| Abstract|| |
Renal cortical necrosis (RCN) is characterized by patchy or diffuse destruction of all the elements of renal cortex resulting from significantly diminished renal arterial perfusion due to vascular spasm and microvascular injury. It is a rare cause of acute kidney injury (AKI) in developed countries with frequency of 1.9%—2% of all patients of AKI. In contrast, the incidence of RCN is higher in developing countries ranging from 6%–7%. Obstetric complication is the main cause of RCN, earlier it was about 20%–30% which has been declining to 5% in the Indian subcontinent during the past two decades. The aim of this study is to review five consecutive cases of RCN diagnosed within very short span of time. Histopathologically, diagnosed five cases of RCN during one-month span in September 2016 at Armed Forces Institute of Pathology, Dhaka were included in this study. All the cases were referred cases from a tertiary level obstetric center of Dhaka city; the mean age was 24.2 ± 3.4 years. All the cases had the history of postpartum hemorrhage followed by septicemia. They all presented with acute renal failure dependent on hemodialysis for >21 days. On histological examination, three (60%) had patchy RCN and two (40%) had diffuse RCN. Two (40%) showed coagulative necrosis of all the glomeruli, two (40%) showed coagulative necrosis of >50% of glomeruli, and in one (20%) case necrosis of about 25% of glomeruli. One of the glomeruli showed global sclerotic change of most of the glomeruli. In all the cases, interstitium showed moderate focal lymphocytic infiltration and mild edema. Among all, one (20%) was found with immunoglobulin A nephropathy as an associated diagnosis. RCN is still encountered as an obstetric complication in our setting and this type of grave consequences should be prevented by better monitoring of pregnancies.
|How to cite this article:|
Jaynul Islam SM, Akhter S, Hossain MS. Renal Cortical Necrosis; Five Consecutive Cases within Short Span of Time. Saudi J Kidney Dis Transpl 2019;30:919-23
|How to cite this URL:|
Jaynul Islam SM, Akhter S, Hossain MS. Renal Cortical Necrosis; Five Consecutive Cases within Short Span of Time. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2020 Dec 2];30:919-23. Available from: https://www.sjkdt.org/text.asp?2019/30/4/919/265469
| Introduction|| |
Pregnancy-related acute kidney injury (AKI) is a rare complication in high-income countries, with an estimated incidence from 1.5 to 4.5/10,000 deliveries. Renal cortical necrosis (RCN) is defined as ischemic destruction of the renal cortex secondary to a prolonged decrease in renal arterial perfusion (vascular spasm, microvascular injury, or intravascular coagulation). Obstetric RCN is especially associated with massive hemorrhage due to placenta previa, abruptio placentae, postpartum hemorrhage (PPH), or other severe complications such as amniotic fluid embolism and septic abortions. The incidence of pregnancy- related RCN is also declining in developing countries, but it remains still high in South East Asia. In Eastern India, it was estimated 5.2% and in Pakistan, it was 30% of pregnancy- related AKI. RCN also carries high morbidity and mortality in South East Asia, ranging from 26% to 93.3%.
Two cases of RCN were reported following acute pancreatitis from Bangladesh, but no data could be retrieved on postpartum RCN from the literature. However, one study carried out in the largest public hospital at Dhaka during 2007–2008 found prevalence of pregnancy-related AKI as 21.6%. However, most of these AKIs were not evaluated histo- logically. Here, we are presenting clinico- pathological spectrum of five cases of post- partum RCN diagnosed histologically all of which occurred within very short period (30 days).
