From Wikipedia, the free encyclopedia
Renal cortical necrosis
Other namesDiffuse bilateral renal cortical necrosis (BRCN), diffuse cortical necrosis, acute cortical necrosis, acute kidney failure with acute cortical necrosis
Specialty Nephrology

Renal cortical necrosis (RCN) is a rare cause of acute kidney failure. The condition is "usually caused by significantly diminished arterial perfusion of the kidneys due to spasms of the feeding arteries, microvascular injury, or disseminated intravascular coagulation" and is the pathological progression of acute tubular necrosis. [1] It is frequently associated with obstetric catastrophes such as abruptio placentae and septic shock, and is three times more common in developing nations versus industrialized nations (2% versus 6% in causes of acute kidney failure).[ citation needed]

Causes

Adults

Babies

Pathophysiology

The exact pathologic mechanism for RCN is unclear, however the onset of small vessel pathology is likely an important aspect in the cause of this condition. In general the renal cortex is under greater oxygen tension and more prone to ischemic injury, especially at the level of the proximal collecting tubule, leading to its preferential damage in a sudden drop in perfusion. Rapidly corrected acute renal ischemia leads to acute tubular necrosis, from which complete recovery is possible, while more prolonged ischemia may lead to RCN. Pathologically, the cortex of the kidney is grossly atrophied with relative preservation of the gross structure of the medulla. The damage is usually bilateral owing to its underlying systemic causes, and is most frequently associated with pregnancy (>50% of cases). [1] It accounts for 2% of all cases of acute kidney failure in adults and more than 20% of cases of acute kidney failure during late pregnancy. [15] [16]

Diagnosis

While the only diagnostic "gold standard" mechanism of diagnosis en vivo is via kidney biopsy, the clinical conditions and blood clotting disorder often associated with this disease may make it impractical in a clinical setting. Alternatively, it is diagnosed clinically, or at autopsy, with some authors suggesting diagnosis by contrast enhanced CT. [17]

Treatment

Patients will require dialysis to compensate for the function of their kidneys.

Prognosis

Cortical necrosis is a severe and life-threatening condition, with mortality rates over 50%.[ citation needed] Those mortality rates are even higher in neonates with the condition due to the overall difficult nature of neonatal care and an increased frequency of comorbid conditions. The extent of the necrosis is a major determinant of the prognosis, which in turn is dependent on the duration of ischemia, duration of oliguria, and the severity of the precipitating conditions. Of those that survive the initial event, there are varying degrees of recovery possible, depending on the extent of the damage.

