Magnesium Aluminate Nanoparticles for Chemical Detoxification of Sarin and Soman.

The solutions of Mg(NO3)2, Al(NO3)3, and (NH4)2CO3 were mixed at pH 8 and then heated at 95 °C for 4 h, aged at room temperature for 16 h, and calcined at 650 °C for 4 h to obtain magnesium aluminate nanoparticles. The obtained materials exhibited spinel structure with the particle size being 6 to 26 nm. The nanoparticles demonstrated type IV nitrogen adsorption isotherm, typical of mesoporosity with a surface area of 325 m²/g. They were utilized for studies on chemical detoxification of deadly chemical warfare agents such as sarin and soman. Our results showed that the magnesium aluminate nanoparticles effectively decontaminated more than 99% of sarin and soman within 8-10 min when used at a ratio of 1:50-60% w/w.

The Role of p53 Gene in Cervical Carcinogenesis.

AIM: To investigate the role of p53 gene in cervical carcinogenesis. MATERIALS AND METHODS: A total 50 cases and controls were taken after setting exclusion criteria. Venous blood (3 ml) samples were collected in sterile EDTA sterile vials. Both punch biopsy of cervical growth in cases and biopsy from cervix after hysterectomy in controls were performed. Genomic DNA was extracted from tissue and blood using standard protocol of Miller et al. 1994 using chloroform-phenol method. Gene was amplified using specific forward and reverse primers and p53 gene expressions were studied. The present study of p53 gene regulation analyzed the expression of 279-bp bands on 1.5 agarose gel. OBSERVATIONS: Out of the total 50 samples of cases and controls, we were able to isolate DNA from 38 cases and 28 controls in blood and in 22 cases and 22 controls in tissue. In cases of carcinoma cervix, p53 expression is either downregulated or absent in 71.06 % of cases compared to 50 % of controls in blood and 72.73 % of cases compared to 59.09 % of controls in tissue, but these figures were not statistically significant (p = 0.67 and p = 0.167, respectively). p53 positivity rate was only in 27.78 % of squamous cell cancer and 50 % of adenocarcinoma. Three out of nine patients (33.3 %) with L.N. positive status have p53 gene positivity, whereas 23 % (3 out of 13) with L.N. negative status have p53 gene positivity, which is not significantly associated. In our study, p53 overexpression increases with the various stages of cervical cancer. CONCLUSION: In our study, we found that there is the increased frequency of upregulation or overexpression of p53 gene in control in both blood (50 %) and tissue (40.9 %), but this association is statistically nonsignificant. In the present study, there is a lack of relationship between p53 overexpression and prognosis in the cervical cancer patients. However, our study lacked larger sample size which otherwise would have been able to lend support to truly significant findings through much larger combined and comparative datasets.

Changing picture of acute kidney injury in pregnancy: Study of 259 cases over a period of 33 years.

The incidence of acute kidney injury (AKI) in pregnancy is declining in developing countries but still remains a major cause of maternal and fetal morbidity and mortality. The aim of the study was to analyze the changing trends in pregnancy related AKI (PR-AKI) over a period of thirty-three years. Clinical characteristics of PR-AKI with respect to incidence, etiology and fetal and maternal outcomes were compared in three study periods, namely 1982-1991,1992-2002 and 2003-2014. The incidence of PR-AKI decreased to 10.4% in 1992-2002, from 15.2% in 1982-1991, with declining trend continuing in 2003-2014 (4.68%).Postabortal AKI decreased to 1.49% in 2003-2014 from 9.4% in 1982-1991of total AKI cases. The AKI related to puerperal sepsis increased to 1.56% of all AKI cases in 2003-2014 from 1.4% in 1982-1991. Preeclampsia/eclampsia associated AKI decreased from 3.5% of total AKI cases in 1982-1991 to 0.54% in 2003-2014. Pregnancy associated - thrombotic microangiopathy and acute fatty liver of pregnancy were uncommon causes of AKI. Hyperemesis gravidarum associated AKI was not observed in our study. Incidence of renal cortical necrosis (RCN) decreased to 1.4% in 2003-2014 from 17% in 1982-1991.Maternal mortality reduced to 5.79% from initial high value 20% in 1982-1991. The progression of PR-AKI to ESRD decreased to1.4% in 2003-2014 from 6.15% in 1982-1991. The incidence of PR-AKI has decreased over last three decades, mainly due to decrease in incidence of postabortal AKI. Puerperal sepsis and obstetric hemorrhage were the major causes of PR-AKI followed by preeclampsia in late pregnancy. Maternal mortality and incidence and severity of RCN have significantly decreased in PR-AKI. The progression to CKD and ESRD has decreased in women with AKI in pregnancy in recent decade. However, the perinatal mortality did not change throughout study period.

