| Abstract|| |
The incidence of acute kidney injury in pregnancy (P-AKI) has markedly decreased over the last three decades in India, particularly due to decreased incidence of postabortion AKI. However, P-AKI still accounts for 3%–5% of cases of total AKI. Postabortion sepsis has decreased to between 0.9% and 1.5% in 2014 from 9.4% in 1980–1990 in the new millennium. Currently, in India, majority of P-AKI (70%–90%) occurs in the postpartum period and in late 3rd trimester similar to the developed countries, but causes are different. We observed that preeclampsia/eclampsia is the most common cause of P-AKI in the late 3rd trimester and postpartum period followed by puerperal sepsis and postpartum hemorrhage (PPH). Both puerperal sepsis and PPH are treatable and preventable etiologies of P-AKI. Timely and aggressive management of antepartum hemorrhage (APH/PPH) and puerperal sepsis are required to reduce the burden of P-AKI in developing countries. Specific-pregnancy disorders such as P-aHUS/thrombotic thrombocytopenic purpura, pregnancy-associated thrombotic microangiopathy, and acute fatty liver of pregnancy are the uncommon/rare causes of P-AKI in India and possibly also because of the lack of awareness toward diagnosis. Despite decreasing incidence of P-AKI, fetal mortality remained high and unchanged. However, maternal mortality has decreased to 5% from initial high mortality of 20%–25%. The incidence and severity of renal cortical necrosis have significantly decreased at our center.
|How to cite this article:|
Prakash J, Prakash S, Ganiger VC. Changing epidemiology of acute kidney injury in pregnancy: A journey of four decades from a developing country. Saudi J Kidney Dis Transpl 2019;30:1118-30
|How to cite this URL:|
Prakash J, Prakash S, Ganiger VC. Changing epidemiology of acute kidney injury in pregnancy: A journey of four decades from a developing country. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2020 Jan 23];30:1118-30. Available from: http://www.sjkdt.org/text.asp?2019/30/5/1118/270268
| Introduction|| |
Acute kidney injury in pregnancy (P-AKI) merits special attention because it involves risk to two lives (mother and fetus). It is largely due due to potentially preventable obstetric complications.,,, Socioeconomic and environmental factors are accountable for huge differences in the incidence, causes, and outcome of PAKI in developed countries compared with developing countries.,, With the liberalization of abortion law and improved obstetric care in developed countries, P-AKI is now an uncommon occurrence., From 1958 to 1994, the incidence of P-AKI has decreased from 1/3000 to 1/18,000 with respect to total pregnancies and from 43% to 0.5% with respect to the total number of acute renal failure. The incidence of P-AKI has declined significantly over the last three decades in developing countries but still accounts for 5%–20% of total AKI.,, In a recent study of P-AKI from India, its prevalence among all cases of AKI has decreased from 15% in 1980 to 10% in the 1990s., Our current study revealed P-AKI constitutes 4.68% of total AKI in 2003–2014 in the Eastern part of India.
During the first trimester of gestation, AKI develops most often due to hyperemesis gravidarum or septic abortion. Septic abortion was the most common cause of P-AKI in the 1980s and 1990s in India.,,, However, postabortion AKI has decreased to 1.49% in 2003–2014 from 9.4% in 1982–1991 of total AKI cases. Prevention of unwanted pregnancy and avoidance of septic abortion are keys to eliminating abortion associated – AKI in early pregnancy. We have not seen AKI on account of hyperemesis gravidarum over a period of 34 years at our center. This is possibly due to under-reporting or mild nature of renal dysfunction (i.e., prerenal azotemia). In the late third trimester and around delivery, the causes of P-AKI are similar but differ in frequency between developing and developed countries. In developing countries, the most common contributing factors to P-AKI are puerperal sepsis, postpartum hemorrhage (PPH), intrauterine fetal death, and preeclampsia;, whereas in developed countries, the most common causes of P-AKI are preeclampsia, hemolysis-elevated liver enzymes-low platelet (HELLP) syndrome, hemorrhage by abruption placenta, thrombotic microangiopathies (TMAs) and acute fatty liver of pregnancy (AFLP), in decreasing order of frequency., Pregnancy-associated thrombotic microangiopathies (aHUS/TTP) and AFLP are rare causes of AKI during pregnancy in developing counties. In this review, the changing picture of AKI in pregnancy will be discussed, with particular reference to the experience in India, as an example of a developing emerging country.