References

  1. ^ a b Deverajan, Prasad (May 26, 2011). Langman, Craig B (ed.). "eMedicine: Renal Cortical Necrosis". Medscape. Retrieved 27 March 2012.
  2. ^ Singh, B.; Gupta, A.; Mahajan, S.; Gupta, R. (2012). "Acute cortical necrosis and collapsing glomerulopathy in an HIV-infected patient: A rare clinical scenario". Saudi Journal of Kidney Diseases and Transplantation. 23 (2): 363–366. PMID  22382240.
  3. ^ Kumar, S.; Sharma, A.; Sodhi, K. S.; Wanchu, A.; Khandelwal, N.; Singh, S. (2012). "Renal cortical necrosis, peripheral gangrene, perinephric and retroperitoneal haematoma in a patient with a viper bite". Tropical Doctor. 42 (2): 116–117. doi: 10.1258/td.2011.110281. PMID  22316624. S2CID  21121415.
  4. ^ Jung, Y. S.; Shin, H. S.; Rim, H.; Jang, K.; Park, M. H.; Park, J. -S.; Lee, C. -H.; Kim, G. -H.; Kang, C. M. (2012). "Bilateral Renal Cortical Necrosis Following Binge Drinking". Alcohol and Alcoholism. 47 (2): 140–142. doi: 10.1093/alcalc/agr154. PMID  22215004.
  5. ^ Jha, R.; Narayan, G.; Swarnalata, G.; Shiradhonkar, S.; Rao, B. S.; Sinha, S. (2011). "Acute cortical necrosis following renal transplantation in a case of sickle cell trait". Indian Journal of Nephrology. 21 (4): 286–288. doi: 10.4103/0971-4065.78066. PMC  3193676. PMID  22022093.
  6. ^ Uppin, M. S.; Rajasekhar, L.; Swetha, H.; Srinivasan, V. R.; Prayaga, A. K. (2010). "Renal cortical necrosis at presentation in a patient with systemic lupus erythematosus: An autopsy case report". Clinical Rheumatology. 29 (7): 815–818. doi: 10.1007/s10067-010-1395-5. PMID  20169460. S2CID  22280989.
  7. ^ a b Huang, C. C.; Huang, J. K. (2011). "Sepsis-Induced Acute Bilateral Renal Cortical Necrosis". Nephrology. 16 (8): 787. doi: 10.1111/j.1440-1797.2011.01478.x. PMID  22029648. S2CID  30964151.
  8. ^ Kim, J. O.; Kim, G. H.; Kang, C. M.; Park, J. S. (2011). "Bilateral Acute Renal Cortical Necrosis in SLE-Associated Antiphospholipid Syndrome". American Journal of Kidney Diseases. 57 (6): 945–947. doi: 10.1053/j.ajkd.2011.02.381. PMID  21514023.
  9. ^ Novembrino, C.; De Giuseppe, R.; De Liso, F.; Bonara, P.; Bamonti, F. (2010). "Vitamin deficiency and renal cortical necrosis". The Lancet. 376 (9736): 160. doi: 10.1016/S0140-6736(10)61101-4. PMID  20638557. S2CID  42150606.
  10. ^ Kumar, S.; Krishna, G. S.; Kishore, K. C.; Sriram, N. P.; Sainaresh, V. V.; Lakshmi, A. Y. (2009). "Bilateral renal cortical necrosis in acute pancreatitis". Indian Journal of Nephrology. 19 (3): 125. doi: 10.4103/0971-4065.57112. PMC  2859480. PMID  20436735.
  11. ^ Baliga, K. V.; Narula, A. S.; Khanduja, R.; Manrai, M.; Sharma, P.; Mani, N. S. (2008). "Acute Cortical Necrosis inFalciparumMalaria: An Unusual Manifestation". Renal Failure. 30 (4): 461–463. doi: 10.1080/08860220801964293. PMID  18569922.
  12. ^ Toh, H. -S.; Cheng, K. -C.; Kuar, W. -K.; Tan, C. -K. (2008). "The Case ∣ Generalized petechiae and acute renal failure". Kidney International. 73 (12): 1443–1444. doi: 10.1038/ki.2008.143. PMID  18516063.
  13. ^ Leroy, F.; Bridoux, F.; Abou-Ayache, R.; Belmouaz, S.; Desport, E.; Thierry, A.; Bauwens, M.; Touchard, G. (2008). "Nécrose corticale rénale bilatérale induite par la quinine". Néphrologie & Thérapeutique. 4 (3): 181–186. doi: 10.1016/j.nephro.2008.01.001. PMID  18343736.
  14. ^ Sastre López, A.; Gago González, E.; Baños Gallardo, M.; Gómez-Huertas, E.; Ortega Suárez, F. (2007). "All-trans retinoic acid syndrome corrected and renal cortical necrosis". Anales de Medicina Interna. 24 (11): 551–553. doi: 10.4321/s0212-71992007001100009. PMID  18275266.
  15. ^ Prakash, J.; Niwas, S. S.; Parekh, A.; Pandey, L. K.; Sharatchandra, L.; Arora, P.; Mahapatra, A. K. (2010). "Acute kidney injury in late pregnancy in developing countries". Renal Failure. 32 (3): 309–313. doi: 10.3109/08860221003606265. PMID  20370445. S2CID  37285787.
  16. ^ Pertuiset, N.; Grünfeld, J. P. (1994). "Acute renal failure in pregnancy". Baillière's Clinical Obstetrics and Gynaecology. 8 (2): 333–351. doi: 10.1016/s0950-3552(05)80324-4. PMID  7924011.
  17. ^ Kim, H. J.; Cho, O. K. (1996). "CT scan as an important diagnostic tool in the initial phase of diffuse bilateral renal cortical necrosis". Clinical Nephrology. 45 (2): 125–130. PMID  8846525.

