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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2013  |  Volume : 24  |  Issue : 4  |  Page : 725-730
Renal cortical necrosis in tropics

1 Department of Nephrology, Osmania General Hospital, Hyderabad, Andhra Pradesh, India
2 Department of Pathology, Apollo Hospital, Hyderabad, Andhra Pradesh, India

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Date of Web Publication24-Jun-2013


The aim of this study is to review cases of renal cortical necrosis (RCN) that were seen on renal biopsy at our center over a period of seven years. All renal biopsy records over seven years at the Osmania General Hospital were reviewed to identify patients with histologically proven RCN. The demographic, clinical, laboratory investigations and follow-up data were noted. There were a total of 105 patients with RCN. The mean age was 28.13 ± 12.40 years. Forty-one cases (39.04%) resulted from obstetric complications. The most common histology type of RCN was patchy cortical necrosis in 65 patients (62%). All patients required dialysis, and the mean duration of dialysis was 3 ± 1 weeks. Thirty-three (31.42%) patients progressed to end-stage kidney disease while three patients underwent renal transplantation. Ten (9.5%) patients succumbed to acute kidney injury. The remaining patients recovered sufficient renal function and were dialysis-independent till the last follow-up. RCN is an important cause of chronic kidney disease. Obstetric complications are the leading cause of RCN in our setting. An early renal biopsy, especially in cases of anuric renal failure, helps in establishing the diagnosis.

How to cite this article:
Sahay M, Swarnalata, Swain M, Padua M. Renal cortical necrosis in tropics. Saudi J Kidney Dis Transpl 2013;24:725-30

How to cite this URL:
Sahay M, Swarnalata, Swain M, Padua M. Renal cortical necrosis in tropics. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2021 Sep 21];24:725-30. Available from: https://www.sjkdt.org/text.asp?2013/24/4/725/113864

   Introduction Top

Renal cortical necrosis (RCN) is a rare but important cause of renal failure in developing countries. Although RCN is a rare cause of acute kidney injury (AKI) in the developed world, [1] it still continues to be an important cause of morbidity and mortality in developing countries. [2],[3],[4],[5],[6] The damage is permanent and functional loss is irreversible. Most cases of RCN progress to end-stage renal disease (ESRD). The incidence however is declining. [7]


Cortical necrosis occurs secondary to ischemic necrosis of the renal cortex due to diminished renal arterial perfusion secondary to vascular spasm, microvascular injury or disseminated intravascular coagulation (DIC). Cases are usually bilateral. In most cases, the medulla, juxtamedullary cortex and a thin rim of sub-capsular cortex are spared. If the vasospasm is short lived with early restoration of vascular flow, acute tubular necrosis occurs. In hemo-lytic uremic syndrome (HUS) and septic abortion, endotoxin-mediated endothelial damage also plays a significant role. Under normal circumstances, when endothelial injury occurs, the local release of nitric oxide (endothelium-derived relaxing factor) minimizes thrombus formation by diminishing platelet aggregation. If, however, the endothelial dysfunction is severe, nitric oxide release is impaired and thrombus formation ensues. In abruptio placenta, hypercoagulable state, endothelial injury and intravascular thrombosis contribute to RCN. [8]

This study was carried out to determine the varied etiologies, clinical course and outcome of cortical necrosis in a developing country.

   Materials and Methods Top

There were 2997 renal biopsies performed at the Osmania General Hospital during the seven-year period from January 2004 till December 2010. All renal biopsy records of patients with cortical necrosis over these seven years were reviewed and demographic data, clinical presentation, laboratory data and outcome were recorded. The renal biopsy specimens were processed and stained with hematoxylin and eosin stain. RCN was divided into two groups using standard histological criteria: Diffuse cortical necrosis (DCN) was defined as confluent global cortical destruction of the cortex involving the columns of Bertini with preservation of a thin rim of sub-capsular and juxtamedullary tissue in few cases. DCN is associated with irreversible renal failure. Patchy cortical necrosis (PCN) is characterized by contiguous area of necrosis involving one-third to one-half of the entire cortex. [9] PCN may be associated with partial recovery of renal function. The data were statistically analyzed using SPSS version 14.