| Diagnosis of AKI in Pregnancy|| |
The validated definition of AKI in pregnancy is not yet established in the literature. The use of Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease (RIFLE) classification in pregnant women needs further study and is not consensual. The prognostic utility of RIFLE had been demonstrated in nonpregnant women, but only a few studies have reported its application in pregnant women., Pregnancy is associated with physiological increase in glomerular filtration rate (GFR) and renal plasma flow. The GFR can reach 40%–50% of baseline throughout pregnancy and subsides in the first 3 months postpartum. Renal plasma flow can increase up to 85% in the second trimester of pregnancy. These hemodynamic changes result in a decrease of serum creatinine in pregnancy to 0.4–0.5 mg/dL and blood urea nitrogen (BUN) to 8–10 mg/dL. The knowledge of this physiological adaption in pregnancy is of clinical importance because serum creatinine and BUN of 1.0 mg/dL and 13 mg/dL, respectively, would be considered normal in the nonpregnant individual but reflects renal impairment in a pregnant woman. Therefore, the diagnosis of AKI in pregnancy is based on increase in the serum creatinine. A creatinine level of ≥1 mg/dL or a rapid rise (by definition in 48 h) of 0.5 mg/dL above baseline should be investigated for evidence of AKI. The following criteria for the diagnosis of AKI in pregnant women may be used (any of the three); (1) Sudden increase in the serum creatinine of >1 mg/dL, (2) Oliguria/anuria and (3) Need for dialysis. We have used these criteria for the diagnosis of AKI in pregnancy in our study.
| Incidence of Pregnancy-Related Acute Kidney Injury|| |
AKI is a rare complication of pregnancy in the developed world. With the legalization of abortion, screening of hypertensive complications of pregnancy and overall improved antenatal care, the incidence of P-AKI has declined significantly in most developed countries. Stratta et al. reported the incidence of P-AKI in developed countries has declined from about 1/3,000 to 1/15,000–1/20,000 pregnancies since 1960. In a recent study from Canada, AKI occurred in 1/10000 pregnancies among 1.9 million pregnant women over a period of 15 years. In contrast, in developing countries obstetrical complications account for 15%–25% of total AKI and the most common cause of P-AKI is septic abortion. The main reasons leading to the persistent high incidence of P-AKI in developing countries are septic abortions usually performed in unhygienic conditions without adequate medical monitoring; overall poor follow-up of pregnancy, absence of medical facilities in rural areas and relatively late referral of patients with these conditions. However, the incidence of P-AKI is declining even in developing countries. Obstetrical complications constitute 9%–13% of total AKI cases in India and Pakistan.,,, The incidence of P-AKI has decreased from 15.2% in 1982–1991 to 10.4% in 1992–2002 with the declining trend continuing in 2003–2014 (4.68%) at our center over a period of three decades. We have earlier reported AKI occurring in 1.78% of total deliveries (1 in 56 births) in the third trimester of pregnancy with maternal mortality of 20%. The decreasing trend in P-AKI was also noted in other Indian studies, sepsis being the most common cause. Thus, the incidence of P-AKI in developing countries accounts for 5%-8% of total AKI cases., In contrast to India, a recent study from Pakistan reported an increase in pregnancy-related AKI in the last 10 years. This is possibly due to the lack of adequate primary health-care facilities and immoral practice of induced abortion to kill the fetus in early pregnancy.
| Causes and Timing of Pregnancy-Related Acute Kidney Injury|| |
The development of AKI during pregnancy follows bimodal distribution with two incidence peaks; one in the first trimester and other in the third trimester and postpartum period., During the first trimester of gestation, AKI develops most often due to septic abortion and hyperemesis gravidarum. The first peak has almost been eliminated in developed countries due to virtual disappearance of septic abortion.,, Currently, hyperemesis gravidarum is the most common cause of AKI in the first trimester in the developed world. This is however rare in India. The most likely causes are; (1) under-reporting and (2) mild nature of AKI (i.e., prerenal azotemia).
The third trimester AKI is due to late obstetrical complications, including puerperal sepsis, ante or PPH, intrauterine death, preeclampsia, thrombotic-microangiopathy (TMA), and AFLP. P-AKI occurs mainly (75%–85%) during the late third trimester and around delivery in most countries, including developing countries., Preeclampsia is the most common etiology of P-AKI even in developing countries., However, puerperal sepsis is the main cause of PAKI in the postpartum period in certain parts of India followed by PPH.,, In contrast to the developed world, pregnancy-associated TMA (P-TMA) and AFLP are uncommon/rare causes of AKI in pregnancy in India and other developing countries.,, Two Indian studies have reported a single case (one each) of postpartum aHUS among their patients with obstetric AKI., It is worth mentioning that AFLP and P-TMA are rare disorders, affecting 1/20,000 and 1/25,000 pregnancies, respectively., Stratta et al noted TMA (aHUS) in two patients (2.4%) in their series of 84 cases of P-AKI over a period of 39 years. In addition to rare diseases, inadequate investigations may account for under-reporting of P-TMA and AFLP as the cause of AKI in pregnant women in our country. The main causes and outcomes of P-AKI in the last 33 years at our center are shown in [Table 1]. The maternal and fetal outcome of P-AKI differs according to the period and place of the study. Studies in the 1970s reported maternal mortality of 55%, while recent studies report mortality to be ~ 15%, and 8%–30% of patients developed ESRD.,,, However, perinatal mortality has remained very high (~45%) and has not changed over a period of three decades. Percentage of P-AKI requiring dialysis has also decreased from 83% in 1982–1991 to 66.6% in 2003–2014. The number of patients with P-AKI progressing to ESRD had declined from 6.15% in 1982–1991 to 1.4% in 2003-2014. Overall, P-AKI may progress to ESRD in 10%–30% of the patients mainly due to renal cortical necrosis.