External links

From Wikipedia, the free encyclopedia
Renal cortical necrosis
Other namesDiffuse bilateral renal cortical necrosis (BRCN), diffuse cortical necrosis, acute cortical necrosis, acute kidney failure with acute cortical necrosis
Specialty Nephrology

Renal cortical necrosis (RCN) is a rare cause of acute kidney failure. The condition is "usually caused by significantly diminished arterial perfusion of the kidneys due to spasms of the feeding arteries, microvascular injury, or disseminated intravascular coagulation" and is the pathological progression of acute tubular necrosis. [1] It is frequently associated with obstetric catastrophes such as abruptio placentae and septic shock, and is three times more common in developing nations versus industrialized nations (2% versus 6% in causes of acute kidney failure).[ citation needed]

Causes

Adults

Babies

Pathophysiology

The exact pathologic mechanism for RCN is unclear, however the onset of small vessel pathology is likely an important aspect in the cause of this condition. In general the renal cortex is under greater oxygen tension and more prone to ischemic injury, especially at the level of the proximal collecting tubule, leading to its preferential damage in a sudden drop in perfusion. Rapidly corrected acute renal ischemia leads to acute tubular necrosis, from which complete recovery is possible, while more prolonged ischemia may lead to RCN. Pathologically, the cortex of the kidney is grossly atrophied with relative preservation of the gross structure of the medulla. The damage is usually bilateral owing to its underlying systemic causes, and is most frequently associated with pregnancy (>50% of cases). [1] It accounts for 2% of all cases of acute kidney failure in adults and more than 20% of cases of acute kidney failure during late pregnancy. [15] [16]

Diagnosis

While the only diagnostic "gold standard" mechanism of diagnosis en vivo is via kidney biopsy, the clinical conditions and blood clotting disorder often associated with this disease may make it impractical in a clinical setting. Alternatively, it is diagnosed clinically, or at autopsy, with some authors suggesting diagnosis by contrast enhanced CT. [17]

Treatment

Patients will require dialysis to compensate for the function of their kidneys.

Prognosis

Cortical necrosis is a severe and life-threatening condition, with mortality rates over 50%.[ citation needed] Those mortality rates are even higher in neonates with the condition due to the overall difficult nature of neonatal care and an increased frequency of comorbid conditions. The extent of the necrosis is a major determinant of the prognosis, which in turn is dependent on the duration of ischemia, duration of oliguria, and the severity of the precipitating conditions. Of those that survive the initial event, there are varying degrees of recovery possible, depending on the extent of the damage.