   Results Top

We identified 105 cases of RCN during the study period. Of these patients, 30 were men and 75 were women (1:2.5). The clinical features are depicted in [Table 1]. There were ten children. Hyperkalemia, hypocalcemia and metabolic acidosis were seen in 23 (21.9%), 13 (12.38%) and 78 (74.28%) patients, respectively. Hemolytic anemia, thrombocytopenia and coagulation abnormalities with low fibrinogen levels and increased fibrin-degradation products were seen in ten (9.5%), 26 (24.76%) and 15 (14.28 %) patients [Table 2].
Table 1: Clinical features.

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Table 2: Laboratory data.

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The common etiologies of RCN are shown in [Table 3]. Forty-one women (39.04%) developed RCN secondary to obstetric problems. Obstetric conditions associated with RCN are shown in [Table 4]. Of the 41 females with obstetric RCN, 21 (53%) were primigravida and 22 (53.6%) had pregnancy-induced hypertension. Among children, five had gastroenteritis, one had snake envenomation and four had HUS as the cause for RCN.
Table 3: Etiology of renal cortical necrosis.

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Table 4: Etiology of obstetric renal cortical necrosis (n = 41).

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The most common histology type of RCN was patchy in 75 patients (71.42%) while the remaining patients had the diffuse form [Figure 1]. Calcification was noted in five (4.75%) patients. Two patients had sub-capsular band on ultrasound. All patients required dialysis, and the mean duration of dialysis was 3 ± 1 weeks. Thirty-three (31.42%) patients progressed to end-stage kidney disease while three patients underwent renal transplantation. Ten (9.5%) patients succumbed to the AKI. Twenty (19 %) patients recovered completely. The remaining patients recovered sufficient renal function and were dialysis-independent till the last follow-up.
Figure 1: Ghost glomeruli diffuse cortical necrosis (H×E).

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   Discussion Top

The frequency of RCN in all patients with AKI is 1.9-2% in the western countries. [1] The incidence of RCN was reported to be 3.12% of all cases of AKI by Jaiprakash [7] and 3.8% at a referral center in North India in Chugh's study. [5]

The first peak of RCN occurs in early infancy and is associated with severe perinatal events. [10] RCN in childhood is usually secondary to HUS or severe volume depletion. The second peak occurs in women of childbearing age because of obstetric causes. The age range in our study was 2-40 years, with a mean of 28.13 ± 12.40 years. In another Indian study, the age range of patients in the non-obstetric group was 18-55 years while in the obstetric group it was between 20 and 38 years. [7] The age of children with HUS was eight months to 12 years. [7] In another study from Pakistan, the mean age group was 26.21 ± 13.01 years. [4] RCN has no racial predilection.

In childhood, RCN equally affects both sexes. In adults, RCN occurs more frequently in women because the most common cause is placental abruption. [7] In our study, 71.42% were women.

Clinical features

RCN may present with oliguric renal failure, hematuria, flank pain, costo-vertebral tenderness with palpable, tender kidneys and shock. Perinatal asphyxia may be seen in neonates. In childhood, it most often complicates HUS or gastroenteritis. In pregnancy, there may be associated abortion, symptoms of eclampsia and vaginal bleeding.

All patients with RCN have severe renal failure at presentation. Oligoanuria of five to 12 days duration was seen in all patients in one study, [7] while in the study by Chugh et al, 78.8% had anuria. [5] Majority of the patients in our study presented with oligoanuric renal failure.

