NORMAL CT NEPHROGRAM
Classic descriptions divide the appearance of the nephrogram into distinct phases (unenhanced,
corticomedullary,
nephrographic and excretory) that are based on the transit of contrast material through the kidney.
The different phases of the nephrogram must be symmetrical (beginning,
time of disappearance and enhancement)
In case of asymmetry,
the renal parenchyma that presents a delay of the nephrogram will be the pathological one
Unenhanced CT Fig. 4 :
- It allows comparing and evaluating contrast uptake in subsequent phases.
- Useful for differential diagnosis between complicated hyperdense cysts / hematomas versus tumor lesions.
The tumor lesions present enhancement,
whereas the cysts and hematomas should not enhance.
- Evaluate urolithiasis and calcifications are best seen without contrast.
After the administration of contrast the first phase is corticomedullary phase Fig. 4 :
- The phase begins between 20-60 seconds after the contrast injection.
- During this phase the glomerular filtration begins and the contrast passes through the renal arteries and cortical nephrons.
- The renal cortex enhances brightly and is clearly differentiated from the medullary kidney that presents minimally enhancing.
- This phase is the best to evaluate the vascular anatomy (maximum enhancement of the renal arteries and veins).
- During this phase a greater enhancement of the aorta (Ao) is observed compared to the inferior vena cava (IVC).
Nephrographic phase Fig. 4 :
- Begins 80-120 seconds after the contrast injection.
- During this phase,
the contrast passes to the medullary collecting ducts.
- Homogeneous enhancement of all renal parenchyma (renal medulla and cortex)
- Best phase to distinguish renal masses.
- A similar enhancement of the aorta and IVC is observed
Excretory,
pyelographic or urographic phase Fig. 4 :
- Begins 180 seconds (3 minutes) after the start of contrast medium injection.
- The contrast material is excreted into renal pelvis.
- Progressive decrease of the nephrogram.
- Best phase to evaluate the collecting system (minor and major calyces,
renal pelvis,
ureter,
bladder)
Fig. 4: Images show different phases of normal CT urogram.
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
ABNORMAL NEPHROGRAPHIC AND PYELOGRAPHICPATTERNS
The CT nephrogram alterations are expressions of impaired contrast medium delivery,
transit,
and excretion by the kidney.
This is strictly related to the inner pathophysiological mechanisms underlying each condition associated with alteration of the renal function Fig. 1 Fig. 3 .
There are seven abnormal nephrographic patterns:
- Unilateral global absence of the nephrogram.
- Patched or segmented absence of the nephrogram.
- Unilateral delayed nephrogram.
- Bilateral persistent or delayed nephrogram.
- Rim nephrogram.
- Reverse rim nephrogram.
- Striated nephrogram.
UNILATERAL GLOBAL ABSENCE OF THE NEPHROGRAM
Absence of renal parenchymal enhancement in the different phases.
Etiology:
-Absence of kidney (agenesis Fig. 5 ,
ectopic Fig. 6 ,
nephrectomy)
-Absence of renal function:
- Complete renal artery occlusion (traumatic,
dissection,
embolism,
thrombosis Fig. 7 ).
- Complete occlusion of the renal vein (thrombosis).
- Complete chronic urinary obstruction + renal atrophy.
- Congenital or acquired absence of nephrons Fig. 8 .
Early recognition of this pattern is important to take the necessary therapeutic measures and avoid irreversible hypoxic damage.
Fig. 7: Absence of a nephrogram due to acute thrombosis of the left renal artery. A) Corticomedullary phase. B) Nephrographic phase. C) Coronal CT MIP reconstruction showing right renal artery obstruction (arrow)
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
PATCHED OR SEGMENTED ABSENCE OF THE NEPHROGRAM
Segmental renal infarction:
-It affects segmental or subsegmental vessels.
-Sharply demarcated,
wedge-shaped areas of absent enhancement.
-The size of the defect is related to the caliber of the affected vessel
-Clinical presentation: Unspecific.
Renal fossa pain,
hematuria,
fever.
-Medical history is fundamental for an etiological diagnosis.
-Etiology:
- Arterial embolisms (most frequent etiology and usually multifocal).
