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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2021  |  Volume : 32  |  Issue : 5  |  Page : 1397-1406
Feto-maternal and renal outcomes of nephrotic syndrome in pregnancy

1 Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of Maternal and Fetal Health, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
3 Department of Pathology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

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Date of Web Publication4-May-2022


Proteinuria can range from subnephrotic to nephrotic amounts during pregnancy, though nephrotic syndrome (NS) is rare (0.012%–0.025%). Without a renal biopsy, this distinction may be difficult at times. The objective of our study was assessing about renal and feto-maternal outcomes of these patients. This study was done in a tertiary-care hospital in north India from 2010 to 2019. We included all pregnant women with nephrotic-range proteinuria, with no signs or symptoms suggestive of pre-eclampsia. We studied their treatment modalities, renal, maternal, and fetal outcomes. Eighteen eligible pregnant women diagnosed with NS with no features suggestive of pre-eclampsia or associated comorbidities were included. The gestational age of presentation was 23.2 ± 1.36 weeks. The average proteinuria was 4.38 ± 0.76 g/day. The patients were managed conservatively without kidney biopsy. About 16.7% of pregnancies had worsening of hypertension and acute kidney injury which recovered after delivery. Anasarca was troublesome for four patients requiring fresh-frozen plasma infusion. All were managed conservatively; however, five patients were started on empirical immunosuppression, all five with steroids, while two required the addition of calcineurin inhibitors as well. All had live births, but 25.7% each had preterm and intrauterine growth restriction while one required neonatal intensive care unit admission. The degree of proteinuria had an impact on maternal and fetal outcomes, especially on risk to pre-eclampsia. NS during pregnancy needs evaluation and counseling. Majority of them can be managed conservatively yet specific therapies can safely be tried among symptomatic ones. Despite good outcomes, a sizeable risk to maternal and fetal complications can occur.

How to cite this article:
Kaul A, Bhaduaria D, Pradhan M, Jain M, Prasad N, Patel M, Gupta A, Sharma R K. Feto-maternal and renal outcomes of nephrotic syndrome in pregnancy. Saudi J Kidney Dis Transpl 2021;32:1397-406

How to cite this URL:
Kaul A, Bhaduaria D, Pradhan M, Jain M, Prasad N, Patel M, Gupta A, Sharma R K. Feto-maternal and renal outcomes of nephrotic syndrome in pregnancy. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2022 May 25];32:1397-406. Available from: https://www.sjkdt.org/text.asp?2021/32/5/1397/344760

   Introduction Top

In normal pregnancy, there is a mild increase in urinary protein excretion, a value exceeding 300 mg/24 h is considered abnormal.[1] Nephrotic syndrome (NS) or nephrotic-range proteinuria is reported to occur in 0.012%–0.025% of all pregnancies.[2] Proteinuria is considered a cardinal feature of pre-eclampsia and the most common cause among females biopsied during pregnancy though proteinuria can appear in pregnancy due to primary renal disease or renal disease secondary to systemic disorders.[3]

A clinical distinction between glomerular diseases and pre-eclampsia is essential, as one requires proper characterization for specific treatment while the other settles with termination of pregnancy. Timing of proteinuria may be helpful sometimes for this distinction. Proteinuria documented before pregnancy or before 20 weeks of gestation suggests glomerular disease while appearance after the 20th week of gestation may suggest preecalmpsia.[4] However, this distinction may at times be difficult and may need renal biopsy to confirm. The decision to perform renal biopsy during pregnancy needs to be weighed based on several factors, including the stage of pregnancy, the severity of the renal disease, response to conservative management and the suspected underlying diagnosis.

