Key points

Introduction

Acute kidney injury (AKI), previously known as acute renal failure, is a condition characterized by a decline in the glomerular filtration rate (GFR) over a short course (hours to days) resulting in azotemia. Although debated, multiple definitions have emerged from groups such as the Acute Dialysis Initiative, the Acute Kidney Injury Network, and the Kidney Disease: Improving Global Outcomes group. However, the clinical presentation generally consists of an increase in creatinine level and, in some cases, oliguria or anuria. AKI usually occurs in the setting of acute and chronic diseases, and is common in the hospital setting, affecting up to 20% of hospitalized patients, as well as up to 36% to 60% of admissions to the intensive care unit (ICU).

The causes of AKI are often divided into prerenal, renal, and postrenal categories. Prerenal causes of AKI are the result of hypoperfusion or hypovolemia, including decreased intake, vomiting, diarrhea, blood loss, heart failure, hepatorenal syndrome, sepsis, and less commonly renal artery stenosis and thrombosis. The most common renal or intrinsic cause of AKI is acute tubular necrosis (ATN). However, other renal causes include glomerular, interstitial, and small-vessel diseases, which may be secondary to vasculitis, infection, or drug reaction, among other causes. Postrenal causes of AKI are obstructive, such as nephrolithiasis, malignancy, and benign prostatic hyperplasia. Regardless of the cause, AKI may lead to complications caused by uremia (encephalopathy, neuropathy, pericarditis), volume overload (dyspnea, pulmonary edema), and electrolyte disturbances (hyperkalemia). These complications are associated with increased mortality in patients who develop AKI. Furthermore, some patients never fully recover their baseline renal function, and may ultimately need long-term dialysis. Of course, this common entity has a great impact on patient outcomes, length of hospital stay, and cost of care.

Although an acute increase in creatinine level is key to the diagnosis of AKI, imaging of the kidneys can provide valuable information for the work-up and management of AKI. Different imaging modalities can be used to evaluate renal anatomy, evaluate renal perfusion, rule out urinary tract obstruction, as well as assess for signs of renal inflammation and edema. This article discusses the utility of the different imaging modalities in characterizing AKI in adults, including ultrasonography (US), computed tomography (CT), magnetic resonance (MR) imaging, and nuclear medicine imaging.

Ultrasonography

The first-choice imaging modality for the kidneys in the context of AKI is US, specifically two-dimensional (2D) gray-scale US, given its ease of use, noninvasiveness, accessibility, low cost, and excellent safety profile. Advances in imaging technology have further improved visualization of the kidneys with US. Furthermore, portable US provides an advantage for imaging critically ill patients in the ICU. Although only approximately 10% of renal US examinations show abnormal findings related to AKI, these can have a significant impact on guiding patient management. A normal US also helps guide management by excluding major structural abnormalities.

Size

Kidney size can help differentiate acute from chronic kidney disease (CKD). Small or atrophic kidneys are often seen with CKD, in which case the patient’s renal function is unlikely to fully recover ( Fig. 1 ). Enlarged kidneys may suggest an infiltrative disease process, including lymphoma and monoclonal gammopathies. Other causes of enlarged kidneys in the setting of AKI include pyelonephritis, ATN, acute interstitial nephritis, and acute proliferative glomerulonephritis (GN). A rarer cause of an enlarged kidney is renal vein thrombosis. In renal transplant patients, an enlarged kidney may be seen in the setting of acute rejection (sensitivity and specificity >80%).

US findings of CKD, including bilateral decreased kidney size and cortical thickness, on longitudinal images of the left ( A ) and right ( B ) kidneys. In another patient, US findings of chronic kidney disease, including markedly increased cortical echogenicity and cortical thinning on longitudinal images of the left ( C ) and right ( D ) kidneys.

([ C, D ] Courtesy of Vincent M. Mellnick, MD, Mallinckrodt Institute of Radiology, St.Louis, MO, USA.)

