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The most common clinical indications include:
Characterization of indeterminate renal lesions detected on prior cross-sectional imaging. This is done most frequently to distinguish a benign lesion such as a renal cyst from a malignant primary or metastatic neoplasm.
Surveillance of patients with genetic syndromes who are at increased risk for renal cell carcinoma (RCC).
Staging and response assessment of patients with renal malignancies.
Pretreatment and post-treatment evaluation of patients undergoing renal transplantation, as well as pretreatment evaluation of live renal donors.
Evaluation of patients with abdominal symptoms or signs (e.g., flank pain, hematuria) that are suspected to be secondary to renal disease.
Assessment for traumatic injury to the kidneys (mainly using contrast-enhanced CT).
Providing guidance for percutaneous biopsy or intervention for renal disease.
The kidneys have an attenuation of 30 to 50 Hounsfield units (HU) on unenhanced CT ( Figure 35-1, A ). On MRI, the renal cortices have low T1-weighted signal intensity relative to the medullary pyramids and low T2-weighted signal intensity relative to the medullary pyramids ( Figure 35-2 ). The normal kidney is “bean shaped” and has a smooth contour. Persistent fetal lobation may sometimes be seen and can give the kidney a lobulated contour.
Unenhanced CT images (but not MR images) are useful to detect renal calcifications that may be related to urinary stone disease, parenchymal calcifications due to varied causes such as hyperparathyroidism, or dystrophic calcifications in renal neoplasms. However, both CT and MR unenhanced images are useful to (1) detect presence of macroscopic fat within a renal mass to establish a specific diagnosis of renal angiomyolipoma (AML), a benign lesion, as well as to (2) serve as a reference of comparison for contrast-enhanced images to determine whether there are enhancing components within a renal lesion. In the vast majority of renal lesions, the presence of a soft tissue enhancing component is suspicious for a malignant lesion such as RCC.
The kidneys receive ≈25% of the cardiac output and therefore enhance avidly and rapidly after contrast administration. Following the intravenous administration of contrast material, sequential phases of enhancement of the kidney are seen as follows:
The arterial phase of enhancement occurs 10 to 30 seconds after contrast administration, where the renal arteries predominantly enhance. This phase is useful for delineation of renal arterial anatomy and pathology, as in preoperative planning for renal donor evaluation or for a complex tumor resection.
The corticomedullary (or cortical) phase of enhancement occurs 25 to 70 seconds after contrast administration. Here, the renal cortices are enhanced but the medullary pyramids have not yet enhanced ( Figure 35-1, B ). In this phase, the intrarenal vasculature and hypervascular renal lesions are seen to best effect. However, some small renal lesions, particularly those located in the medullary pyramids, may be difficult to visualize during this phase of enhancement.
The nephrographic phase of enhancement occurs 60 to 180 seconds after contrast administration, where the renal cortices and medullary pyramids are homogeneously enhanced ( Figure 35-1, C ). In this phase, hypovascular renal lesions and the renal veins are seen to best effect; most renal lesions are seen as areas with less enhancement in the enhanced normal renal parenchyma. Hypervascular renal lesions may also have washout of enhancement relative to the enhanced normal renal parenchyma, and thus are easily identified.
The delayed (or excretory or equilibrium) phase of enhancement occurs starting >120 to 180 seconds after contrast administration, where renal parenchyma decreases in enhancement, and the renal collecting systems increasingly opacify with excreted intravenous contrast material ( Figure 35-1, D ). This phase is most useful to evaluate the collecting systems for urothelial tumors as in a CT urogram and to evaluate the integrity of the collecting systems in patients with severe renal trauma (blunt or penetrating).
CT and MRI play an important role in the preoperative evaluation of renal transplant donors, as well as in the pre- and postoperative evaluation of recipients of renal transplants.
In potential renal donors, preoperative evaluation can be performed with three-phase dynamic contrast-enhanced CT or MRI to delineate the renal arterial, venous, and urothelial anatomy, because anatomic variations are common. This imaging evaluation is also performed to identify any incidental lesions in the abdomen or pelvis of the donors, which may need attention prior to surgery.
In potential renal transplant recipients, preoperative evaluation is helpful to delineate the underlying anatomy and to evaluate for preexisting renal disease. Renal transplants are usually placed in the iliac fossa with vascular anastomosis to the external iliac vasculature and ureteral implantation into the bladder.