Systematic research suggested heterogeneity regarding the pros and cons of kidney biopsy in pregnancy, with the risks of complications being higher in pregnancy than in the postpartum period (7% vs. 1%, respectively) and considered deferring till termination, however, it may be performed under conditions warranting immediate treatment such as sudden renal insufficiency or massive NS of unknown origin.[5] There is consensus that mild or moderate proteinuria in normotensive women and/or asymptomatic microscopic hematuria with well preserved renal function should be monitored closely and biopsy should be deferred to the postpartum period.[6]

In the absence of uncontrolled hypertension (HTN) or renal insufficiency, many consider the perinatal outcomes in pregnant women with NS to be good. Elevated creatinine has been long considered a risk factor for adverse pregnancy outcomes. There exists not enough data to assess for the maternal and fetal outcomes among pregnant females with NS in the absence of significant renal impairment. Usually in such females without significant HTN or renal insufficiency, outcomes are good despite having limited data on this population.[7],[8],[9],[10],[11] The objective of our study was assessing about renal and feto-maternal outcomes of these patients thus advising and managing such high-risk pregnancies.

   Study Protocol Top

This is a retrospective observational study. All women with proteinuria during pregnancy who were referred to the department of nephrology from January 2010 to December 2019 were evaluated. These patients were classified into two groups according to their degree of proteinuria and duration of gestation: Subnephrotic or nephrotic-range proteinuria; and <20 weeks or >20 weeks of gestation at the time of onset of proteinuria. All the patients were screened for the presence of any other systemic illnesses such as diabetes, HTN, and dyslipidemia. All participants had a normal ultrasound scan of the fetus, gestation-appropriate levels of maternal alpha-fetoprotein and beta-human chorionic gonado-tropins, and no clinical or biochemical evidence of pre-eclampsia. None of them underwent renal biopsy during the pregnancy.

These patients were regularly followed up in the department of nephrology and maternal and reproductive medicine initially fortnightly and by 32 weeks they were followed weekly and assessed for their clinical signs of anasarca, ability in doing daily activities, blood pressure, proteinuria, and serum albumin levels. They were watched for any evidence of the development of pre-eclampsia or fetal abnormality on each visit.

All patients were managed conservatively and assessed for the etiology which was easy for patients who presented early <20 weeks while those presenting late >20 weeks needed to be looked for evidence of pre-eclampsia versus primary glomerular disease.

All deliveries were conducted in the department of maternal and reproductive medicine department and the mother and child were assessed by the obstetrician and pediatrician at the time of delivery. The mode of delivery was decided by the treating obstetrician.

All patients were assessed for clinical signs and symptoms and were planned for conservative therapy at first. In those pregnancies where there were clinical signs of worsening symptoms along with proteinuria which was not responding to conservative management were treated with specific therapy without biopsy.

Primary glomerular disease

Any female presenting during pregnancy with proteinuria before 20 weeks of gestation or after 20 weeks with proteinuria had evidence of hypertriglyceridemia, hypoalbuminemia, and no clinical markers for pre-eclampsia were included in this group.


Abrupt onset of HTN after 20 weeks of gestation associated with the appearance of proteinuria with protein excretion >300 mg/day.

Pre-eclampsia superimposed on primary glomerular disease

Among females who had HTN or proteinuria at the start of pregnancy if there was doubling of protein excretion associated with worsening of HTN after 20 weeks of gestation was considered pre-eclampsia in the backdrop of underlying disease.

Treatment offered - conservative

All patients were managed with conservative management in the form of sodium restriction (1.5 g, approximately 60 mEq), bed rest, leg elevation, prophylactic anticoagulation, especially with severe hypoalbuminemia (serum albumin <2.0 mg/dL) along with other risk factors (e.g., bed rest). Those patients with heavy proteinuria with severe hypoalbuminemia developing gross anasarca were admitted and managed with intravenous albumin or fresh-frozen plasma with judicious use of diuretics.

Specific therapy

All pregnant females having clinical signs of worsening anasarca and proteinuria suggestive of underlying glomerular disease not responding to conservative management required empirical treatment with immunosuppression in the form of steroids and or calcineurin inhibitor therapy.