Spectrum of VP1 region genetic variants in the foot-and-mouth disease virus serotype O populations derived from infected cattle tongue epithelium.

RNA virus population exists as a complex distribution of non-identical but closely related sequences known as viral quasispecies. Variant strains are selected from this quasispecies population in response to changing environment. The quasispecies dynamics of a virus existing within an infected host differs from that in a cell culture-adapted population. This study was carried out to explore the genetic variations present in the VP1 coding region of the foot-and-mouth disease (FMD) virus serotype O derived directly from infected cattle tongue epithelium. Molecular clonal populations of two serotype O strains belonging to lineages Ind2001 (IND 30/2011) and PanAsia2 (IND 5/2011) were sequenced at VP1 coding region. For IND 30/2011, 19 clones were sequenced and analysis showed variations at 12 nucleotide positions (nt) resulting in 8 amino acid (aa) replacements. Similarly, for IND 5/2011 virus, 18 clones were sequenced, of which six showed nt variations leading to 3 aa replacements. Most of the variable positions mapped to the surface-exposed loops and some of them were found in the neutralizing antigenic sites (position 81, 149, 169, 186 and 202 of IND 30/2011 and 141 of IND 5/2011), which potentially could be beneficial in rapid adaptive evolution of the virus by giving rise to antigenic variants to overcome neutralizing antibodies. These findings encourage further research into the landscape of the viral quasispecies population in vivo and its implication for viral ecology.

In human alleles specific variation of MTHFR C677T and A1298C associated "risk factor" for the development of ovarian cancer.

Etiopathology of tumor biology is highly complex and ovarian cancer is one of the important gynaecological neoplasia associated with high risk of mortality rate. Methlenetetrahydrofolate reductase (MTHFR) mutation are commonly linked to folate metabolism with increased risk factor for the development of neural tube defects, recurrent pregnancy loss and development of several type of cancer but genetic interaction between two alleles of MTHFR has been poorly defined in ovarian cancer in India. Hence, present study becomes imperative with the aim to assess the alleles frequency of MTHFR (C677T & A1298C) gene polymorphism using PCR based RFLP analysis. The O.R at 95% confidence interval (C.I.) was computed between cases and their respective controls to determine "risk factor". Interestingly, our findings reveals highly significant (p < 0.001) difference in heterozygous (CT) condition of C677T allele by computing odd ratio (0.12 at 95% C.I, 0.021-0.0428; P for trend = 0.001) in controls and (0.34 at 95% C.I, 0.074-1.530; P for trend = 0.198) cases, suggesting that three time increase the "risk factor" for genetic susceptibility of MTHFR "T" allele for the development of ovarian carcinoma.

Genetic diversity of stem cells and their functional impact on the development of neural tube defects in Eastern population of India.