|Table 1: Main causes and outcomes of acute kidney injury in pregnancy in the last 33 years.|
Click here to view
AKI in First Trimester of Pregnancy
In 1970s and 1980s, septic abortion was the most common cause of P-AKI ranging between 50 and 70% of cases.,,, These abortions were conducted by untrained midwives under unhygienic conditions leading to septic abortion and subsequent AKI. The abortion was seldom “spontaneous” as stated by most of these patients. Septic abortion is a catastrophic disease and patient generally presents with high fever, chills, leukocytosis, uterine tenderness, hypotension, and foul-smelling cervical discharge. Sepsis is more common in patients with induced abortion (60%) than in those with spontaneous abortion. The microorganisms are more frequently isolated in vaginal swab culture. Positive blood culture is obtained in about one-third of the patients. The common organisms isolated on culture include anaerobic Streptococci, Bacteriodes fragilis, Streptococcus pyogenes, and Clostridium perfringenes. We have also isolated Gram-positive anaerobic Cocci, Klebsiella, Pseudomonas, Pyocyaneus and Escherichia More Details coli. Since 1980, the incidence of P-AKI in our center has declined due to a decrease in the incidence of septic abortion-related AKI [Figure 1]. The proportion of AKI due to septic abortion has decreased in recent years in other centers in India as well. In the Chandigarh study, post-abortal AKI was reported to decline to 3.5% in 1981–1986 from 13.7% of total AKI cases during 1965–1974. We reported that post-abortal AKI decreased to 7% in 1992–2002 from 9% of total AKI cases in 1982–1991. In our recent study, septic abortion contributed to 1.49% of total AKI cases in 2003–2014. Several studies from other Indian centers have reported that postabortal AKI has decreased markedly [Figure 2].,, Thus, septic abortion-related AKI is declining in India except in Kashmir valley, where 50% of total obstetric AKI was reported to be due to septic abortion. This might be due to regional differences in abortion practices and social stigma attached to abortion. However, the decrease in incidence of postabortal AKI is not uniform throughout the country.,,
|Figure 1: Distribution of cases of pregnancy-related acute kidney injury with respect to the gestational period.|
P-AKI: Acute kidney injury in pregnancy.
Click here to view
|Figure 2: Distribution of cases of pregnancy-related acute kidney injury during different phases of pregnancy.|
P-AKI: Acute kidney injury in pregnancy.
Click here to view
Hyperemesis gravidarum has been emphasized as an important cause of P-AKI in the first trimester of pregnancy in western literature. However, it is rarely reported from developing countries. We have observed no cases of AKI complicating hyperemesis gravidarum in our study in the last three decades, possibly due to under-reporting or mild degree of AKI (prerenal azotemia) associated with hyperemesis gravidarum.
AKI in Third Trimester and Around Delivery
Similar to developed nations, a peak of PAKI in the postpartum period is also recorded in India. Studies from several Indian areas revealed that postpartum AKI contributes to 70%–83% of total pregnancy-associated AKI.,,, We reported that 68% of P-AKI occurred in the postpartum period. The common causes of P-AKI in the postpartum period and around delivery include preeclampsia, HELLP syndrome, PPH, and puerperal sepsis. As already mentioned, pregnancy-associated thrombotic-microangiopathies (aHUS/TTP) and AFLP are rarely diagnosed in India.,,
Preeclampsia is a multisystem disorder unique to human pregnancy. Conventionally, diagnosis is based on new-onset hypertension and proteinuria at ≥20 weeks of gestation or in the absence of proteinuria, hypertension together with evidence of systemic disease (such as thrombocytopenia, elevated liver enzymes, renal dysfunction, pulmonary edema, and visual or cerebral disturbances). The characteristic kidney lesion of preeclampsia is swelling and detachment of glomerular endo-thelial cells leading to capillary lumen obstruction. AKI occurs in approximately 1% of women with severe preeclampsia.,,, PE/E accounts for 15%–20% of P-AKI cases and are the leading causes of AKI worldwide., PE/E was responsible for P-AKI in 43.9% and 35.29% of cases in pregnant women in our own study., Reversal of AKI occurs following delivery of fetus in majority of patients with preeclampsia. However, persistent renal dysfunction and the need of long-term dialysis suggest preexisting hypertension and chronic kidney diseases., The most common histological lesion in the setting of AKI in patients with PE/HELLP syndrome is acute tubular necrosis (ATN).,, However, renal cortical necrosis has been reported in preeclamptic women with AKI.,
Hemolysis, elevated liver transaminases, low platelet count (HELLP) syndrome
HELLP syndrome is sometimes considered as a variant of PE: it occurs only in pregnant women and resolves with delivery, being frequently, but not always, associated with hypertension and proteinuria. However, 20% of pregnant women with HELLP syndrome do not develop hypertension or proteinuria, thus supporting distinct disease., It complicates up to 20% of severe PE and is reported to occur in 1–2 per 10,000 pregnancies., HELLP syndrome generally occurs in the third trimester, but may be diagnosed in the 2nd trimester or in the postpartum.