Maternal and fetal assessment

These patients were looked for any signs of worsening HTN, development of pre-eclampsia, renal dysfunction, clinical signs of worsening anasarca. The fetal growth and maturation were done regularly by the obstetrician by clinical as well as radiological and other investigations on follow-up which was on fortnightly basis till the end of the 32 weeks and then weekly thereafter. Deliveries in all these patients were in hospital under supervision. The baby was managed and assessed in neonatal ICU in the hospital. Those females who appeared to be clinically as pre-eclampsia were followed after pregnancy and their parameters assessed. All patients who continued to show evidence of glomerular illness even after delivery subsequently underwent kidney biopsy and were managed according to the underlying glomerular disease.

   Statistical Analysis Top

Normality of the variables was assessed using the Shapiro-Wilk test. Continuous variables were presented in mean ± standard deviation or median, whereas categorical data in frequency (%) as appropriate. Independent samples t-test/Mann–Whitney U test was used to compare the means/median between the groups. Fisher’s exact test was used to test the association between two categorical variables. P <0.05 was considered statistically significant. The IBM SPSS Statistics version 23.0 (IBM Corp., Armonk, NY, USA) and Med Calc software were used for data analysis.

   Result Top

A total of 44 female patients presented with varying degrees of proteinuria during pregnancy. Three patients each had subnephrotic and nephrotic range of proteinuria in <20 weeks of gestation while 12 showed subnephrotic and 14 had nephrotic range proteinuria beyond 20 weeks of gestation.

A total of 12 patients with varying degrees of proteinuria beyond 20 weeks with worsening HTN suggestive of clinical and biochemical evidence of pre-eclampsia. Eight among them revealed nephrotic range proteinuria [Table 1]. They all were managed conservatively with intensive blood pressure monitoring with good maternal and fetal outcomes. On follow-up within an average of 3.4 weeks, all patients showed resolution of proteinuria with normalization of blood pressures in 10 while two needed to be on one antihypertensive medication.
Table 1: Etiology of proteinuria during pregnancy.

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On clinical assessment and laboratory evidence of hypoalbuminemia, dyslipidemia and no evidence of systemic illnesses with no prior history of HTN or diabetes or any evidence of pre-eclampsia, a diagnosis of underlying glomerular illness was made among three of the patients <20 weeks gestation while 14 patients beyond >20 weeks of gestation. Three patients who had subnephrotic range proteinuria also had suggestion of glomerular illness and were closely followed up, of which one had subsequent worsening of proteinuria which was however managed conservatively. Thus, a total of 18 patients during the pregnancy showed evidence of nephrotic range proteinuria with evidence of dyslipidemia, hypoalbuminemia suggesting an underlying glomerular illness. None of these patients underwent kidney biopsy.

Three patients who had proteinuria before 20 weeks were advised for kidney biopsy, but due to their inherent fear of fetal and maternal risks deferred and were managed conservatively.

Clinical presentation

The average maternal age of patients was 28.1 ± 2.3 years while the average gestational age of presentation was 23.1 ± 1.3 weeks. Fourteen females were multigravida. All patients had edema with or without anasarca. The mean serum creatinine at presentation was was 0.58 ± 0.09 mg% and serum albumin of 2.60 ± 0.8 mg/dL. All patients had stable liver functions. Dyslipidemia was seen all of them. Average degree of proteinuria was 4.36 ± 0.76 g/day. The mean blood pressure at presentation was 114/66 mm Hg.

All pregnancies had live birth with an average weight of 2.75 g ± 600 g. Fifty percent (Patient numbers 1, 3, 5, 8, 9, 12, 14, 16, 18) were born out of cesarian section. Intrauterine growth restriction (IUGR) was seen in five pregnancies (Patients 1, 5, 8, 16, 18). The mean age of gestation at delivery was 33.1 ± 0.3 weeks (range 28–37 weeks). Five (Patients 1, 3, 5, 9, 14) of the 18 were preterm. Of the five who had preterm delivery, three had pre-eclampsia while one had IUGR with fetal distress while the other had cord compression.