Causes of RCN can be divided into two groups: Obstetric and non-obstetric. [11],[12],[13],[14] In the United States, RCN accounts for more than 20% of AKI during the third trimester of pregnancy. In an Indian study, acute cortical necrosis due to obstetric causes was observed in 56.2% of the patients, whereas non-obstetric causes accounted for AKI in 43.8% of the patients. [7] Similar observations were made by Ali (55.5% obstetric RCN) [4] and Chugh (56.6% obstetric RCN). [5] In our study, obstetric causes accounted for 39.04% of the patients. In the literature, obstetric complications mostly responsible include abruptio placenta, septic abortion, eclamptic toxemia, post-partum hemorrhage, intrauterine fetal death, amniotic fluid embolism and puerperal sepsis.

In an Indian study, 78% of obstetric RCN was due to septic abortions. In a study by Ojha et al where RCN was seen in 15.2% of the patients, the incidence was higher (11.9%) in early pregnancy, i.e. post-abortal cases, compared with 3.3% patients who were near term. [7] However, other studies have shown that RCN was more common in late pregnancy (37.1%) as compared with early pregnancy (septic abortion) (19.5%). [5] In our study, RCN was more common near term, and abruptio placenta was the most common cause. Septic abortion was noted only in two cases.

Chugh et al showed that non-obstetric conditions leading to acute cortical necrosis in a study were snake bite (sea snake, cobra, green pit viper, Russell viper) - 14.2%, HUS 11.5%, hyperacute kidney transplant rejection 5.3%, gastroenteritis 4.4%, pancreatitis 3.5%, septicemia 2.7% and drugs 0.9%. [5] Other causes include shock, [15] extensive burns, diabetic keto-acidosis, multiple fractures, hemorrhage, streptococcus pharyngitis, [16] dehydration in infancy or childhood, organophosphorus poisoning [17] and intra-abdominal procedures. [18] In a study, overall, abruptio placenta was the most common obstetric cause, responsible for 50-60% of all cases of RCN, followed by overwhelming infections with septic shock, which comprised 30-40% of the cases. [11] However, in another series, HUS was the main cause of RCN (72%) in the non-obstetric group. [7] Of the cases of HUS, 66.6% patients had D+ HUS associated with diarrhea while 33.3% had D-HUS, especially in the adult age group. [7] In our study, obstetric RCN was the most common etiology while gastroenteritis was the most common etiology in the non-obstetric group.

Neonatal conditions include congenital heart disease, fetal-maternal transfusion, dehydration, perinatal asphyxia, severe hemolytic disease and sepsis. [10]

Imaging studies

Thin cortical shells or tram lines caused by calcification are a radiologic hallmark on plain film, but they develop four to five weeks after the initial insult. [19] The sonogram initially shows enlarged kidneys with reduced blood flow. Cortical tissue becomes shrunken later as the disease progresses. A characteristic finding on ultrasound is the hypoechoic zone. Most renal diseases cause an increase in the echogenicity of the cortex, but, in RCN, a hypoechoic circumferential band on sonography in seen in the sub-capsular area. In our study, this was seen only in two patients. Contrast-enhanced computed tomography (CT) scanning is the most sensitive imaging modality. [20] In seven cases of cortical necrosis in our study where CT was available, it showed characteristic findings. Diagnostic features include absent opacification of the renal cortex with low-attenuation zone and enhancement of the sub-capsular and juxtamedullary areas and medulla without excretion of contrast medium. 99m Technicium Diethylene triamine pentacetic acid (DT-PA) scan reveals markedly diminished perfusion with delayed or no function. Renal scan is the imaging technique of choice to diagnose RCN in transplant kidneys or if contrast-enhanced CT scanning is not available. In the recent literature, magnetic resonance imaging [21] has been reported as a diagnostic tool, but yield occurs later in the illness with approximate latency of ten days. However, renal biopsy remains the mainstay of diagnosis.