References

  1. ^ a b Deverajan, Prasad (May 26, 2011). Langman, Craig B (ed.). "eMedicine: Renal Cortical Necrosis". Medscape. Retrieved 27 March 2012.
  2. ^ Singh, B.; Gupta, A.; Mahajan, S.; Gupta, R. (2012). "Acute cortical necrosis and collapsing glomerulopathy in an HIV-infected patient: A rare clinical scenario". Saudi Journal of Kidney Diseases and Transplantation. 23 (2): 363–366. PMID  22382240.
  3. ^ Kumar, S.; Sharma, A.; Sodhi, K. S.; Wanchu, A.; Khandelwal, N.; Singh, S. (2012). "Renal cortical necrosis, peripheral gangrene, perinephric and retroperitoneal haematoma in a patient with a viper bite". Tropical Doctor. 42 (2): 116–117. doi: 10.1258/td.2011.110281. PMID  22316624. S2CID  21121415.
  4. ^ Jung, Y. S.; Shin, H. S.; Rim, H.; Jang, K.; Park, M. H.; Park, J. -S.; Lee, C. -H.; Kim, G. -H.; Kang, C. M. (2012). "Bilateral Renal Cortical Necrosis Following Binge Drinking". Alcohol and Alcoholism. 47 (2): 140–142. doi: 10.1093/alcalc/agr154. PMID  22215004.
  5. ^ Jha, R.; Narayan, G.; Swarnalata, G.; Shiradhonkar, S.; Rao, B. S.; Sinha, S. (2011). "Acute cortical necrosis following renal transplantation in a case of sickle cell trait". Indian Journal of Nephrology. 21 (4): 286–288. doi: 10.4103/0971-4065.78066. PMC  3193676. PMID  22022093.
  6. ^ Uppin, M. S.; Rajasekhar, L.; Swetha, H.; Srinivasan, V. R.; Prayaga, A. K. (2010). "Renal cortical necrosis at presentation in a patient with systemic lupus erythematosus: An autopsy case report". Clinical Rheumatology. 29 (7): 815–818. doi: 10.1007/s10067-010-1395-5. PMID  20169460. S2CID  22280989.
  7. ^ a b Huang, C. C.; Huang, J. K. (2011). "Sepsis-Induced Acute Bilateral Renal Cortical Necrosis". Nephrology. 16 (8): 787. doi: 10.1111/j.1440-1797.2011.01478.x. PMID  22029648. S2CID  30964151.
  8. ^ Kim, J. O.; Kim, G. H.; Kang, C. M.; Park, J. S. (2011). "Bilateral Acute Renal Cortical Necrosis in SLE-Associated Antiphospholipid Syndrome". American Journal of Kidney Diseases. 57 (6): 945–947. doi: 10.1053/j.ajkd.2011.02.381. PMID  21514023.
  9. ^ Novembrino, C.; De Giuseppe, R.; De Liso, F.; Bonara, P.; Bamonti, F. (2010). "Vitamin deficiency and renal cortical necrosis". The Lancet. 376 (9736): 160. doi: 10.1016/S0140-6736(10)61101-4. PMID  20638557. S2CID  42150606.
  10. ^ Kumar, S.; Krishna, G. S.; Kishore, K. C.; Sriram, N. P.; Sainaresh, V. V.; Lakshmi, A. Y. (2009). "Bilateral renal cortical necrosis in acute pancreatitis". Indian Journal of Nephrology. 19 (3): 125. doi: 10.4103/0971-4065.57112. PMC  2859480. PMID  20436735.
  11. ^ Baliga, K. V.; Narula, A. S.; Khanduja, R.; Manrai, M.; Sharma, P.; Mani, N. S. (2008). "Acute Cortical Necrosis inFalciparumMalaria: An Unusual Manifestation". Renal Failure. 30 (4): 461–463. doi: 10.1080/08860220801964293. PMID  18569922.
  12. ^ Toh, H. -S.; Cheng, K. -C.; Kuar, W. -K.; Tan, C. -K. (2008). "The Case ∣ Generalized petechiae and acute renal failure". Kidney International. 73 (12): 1443–1444. doi: 10.1038/ki.2008.143. PMID  18516063.
  13. ^ Leroy, F.; Bridoux, F.; Abou-Ayache, R.; Belmouaz, S.; Desport, E.; Thierry, A.; Bauwens, M.; Touchard, G. (2008). "Nécrose corticale rénale bilatérale induite par la quinine". Néphrologie & Thérapeutique. 4 (3): 181–186. doi: 10.1016/j.nephro.2008.01.001. PMID  18343736.
  14. ^ Sastre López, A.; Gago González, E.; Baños Gallardo, M.; Gómez-Huertas, E.; Ortega Suárez, F. (2007). "All-trans retinoic acid syndrome corrected and renal cortical necrosis". Anales de Medicina Interna. 24 (11): 551–553. doi: 10.4321/s0212-71992007001100009. PMID  18275266.
  15. ^ Prakash, J.; Niwas, S. S.; Parekh, A.; Pandey, L. K.; Sharatchandra, L.; Arora, P.; Mahapatra, A. K. (2010). "Acute kidney injury in late pregnancy in developing countries". Renal Failure. 32 (3): 309–313. doi: 10.3109/08860221003606265. PMID  20370445. S2CID  37285787.
  16. ^ Pertuiset, N.; Grünfeld, J. P. (1994). "Acute renal failure in pregnancy". Baillière's Clinical Obstetrics and Gynaecology. 8 (2): 333–351. doi: 10.1016/s0950-3552(05)80324-4. PMID  7924011.
  17. ^ Kim, H. J.; Cho, O. K. (1996). "CT scan as an important diagnostic tool in the initial phase of diffuse bilateral renal cortical necrosis". Clinical Nephrology. 45 (2): 125–130. PMID  8846525.

External links


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