Anencephaly and myelomeningocele are the 2 most common forms of neural tube defects (NTDs). During embryogenesis large numbers of extrinsic and intrinsic factors are responsible for the closing of the neural tube. "Stem cells" maintain the pluripotency during differentiation of 3 germ layers, including the neural ectoderm. We examined the role of Oct4, Nanog3, and Sox2 genes in the etiopathology of NTDs in an eastern Indian population using PCR-based DNA analysis. The highest frequency (16%) of complete loss of the Sox2 gene was found in NTDs. The highest frequency (48%) of overexpression (upregulation) was found for Nanog3, while 40% was observed for Oct4 and Sox2. The odds ratio for cases versus controls was from 0.132 at 95% confidence interval = 0.005-1.298 for Nanog3 to 2.316 (0.424-13.812) for Oct4. The highest frequency (77%) of overexpression for Nanog3 and Sox2 was observed in encephalocele and anencephalic patients, while in the comparison of regional variation, i.e., cephalic to caudal regions of NTDs, the highest frequency of downregulation (regression) of Nanog3 and Sox2 was found in lumbosacral myelomeningocele patients. However, cervical myelomeningocele patients had the highest frequency of overexpression in all 3 genes, suggesting that the mutational spectra of stem cells influence the cells of the neural crest in NTDs.

Prevalence of cystathionine beta synthase gene mutation 852Ins68 as a possible risk for neural tube defects in eastern India.

Cystathionine beta synthase gene (CßS) catalyzes the condensation of homocysteine with serine, forming cystathionine by the transsulfuration pathway. Disruption of CßS enzyme activity due to defective folic acid metabolism increases the risk factor for neural tube defects. We evaluated the CßS gene mutation in 25 children with neural tube defects (NTDs), including lumbosacral and thoracic myelomeningocele and open NTDs and mothers of cases, along with 25 healthy children and their mothers, serving as controls. Genomic DNA was isolated to assess the polymorphism of 852Ins68 in the CßS gene using PCR-RFLP analysis and nucleotide sequencing techniques. The 68-bp insertion was observed in one of the 25 NTD cases (lumbosacral myelomeningocele), and in two of the mothers of NTD cases. Statistical analysis was carried out using the Fischer exact probability test, which showed a lack of significance (P > 0.05), but the odds ratio of 2.08 with 95% confidence interval of 0.17-24.6 in NTDs mother was quite high because of the small sample size. However, the study was further extended to find out the involvement of specific nucleotide sequences, which again confirmed the 852Ins68 insertion and replacement of nucleotides (TCCAT to GGGG) in lumbosacral myelomeningocele (due to other category of NTDs), suggesting that it could be an independent risk factor for birth defects, including NTDs.

Serological evidence of foot-and-mouth disease virus infection in randomly surveyed goat population of Orissa, India.

India is endemic for foot-and-mouth disease (FMD), and goats constitute the second largest susceptible population of domestic livestock. FMD surveillance and control strategies in the country largely ignore small ruminants, known to be critical in the epidemiology of the disease. Here, serological investigations were carried out to generate estimates of antibody prevalence in goats of Orissa state to both non-structural (NSP-Ab) and structural proteins (SP-Ab) of FMD. The apparent overall NSP-Ab and SP-Ab seroprevalences were 38% and 20.7%, respectively, which signifies a very high level of FMD virus circulation in the goat population despite the lack of clinical signs in this species. The apparent prevalence of NSP-Ab and SP-Ab was positively correlated in the sampling areas. Interestingly, the values found for NSP-Ab prevalence were almost consistently higher than those found for SP-Ab prevalence. This could have been attributable to either issues related to sensitivity and specificity of the test systems employed or differences in the post-infection kinetics of NSP- and SP-Ab. The pattern that emerged from SP-Ab analysis indicated goats being infected with all three prevalent serotypes (O, A and Asia 1) and reinforces the concept that non-vaccinated goats can be exploited as tracer animals for detecting serotypes involved in outbreaks. The results underscore the requirement to bring caprine species under comprehensive surveillance and vaccination campaigns to check silent amplification, excretion and transmission of the virus.

Loss of the AZFc region due to a human Y-chromosome microdeletion in infertile male patients.