Kidney biopsy is indicated if the diagnosis is unclear. The tubular cells show necrosis with infiltration of leukocytes. The glomeruli may be necrotic and thrombosis of the arterioles can be seen. The medulla and a thin rim of sub-capsular tissue are preserved because the arteries supplying these regions are not involved. Calcification at the junction of the necrotic and viable tissue is seen, with the earliest appearance reported as six days after insult. [22] Studies have shown that patients with thrombotic micro-angiopathy (TMA) involving the arteries have a higher likelihood of progressing into acute cortical necrosis compared with patients with predominant glomerular TMA. In a study, DCN was the dominant lesion in 71.9% patients, and the remaining 28% patients had PCN. [7] Renal histology showed DCN in 62.8% patients and patchy lesions in 37.2% patients in a study by Chugh, [5] whereas PCN was the most common histology type (77.8%) in another study. [4] In our series, DCN was observed in 28.6% patients and PCN in 71.4% patients. RCN was found to be 0.2% in autopsy studies. [22]

AKI is typical in patients with RCN, with associated complications (eg, hyperkalemia, fluid overload). Variable survival has been noted in patients with RCN. [23],[24],[25] Twenty percent to 40% of the patients have partial recovery, with a creatinine clearance that stabilizes between 15 and 50 mL/min. In our series, 20% of the patients recovered while 31.42% patients progressed to ESRD. In Ojha's study, 19.2% had a partial recovery while 28% progressed to ESRD. In the same study, the mortality decreased from 72% in 1984 to 19% in 1995. [7] Dialysis-free survival of as long as 12 years has been recorded. [5] Various causes of mortality are severe uremia, pulmonary edema, hyperkalemia, gastrointestinal hemorrhage and septicemia. Prognosis and survival of patients with cortical necrosis has improved markedly in developed countries due to the availability of hemodialysis and renal transplant therapy. In untreated patients, the mortality rate exceeds 50%.

   Limitations of the study Top

All patients did not come for regular monthly follow-up. Some cases of patchy cortical necrosis may have been misclassified as DCN, as classification was based on renal biopsy and renal angiogram was not performed in all patients.

   Conclusion Top

RCN is an important cause of chronic kidney disease. Obstetric complications are the leading cause of RCN in our setting. An early renal biopsy, especially in cases of anuric renal failure, helps in establishing the diagnosis.

   Conflict of interest Top

The authors have no conflict of interest to declare.