Fifty percent (Patient number – 1, 3, 5, 8, 9, 12, 14) underwent cesarean section. Labor occurred spontaneously among them except for patient numbers 4 and10 which had to be induced due to poor progression of labor. None of the patients who had evidence of pre-eclampsia required early termination of pregnancy, seizure, or bleeding during pregnancy or peripartum period.

During puerperium, none of them had any evidence of infection, excessive bleeding, or postpartum hemorrhage. There were no episodes of thrombosis.

None of the neonates had any evidence of neonatal asphyxia or hypoglycemia. Neonate numbers 11, 15, 18 developed physiological jaundice with one requiring phototherapy and settled within seven days. The average stay was around five days.

Renal outcomes of nephrotic syndrome in pregnancy

Acute kidney injury with NS was observed in three of our patients (patient numbers 9, 14, 17) with a rise of serum creatinine of 0.45 to 1.4 mg/dL. None of our patients required dialysis during pregnancy. All three had resolution of their creatinine post-delivery. Patient number 1 had worsening of renal functions with preeclampsia underwent preterm delivery at 28 weeks gestation. Patient number 5 had worsening of HTN with proteinuria needed empirical start of steroids with IUGR and preterm delivery at 30 weeks. Three patients (Patient numbers 1, 9, and 14) had systolic or diastolic blood pressure rise of more than 20 mm Hg from baseline during late pregnancy with clinical evidence of pre-eclampsia which was managed conservatively and fetal and maternal well-being was followed up intensively with in hospital admission.

Patients who developed AKI during pregnancy had greater risk to preterm and IUGR [Table 3]. The patients with peak proteinuria during pregnancy were associated with increased risk of preterm and IUGR.
Table 3: Distribution of clinical values in pregnancy outcomes (n=18).

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On evaluating the maternal and fetal complication with degree of proteinuria during pregnancy, proteinuria significantly correlated with adverse outcomes of preeclampsia (P <0.05) [Table 2], [Table 3].
Table 2: Change in proteinuria (%) and its relationship with pregnancy outcomes (n=18).

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Treatment offered for nephrotic range proteinuria during [Table 4]
Table 4: Renal outcomes of nephrotic syndrome in pregnancy.

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Patients 1, 5, 7, 9, 14, and 17 needed to be admitted in view of worsening anasarca average around 28 weeks of pregnancy requiring albumin and plasma infusion while others were managed with salt restriction, bed rest and limb elevation. Prophylactic anticoagulant in form of enoxaparin 40 mg/day was used in two patients while two received 5000 U of heparin twice daily (Patient 1, 5, 14, and 17) who had serum albumin levels <2 mg/dL with gross anasarca. There was no report of adverse effects such as bleeding, abruption, or subchorionic hematoma.

Specific treatment given during pregnancy [Table 4]

Proteinuria worsened in patient numbers 1, 5, 9, 14, and 17 and they needed to be empirically started on steroids (1 g/kg body weight) at 24, 25, 28, 29, 30, and 32 weeks of pregnancy respectively with some relief in the degree of proteinuria in patients 1, 9, and 14 (decreased from 5.5, 5.7, 6 g/day) to 4.8, 4.5, and 4.1 g/day at term. However patient numbers 5 and 17 had significant proteinuria of 7.8 and 7.9 g/day which worsened despite steroids and had to be added with cyclosporine 3 g/kg at 30 weeks of pregnancy with some relief proteinuria decreased to 6.2 and 5.9 g/day. None of the patients who received steroids or cyclosporine had worsening of hyperglycemia, thrombotic tendencies, or wound infection.

