medicine. 164 (6): 406–16. doi: 10.7326/M15-1456 . PMID   26830221.
  5. 1 2 3 4 5 6 7 Nyman, Ulf; Ahlkvist, Joanna; Aspelin, Peter; Brismar, Torkel; Frid, Anders; Hellström, Mikael; Liss, Per; Sterner, Gunnar; Leander, Peter (2018). "Preventing contrast medium-induced acute kidney injury". European Radiology. 28 (12): 5384–5395. doi:10.1007/s00330-018-5678-6. ISSN   0938-7994. PMID   30132106. S2CID   52057355.
  6. ↑ Mehran R, Aymong ED, Nikolsky E, et al. (2004). "A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation". J. Am. Coll. Cardiol. 44 (7): 1393–9. doi:10.1016/j.jacc.2004.06.068. PMID   15464318.
  7. ↑ Kalgi Modi, Scott C. Dulebohn (2017). Contrast-Induced Nephropathy. StatPearls Publishing. PMID   28846220. CC-BY-4.0
  8. 1 2 Yang, Xiaoming; Hiremath, Swapnil; Akbari, Ayub; Shabana, Wael; Fergusson, Dean A.; Knoll, Greg A. (2013). "Prevention of Contrast-Induced Acute Kidney Injury: Is Simple Oral Hydration Similar To Intravenous? A Systematic Review of the Evidence". PLOS ONE. 8 (3): e60009. Bibcode:2013PLoSO...860009H. doi: 10.1371/journal.pone.0060009 . ISSN   1932-6203. PMC   3608617 . PMID   23555863.
  9. 1 2 Subramaniam, RM; Suarez-Cuervo, C; Wilson, RF; Turban, S; Zhang, A; Sherrod, C; Aboagye, J; Eng, J; Choi, MJ; Hutfless, S; Bass, EB (15 March 2016). "Effectiveness of Prevention Strategies for Contrast-Induced Nephropathy: A Systematic Review and Meta-analysis". Annals of Internal Medicine. 164 (6): 406–16. doi: 10.7326/m15-1456 . PMID   26830221.
  10. ↑ Sinert R, Doty CI (2007). "Evidence-based emergency medicine review. Prevention of contrast-induced nephropathy in the emergency department". Annals of Emergency Medicine. 50 (3): 335–45, 345.e1–2. doi:10.1016/j.annemergmed.2007.01.023. PMID   17512638.
  11. ↑ Bagshaw SM, Ghali WA (2005). "Theophylline for prevention of contrast-induced nephropathy: a systematic review and meta-analysis". Arch. Intern. Med. 165 (10): 1087–93. doi:10.1001/archinte.165.10.1087. PMID   15911721.
  12. ↑ Gleeson TG, Bulugahapitiya S (2004). "Contrast-induced nephropathy". AJR Am J Roentgenol. 183 (6): 1673–89. doi:10.2214/ajr.183.6.01831673. PMID   15547209.
  13. ↑ Kellum J, Leblanc M, Venkataraman R (2006). "Renal failure (acute)". Clinical Evidence (15): 1191–212. PMID   16973048.
  14. ↑ Sadat U, Usman A, Gillard JH, Boyle JR (2013). "Does ascorbic acid protect against contrast-induced acute kidney injury in patients undergoing coronary angiography: a systematic review with meta-analysis of randomized, controlled trials". J Am Coll Cardiol. 62 (23): 2167–75. doi: 10.1016/j.jacc.2013.07.065 . PMID   23994417.
  15. ↑ Putzu, Alessandro; Berto, Martina Boscolo; Belletti, Alessandro; Pasotti, Elena; Cassina, Tiziano; Moccetti, Tiziano; Pedrazzini, Giovanni (2017). "Prevention of Contrast-Induced Acute Kidney Injury by Furosemide With Matched Hydration in Patients Undergoing Interventional Procedures". JACC: Cardiovascular Interventions. 10 (4): 355–363. doi:10.1016/j.jcin.2016.11.006. PMID   28231903.
  16. ↑ Mattathil, Stephanie; Ghumman, Saad; Weinerman, Jonathan; Prasad, Anand (2017-10-01). "Use of the RenalGuard system to prevent contrast-induced AKI: A meta-analysis". Journal of Interventional Cardiology. 30 (5): 480–487. doi: 10.1111/joic.12417 . ISSN   1540-8183. PMID   28870002. S2CID   27646564.
  17. ↑ Barrett BJ, Parfrey PS (2006). "Clinical practice. Preventing nephropathy induced by contrast medium". N. Engl. J. Med. 354 (4): 379–86. doi:10.1056/NEJMcp050801. PMID   16436769.
  18. 1 2 3 4 5 Ellis, JH; Davenport, MS; Dillman, JR; Hartman, RP; Herts, BR; Jafri, SZ; Kolbe, AB; Laroia, A; Cohan, RH; MacDonald, RJ; Needleman, L; Newhouse, JH; Pahade, JK; Sirlin, CB; Wang, CL; Wasserman, N; Weinreb, JC (2017). ACR Manual on Contrast Media. American College of Radiology. pp. 35–46. ISBN   978-1-55903-012-0 . Retrieved 20 November 2020.
  19. 1 2 3 4 5 6 7 8 Mehran, Roxana; Dangas, George D.; Weisbord, Steven D. (30 May 2019). "Contrast-Associated Acute Kidney Injury". New England Journal of Medicine. 380 (22): 2146–2155. doi:10.1056/NEJMra1805256.
  20. ↑ Kooiman, Judith; Pasha, Sharif M.; Zondag, Wendy; Sijpkens, Yvo W. J.; Molen, Aart J. van der; Huisman, Menno V.; Dekkers, Olaf M. (2012-10-01). "Meta-analysis: Serum creatinine changes following contrast enhanced CT imaging". European Journal of Radiology. 81 (10): 2554–2561. doi:10.1016/j.ejrad.2011.11.020. ISSN   0720-048X. PMID   22177326. S2CID   6307799.
  21. ↑ Brar, Somjot S.; Aharonian, Vicken; Mansukhani, Prakash; Moore, Naing; Shen, Albert Y.-J.; Jorgensen, Michael; Dua, Aman; Short, Lindsay; Kane, Kevin (2014-05-24). "Haemodynamic-guided fluid administration for the prevention of contrast-induced acute kidney injury: the POSEIDON randomised controlled trial". Lancet. 383 (9931): 1814–1823. doi:10.1016/S0140-6736(14)60689-9. ISSN   1474-547X. PMID   24856027. S2CID   7882106.
  22. ↑ John Mandrola (2017-03-07). "Contrast-Induced Nephropathy: Signal or Noise?". Medscape. Retrieved 2017-09-28.
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