Infertility is a major reproductive health threat; the frequency of male infertility due to Y-chromosome microdeletions is 13-18% in the human population; these microdeletions involve recurrent loss of three non-overlapping regions designated as AZFa, AZFb and AZFc, associated with spermatogenic failure. Several contradictory reports have been published regarding deletion frequency based on sequence-tagged site markers and genotype-phenotype correlation. We examined the prevalence of Yq- deletion in 64 clinically diagnosed infertile male patients. We found a 3% frequency of microdeletion of the AZFc region; hormone profiles (FSH, LH and testosterone) showed significantly (P < 0.001) elevated levels compared to controls. No mutations were observed in the AZFa and AZFb regions, perhaps due to the selective use of sequence-tagged site markers.

Spectrum of kidney diseases in patients with preeclampsia-eclampsia.

AIM: The aim of this study was to analyse the clinical spectrum of renal manifestation of preeclampsia in pregnant women. METHOD: Diagnosis of preeclampsia was made using two cardinal feature of the disease after 20th weeks of gestation in previously normotensive and nonproteinuric women: (1) Blood pressure > 140/90 mm Hg and (2) urinary protein excretion of > 300 mg/24 hour. The patients with renal manifestations were followed up to 12 weeks postpartum or till death whichever was earlier. RESULT: Of 1805 pregnant women, preeclampsia was diagnosed in 106 (5.87%) patients. Primiparity constitutes 53.77% of total patients. Hypertension and proteinuria were observed in all patients. Hyperuricemia was observed in 93.65% of cases. Acute renal failure occurred in 22 patients. Dialysis support was needed in only four cases of ARF with complete recovery of renal function in 82% of cases. HELLP syndrome was seen in 16 (preeclampsia 5; eclampsia 11) patients. Sixty six patients (Death 13 and lost to follow up 27) were followed for 12 weeks. The renal parameters (Hypertension, Proteinuria and renal function) returned to normal in all except in two patients. Renal biopsy in these two cases revealed FSGS and MPGN in one each. CONCLUSION: The incidence of preeclampsia was 5.87%. Nephrotic syndrome was observed in 11.32% of patients. Acute renal failure occurred in 20.8% of patients. Hypertension, proteinuria and renal function resolved to normal over a average period of 35.8 days in all survivors. The overall mortality was 12%. Neurological complication, pulmonary edema and multiple organ failure were the causes of death.

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.

BACKGROUND: Renal cortical necrosis (RCN) accounts for 2% of all cases of acute renal failure (ARF) in adults and 15-20% of ARF during the third trimester of pregnancy in developed nations. However, RCN incidence is higher in developing countries ranging from 6-7% of all cases of acute renal failure. The present study describes changing trends in the clinical spectrum of RCN in patients with ARF in Eastern India. METHODS: Patients with ARF suspected to have RCN on clinical grounds underwent percutaneous renal biopsy. Patients showing cortical necrosis on histology were included in the present study. Diffuse and patchy cortical necrosis was classified based on standard histological criteria. The patients with cortical necrosis were studied over a period of 22 years; from July 1984 to December 2005. The results of our observation were compared with respect to etiology, incidence, prognosis and outcome of renal cortical necrosis in two study periods; namely, 1984-1994 and 1995-2005. RESULTS: The incidence of RCN was 3.12% of all cases of ARF of diverse etiology. RCN was observed in 57 patients; obstetric 32 (56.2%); non-obstetric 25 (43.8%). Diffuse cortical necrosis was the dominant lesion in 41 (71.9%) patients and the remaining 16 (28%) patients had patchy cortical necrosis. The overall incidence of RCN in obstetric ARF was 15.2%; the incidence being higher (11.9%) in the post-abortal group in comparison to 3.3% in late pregnancy. RCN had occurred complicating abruptio placentae, puerperal sepsis and postpartum haemorrhage (PPH) in late pregnancy, while septic abortion was the sole cause of RCN in early pregnancy. Haemolytic uraemic syndrome (HUS) was the major (31.5%) cause of RCN in the non-obstetric group and miscellaneous factors were responsible in seven (12.3%) patients. Partial recovery of renal function was observed in 11 (19.2%), and 16 (28%) patients had progressed to ESRD. The incidence of RCN decreased from 6.7% in 1984-1994 to 1.6% in 1995-2005 of total ARF cases. RCN following obstetrical complication decreased significantly; 4.7% in the 1990s to 0.5% of the total ARF cases, in the 2000s. The mortality decreased to 19% in 1995-2005 from the initial high mortality of 72% in 1984-1994. The renal prognosis improved as a result of the decreased mortality of patients. CONCLUSION: We observed a decreasing trend in the incidence of RCN in patients with ARF in recent years, which is associated with increased patient survival and better renal prognosis. This improvement was mainly due to declining incidence and severity of RCN in obstetrical ARF.