Treatment offered for nephrotic syndrome following delivery

All patients underwent kidney biopsy around 26.7 ± 4 days after delivery except patient number 10 wherein it was performed three months after delivery. Histological diagnosis on kidney biopsy done post delivery revealed immunoglobulin A (IgA) in five while focal segmental glomerulosclerosis (FSGS) in four of them. Patient numbers 1 and 9 who were started on steroids during pregnancy had biopsy-proven FSGS continued on steroids for three months with complete remission in patient number 1 while the other required to be started on cyclosporine 3 mg/Kg post delivery following which she went into remission and stayed in remission even after stopping therapy for 2.3 years. Patient numbers 2, 7, 8, 13, and 15 with IgA nephropathy were given oral steroids and fish oil with complete remission in all five.

Patient number 17 who had biopsy-proven membranous was already started on cyclosporine (3 mg/kg) during pregnancy was continued with low dose steroids with partial remission proteinuria at last follow-up was 1.4 g/day, while two patients (patient numbers 6 and 10) was treated post delivery with low dose steroid (5 mg/kg with tacrolimus at 0.8 mg/kg with excellent response within 4 to 6 months). All patients (patient numbers 3, 11 and 12) with MCD responded well to steroids, one patient (patient number 4) with membranous was treated with cyclical therapy of steroids and endoxan with remission achieved after three cycles. While patient 16 was non-IgA mesangio proliferation and patient number 18 was MPGN both responded well to oral steroids and went into remission after 2.5 and 8.7 months respectively.

   Discussion Top

Nephrotic range proteinuria during pregnancy needs careful evaluation and distinction between renal diseases and pre-eclampsia which is essential for clinical management. There are scarce data on the assessment for the maternal and fetal outcomes among pregnant females with NS in the absence of significant renal impairment. Our study is a retrospective analysis of 18 pregnancies who presented with NS at an average gestation of 23.1 ± 1.3 weeks; none of the females underwent kidney biopsy. Average proteinuria was around 4.36 ± 0.76 g/day. All were managed conservatively except for five patients who required immuno-suppression without kidney biopsy, steroids in all while two required in addition calcineurin inhibitors. Proteinuria during pregnancy correlated with maternal and fetal complications. About 16.5% of pregnancies had developed pre-eclampsia and AKI while 27.8% of pregnancies resulted in preterm and low birth weight babies.

There have been various studies which have looked into outcomes in specific glomerulopathies.[7] Systematic research suggested heterogeneity regarding the pros and cons of kidney biopsy in pregnancy, with the risks of complications being higher in pregnancy than in the postpartum period (7% vs. 1%, respectively) and could be deferred till termination.[6] In the absence of renal failure or HTN, outcomes of such pregnancies are good.[12] With limited data on NS in relation to pregnancy course and outcomes.[13],[14] it was worthwhile looking into such pregnancies with NS in absence of kidney biopsy for feto-maternal and renal outcomes.

Anti proteinuric therapy like angiotensin-converting enzyme inhibitors and receptor blockers are contraindicated during pregnancy because of their unwanted side-effects. The use of diuretics is discouraged because of the theoretical risk of impairing the normal pregnancy-associated expansion of plasma volume, possibly decreasing placental perfusion, still, there is no clear evidence of adverse fetal effects with thiazide or loop diuretics, and their use is occasionally indicated for severe, intractable edema.[15] In our study population, majority of them required salt restriction, bed rest, and limb elevation. Anasarca for edema control however it became difficult to be managed in four patients who required admission and treatment with low dose loop diuretics along with intravenous fresh frozen plasma keeping a watch over placental perfusion and weight. Albumin has been assigned to pregnancy category C by the Food and Drug Administration. It is not known whether albumin can cause fetal harm when administered to a pregnant woman. Albumin should only be given during pregnancy when the benefit outweighs the risk. Case reports have clearly shown benefits in terms of reducing anasarca with no adverse effects of fresh frozen plasma and albumin.[7] One needs to weigh the risk and benefits while managing them during pregnancy.