AKI is reported in 3%–15% cases of HELLP syndrome and overall, it may account for 40% of P-AKI and may increase up to 60% of cases in severe form of the disease (i.e., HELLP syndrome).,,, The HELLP syndrome contributes to AKI in 8%–10% of patients in Indian studies., Majority (93%–100%) of patients with the HELLP syndrome-related AKI has excellent prognosis with near complete recovery of renal function.,, Both preeclampsia and HELLP syndrome are antiangiogenic state characterized by increased circulatory concentration of sFlt-1 and endoglin. Kidney biopsy study reveals typical features of TMA in <15% of patients with HELLP associated AKI.
Acute fatty liver of pregnancy
AFLP is a rare disorder with an incidence of 1/7,000 ίΰ 1/20,000 pregnancies.,, It affects women in the 3rd trimester of pregnancy and is characterized by the sudden onset of acute liver failure with coagulopathy. AFLP is a diagnosis of exclusion, once viral hepatitis and biliary obstruction have been ruled out. The presence of lipid micro vesicular infiltration of hepatocytes without inflammation and necrosis is a typical finding in patients with AFLP. AKI is seen in 20%–100% of cases, and its etiology is multifactorial., The various factors contributing to AKI in AFLP include; hypovolemia, co-existing preeclampsia, coagulopathy, hepatic failure, and intra-abdominal hemorrhage. AKI in patients with AFLP is mostly mild and usually does not require dialysis support., In most women, there is complete liver and kidney recovery after delivery. AKI is usually nonoliguric and ATN can occur in the setting of hemorrhage-induced hypovolemia.
Urgent and immediate delivery of fetus is associated with favorable maternal and fetal prognosis. Earlier studies have reported very high rate (85%) of maternal and fetal mortality in women with AFLP. However, a recent case series reported maternal and perinatal mortality ranging between 10% and 20%.,
Thrombotic-microangiopathy of pregnancy (P-TMA)
Thrombotic-microangiopathy of pregnancy is a rare disorder occurring in 1/25,000 pregnancies. It is reported to occur de novo during pregnancy and may relapse in subsequent pregnancies as well. P-TMA accounts for 8%–18% of all cases of TMA. Depending on the dominant mode of clinical presentation, two clinical forms of syndromes have been described; (a) thrombotic-thrombocytopenic purpura (TTP) and (b) hemolytic uremic syndrome (HUS). TTP is often diagnosed before delivery with highest risk during late 3rd trimester, because of progressive decrease in AD AMTS-13 activity and simultaneous steadily increase in plasma concentration of VWF during normal gestation. Atypical HUS (aHUS) mainly occurs in the first six months postpartum. Pregnancy and delivery are uneventful in majority of the patients. Complement alternative pathway (CAP) dysregulation is associated with P-TMA and mainly (80%) occurs during the postpartum period and 80% of patients reached ESRD during the first aHUS episode and 80% of P-HUS had CAP dysregulation in CFH and CFI encoding gene. The clinical feature of aHUS is similar to TTP, but renal involvement is more severe and the neurological manifestation is rare.
Differential diagnosis of TMA-associated AKI in pregnancy
TMA-associated AKI in pregnant women has several common clinical features such as micro-angiopathic hemolytic anemia, decreased platelet count and acute renal dysfunction. Thus, the presence of TMA and AKI in pregnancy is one of the most challenging differential diagnoses. However, the exact diagnosis of these syndromes is mandatory to make an appropriate therapeutic decision, which may save the life of both mother and fetus. [Table 2] summarizes the clinical and laboratory features of TMA-associated AKI in pregnancy. Delivery of fetus improves the clinical manifestation of AFLP and preeclampsia/HELLP syndrome. However, there is no benefit of delivery in patients with P-TMA (aHUS/TTP). Plasma exchange is the first line of treatment for patients with HUS/TTP. The important clinical clues to distinguish between these syndromes are given below.
|Table 2: Comparison of clinical and laboratory characteristics of HELLP, TTP, HUS, and AFLP.|
Click here to view
A. Distinguishing AFLP from HELLP syndrome
- Hypoglycemia and coagulopathy are the key features of AFLP
- Liver dysfunction is the dominant presentation with elevated aminotransferases and bilirubin level in AFLP
- Ammonia level is elevated in AFLP
- Profoundly depressed anti-thrombin level is seen in AFLP
- Hemolysis and thrombocytopenia are either mild or absent in AFLP, while it is moderate to severe in HELLP syndrome.