Post-transplant evaluation in renal transplant recipients is primarily focused on the detection of vascular, renal parenchymal, or urothelial complications. Although ultrasonography (US) is often the initial imaging modality to evaluate these patients, CT and MRI may be used for problem-solving. Commonly encountered vascular complications following renal transplantation include thrombosis or stenosis of the transplant renal arteries or veins, renal arteriovenous fistula (AVF), and renal arterial pseudoaneurysm formation (the latter two are often a complication of percutaneous biopsy of a renal transplant). Commonly encountered urothelial complications following renal transplantation include ureteral obstruction and leak at the site of ureteral anastomosis to the urinary bladder; such urologic complications account for 10% of postoperative complications in renal transplants and are an important cause of transplant failure. Other important complications seen in renal transplants include urolithiasis, peritransplant fluid collection (abscess, hematoma, lymphocele, or urinoma), renal infarct, acute tubular necrosis (ATN), transplant rejection, and post-transplant lymphoproliferative disorder (PTLD).
A horseshoe kidney is the most common type of congenital renal fusion anomaly, occurring in 1 in 500 people, in which the lower poles of the kidneys are attached to each other across the midline, leading to a “horseshoe” configuration. The region of connection, called the isthmus, is composed of fibrous tissue or functioning renal parenchyma and is located just inferior to the inferior mesenteric artery ( Figure 35-3 ).
Patients with a horseshoe kidney are generally asymptomatic but have an increased risk of a malformed ureteropelvic junction with resultant obstruction, vesicoureteral reflux (VUR), nephrolithiasis, renal traumatic injury to the isthmus in blunt abdominal trauma, urinary tract infections, and renal neoplasms including Wilms tumor and urothelial carcinoma.
A renal cyst is the most common benign renal lesion. It occurs with increasing frequency with increasing age and may be seen in up to one third of adults over the age of 60. It is round or oval in shape and is composed of simple fluid with a smooth thin wall. On CT, a simple renal cyst will have fluid attenuation (0 to 20 HU) on CT, and on MRI, it will have low signal intensity on T1-weighted images, very high signal intensity on T2-weighted images, and very high signal intensity on heavily T2-weighted images relative to renal parenchyma. Simple cysts do not demonstrate enhancement ( Figure 35-4 ).
Sometimes, a cyst can become minimally complex secondary to hemorrhage or infection. When this occurs, on CT, the attenuation of the cyst contents will be higher than that in simple cysts. On MRI, the T1-weighted signal intensity of the cyst contents will be variably increased, and its T2-weighted signal intensity will be variably decreased relative to that of simple cysts. In addition, internal septations, fluid-debris levels, calcifications, or wall thickening may also be seen. However, no enhancing components will be present ( Figure 35-5 ).
A cystic nephroma is a rare benign cystic renal neoplasm. In adults, it most commonly occurs in women in the fifth through seventh decades of life. It also occurs in young boys in the first decade of life. On CT and MRI, a well-circumscribed cystic renal lesion is typically seen, usually with multiple variably enhancing internal septations, and sometimes with herniation into the renal collecting system ( Figure 35-6 ), which is a characteristic feature. Solid enhancing components, hemorrhage, venous extension, regional lymphadenopathy, and distant metastatic disease are generally not seen. However, surgical resection is generally performed because it is extremely difficult to distinguish a cystic nephroma from a cystic RCC.
The Bosniak classification system ( Table 35-1 ) utilizes specific CT or MR imaging features to help classify cystic renal lesions into those that are likely benign (and do not require surgical resection) from those that are likely malignant (and thus require surgical resection).
CATEGORY | IMAGING FEATURES | MANAGEMENT |
---|---|---|
I: simple cyst | Fluid attenuation (CT) Fluid signal intensity (MRI) Thin smooth wall No enhancement |
100% benign No further follow-up |
II: minimally complex cyst | Fine calcifications or a short segment of slightly thickened calcification (CT) Few thin internal septations without enhancement Homogeneously hyperattenuating (>20 HU) and nonenhancing but ≤ 3 cm and not fully intrarenal (CT) Increased T1-weighted signal intensity or slightly decreased T2-weighted signal intensity relative to simple fluid but nonenhancing (MRI) |
100% benign No further follow-up |
IIF: probable minimally complex cyst | Small nodular calcifications (CT) Multiple thin internal septations without enhancement Minimal smooth thickening of wall or internal septations Homogeneously hyperattenuating (>20 HU) and nonenhancing but either ≤ 3 cm and fully intrarenal or >3 cm (CT) |
95% benign Follow-up imaging |
III: probable cystic renal neoplasm | Thick or irregular walls or internal septations with enhancement | >50% malignant Surgical resection |
IV: cystic renal neoplasm | Solid nodular components with enhancement | >95% malignant Surgical resection |
The various conditions that lead to polycystic kidney disease may be subdivided into nonheritable causes and heritable causes.