   References Top

1.Schreiner GE. Bilateral cortical necrosis. In: Hamburger J, Grunfeld JP, eds. Nephrology. New York: Wiley; 1979. p. 411-30.  Back to cited text no. 1
2.Prakash J, Tripathi K, Pandey LK, Shahai S, Usha, Srivastava PK. Spectrum of renal cortical necrosis in acute renal failure in Eastern India. Postgrad Med J 1995;71:208-10.  Back to cited text no. 2
3.Sakhuja V, Chugh KS. Renal cortical necrosis. Int J Artif Organs 1986;9:145-6.  Back to cited text no. 3
4.Ali SS, Rizvi SZ, Muzaffar S, Ahmad A, Ali A, Hassan SH. Renal cortical necrosis: A case series of nine patients & review of literature. J Ayub Med Coll Abbottabad 2003;15:41-4.  Back to cited text no. 4
5.Chugh KS, Jha V, Sakhuja V, Joshi K. Acute renal cortical necrosis a study of 113 patients. Ren Fail 1994;16:37-47.  Back to cited text no. 5
6.Prakash J, Sen D, Kumar NS, Kumar H, Tripathi LK, Saxena RK. Acute renal failure due to intrinsic renal diseases: Review of 1122 cases. Ren Fail 2003;25:225-33.  Back to cited text no. 6
7.Prakash J, Vohra R, Wani IA, et al. Decreasing incidence of renal cortical necrosis in patients with acute renal failure in developing countries: a single-centre experience of 22 years from Eastern India. Nephrol Dial Transplant 2007;22:1213-7.  Back to cited text no. 7
8.Chris VG, Willem P, Jef A, Jos V, Paul JD. Activation of both coagulation and fibrinolysis in childhood hemolytic uremic syndrome. Kidney Int 1998;54:1324-30.  Back to cited text no. 8
9.Jennette JC, Robert H. Acute ischemic and toxic tubular injury and other ischemic renal injury in "Heptinstall"s Pathology of the Kidney". In: Jennette JC, Olson JL, Schwartz MM, Silva FG, eds. 6 th ed. Philadelphia: Lippincott Williams & Wilkins; 2006 p. 1145-88.  Back to cited text no. 9
10.Campbell AC, Henderson JL. Symmetrical cortical necrosis of the kidneys in infancy and childhood. Arch Dis Childhood 1949;24:269-85.  Back to cited text no. 10
11.Prakash J, Tripathi K, Pandey LK, Gadela SR. Renal cortical necrosis in pregnancy-related acute renal failure. J Indian Med Assoc 1996; 94:227-9.  Back to cited text no. 11
12.Sheehan HL, Moore HC. Renal cortical necrosis and the Kidney of concealed Accidental Haemorrhage. Oxford: Blackwell;1952.  Back to cited text no. 12
13.Chugh KS, Singhal PC, Sharma BK, et al. Acute renal failure of obstetric origin. Obstet Gynaecol 1976;48:642-6.  Back to cited text no. 13
14.Ober WE, Reid DE, Rommy SL, Merril JP. Renal lesions and acute renal failure in pregnancy. Am J Med 1956;21:781.  Back to cited text no. 14
15.McFarlane D. Focal renal cortical necrosis in a fatal case of shock. J Pathol Bacteriol 1941;52: 406-8.  Back to cited text no. 15
16.Sandra WM, Nancy EG, Robert PE. Renal cortical necrosis following streptococcal infection. Arch Intern Med 1977;137:1196-7.  Back to cited text no. 16
17.Perry JW. Phosphorus poisoning with cortical necrosis of the kidneys, a report of two fatal cases. Australas Ann Med 1953;2:94-8.  Back to cited text no. 17
18.Palapattu GS, Barbaric Z, Rajfer J. Acute bilateral renal cortical necrosis as a cause of postoperative renal failure. Urology 2001;58: 281.  Back to cited text no. 18
19.Orom S, Ron G, Pell L, Winteler J. Renal cortical calcification after snake bite. Am Heart J. 1964;67:714-5.  Back to cited text no. 19
20.Rathod K, Garg A, Chavhan G, Rathod N. Computed tomography as a diagnostic tool in acute renal cortical necrosis. J Assoc Physicians India 2002;50:1451-2.  Back to cited text no. 20
21.Jeong JY, Kim SH, Sim JS, et al. MR findings of renal cortical necrosis. J Comput Assist Tomogr 2002;26:232-6.  Back to cited text no. 21
22.Solez K. Pathology of kidney, 3 rd ed. Boston: Little Brown and Co.; 1983. p. 1121-33.  Back to cited text no. 22
23.Deutsch V, Frankl O, Drony Y, Eliahou, Braf ZF. Bilateral renal cortical necrosis with sur­vival through the acute phase with a note on the value of selective nephroangiography. Am J Med 1971;50:828-34.  Back to cited text no. 23
24.Walls J, Schorr WJ, Kerr DN. Prolonged oligu-ria with survival in acute bilateral cortical necrosis. Br Med J 1968;4:220-2.  Back to cited text no. 24
25.Groshong TD, Taylor AA, Nolph KD, Esterly J, Maher JF. Renal function following cortical necrosis in childhood. J Pediatr 1971;79:267-75.  Back to cited text no. 25

Correspondence Address:
Manisha Sahay
Department of Nephrology, Osmania General Hospital, Hyderabad, Andhra Pradesh
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DOI: 10.4103/1319-2442.113864

PMID: 23816721

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  [Table 1], [Table 2], [Table 3], [Table 4]


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