Echogenicity

Parenchymal echogenicity of the kidneys is compared with the adjacent liver and spleen and can also help characterize AKI. Markedly increased renal cortical echogenicity is seen in CKD (see Fig. 1 ). Infiltrative diseases, such as ATN, monoclonal gammopathy, as well as proliferative and crescentic GN, show increased renal cortical echogenicity and loss of the normal corticomedullary differentiation ( Fig. 2 ). In contrast, renal parenchymal edema appears hypoechoic on US. Pyelonephritis can be seen as decreased renal cortical echogenicity with loss of the corticomedullary differentiation, but may also appear as a focus of masslike enlargement or increased echogenicity as well. More focal hypoechoic foci/fluid collections in the context of suspected pyelonephritis can be seen in the setting of abscess formation ( Fig. 3 ). The presence of a hypoechoic band surrounding the kidney may be seen in the setting of acute cortical necrosis.

US findings of increased renal echogenicity, which may be seen in ATN, monoclonal gammopathy, as well as proliferative and crescentic GN.

US findings of pyelonephritis in a transplanted kidney on 2D ( A ) and Doppler ( B ) images. The findings, including decreased cortical echogenicity, echogenic renal sinus fat, and increased Doppler flow, are seen in the context of infection.

Obstruction

US can be used to detect signs of obstruction involving the renal collecting system, ureters, or bladder. This is one of the most important causes of AKI to diagnose by imaging because the treatment is typically centered on relieving the obstruction by catheter placement, stenting, or urinary diversion. Hydronephrosis, manifested with calyceal dilatation on US, can be seen in the context of nephrolithiasis ( Fig. 4 ), or a urinary outlet obstruction caused by an intrinsic or extrinsic cause such as a mass. Calyceal dilatation may also be secondary to urinary tract infection, physiologic dilatation in pregnancy, and in patients with diabetes insipidus. Doppler imaging may also be used to assess for obstruction, with the unilateral absence of a ureteric jet suggesting obstruction.

US findings of a midureteric renal calculus on 2D ( A ) and Doppler ( B ) images. The stone seems echogenic with posterior shadowing on the 2D-image, with twinkle artifact ( arrow ) evident on Doppler.

Renal Transplant

US is generally the first-line imaging test for assessment of renal transplant patients, particularly in the context of a increasing creatinine level. A diminished renal function may be the result of hyperacute, acute ( Fig. 5 ), or chronic rejection ( Fig. 6 ), among other causes that may also occur in the native kidney, such as ATN and drug nephrotoxicity. US may show a variety of different findings in the context of AKI, including increased size of the kidney, increased or decreased cortical echogenicity, loss of corticomedullary differentiation, prominent pyramids, thickening of the collecting system, and effacement of the central sinus echo complex. In the setting of chronic transplant rejection, thinning of the renal cortex and mild hydronephrosis may be seen. Furthermore, Doppler US may be used for assessment of renal transplants, with an RI greater than 0.8 being a nonspecific indicator of renal transplant dysfunction. Reversal of diastolic flow may also be seen with chronic rejection, but is much less common.

US findings of acute renal transplant rejection (postoperative day 10) on 2D ( A ) and Doppler ( B ) images showing an increasing RI (R = 1.00) with high-resistance systolic flow and loss of diastolic flow.

US findings of chronic renal transplant rejection (5 years posttransplant) with gradually increased renal cortical echogenicity and atrophy on 2D images ( A ), and an increasing RI (R = 0.84) on Doppler images ( B ).

Computed tomography

Abdominal and pelvic CT can serve as a valuable second-line imaging test for assessing patients with AKI when the initial US is inconclusive. Although the topic is much debated, the use of intravenous (IV) contrast for a CT scan is avoided whenever possible in the setting of AKI. The findings of both unenhanced CT (UECT) and contrast-enhanced CT (CECT) are discussed, because contrast administration can provide relevant additional information on the renal parenchyma and corticomedullary differentiation.

Obstruction

An unenhanced CT scan of the abdomen and pelvis can detect nephrolithiasis leading to obstructive AKI. This finding is especially important in the setting of a solitary kidney or bilateral obstructive nephrolithiasis ( Fig. 7 ). A CT scan can also show findings of hydronephrosis, hydroureter, as well as perinephric and periureteric stranding in the context of nephrolithiasis, even after a stone has passed. This finding may be particularly useful in the context of a negative or inconclusive/nondiagnostic initial renal US scan; for example, one that shows hydronephrosis but no definite obstructive stone.

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