Victim Of Medical Investigation or Treatment: contrast associated acute kidney injury

Abstract

10 PRACTICAL DIABETES Vol. 38 No. 1 Copyright © 2021 John Wiley & Sons A 84-year-old woman with type 2 diabetes for 13 years became generally unwell; long-term control of her diabetes, hypertension and dyslipidaemia was poor. Investigations revealed a chest infection and her creatinine had risen from 111 to 429μmol/L over seven days (Table 1). Plasma osmolality, and urine ketone levels were normal. She had taken a stable dose of perindopril for several years and was not taking any other nephrotoxic drugs. She had not been obviously hypotensive or hypovolaemic; renal ultrasound was normal. She had a previous history of breast cancer and deep vein thrombosis. She had recently been dyspnoeic with clear chest X-ray but raised D-dimer (1241ng/ml); computed tomography pulmonary angiogram (CTPA) was performed three days before admission with prior eGFR 46ml/min/1.73m2 and creatinine level 111μmol/L. She fulfilled the criteria for contrast induced acute kidney injury (CI-AKI), i.e. an increase in serum creatinine of 25% or 26.5μmol/L, a temporal relationship to the contrast agent (generally two to three days), and other causes of renal impairment excluded.1,2 Risk factors for CI-AKI2,3 are: age; female gender; diabetes mellitus; hypertension; renal impairment; heart failure; myeloma; albuminuria; anaemia; hypovolaemia; nephrotoxic drugs; hypoalbuminaemia; higher glucose level; and higher LDL level. The patient had several risk factors: age, gender, diabetes, hypertension, renal impairment, hyperglycaemia, raised LDL level, and ACE inhibitor use. Characteristics of the contrast (intra-arterial, non-ionic, hyperosmolar or larger volumes) also increase the risk of CI-AKI,1–3 but modern weight-based contrast dosing minimises this. Some risk factors can be modified, some cannot. Lower baseline renal function increases the risk of CI-AKI. An eGFR of 45ml/min/1.73m2 was often taken as a cut off for using intravenous contrast.1 In elderly patients, the Cockcroft Gault formula may be closer to the glomerular filtration rate than the formulae used by the laboratories4 but this patient’s baseline Cockcroft Gault eGFR was identical: 46ml/ min/1.73m2. Different guidelines give different eGFR thresholds from 30 to 60ml/min/1.73m2 for developing CI-AKI.5 Risk stratification models, often derived from cardiology patients with intra-arterial contrast and cardiac disease (both CI-AKI risk factors), may be inappropriate for other patients.6 To avoid CI-AKI, one can consider other imaging modalities, hold potentially nephrotoxic drugs 24 hours before contrast, preload with intravenous normal saline and use safest contrast.2,3 Systematic community control of glucose, cholesterol and blood pressure might have helped this patient; there was no time to achieve this as an inpatient since pulmonary emboli on CTPA can disappear within 48 hours. Treatment is avoidance, general support, and hydration; dialysis removes contrast,7 but is rarely required. The management of metformin with contrast is controversial. The Royal College of Radiologists3 cites a lack of valid evidence regarding metformin-associated lactic acidosis due to contrast, but suggests that if the eGFR is under 60, the clinician and radiologist should liaise regarding temporary metformin cessation. Other guidance8 suggests holding the metformin if eGFR is under 30 and restarting it if eGFR is unchanged, which contrasts to the metformin Summary of Product Characteristics9 that advises avoiding metformin at this eGFR and halting metformin in conditions that might alter renal function. In conclusion, contrast enhanced scans provide much useful information, but one must be aware of the hazards and their risk factors; liaison with the radiology department is invaluable.