Fig. 9 Fig. 10
- Arterial or venous thrombosis,
vasculitis Fig. 11 .
- Pyelonephritis: interstitial edema secondary to infection can cause ischemic areas due to compression of vascular structures.
Fig. 12
- Hemodynamic changes in septic shock.
Fig. 13
- Areas of post-radiofrequency necrosis in the treatment of renal neoplasms or metastases Fig. 19 .
Space-occupying lesion:
-Cysts,
neoplasms,
abscesses. Fig. 14 Fig. 15 Fig. 16 Fig. 17
Post-traumatic injuries:
-Kidney contusion.
-kidney lacerations.
Fig. 18
Fig. 10: Renal infarction due to embolism after contralateral nephrectomy. Enhanced CT images show a sharply demarcated, wedge-shaped area of absent enhancement, suggestive of renal infarction. A) Corticomedullary phase B) Nephrographic pase.
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
Fig. 12: Patched areas of focal absence of nephrogram in both kidneys in a patient with fever and bacteriuria, findings suggestive of ischemic changes due to acute pyelonephritis.
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
Fig. 14: Renal cyst (arrow) with absence of enhancement in the different phases and hypodense in the phase without contrast. Renal cell carcinoma (arrowhead) with enhancement in the corticomedullary phase, hypodense in the following phases and isodense in the unenhanced CT.
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
UNILATERAL DELAYED PYELOGRAM OR NEPHROGRAM.
Increase in mean transit time of the contrast in the affected kidney.
The diseased kidney is delayed in either the angiographic or nephrographic phase while the normal kidney is in the nephrographic or pyelographic phase,
respectively
Etiology:
-Renal artery stenosis: Fig. 20
- It produces a decrease in the hydrostatic pressure in the glomerular capillary ⇒ decrease glomerular filtration rate (GFR).
- Chronic hypoperfused kidney ⇒ Small or atrophic kidney.
-Renal vein thrombosis:
- It produces a retrograde increase in renovascular pressure that decreases arterial perfusion ⇒ decrease GFR.
- It produces intersticial edema in Kidney parenchyma ⇒ compression of collecting ducts ⇒ increase retrograde pressure to Bowman's capsule ⇒ decrease GFR.
- Enlarged kidney and renal vein.
- The tumor venous thrombus will present enhancement (Fig. 21) and the non-malignant venous thrombus will not.
Fig. 22
Fig. 21: Renal vein (x) and inferior vena cava tumor thrombus in renal cell carcinoma. Right kidney in nephrographic phase with left delayed nephrogram (corticomedullary phase). Note enlarged left kidney and renal vein due to venous congestion. The tumor thrombus show enhancement (x).
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
Fig. 22: Non-malignant left renal vein thrombosis (arrow) with delayed nephrogram. A) Right kidney in nephrographic phase, left kidney in corticomedullary phase. B) Left excretory phase is not observed.
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
-Obstructive uropathy: Fig. 23
- Obstruction any point of the urinary tract ⇒ increase retrograde pressure ⇒ increase pressure in the Bowman's capsule and in the renal parenchyma ⇒ decrease GFR.
- Enlarged renal pelvis,
ureter or bladder.
Fig. 23: Left pelviureteric junction stenosis with delayed nephrogram and dilatation of the renal pelvis and calyces secondary to chronic obstruction. A) Corticomedullary phase. B) Nephrographic phase . C) Excretory phase, does not show excretion of contrast material to the left excretory system.
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
-Extrinsic compression: Fig. 24
- Subcapsular or perirenal collections.
- Increase intrarenal pressure ⇒ decrease in renal arterial perfusion ⇒ decrease GFR.
-Unilateral poor nephron function due acute pyelonephritis.
BILATERAL PERSISTENT NEPHROGRAM OR BILATERAL DELAYED PYELOGRAM
Both kidneys remain in the corticomedullary or nephrographic phase for more than 3 minutes after contrast administration.
The mechanism of this pattern is slow progression of contrast material through both kidney.
Etiology:
-Systemic hypotension (Shock): Fig. 25
- The decrease in systolic blood pressure produces activation of the renin-angiotensin-aldosterone system and there will be a slow progression of contrast through the collecting duct system with a greater reabsorption of water and sodium.