Non-heritable/idiopathic causes include the following conditions:
Multiple incidental renal cysts : When cysts involve the renal pelvis, they may either be secondary to (1) peripelvic (renal sinus) cysts that arise from the renal hilar lymphatics, which are usually small, multiple, and bilateral; or (2) parapelvic cysts that arise from the renal cortex and extend into the renal sinus fat, which are more commonly solitary and unilateral.
Localized cystic renal disease : This is a rare idiopathic benign condition in which a unilateral cluster of tightly spaced variably sized cysts are seen within a kidney. Presence of intervening normally enhancing renal parenchyma and the lack of a surrounding capsule are additional imaging features that are suggestive of this diagnosis (see Figure 35-4 ).
Multicystic dysplastic kidney (MCDK) : This is a nonheritable developmental disorder that is often diagnosed in utero, where one kidney is partially or completely replaced by a cluster of nonfunctioning noncommunicating cysts, sometimes with atrophy of the ipsilateral ureter, renal collecting system, and renal vasculature. Compensatory hypertrophy of the contralateral kidney is often present as well.
Acquired cystic renal disease of dialysis (ACKD) : Multiple renal cysts may occur in patients with end-stage renal disease and increase in frequency in proportion to the duration of dialysis. Multiple simple or complex cysts of varying size are typically seen throughout the small shrunken kidneys.
Lithium-induced nephrotoxicity : This is secondary to long-term lithium therapy (usually in patients with depression or schizophrenia), where multiple subcentimeter (usually 1 to 2 mm) uniformly distributed cysts are seen throughout the normal-sized kidneys ( Figure 35-7 ).
Glomerulocystic kidney disease (GCKD) : This is a rare form of cystic renal disease that is most often seen in neonates and young children, where multiple small cysts are predominantly seen in the subcapsular cortices of the kidneys which may be normal or small in size.
Heritable causes include the following conditions:
Autosomal dominant polycystic kidney disease (ADPKD) : This is the most common heritable renal disorder. It typically presents in the third through fourth decades of life, where about 50% of patients develop end-stage renal disease, and is associated with an increased risk of cardiac valve abnormalities and intracranial aneurysms. Multiple cysts are typically seen bilaterally in the kidneys, which may be normal in size but can also be enormously enlarged. The cysts may be simple or minimally complex ( Figure 35-8 ). Cysts are also commonly seen in the liver and less commonly seen in the pancreas, spleen, ovaries, and testes.
Autosomal recessive polycystic kidney disease (ARPKD) : This is a rare heritable renal disorder, which may be diagnosed in utero, in neonates and infants, in children, or in adults but most often presents at the age of 2.5 years. Multiple uniform 1- to 2-mm tubular cysts are typically seen, predominantly in a medullary location, but sometimes larger 1- to 2-cm cysts are also encountered within the kidneys (which are typically large in size). Associated findings of congenital hepatic fibrosis, portal hypertension (including splenomegaly and ascites), and biliary cystic disease are typically present as well.
von Hippel Lindau (vHL) syndrome : This is an autosomal dominant condition that is associated with development of renal cysts, RCC, pheochromocytomas, pancreatic cysts, pancreatic neoplasms including serous cystadenoma and neuroendocrine tumors, and central nervous system hemangioblastomas. In vHL syndrome, simple-appearing renal cysts often contain small foci of RCC.
Tuberous sclerosis (TS) : This is the second most common phakomatosis (after neurofibromatosis type 1) and is an autosomal dominant condition that leads to hamartoma formation in the various organs of the body. Multiple bilateral renal AMLs are typically seen, which may enlarge and replace the kidneys, often in association with multiple renal cysts. Fat-containing hepatic AMLs and uniformly distributed cystic lung disease are additional suggestive imaging findings that may also be seen.
Medullary cystic renal disease : This condition usually occurs in children and young adults. Multiple small 1- to 1.5-cm cysts are seen at the corticomedullary junctions in the kidneys (which are typically small in size).
For the answer, see Box 35-1 .
Cystic lesions
Renal cyst
Cystic nephroma
Renal abscess
Renal hematoma
Cystic/necrotic renal malignancy (RCC, metastasis)
Solid lesions
Renal contusion
Renal infarct
Focal pyelonephritis
Renal AML
Renal oncocytoma
Solid renal malignancy (RCC, lymphoma, metastasis, urothelial cancer extending from collecting system)
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