B. Distinguishing TTP/aHUS (P-TMA) from HELLP syndrome
- Isolated lactate dehydrogenase (LDH) increase with normal SGOT/SGPT, (LDH/ AST ratio - 25:1) favor HUS/TTP
- Coagulation abnormalities such as elevated antithrombin, D-dimer and high fibrinogen level are absent in HUS/TTP, while they are common in HELLP syndrome.
- The presence of proteinuria, hematuria, and RBC casts in urine favors aHUS and only isolated proteinuria occurs in HELLP syndrome
- Liver involvement is a hallmark of HELLP syndrome, is rare in patients with aHUS (severely increased hepatic transaminases level strongly suggests HELLP syndrome).
C. Preeclampsia/HELLP syndrome Both preeclampsia and HELLP syndrome have similar clinical features with increased circulatory concentration of sFlt-1 in maternal blood. HELLP syndrome is considered to be a form of severe preeclampsia. The following points may provide clues to distinguish HELLP syndrome from preeclampsia.
- Thrombocytopenia is often the first sign of HELLP syndrome in pregnant women
- Proteinuria and/or hypertension may be absent in 20% cases of HELLP syndrome while hypertension is a constant feature of preeclampsia
- Systemic manifestations (i.e., elevated SGOT, SGPT, kidney dysfunction, low platelet count, increased LDH and cerebral symptoms) in the absence of proteinuria and hypertension suggest the diagnosis of HELLP syndrome in gravid women.
| Renal Cortical Necrosis (RCN) in Pregnancy|| |
RCN is characterized by ischemic destruction of all the elements of renal parenchyma (glomeruli, blood vessels, and interstitium) in the involved area of cortex. The lesions are secondary to the markedly reduced renal arterial perfusion usually resulting from intravascular coagulation, vascular spasm and microvascular injury. It is a rare lesion that accounts for <2% of all cases of ARF in developed countries. Overall, obstetric complications are the most common (50%–70%) cause of RCN, while nonobstetric conditions causes RCN in approximately 20%–30% of all cases of cortical necrosis., Septic abortion, puerperal sepsis, preeclampsia/HELLP syndrome, abruptio placentae and PPH are the pregnancy-related conditions causing RCN. Renal cortical necrosis due to obstetric complications was noted in 56% and 61% of cases, respectively in our previous study., However, the incidence of cortical necrosis in P-AKI has significantly (P <0.001) decreased from 17% in 1982–1991 ίΰ 2.4% after 2000s. In our experience, renal cortical necrosis was noted in 17% (11/65), 2.4% (3/125) and 1.44% (1/68) patients of obstetric AKI in 1982–1991 1992–2002 and 2003–2014, respectively™ [Figure 3]. Septic abortion was the most common cause of RCN in the first two study periods but no case of septic abortion-induced RCN was observed in the last decade. Currently, RCN accounts for 3% of all causes of AKI in our study. In another study, the overall incidence of RCN in obstetric AKI was 15.2%, and it has decreased significantly from 4.7% in 1984–1994 to 0.5%in 1999–2005 of total AKI cases. The reported incidence of RCN in India and Pakistan varies between 23% and 42.8% of all patients with obstetric AKI. [Table 3] RCN was due to obstetrical causes in 9% of patients with P-AKI in a study from Pakistan.
|Figure 3: Distribution of renal lesions; acute tubular necrosis versus renal cortical necrosis in patients with acute kidney injury in pregnancy in three study periods.|
Click here to view
|Table 3: Renal cortical necrosis in obstetric acute kidney injury from developing countries: A comparative study.|
Click here to view
Septic abortion was an important cause of RCN in India in 1908s and 1990s. However, puerperal sepsis and PPH are the dominant cause of RCN in patients with P-AKI in 2000s. The possible mechanisms of RCN in patients with septic abortion and puerperal sepsis are: sepsis-induced hypotension, disseminated intravascular coagulation contributing to poor renal perfusion and possibly endotoxinmediated endothelial injury leading to endovascular thrombosis and subsequent renal ischemia. In contrast to septic abortion in developing countries, the most common (50%–60%) obstetric cause of RCN is abruptio placentae in developed countries. Although RCN has virtually disappeared in high - income countries, 18 cases of RCN occurred in France following PPH in recent years (2009–2013). The possible mechanism of RCN in these 18 patients are in the setting of gravid endothelium, the conjunction of disseminated intravascular coagulation and the use of anti-fibrinolytic agent (tranexamic acid) may give rise to a risk for uncontrolled clotting in the renal cortex and subsequent development of irreversible partial or diffuse cortical necrosis.