| Materials and Methods|| |
Histopathologically, diagnosed five cases of RCN during a one month span from September 1, 2016, to September 30, 2016, at Armed Forces Institute of Pathology, Dhaka were included in this study. Two renal biopsy samples from each patient were received, one in formalin for routine paraffin sections and one in normal saline for direct immunofluo- rescence study. For histopathological diagnosis Hematoxyline and Eosin, Periodic Acid Schiff, Masson trichrome, and Methanamine silver stains are used for light microscopy. Direct immunofluorescence study was done using immunoglobulin (Ig) G, A, M, C3, C1q, Kappa and Lambda for each case. All the cases were referred to cases from a tertiary level obstetric center of Dhaka city. Clinical information was retrieved from clinical data of the patients. RCN was further categorized histologically as diffuse cortical necrosis when confluent global necrosis was found involving more than half of the entire cortical tissue and focal cortical necrosis when confluent cortical necrosis was found involving one-third to one half of the entire cortical area. Data were analyzed using the Statistical Package for the Social Sciences version 20 (IBM Corp., Armonk, NY, USA).
| Results|| |
Among histologically-proven five cases of RCN, the mean age was 24.2 ± 3.4 years. All the cases had the history of full-term pregnancy followed by delivery either by lower uterine cesarean section or by normal vaginal delivery. Four of the patients had the history of septicemia followed by renal failure, one had the history of PPH with septicemia, and one of the patients had the history of PPH only. All five cases presented with acute renal failure (ARF) were managed with supportive management and were dependent on hemodialysis (HD) for >21 days at a dose 25–30 mL/kg/h. The patients had significant proteinuria ranging from 1 (+) to 3 (+) along with mild [2-4/high-power field (HPF)] to severe (20–30/HPF) hematuria. Serum creatinine level during presentation was from 3.0–8.8 mg/dL. On histo-logical examination, three (60%) had patchy RCN and two (40%) had diffuse RCN. Two (40%) showed coagulative necrosis of all the glomeruli, two (40%) showed coagulative necrosis of >50% of glomeruli and in one (20%) case, necrosis of about 25% of glomeruli [Figure 1]. One of the cases showed global sclerotic change of most of the glomeruli. In all the cases, interstitium showed moderate focal lymphocytic infiltration and mild edema [Table 1]. Among these cases, one (20%) was found with IgA nephropathy as an associated diagnosis [Figure 2].
|Table 1: Demographic and morphologic, biochemical, and morphologic characteristics of renal cortical necrosis.|
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|Figure 1: Coagulative necrosis of glomerulus and tubules (680 x 512 pixel).|
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|Figure 2: Mesangial immunoglobulin A deposits in case 5 (680 x 512 pixel).|
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| Discussion|| |
RCN is a potentially fatal variety of kidney disease with adverse and serious outcomes. The total ischemic necrosis of all the elements (glomeruli, blood vessel and tubule) of the affected area of renal cortex is a typical histo-logical feature of RCN. Obstetric complications (septic abortion, puerperal sepsis, abruptio placentae, PPH, and eclampsia) are the main (60%–70%) causes of RCN in developing countries. The remaining 30%–40% cases of RCN are caused by nonobstetrical causes, mostly due to nonobstetrical sepsis and hemo-lytic uremic syndrome. In Bangladesh, septi-cemia and preeclampsia were found to be main causes of pregnancy-related ARF followed by PPH, antepartum hemorrhage, ruptured ectopic pregnancy. In most of the situation, this pregnancy-related AKI are not evaluated histologically. Recently, possibly due to recent improvement of renal pathology infrastructure and expertise, postpartum AKI cases are biop- sied in case of persistent renal dysfunction even after continued management effort of AKI.
Cortical necrosis occurs secondary to ische-mic necrosis of the renal cortex due to diminished renal arterial perfusion secondary to vascular spasm, microvascular injury, or disseminated intravascular coagulation. In case of severe endothelial insult nitric oxide release is impaired and thrombus formation ensues. In abruptio placenta, hypercoagulable state, endo-thelial injury and intravascular thrombosis contribute to RCN.
The most characteristic clinical features of the disease are anuria. Flank pain, hematuria, fever, and hypovolemia have also been documented as presenting features. The usual course is progression to terminal renal failure and recovery is rare. In our study, all five cases presented with anuria with raised crea-tinine level. Four patients had the history of postpartum sepsis, one had the history of PPH with sepsis and one had only PPH.