Hypertension in pregnancy: hospital based study.

Eighteen hundred two pregnant women consisting of 750 primigravida and 1,052 multigravida were screened for hypertension between July 2000 to June 2002. Hypertension was noted in 97 (5.38%) patients. Twenty five patients were lost to follow up and only 72 patients were included in the final study. The age of the patients ranged between 19 to 32 (mean +/- SD = 24.75 +/- 3.36) years. The majority of patients 41 (57%) were primigravida and 31 (43%) were multigravida. Of 31 multigravida, vast majority (84%) of patients were found to be hypertensive in the third trimester. Only 5 (16%) patient had hypertension in the first trimester. Stage I, II and III hypertension were noted in 18%, 50% and 32% of patients respectively as per JNC-VI criteria. Preeclampsia (PE) was seen in 44.44% (n=32), eclampsia in 40.28% (n=29), HELLP syndrome in 6.94% (n=5), chronic hypertension (HTN) with superimposed PE in 6.94% (n=5) and chronic HTN in 1.38% (n=1). Of the 6 patients with chronic hypertension 50% (3) had essential HTN. Acute renal failure (S. creat > 3 mg/dl) was seen in 7 patients and 4 required dialytic support. Maternal mortality was 5.55% (4) and perinatal death occurred in 37.5% (27) of deliveries. Low birth weight was seen in 66.66% (48) of births. Hypertension complicated 5.38% of all pregnancies in our study. Preeclampsia-eclampsia and its variants remain the major cause of hypertension in pregnant women. Hypertension during pregnancy is responsible for high fetal mortality and low birth weight.

Acute renal failure in pregnancy in a developing country: twenty years of experience.

UNLABELLED: Acute renal failure (ARF) has become a rare complication of pregnancy in developed countries. The aim of this study was to describe changing trends in pregnancy-related acute renal failure (PR-ARF) in two successive periods; 1982-1991 and 1992-2002. From July 1982 to December 2002, 190 cases of PR-ARF were observed in Eastern India (11.6% of total number of ARF needing dialysis). Obstetrical complications were causative factors for ARF in 15% (65/426) and 10% (125/1201) of patients in the two periods, respectively. The incidence of PR-ARF fell from 15% in 1982-1991 to 10% in 1992-2002, with respect to the total number of acute renal failure cases. Post-abortal ARF showed a declining trend, 9% in the 1980s to 7% in the 2000s, of the total number of ARF cases. Preeclampsia-eclampsia was the cause of obstetrical ARF in 23% (1982-1991) and 14.4% (1992-2002) of cases in these two periods. The percentage of total ARF due to eclampsia declined from 3.5% during the period 1982-1991 to 1.4% in 1992-2002. Puerperal sepsis contributed to 0.8% of total ARF in recent years, compared to 2.4% in the earlier period. The incidence of cortical necrosis decreased significantly (p < 0.001) from 17% in 1982-1991 to 2.4% in the 2000s. The maternal mortality reduced to 6.4% in 1992-2002 from initial high mortality of 20% in the period of 1982-1991. CONCLUSION: PR-ARF which remained high in the initial period has decreased in recent years. This is associated with a declining trend in

MTHFR C677T and A1298C polymorphisms are risk factors for Down's syndrome in Indian mothers.

