Persistent nephrogram sign heralding contrast-induced nephrotoxicity

Clinical History

An elderly lady was brought to Hospital with fever and dyspnoea. Medical history included hypertensive cardiac disease, chronic obstructive pulmonary disease, and diabetes mellitus (oral medication containing metformin had just been discontinued due to metabolic decompensation). On admission, laboratory tests disclosed metabolic acidosis, markedly raised inflammatory signs and plasma D-dimer.

Imaging Findings

Initial chest x-rays and CT depicted pneumonic-atelectatic consolidation involving most of the right upper lung lobe associated with stenosis of the afferent lobar bronchus, but ruled out pulmonary thromboembolism. Thoracic CT was performed on a 64-slice multidetector scanner with injection of 80 ml of 370 mgI/ml iodinated contrast medium (CM) plus 40 ml saline flush. Initial serum creatinine (SCr) level was 85 micromol/L (0,97 mg/dL), estimated Glomerular Filtration Rate (eGFR) in the range 30-40 ml/min.

The patient was treated with antibiotics, insulin and parenteral hydration with bicarbonate solution.
The next day at dawn (18 hours after thoracic CT) emergency abdomino-pelvic CT was requested to investigate peritonitis clinical picture due to suspected diverticulitis. At scout-view and unenhanced scans opacification of renal parenchyma (“persistent nephrogram sign”) and collecting systems was seen, and no more intravenous contrast was given. Renal cortical attenuation (RCA) was measured in the range 210-240 HU bilaterally. Acute uncomplicated diverticulitis was confirmed, along with hypodense liver lesions and adrenal masses suspicious for metastases.
During three days of hospitalization, SCr levels progressively raised as shown in Fig. 2, and medical treatment was not sufficient to overcome sepsis and metabolic acidosis.

Discussion

Contrast-induced nephropathy (CIN) is defined as an acute decline in renal function (an increase in SCr by more than 25% or 44 micromol/L (0.5 mg/dl) occurring within 3 days following administration of iodinated CM ,in the absence of an alternative cause.
CIN pathophysiology includes direct toxic effects of CM on tubular cells and reduction in renal perfusion.
Currently CIN represents the third cause of hospital-acquired renal failure, and increases mortality independently of other factors. Increasingly recognized although probably underdiagnosed, CIN manifests as a transient increase in SCr levels peaking at 4-7 days and returning to baseline in 1-2 weeks, sometimes witholiguria.

Exceptional in patients without risk factors, CIN occurs in 10-30% of patents with risk factors, the greatest being a baseline renal insufficiency. European Society of Urogenital Radiology (ESUR) guidelines for renal adverse reactions define risk factors for CIN as patient-related (including eGFR less than 60ml/min or raised SCr particularly if secondary to diabetic nephropathy, dehydration, congestive heart failure, advance age, concurrent therapy with nephrotoxic drugs) and CM-related (high osmolality agents, large or repeated doses).

The persistent nephrogram sign, observed 24-48 hours after intravenous CM, has been described in 1980 as the prolongation of renal radiographic opacity associated with the development of renal failure; this appearance was associated both with pre-existing renal impairment and with renal failure caused by and developing during urography.
In the CT era, measurements of renal cortical attenuation (RCA) indicated that RCA over 108-140 HU one day after intravenous CM represents an early indicator of CIN, while RCAs ranging 55-110 HU indicate patients at high risk.

Although uncertainty exists about its long-term effects, sometimes CIN can lead to permanent renal failure and very rarely the requirement for ongoing dialysis.

Identification of patients at risk for CIN following published guidelines is critical. Measurement of renal function as SCr can be waived only in emergency situations when the procedure cannot be deferred, and is mandatory in patients with known previously raised SCr, diabetics, with history of hypertension or renal disease, and who will receive intra-arterial contrast medium. eGFR calculated using the Cockroft-Gault or the Modification of Diet in Renal Disease (MDRD) equations helps in risk stratification. Diabetics taking metformin should be identified and treated according to ESUR guidelines.

In patients at risk for CIN, repeated imaging studies with CM within a short period of time should be avoided. Unenhanced acquisitions or alternative imaging modalities should be considered. Prophylactic measures include use of low-or iso-osmolar CM, injection of the lowest dose of CM consistent with a diagnostic result, discontinuation of nephrotoxic drugs and parenteral hydration. Drugs such as N-acetylcysteine may be given, but up to date no pharmacological therapy has been shown to offer consistent protection against CIN. Dialysis immediately after CM administration is unnecessary.

Differential Diagnosis List

Final Diagnosis

Contrast media-induced nephrotoxicity

URL:	https://eurorad.org/case/8957
DOI:	10.1594/EURORAD/CASE.8957
ISSN:	1563-4086