Renal imaging may be useful in providing arguments for cortical necrosis and giving an assessment of the extent of damage. When the renal biopsy is difficult or even impossible, imaging, particularly computed tomography and magnetic resonance imaging is a great contribution to confirm the diagnosis. Renal biopsy is the “gold standard” in the diagnosis of cortical necrosis. On histology, all components of the kidney are affected. Different pathologic forms of cortical necrosis are found. Most of the studies reported diffuse cortical necrosis as more prevalent than patchy cortical necrosis,, whereas Sahay et al have reported patchy cortical necrosis in 71.4% and diffuse cortical necrosis in 28.6% renal biop-sies. In this study, we got predominantly (80%) diffuse cortical necrosis. One of our cases was found with mesangial IgA deposits in the glomeruli. The case also had diffuse glomerulosclerosis associated with focal RCN. Possibly, she had postpartum RCN superimposed on IgA nephropathy.
In fact, in our study, total clinical data of the cases regarding prenatal duration was not available. Since the patients were from another tertiary level hospital of Dhaka, some details of management and follow-up of the patients could not be retrieved. As standard management protocol of AKI, all of them were managed by supportive therapy along with maintenance HD. The study comprises only five cases which is actually an extended series case reports, and hence, it does not reflect the epidemiological scenario of the community. However, the occurrence of multiple cases of RCN within a very short period points to the fact that proper antenatal care should be offered and available so as to avoid this serious complication of pregnancy.
| Conclusion|| |
Although renal cortical necrosis has a declining trend in developed counties as well as in our neighboring country, it is still commonly encountered as an obstetric complication in our setting. This type of grave consequences should be prevented by better monitoring of pregnancies.
Conflict of interest: None declared.
| References|| |
Callaghan WM, Creanga AA, Kuklina EV. Severe maternal morbidity among delivery and postpartum hospitalizations in the United States. Obstet Gynecol 2012;120:1029-36.
László FA. Renal cortical necrosis. Experimental induction by hormones. Contrib Nephrol 1981; 28:1-216.
Grünfeld JP, Ganeval D, Bournérias F. Acute renal failure in pregnancy. Kidney Int 1980; 18:179-91.
Kim HJ. Bilateral renal cortical necrosis with the changes in clinical features over the past 15 years (1980-1995). J Korean Med Sci 1995; 10:132-41.
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.
Ali A, Ali MA, Ali MU, Mohammad S. Hospital outcomes of obstetrical-related acute renal failure in a tertiary care teaching hospital. Ren Fail 2011;33:285-90.
Hassan I, Junejo AM, Dawani ML. Etiology and outcome of acute renal failure in pregnancy. J Coll Physicians Surg Pak 2009;19: 714-7.
Rahman H. Etiology and outcome of acute kidney injury; a comprehensive study in four tertiary level hospital of Dhaka. J Paediatr Nephrol2017;5:1-5.
Rahman S, Gupta RD, Islam N, et al. Pregnancy related acute renal failure in a tertiary care hospital in Bangladesh. J Med 2012;13:129-32.
Prakash J, Singh VP. Changing picture of renal cortical necrosis in acute kidney injury in developing country. World J Nephrol 2015;4: 480-6.
Sahay M, Swarnalata, Swain M, Padua M. Renal cortical necrosis in tropics. Saudi J Kidney Dis Transpl 2013;24:725-30.
] [Full text]
Shah VB, Deokar M, Vyankatesh A, Patil PA. Renal cortical necrosis-An autopsy series of 15 cases with review of literature. Bombay Hosp J 2010;52:317-20.
François M, Tostivint I, Mercadal L, et al. MR imaging features of acute bilateral renal cortical necrosis. Am J Kidney Dis 2000;35: 745-8.
Gwendolyn F, Sumitha B, Ellerhea F. Renal cortical necrosis at autopsy: A 12 year experience at a tertiary care center in Mumbai. Int J Med Res Rev 2017;5:626-34.
Sheikh Mohammad Jaynul Islam
Armed Forces Institute of Pathology, Dhaka
[Figure 1], [Figure 2]