| Summary|| |
The incidence of P-AKI had declined significantly over the last three decades in India, mainly due to marked decreased incidence of postabortal AKI. Currently in India, P-AKI mainly (70%–90%) occurs in the late 3rd trimester and in the postpartum period, similar to the developed countries. Preeclampsia is the most common cause of P-AKI followed by puerperal sepsis and PPH in our country. P-TMA and AFLP are the rare/uncommon causes of AKI in pregnancy in most developing countries, including India. In the past, septic abortion was the commonest cause of RCN in India. However, puerperal sepsis and PPH are the dominant cause of RCN in recent years. Further, incidence and severity of RCN have markedly decreased at our center. The maternal mortality has reduced to 5% from initial high mortality of 20%–25%. Overall prognosis of P-AKI has improved but perinatal mortality remained still high, despite good prognosis of AKI in pregnancy.
Conflict of interest: None declared.
| References|| |
Prakash J, Tripathi K, Usha, Pandey LK, Srivastava PK. Pregnancy-related acute renal failure in Eastern India. J Nephrol 1995;8:214-8.
Chugh KS, Singhal PC, Sharma BK, Pal Y, Mathew MT, Dhall K, et al. Acute renal failure of obstetric origin. Obstet Gynecol 1976:48: 642-6.
Prakash J, Tripathi K, Singh RG. Acute renal failure in pregnancy. J Obstet Gynaecol India 1985:25:233-8.
Prakash J, Tripathi K, Malhotra V, Kumar O, Srivastava PK. Acute renal failure in Eastern India. Nephrol Dial Transplant 1995:10:2009-12.
Jayakumar M, Prabahar MR, Fernando EM, et al. Epidemiologic trend changes in acute renal failure – A tertiary center experience from South India. Ren Fail 2006:28:405-10.
Prakash J, Pant p, Prakash S, et al. Changing picture of acute kidney injury in pregnancy: Study of 259 cases over a period of 33 years. Indian J Nephrol 2016:26:262-7.
Prakash J, Kumar H, Sinha DK, et al. Acute renal failure in pregnancy in a developing country: Twenty years of experience. Ren Fail 2006:28:309-13.
Stratta P, Besso L, Canavese C, et al. Is pregnancy-related acute renal failure a disappearing clinical entity? Ren Fail 1996:18: 575-84.
Hildebrand AM, Liu K, Shariff SZ, Ray JG, Sontrop JM, Clark WF, et al. Characteristics and outcomes of AKI treated with dialysis during pregnancy and the postpartum period. J Am Soc Nephrol 2015:26:3085-91.
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.
Kumar KS, Krishna CR, Kumar vs. Pregnancy related acute renal failure. J Obstet Gynaecol India 2006:56:308-10.
Goplani KR, Shah PR, Gera DN, et al. Pregnancy-related acute renal failure: A singlecenter experience. Indian J Nephrol 2008:18: 17-21.
Piccoli GB, Conijn A, Attini R, Biolcati M, Bossotti C, Consiglio V. Pregnancy in chronic kidney disease: Need for a common language. J Nephrol 2011:24:282-99.
Abosaif NY, Tolba YA, Heap M, Russell J, El Nahas AM. The outcome of acute renal failure in the intensive care unit according to RIFLE: Model application, sensitivity, and predictability. Am J Kidney Dis 2005;46:1038-48.
Silva GB Jr., Monteiro FA, Mota RM, et al. Acute kidney injury requiring dialysis in obstetric patients: A series of 55 cases in Brazil. Arch Gynecol Obstet 2009:279:131-7.
Maynard SE, Karumanchi SA, Thadhani R. Hypertension and kidney disease in pregnancy. In: Brenner BM, Rector B, editors. The Kidney. 8th
ed. Philadelphia: Saunders Elsevier; 2008. p. 1567-95.
Grünfeld JP, Ganeval D, Bournérias F. Acute renal failure in pregnancy. Kidney Int 1980; 18:179-91.
Stratta P, Canavese C, Dogliani M, Todros T, Gagliardi L, Vercellone A. Pregnancy-related acute renal failure. Clin Nephrol 1989:32:14-20.
Grünfeld JP, Pertuiset N. Acute renal failure in pregnancy: 1987. Am J Kidney Dis 1987:9: 359-62.
Selcuk NY, Tonbul HZ, San A, Odabas AR. Changes in frequency and etiology of acute renal failure in pregnancy (1980-1997). Ren Fail 1998:20:513-7.
Prakash J, Niwas SS, Parekh A, et al. Acute kidney injury in late pregnancy in developing countries. Ren Fail 2010:32:309-13.
Chugh KS, Sakhuja V, Malhotra HS, Pereira BJ. Changing trends in acute renal failure in third-world countries – Chandigarh study. Q J Med 1989:73:1117-23.