Though histopathology among NS helps in management during pregnancy. However, with increased risk evidence from literature, novel diagnostic approaches, such as the possibility of testing for anti-PLA2R (M-type phospholipase A2 receptor)[17] to detect membranous nephropathy or of analyzing the patterns[7] of proteinuria and ruling out pre-eclampsia can to some extent help in a change in management. Steroids were most commonly chosen to treat glomerular lesion. Sometimes empirical therapy with steroids in NS in pregnancy may need to be started. Steroids are generally safe during pregnancy. Prednisone does not represent a major teratogenic risk in humans at therapeutic doses.[18] The major concern is of worsening maternal glucose and blood pressure control, premature rupture of membranes, and infection. However, none of our patients showed any evidence of any complications due to steroids. Steroids significantly decreased proteinuria in three of the five patients in our study group when used empirically during pregnancy.

Studies in pregnant rats have generally shown no effect of cyclosporine on organogenesis, although some renal proximal tubular cell damage can occur.[19],[20] Cyclosporine <4 mg/kg should be maintained among renal transplant contemplating pregnancy, metabolism appears to be increased during pregnancy and higher doses may be required to maintain plasma levels in the therapeutic range.[21] Some of the pregnancies in cyclosporine-treated women were complicated by pre-eclampsia. In our study group usage of cyclosporine in two of our patients’ refractory to conservative treatment showed good response to treatment with good therapeutic levels maintained at a dose of 3 mg/kg with no worsening HTN or renal failure. It needs larger prospective studies to reciprocate these findings.

Mackey observed that despite having heavy proteinuria or gross edema during pregnancy, patients did not undergo termination of pregnancy and only were indicated when there was the deterioration of renal failure or HTN.[10] In our study population, majority were managed conservatively with 100% live births however pregnancy with NS was found to be associated with the risk of preeclampsia, pre-term birth, and IUGR. The degree of proteinuria was associated with maternal and fetal complications. Literature has shown that proteinuria was the only predictor of a poor maternal and fetal outcome.[16],[20],[21],[22]

Piccoli et al[5] found that adverse outcomes were more common in patients with chronic kidney disease compared with those without, i.e., preterm delivery (44% vs. 5%), cesarean section (44% vs. 25%), and neonatal intensive care unit admission (26% vs. 1%). While the presence of NS due to renal disease, in the absence of significant renal insufficiency or HTN, has been described to have minimal effects on the natural course of renal disease or maternal-fetal outcomes.[11] In our study population, the mean serum creatinine was <1.5 mg% despite normal renal functions and initial normal blood pressures worsening proteinuria added to the poorer maternal and fetal outcomes. A larger prospective study is required to confirm these findings.

   Conclusion Top

Nephrotic range proteinuria during pregnancy needs careful distinction between etiologies as it affects clinical outcome and management. Renal biopsy in women with native kidney disease presenting with nephrotic range proteinuria can be deferred during gestation understanding its complications. Majority of these women are managed conservatively yet specific therapies especially immunosuppression can safely be tried among females who are symptomatic. Such pregnancies need detailed counseling. Though the outcomes are good yet a sizeable risk of maternal and fetal complications can occur. Thus, a multidisciplinary approach while managing these pregnancies needs to be adopted.

Conflict of interest: None declared.

