Acute Renal Failure in Pregnancy in a Developing Country: Twenty Years of Experience

Prakash, Jai; Kumar, Hemant; Sinha, D. K.; Kedalaya, P G; Pandey, Laxmi; Srivastava, Pramod K.; Raja, R; Usha, .

doi:10.1080/08860220600583658

Cited by 72 publications

(72 citation statements)

References 8 publications

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“…The specific factors leading to the persistent high incidence of P-AKI in developing countries include septic abortions usually performed in the absence of adequate medical monitoring, overall poor follow-up of pregnancy with limited screening of hypertensive complications of pregnancy, and relatively late referral of patients with these disorders. However, the incidence of P-AKI is declining even in developing countries (5,6). In a recent survey of P-AKI in an Indian nephrology center, the prevalence of P-AKI among all cases of AKI decreased from 15% in the 1980s to 10% in the 1990s.…”

Section: Incidence Of P-akimentioning

confidence: 99%

Obstetric Nephrology

Fakhouri

Vercel

Frémeaux‐Bacchi

2012

Clinical Journal of the American Society of Nephrology

147

121

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Summary AKI in pregnancy remains a cause of significant fetomaternal mortality and morbidity, particularly in developing countries. Hypertensive complications of pregnancy (preeclampsia/eclampsia or hemolysis, elevated liver enzymes, and low platelets count syndrome) are the leading cause of AKI in pregnancy worldwide. Thrombotic microangiopathy is another peculiar and devastating cause of AKI in pregnancy. During the last decade, our understanding, and in some cases, our management, of these causes of AKI in pregnancy has dramatically improved. For instance, convincing data have linked pre-eclampsia/eclampsia to an increase in circulating antiangiogenic factors soluble Flt 1 and endoglin, which induce endothelial cell dysfunction, hypertension, and proteinuria. Several distinct pathogenic mechanisms underlying thrombotic microangiopathy, including thrombotic microangiopathy occurring during pregnancy, have been established. Thrombotic microangiopathy, which can present as hemolytic uremic syndrome or thrombotic thrombocytopenic purpura, can be reclassified in four potentially overlapping subtypes: disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 deficiency-related thrombotic microangiopathy, complement alternative pathway dysregulation-related thrombotic microangiopathy, secondary thrombotic microangiopathy (verotoxin and antiangiogenic drugs), and thrombotic microangiopathy of undetermined mechanism. In most cases, pregnancy is only a precipitating factor for thrombotic microangiopathy. Treatment of thrombotic microangiopathy occurring during pregnancy should be tailored to the underlying pathogenic mechanism: (1) restoration of a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 serum activity in the setting of thrombotic thrombocytopenic purpura through plasma exchanges and in some cases, B cell-depleting therapy and (2) inhibition of complement alternative pathway activation in atypical hemolytic uremic syndrome using antiC5 blocking antibody (eculizumab).

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Section: Incidence Of P-akimentioning

confidence: 99%

Obstetric Nephrology

Fakhouri

Vercel

Frémeaux‐Bacchi

2012

Clinical Journal of the American Society of Nephrology

147

121

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“…11 The incidence of RCN has declined from 17% in 1982-1991 to 2.4% in 1992-2002 in obstetric AKI in our recent publication. 21 RCN was observed in 2.3% of patients in third trimester AKI in our another study. 22 Renal cortical necrosis occurred in 1.4% of patients with obstetric AKI in 2003-2014 in the present study.…”

Section: Discussionmentioning

confidence: 99%

Renal cortical necrosis is a disappearing entity in obstetric acute kidney injury in developing countries: our three decade of experience from India

et al. 2015

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Rational: Obstetrical complications are the commonest causes of Renal Cortical Necrosis (RCN). However, the overall incidence of RCN in obstetric acute kidney injury in developing countries has been decreasing in recent years. Objective: The aim of this study was to evaluate the changing profile of RCN in obstetric AKI over the last three decades. Methods: This single center study included patients with biopsy proven renal cortical necrosis over a period of 32 years from 1982 to 2014. The diagnosis of RCN was suspected in patients with prolonged AKI (44 weeks) with absolute anuria in the setting of hemorrhage, hypotension and sepsis; and was confirmed by renal biopsy. The changing pattern in the incidence, etiology and outcome of RCN in patients with obstetric AKI was compared in the three study periods, namely 1982-1991, 1992-2002 and 2003-2014. Results: Over a period of 32 years, RCN was diagnosed in 15/259(5.8%) cases of obstetric AKI. Diffuse and patchy cortical necrosis were noted in 8(53.3%) and 7(46.7%) patients, respectively. RCN occurred in 17%(11/65), 2.4%(3/125) and 1.44%(1/69) patients in 1982-1991, 1992-2002 and 2003-2014, respectively. Septic abortion was commonest cause of RCN in the first two study periods but no case was observed in last decade. The decrease in incidence of RCN over the three decades was statistically significant (p-value50.001). Maternal mortality decreased to zero in 2003-2014 from 72.7% in 1982-1991. Conclusions: The incidence of RCN in obstetric AKI in developing countries has declined low enough to label it as a disappearing entity.

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“…41 Recent estimates suggest that the incidence of AKI from obstetric causes is less than 1 in 20,000 pregnancies. 42 When AKI occurs early in pregnancy (12 to 18 weeks), it is usually in association with septic abortion or volume depletion due to hyperemesis gravidarum.…”

Section: Acute Kidney Injury In Pregnancymentioning

confidence: 99%