Fig. 25: Enhanced CT images show bilateral persistent nephrogram 30 minutes after intravenous contrast administration in a patient with hypovolemic shock. Note the collapse of the inferior vena cava (arrow) and the absence of contrast in both the aorta (arrowhead) and the inferior vena cava.
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
-Acute tubular necrosis:
- Retention of contrast inside the renal tubules due to epithelial tubule cells lesion or intratubular detritus that originates mechanical intrarenal obstruction of the tubules
- There are multiple causes such as renal ischemia or nephrotoxicity (contrast,
myoglobinuria,
hemoglobinuria ...).
- We must suspect it when we see persistence of the nephrogram 12-24 hours after the administration of contrast.
It is important because this finding precedes the development of oliguria and the elevation of creatinine and allows us to establish an early treatment.
RIM NEPHROGRAM
The diseased kidney only has a thin (2-4 mm) peripheral band of cortical opacification within the subcapsular zone and centrally in the cortex immediately adjacent to the medulla.
The remaining renal parenchyma does not enhance.
Fig. 26
It is the result of occlusion of main renal arteries or veins, with a compensatory circulation to the subcapsular region by collateral flow through capsular,
periureteric and peripelvic vessels.
The rim nephrogram is not observed immediately after the renal infarction and may take several days to establish.
The rim nephrogram is highly suggestive of renovascular compromise and allows us to differentiate it from pyelonephritis where it will be absent.
Fig. 26: Rim nephrogram (arrow) secondary to renal infarction. A) Coronal and B) axial CT images show a geographic area of nephrographic abscense in the left kidney with enhancement in subcapsular region (arrow) as result of collateral blood flow.
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
REVERSE RIM NEPHROGRAM
We will observe enhancement of the renal medulla and absence of enhancement of the renal cortex.
A peripheral ring of subcapsular enhancement can be observed due to collateral flow through the capsular vessels.
This pattern is almost always identified in the setting of acute cortical necrosis.
Acute cortical necrosis: Fig. 27
- Ischemic necrosis of the renal cortex.
Sparing renal medulla.
- The process is diffuse and bilateral in most cases.
- Etiology: prolonged systemic hypotension (obstetric complications,
sepsis),
post-transfusional reactions,
haemolytic uraemic syndrome,
transplant rejection,
severe dehydration.
- There will be cortex atrophies ⇒ cortical nephrocalcinosis.
Fig. 27: Enhanced CT image shows inverted rim nephrogram in a patient with acute cortical necrosis due to post transfusion syndrome.
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
STRIATED NEPHROGRAM
The normal homogenous nephrographic pattern is replaced by alternating bands of high and low attenuation.
Fig. 28
These bands have a radial arrangement similar to the collecting ducts and extend from the renal capsule to the papilla.
The low attenuation bands may be due to collecting tubules that do not contain contrast or edema between the nephrons.
High attenuation bands may be due to normal attenuation of the parenchyma or hyperatenuation due to tubular obstruction (due to pus in pyelonephritis,
proteinuria,
myoglobulinuria) that causes increased water absorption with increased contrast concentration in the collecting tubules.
The most frequent etiology is pyelonephritis.
It also occurs in renal contusion,
hypotension,
autosomal recessive polycystic kidney disease,
urinary obstruction and renal vein thrombosis.
Fig. 28: Enhanced CT images show bilateral striated nephrogram secondary to acute pyelonephritis. There are alternating bands of enhanced and nonenhanced renal parenchyma.
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.
Emphysematous pyelonephritis
-Kidney infection with gas formation within or around the kidneys.
-High mortality
-More common in immunocompromised individuals or diabetes mellitus.
-CT: Fig. 29
- Best diagnostic modality.
- Striated nephrogram with gas or bubbles.
- Necrotic areas / abscesses.
- Fluid collections with gas-fluid levels.
Fig. 29: Contrast-enhanced CT images shows a striated nephrogram due to the presence of interstitial gas (arrowheads) in the right renal parenchyma. Renal hypocaptation foci of patchy distribution and perirenal gas (arrows) are shown. Radiological findings suggestive of emphysematous pyelonephritis.
References: Department of Radiology, Hospital Universitario de Donostia. San Sebastián.