1. Renal cortical necrosis is a rare form of acute kidney injury caused by ischemic necrosis of the renal cortex. It is characterized by hypoechoic cortical rims on ultrasound and lack of cortical enhancement with preserved medullary enhancement on CT. 2. Obstetric complications like eclampsia, abruptio placentae, and septic abortion account for over 50% of cases. Other causes include shock, sickle cell anemia, and renal transplant rejection. 3. On imaging, renal cortical necrosis appears as hypoechoic cortical rims on ultrasound, lack of cortical enhancement with CT, and cortical calcifications appearing as "tram lines" on x-ray after 4 weeks. This

1. Renal Cortical Necrosis
Dr.Mohamed Soliman,MSC

2. shock
eclampsia
septic abortion
sickle cell anemia
renal allograft rejection
disseminated intravascular coagulopathy
Abruptio placentae
Case
scenario
Prolonged anuria
oliguria;
azotemia,
hyperkalemia,
metabolic acidosis

3. • Size
• Parynchma
• Cortical thickness
• Echogenicity
• Color Doppler

4. Bilateral lack of renal
cortical enhancement
preserved medullary enhancement

5. Definition
Rare form of acute renal injury characterized by ischemic necrosis of renal cortex

6. General features
Best diagnostic clue
○ CECT:↓ enhancement of renal cortex with preserved enhancement of medulla and thin
rim of subcapsular cortical tissue best shows pathophysiology
• Location
○ Usually extensive and bilateral
• Best imaging tool
○ Sonography for exclusion of collecting system dilatation
○ Characteristic ultrasound appearance (hypoechoic cortical rim) suggests acute cortical
necrosis in appropriate clinical context

7. • Acute cortical necrosis: ↓ renal cortical echogenicity
• Chronic cortical necrosis diffuse ↑ cortical echogenicity and acoustic shadow due to
cortical calcification
• Color Doppler : marked or no color flow
• Characteristic ultrasound appearance (hypoechoic cortical rim) sign.

8. Radiographic findings
Cortical calcification
Dual linear opacities paralleling cortico-medullary line
("tram line" sign), which is usually seen after 4 weeks

9. • non contrast
○ Calcifications in renal cortex and columns of Bertin may indicate prior cortical
necrosis
contrast
○ Acute necrosis: ↓ enhancement of renal cortex
○ Preserved enhancement of thin rim of subcapsular cortical tissue due to
separate capsular blood supply
○ Preserved medullary enhancement
○ ↓ excretion of contrast media into collecting system

10. No cortical
enhancement preserved
medullary
enhancement

11. subcapsular
calcifications
shock caused
by a
ruptured
abdominal
aortic
aneurysm.
aortic wall and
endograft.

12. • T1WI
○ ↓ signal intensity inner cortex and columns of Bertin
• T2WI
○ ↓ signal intensity inner cortex and columns of Bertin
○ ↑ signal intensity subcapsular rim

13. Patient with sickle cell anemia
reversal of the usual corticomedullary
pattern, with the cortex being
hypointense to the medulla.
hemosiderin deposition or cortical
necrosis,

14. Acute Tubular Necrosis
• Persistent nephrogram on NECT (after prior
contrast administration)
• US: ↑ renal size and echogenicity

15. Renal Infarction
• CECT: Nonenhancing wedge-
shaped area of renal parenchyma
with enhancing capsular rim Renal
Vein Thrombosis
• Occluded renal vein with renal
enlargement and delayed renal function
• MR: Low signal intensity in outer
medulla

16. 1. Abruptio placentae
2. septic abortion
3. eclampsia
4. Hemolytic uremic syndrome
5. disseminated intravascular coagulopathy
6. Shock
7. sickle cell anemia
8. renal allograft rejection
• Complete cortical necrosis : Global
ischemic necrosis of cortex with
preservation of thin subcapsular rim of
tissue
• Patchy cortical necrosis : Multiple
contiguous areas of necrosis involving up to
½ of cortex

17. • Epidemiology
○ Rare cause of acute kidney injury (AKI) in developed countries
○ More common in infants and young women
○ Obstetric complications account for > 50% of cases
Natural History & Prognosis
• Poor prognosis
• Evolution toward chronic renal failure and end-stage renal disease
• Mortality > 50% if untreated
Treatment
• Treatment of underlying cause
• Dialysis; transplantation

18. 1. Clinical : eclampsia – transplantation allograft rejection -..etc
2. US : hypoechoic cortical rim sign
3. Doppler: no or marked decreased color flow .
4. Acute cortical necrosis: ↓ renal cortical echogenicity
5. chronic: diffuse ↑ cortical echogenicity +acoustic shadow (cortical calcification)
6. X ray : Cortical calcification ("tram line" sign), which is usually seen after 4 weeks
7. CT Calcifications in renal cortex and columns of Bertin .
8. Acute necrosis: ↓ enhancement of renal cortex
9. Preserved enhancement of thin rim of subcapsular cortical tissue due to separate
capsular blood supply
10.Preserved medullary enhancement
11.↓ excretion of contrast media into collecting system
•

19. right kidney in a patient
with sickle cell anemia
developing renal cortical
necrosis shows decreased
renal cortical echogenicity compared
to medulla.

20. Axial CECT in the same patient
shows bilateral lack of renal
cortical enhancement and
preserved medullary enhancement
compatible with bilateral renal cortical
necrosis.

21. Axial NECT shows subcapsular
calcifications in both kidneys,
indicative of renal cortical necrosis
following shock caused by a
ruptured abdominal aortic aneurysm.
Note the aortic wall and endograft.

22. Axial T1WI GRE in a patient
with sickle cell anemia shows
reversal of the usual corticomedullary
pattern, with the cortex being
hypointense to the medulla.
This may be due to hemosiderin
deposition or cortical necrosis, both of
which can be seen in patients
with sickle cell disease