Down's syndrome (DS), a chromosomal disorder due to trisomy 21, results mostly from nondisjunction in maternal meiosis. The present case-control study examined the association of genetic polymorphisms with predisposition to nondisjunction. Two common polymorphisms (SNPs), C677T and A1298C, in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene involved in folate metabolism, are known to lower the activity of this enzyme. Three hundred and fourteen mothers (with DS children and controls), mostly from the eastern states of India, were genotyped for the two above-mentioned SNPs. Significant association with both of these SNPs were detected, more specifically, in the mothers of DS children homozygous for the polymorphic alleles 677 T and 1298 C. The relative risk of T (C677T) and C (A1298C) homozygosity in mothers for DS-affected pregnancy was 7 (OR 7.67, 95% CI 1.67-35.08, P=0.003) and 4 (OR 4.40, 95% CI 1.45-13.26, P=0.008), respectively. Moreover, all 677TT mothers studied were less than 31 years of age, whereas no correlation with maternal age was observed for A1298C genotypes. Interestingly, all of the young 677TT mothers had either a first- or secondborn child with DS. Thus, this study reports that young Indian mothers with TT genotypes are genetically predisposed to nondisjunction due to abnormal folate metabolism.

Effects of metformin treatment on luteal phase progesterone concentration in polycystic ovary syndrome.

The causes of luteal phase progesterone deficiency in polycystic ovary syndrome (PCOS) are not known. To determine the possible involvement of hyperinsulinemia in luteal phase progesterone deficiency in women with PCOS, we examined the relationship between progesterone, luteinizing hormone (LH) and insulin during the luteal phase and studied the effect of metformin on luteal progesterone levels in PCOS. Patients with PCOS (19 women aged 18-35 years) were treated with metformin (500 mg three times daily) for 4 weeks prior to the test cycle and throughout the study period, and submitted to ovulation induction with clomiphene citrate. Blood samples were collected from control (N = 5, same age range as PCOS women) and PCOS women during the late follicular (one sample) and luteal (3 samples) phases and LH, insulin and progesterone concentrations were determined. Results were analyzed by one-way analysis of variance (ANOVA), Duncan's test and Karl Pearson's coefficient of correlation (r). The endocrine study showed low progesterone level (4.9 ng/ml) during luteal phase in the PCOS women as compared with control (21.6 ng/ml). A significant negative correlation was observed between insulin and progesterone (r = -0.60; P < 0.01) and between progesterone and LH (r = -0.56; P < 0.05) concentrations, and a positive correlation (r = 0.83; P < 0.001) was observed between LH and insulin. The study further demonstrated a significant enhancement in luteal progesterone concentration (16.97 ng/ml) in PCOS women treated with metformin. The results suggest that hyperinsulinemia/insulin resistance may be responsible for low progesterone levels during the luteal phase in PCOS. The luteal progesterone level may be enhanced in PCOS by decreasing insulin secretion with metformin.

Effects of metformin treatment on luteal phase progesterone concentration in polycystic ovary syndrome

The causes of luteal phase progesterone deficiency in polycystic ovary syndrome (PCOS) are not known. To determine the possible involvement of hyperinsulinemia in luteal phase progesterone deficiency in women with PCOS, we examined the relationship between progesterone, luteinizing hormone (LH) and insulin during the luteal phase and studied the effect of metformin on luteal progesterone levels in PCOS. Patients with PCOS (19 women aged 18-35 years) were treated with metformin (500 mg three times daily) for 4 weeks prior to the test cycle and throughout the study period, and submitted to ovulation induction with clomiphene citrate. Blood samples were collected from control (N = 5, same age range as PCOS women) and PCOS women during the late follicular (one sample) and luteal (3 samples) phases and LH, insulin and progesterone concentrations were determined. Results were analyzed by one-way analysis of variance (ANOVA), Duncan's test and Karl Pearson's coefficient of correlation (r). The endocrine study showed low progesterone level (4.9 ng/ml) during luteal phase in the PCOS women as compared with control (21.6 ng/ml). A significant negative correlation was observed between insulin and progesterone (r = -0.60; P < 0.01) and between progesterone and LH (r = -0.56; P < 0.05) concentrations, and a positive correlation (r = 0.83; P < 0.001) was observed between LH and insulin. The study further demonstrated a significant enhancement in luteal progesterone concentration (16.97 ng/ml) in PCOS women treated with metformin. The results suggest that hyperinsulinemia/insulin resistance may be responsible for low progesterone levels during the luteal phase in PCOS. The luteal progesterone level may be enhanced in PCOS by decreasing insulin secretion with metformin.