   References Top

Higby K, Suiter CR, Phelps JY, Siler-Khodr T, Langer O. Normal values of urinary albumin and total protein excretion during pregnancy. Am J Obstet Gynecol 1994;171:984-9.  Back to cited text no. 1
Cohen AW, Burton HG. Nephrotic syndrome due to preeclamptic nephropathy in a hydatidiform mole and coexistent fetus. Obstet Gynecol 1979;53:130-4.  Back to cited text no. 2
Côté AM, Sauvé N. The management challenges of non-preeclampsia-related nephrotic syndrome in pregnancy. Obstet Med 2011; 4:133-9.  Back to cited text no. 3
Beller FK, Dame W. Morphological alterations in the kidney during preeclampsia: A preliminary communication. Perspect Nephrol Hypertens 1976;5:155-6.  Back to cited text no. 4
Piccoli GB, Daidola G, Attini R, et al. Kidney biopsy in pregnancy: Evidence for counselling? A systematic narrative review. BJOG 2013;120:412-27.  Back to cited text no. 5
Lindheimer MD, Katz AI. Gestation in women with kidney disease: Prognosis and management. Baillieres Clin Obstet Gynaecol 1994;8:387-404.  Back to cited text no. 6
Hamilton P, Myers J, Gillham J, Ayers G, Brown N, Venning M. Urinary protein selectivity in nephrotic syndrome and pregnancy: Resurrection of a biomarker when renal biopsy is contraindicated. Clin Kidney J 2014;7:595-8.  Back to cited text no. 7
Lamkee MJ, Bratvold GE. Renal glomerulo-tubular mechanisms during toxemia of pregnancy. West J Surg Obstet Gynecol 1961; 69:121-8.  Back to cited text no. 8
McKay DB, Josephson MA. Pregnancy after kidney transplantation. Clin J Am Soc Nephrol 2008;3 Suppl 2:S117-25.  Back to cited text no. 9
Mackay EV. Pregnancy and renal disease: A ten year survey. Aust N Z J Obstet Gynaecol 1963;3:21-34.  Back to cited text no. 10
Strauch BS, Hayslett JP. Kidney disease and pregnancy. Br Med J 1974;4:578-82.  Back to cited text no. 11
Piccoli GB, Cabiddu G, Attini R, et al. Risk of adverse pregnancy outcomes in women with CKD. J Am Soc Nephrol 2015;26:2011-22.  Back to cited text no. 12
Studd JW, Blainey JD. Pregnancy and the nephrotic syndrome. Br Med J 1969;1:276-80.  Back to cited text no. 13
Lo JO, Kerns E, Rueda J, Marshall NE. Minimal change disease in pregnancy. J Matern Fetal Neonatal Med 2014;27:1282-4.  Back to cited text no. 14
Sebestyen A, Varbiro S, Sara L, et al. Successful management of pregnancy with nephrotic syndrome due to preexisting membranous glomerulonephritis: A case report. Fetal Diagn Ther 2008;24:186-9.  Back to cited text no. 15
Debiec H, Ronco P. PLA2R autoantibodies and PLA2R glomerular deposits in membranous nephropathy. N Engl J Med 2011; 364:689-90.  Back to cited text no. 16
Mason RG, Thomson AW, Whiting PH, et al. Cyclosporine induced fetotoxity in the rat. Transplantation 1985;39:23-40.  Back to cited text no. 17
Whittier WL, Korbet SM. Timing of complications in percutaneous renal biopsy. J Am Soc Nephrol 2004;15:142-7.  Back to cited text no. 18
Hou S. Pregnancy in renal transplant recipients. Adv Chronic Kidney Dis 2013;20:253-9.  Back to cited text no. 19
Park EJ, Jung H, Hwang J, et al. Pregnancy outcomes in patients with systemic lupus erythematosus: A retrospective review of 62 pregnancies at a single tertiary center in South Korea. Int J Rheum Dis 2014;17:887-97  Back to cited text no. 20
Liu Y, Ma X, Lv J, et al. Risk factors for pregnancy outcomes in patients with IgA nephropathy: A matched cohort study. Am J Kidney Dis 2014;64:730-6.  Back to cited text no. 21
Packham DK, North RA, Fairley KF, Whitworth JA, Kincaid-Smith P. Membranous glomerulonephritis and pregnancy. Clin Nephrol 1987;28:56-64.  Back to cited text no. 22

Correspondence Address:
Anupma Kaul
Department of Nephrology, Sanjay Gandhi Post-Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.344760

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