Gopalakrishnan N, Dhanapriya J, Muthukumar P, et al. Acute kidney injury in pregnancy – A single center experience. Ren Fail 2015:37: 1476-80.
Naqvi R, Ahmed E, Sheikh R, Rizvi A. Obstetrical acute kidney injury: 25 years experience from nephrology care unit in Pakistan. Open Access Libr J 2015;2:e1778.
Arrayhani M, El Youbi R, Sqalli T. Pregnancy-related acute kidney injury: Experience of the nephrology unit at the university hospital of Fez, Morocco. ISRN Nephrol 2013:2013: 109034.
Mishra Vineet V, Goyal Preeti A, Aggarwal Rohina S, et al. A single-centre experience of obstetric acute kidney injury. J Obstet Gynaecol India 2016:66:207-11.
Eswarappa M, Madhyastha PR, Puri S, et al. Postpartum acute kidney injury: A review of 99 cases. Ren Fail 2016:38:889-93.
Sivakumar V, Sivaramakrishna G, Sainaresh VV, et al. Pregnancy-related acute renal failure: A ten-year experience. Saudi J Kidney Dis Transpl 2011:22:352-3.
Matthews JH, Benjamin S, Gill DS, Smith NA. Pregnancy-associated thrombocytopenia: Definition, incidence and natural history. Acta Haematol 1990:84:24-9.
Knight M, Nelson-Piercy C, Kurinczuk JJ, Spark P, Brocklehurst P; UK Obstetric Surveillance System. A prospective national study of acute fatty liver of pregnancy in the UK. Gut 2008:57:951-6.
Najar MS, Shah AR, Wani IA, et al. Pregnancy related acute kidney injury: A single center experience from the Kashmir Valley. Indian J Nephrol 2008:18:159-61.
Patel ML, Sachan R, Radheshyam, Sachan P. Acute renal failure in pregnancy: Tertiary centre experience from North Indian population. Niger Med J 2013:54:191-5.
Hill JB, Yost NP, Wendel GD Jr. Acute renal failure in association with severe hyperemesis gravidarum. Obstet Gynecol 2002:100:1119-21.
Arora N, Mahajan K, Jana N, Taraphder A. Pregnancy-related acute renal failure in Eastern India. Int J Gynaecol Obstet 2010:111: 213-6.
Hassan I, Junejo AM, Dawani ML. Etiology and outcome of acute renal failure in pregnancy. J Coll Physicians Surg Pak 2009; 19:714-7.
Thornton JG, Macdonald AM. Twin mothers, pregnancy hypertension and pre eclampsia. Br J Obstet Gynaecol 1999:106:570-5.
Sibai BM, Ramadan MK. Acute renal failure in pregnancies complicated by hemolysis, elevated liver enzymes, and low platelets. Am J Obstet Gynecol 1993:168:1682-7.
Gui A, Asian H, Cebeci A, Polat I, Ulusoy S, Ceylan Y. Maternal and fetal outcomes in HELLP syndrome complicated with acute renal failure. Ren Fail 2004:26:557-62.
Haddad B, Barton JR, Livingston JC, Chahine R, Sibai BM. Risk factors for adverse maternal outcomes among women with HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome. Am J Obstet Gynecol 2000:183:444-8.
Mattar F, Sibai BM. Eclampsia. VIII. Risk factors for maternal morbidity. Am J Obstet Gynecol 2000:182:307-12.
Fakhouri F, Vercel C, Frémeaux-Bacchi V. Obstetric nephrology: AKI and thrombotic microangiopathies in pregnancy. Clin J Am Soc Nephrol 2012;7:2100-6.
Drakeley AJ, Le Roux PA, Anthony J, Penny J. Acute renal failure complicating severe preeclampsia requiring admission to an obstetric intensive care unit. Am J Obstet Gynecol 2002; 186:253-6.
Kahra K, Draganov B, Sund S, Hovig T. Postpartum renal failure: A complex case with probable coexistence of hemolysis, elevated liver enzymes, low platelet count, and hemolytic uremic syndrome. Obstet Gynecol 1998; 92:698-700.
Abraham KA, Kennelly M, Dorman AM, Walshe JJ. Pathogenesis of acute renal failure associated with the HELLP syndrome: A case report and review of the literature. Eur J Obstet Gynecol Reprod Biol 2003;108:99-102.
Fang JT, Chen YC, Huang CC. Unusual presentation of mesangial proliferative glomerulonephritis in HELLP syndrome associated with acute renal failure. Ren Fail 2000:22:641-6.
Sibai BM. Diagnosis, controversies, and management of the syndrome of hemolysis, elevated liver enzymes, and low platelet count. Obstet Gynecol 2004:103:981-91.
Barton JR, Sibai BM. Gastrointestinal complications of pre-eclampsia. Semin Perinatol 2009:33:179-88.