Antiovarian antibody in premature ovarian failure.

Premature ovarian failure is a syndrome consisting of primary or secondary amenorrhoea, hypergonodotropiremia and hypoestrogenemia in women under the age of 40. An autoimmune mechanism was suggested as possible etiology when Vallolton and Forbes in 1966-67 found antibodies to the cytoplasm of rabbit ova in 29 of 232 tested sera. Immune mechanism in the pathogenesis of premature ovarian failure (POF) is suggested by association of autoimmune phenomenon with POF in some cases and demonstration of circulating antibodies to ovary in serum samples from women with POF. The incidence of presence of antiovarian antibody of POF patients has been reported earlier. Evidence of autoimmunity is present in 18-92% of patients with POF. In the present study we have studied 18 cases of POF without any overt manifestation of autoimmune disorder but the antiovarian antibody was detected, with the idea that this autoantibody might be the cause of ovarian dysfunction which is evident in POF. Presence of antiovarian antibody in 16.67% cases with POF in our study that ovarian antibodies may play a role in or reflect an autoimmune process responsible for the development of POF.

Renal cortical necrosis in pregnancy-related acute renal failure.

Of 63 patients of obstetrical acute renal failure, 15 cases (23.8%) had biopsy proven bilateral renal cortical necrosis. Remaining 48 patients (76.2%) had acute tubular necrosis. Eight of 39 cases in early pregnancy had cortical necrosis (postabortum) and 7 of 24 patients in late pregnancy revealed cortical necrosis. Diffuse and patchy cortical necroses were seen in 12 and 3 patients respectively. The incidence of cortical necrosis was almost equal in both early as well as late pregnancies. The high incidence (20.5%) of cortical necrosis following septic abortion remains the interesting feature of the present study in contrast to very low incidence (1.5%) of cortical necrosis in postabortum group in developed countries. The death occurred in most patients (14 ie, 93.3%) of cortical necrosis because of uraemic complications and sepsis.

Spectrum of renal cortical necrosis in acute renal failure in eastern India.

Renal cortical necrosis is an uncommon cause of acute renal failure. We report 23 cases of biopsy-proven renal cortical necrosis which constituted 6.3% (23/363) of all cases of acute renal failure studied over a period of seven years (1985-92). The patients were divided into two groups: obstetric and non-obstetric. Obstetric complications were responsible for renal cortical necrosis in 15 (65.2%) patients while non-obstetric conditions accounted for the remaining eight (34.8%) cases. The overall incidence of cortical necrosis in obstetric acute renal failure was 15/63 (23.8%) patients, the incidence being nearly equal in early (20.5%) and late (29%) pregnancy. Post-abortum renal failure was the sole cause of cortical necrosis in early pregnancy in the obstetric group. Haemolytic uraemic syndrome (three patients) and septicaemia (two patients) were the main cause of necrosis in the non-obstetric group. The cortical necrosis was diffuse and patchy in 17 and six patients, respectively. The disease had a fatal prognosis in 20 (87%) patients; mortality was due to uraemic complications and infections in the majority of patients. The high frequency of post-abortum renal cortical necrosis in our patients is similar to the experience of other Indian workers.

Birthweight: its relationship with maternal and newborn skinfold thickness.

Two hundred and forty seven pregnant women at term and their offsprings were studied. Maternal skinfold thickness was measured from ten different sites and newborn skinfold thickness was measured from four different sites in each set of cases. Maternal skinfold thickness was positively correlated with the birthweight and skinfold thickness of the offspring. The birthweight was also positively correlated with the skinfold thickness of offspring. The maternal axillary sites and offspring's subscapular site had higher inter correlation as well as with the birthweight of offspring.