Pan C, Perumalswami PV. Pregnancy-related liver diseases. Clin Liver Dis 2011:15:199-208.
Piccini P, Gallo G. Diagnosis and management of HELLP syndrome. In: Ronco C, Bellomo R, Kellum J, editors. Critical Care Nephrology. 2nd
ed. Philadelphia, PA: Saunders; 2009. p. 337-40.
Haddad B, Barton JR, Livingston JC, Chahine R, Sibai BM. HELLP (hemolysis, elevated liver enzymes, and low platelet count) syndrome versus severe preeclampsia: Onset at, or 528.0 weeks’ gestation. Am J Obstet Gynecol 2000:183:1475-9.
Abraham KA, Connolly G, Farrell J, Walshe JJ. The HELLP syndrome, a prospective study. Ren Fail 2001:23:705-13.
Sibai BM, Ramadan MK, Usta I, Salama M, Mercer BM, Friedman SA. Maternal morbidity and mortality in 442 pregnancies with hemolysis, elevated liver enzymes, and low platelets (HELLP syndrome) Am J Obstet Gynecol 1993:169:1000-6.
Selçuk NY, Odabas AR, Cetinkaya R, Tonbul HZ, San A. Outcome of pregnancies with HELLP syndrome complicated by acute renal failure (1989-1999). Ren Fail 2000:22:319-27.
Castro MA, Fassett MJ, Reynolds TB, Shaw KJ, Goodwin TM. Reversible peripartum liver failure: A new perspective on the diagnosis, treatment, and cause of acute fatty liver of pregnancy, based on 28 consecutive cases. Am J Obstet Gynecol 1999:181:389-95.
Usta IM, Barton JR, Amon EA, Gonzalez A, Sibai BM. Acute fatty liver of pregnancy: An experience in the diagnosis and management of fourteen cases. Am J Obstet Gynecol 1994:171:1342-7.
Koroshi A, Babameto A. Acute renal failure during acute fatty liver of pregnancy. Nephrol Dial Transplant 2002:17:1110-2.
Kaplan MM. Acute fatty liver of pregnancy. N Engl J Med 1985:313:367-70.
Fesenmeier MF, Coppage KH, Lambers DS, Barton JR, Sibai BM. Acute fatty liver of pregnancy in 3 tertiary care centers. Am J Obstet Gynecol 2005:192:1416-9.
Ko H, Yoshida EM. Acute fatty liver of pregnancy. Can J Gastroenterol 2006:20:25-30.
Westbrook RH, Yeoman AD, Joshi D, et al. Outcomes of severe pregnancy-related liver disease: Refining the role of transplantation. Am J Transplant 2010:10:2520-6.
Veyradier A, Obert B, Houllier A, Meyer D, Girma JP. Specific von Willebrand factor-cleaving protease in thrombotic microangiopathies: A study of 111 cases. Blood 2001; 98:1765-72.
Ruggenenti P, Cravedi P, Remuzzi G. Thrombotic microagniopathies including hemolytic uremic syndrome. In: Floege J, Johnson R, Feehally J, editors. Comprehensive Clinical Nephrology. 4th
ed. Philadelphia, PA: Mosby; 2010. p. 344-55.
Matlin RA, Gary NE. Acute cortical necrosis. Case report and review of the literature. Am J Med 1974;56:110-8.
Kleinknecht D, Grünfeld JP, Gomez PC, Moreau JF, Garcia-Torres R. Diagnostic procedures and long-term prognosis in bilateral renal cortical necrosis. Kidney Int 1973:4:390-400.
Prakash J, Tripathi K, Pandey LK, Gadela SR, Usha. Renal cortical necrosis in pregnancy-related acute renal failure. J Indian Med Assoc 1996:94:227-9.
Prakash J, Pant P, Singh AK, et al. Renal cortical necrosis is a disappearing entity in obstetric acute kidney injury in developing countries: Our three decade of experience from India. Ren Fail 2015:37:1185-9.
Prakash J, Singh VP. Changing picture of renal cortical necrosis in acute kidney injury in developing country. World J Nephrol 2015:4: 480-6.
68 Naqvi R, Akhtar F, Ahmed E, et al. Acute renal failure of obstetrics origin during 1994 at our centre. Renal Fail 1996:18:681-3.
Ansari MR, Laghari MS, Solangi KB. Acute Renal Failure in Pregnancy: One year observational study at Liaquat University Hospital, Hyderabad. J Pak Med Assoc 2008:58:61-4.
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(3):285-90.
Frimat M, Decambron M, Lebas C, et al. Renal cortical necrosis in postpartum hemorrhage: A case series. Am J Kidney Dis 2016:68:50-7.
Department of Nephrology, Institute of Medical Sciences, Banaras Hindu University, Varanasi - 221 005, Uttar Pradesh
[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3]