Home About us Current issue Back issues Submission Instructions Advertise Contact Login   

Search Article 
  
Advanced search 
 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 3056 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 
 


 
Table of Contents   
ORIGINAL ARTICLE  
Year : 2017  |  Volume : 28  |  Issue : 2  |  Page : 279-284
Spectrum of renal injury in pregnancy-induced hypertension: Experience from a single center in India


1 Department of Nephrology, M. S. Ramaiah Medical College, Bengaluru, Karnataka, India
2 Department of Pharmacy, M. S. Ramaiah Medical College, Bengaluru, Karnataka, India

Click here for correspondence address and email

Date of Web Publication23-Mar-2017
 

   Abstract 

Pregnancy-induced hypertension (PIH) is a known complication of late pregnancy and is an important cause of maternal and fetal morbidity and mortality. Data on clinical profile, especially renal profile of preeclampsia and eclampsia in Indian women are lacking. The aim of our study was to examine the renal profile and clinical outcomes of patients diagnosed with PIH in our institution with a focus on the spectrum of acute kidney injury (AKI). In this prospective, observational study, 347 patients with a diagnosis of preeclampsia-eclampsia, who were undergoing treatment at the M. S. Ramaiah Medical College, were included in the study. The study duration was from 2010 to 2014. Details regarding epidemiologic data, obstetric data, laboratory parameters as well as maternal, renal, and fetal outcomes were noted. Patients with preexisting hypertension, diabetes mellitus, or chronic kidney disease were excluded from analysis. The overall incidence of preeclampsia was 3.4%. Hemolysis, elevated liver enzymes, and low platelets syndrome was seen in 31 patients (9%); 56 patients (19%) had AKI with a mean serum creatinine of 3.2 mg/dL and mean proteinuria of 2.8 g/24 h. Nineteen patients required dialysis. Persistent renal failure was seen in 2.5% of the cohort. Maternal mortality was 2.5%, largely secondary to sepsis. Primiparity was a major risk factor. In this study, we found a low rate of preeclampsia in a low-to-moderate risk cohort, with an incidence of AKI and maternal mortality consistent with reported literature.

How to cite this article:
Eswarappa M, Rakesh M, Sonika P, Snigdha K, Midhun M, Kaushik K, Chennabasappa GK, Sujeeth B. Spectrum of renal injury in pregnancy-induced hypertension: Experience from a single center in India. Saudi J Kidney Dis Transpl 2017;28:279-84

How to cite this URL:
Eswarappa M, Rakesh M, Sonika P, Snigdha K, Midhun M, Kaushik K, Chennabasappa GK, Sujeeth B. Spectrum of renal injury in pregnancy-induced hypertension: Experience from a single center in India. Saudi J Kidney Dis Transpl [serial online] 2017 [cited 2018 Dec 18];28:279-84. Available from: http://www.sjkdt.org/text.asp?2017/28/2/279/202790

   Introduction Top


Acute kidney injury (AKI) in pregnancy is largely a preventable problem usually resulting from obstetric complications and not intrinsic renal disease. Thus, pregnancy-related AKI is more a public health problem than a nephrologic problem.[1] Pregnancy-induced hypertension (PIH) is defined as hypertension (blood pressure >140/90) which occurs for the first time after week 20 of pregnancy.[2] Preeclampsia, eclampsia, hemolysis, elevated liver enzymes and low platelets (HELLP), and more severe forms of PIH are important causes of maternal and fetal morbidity and mortality.[3],[4],[5]

In pregnancy, AKI occurs with a bimodal distribution. A peak in early pregnancy is associated with infection, particularly septic abortion, whereas a third-trimester peak is associated with late obstetric complications such as preeclampsia, abruptio placenta, post-partum hemorrhage, amniotic fluid embolism, and retained dead fetus.[6],[7] Renal dysfunction in the form of AKI and/or proteinuria can be seen in up to 7%–10% cases of PIH in varying degrees of severity.[8] While complete renal recovery takes place in the majority of cases,[9] some cases may culminate in persistent renal failure and end-stage renal disease. We present our experience with 347 patients with preeclampsia-eclampsia.


   Materials and Methods Top


In this prospective observational study, 347 pregnant patients with a diagnosis of PIH were admitted to our institution from 2010 to 2014. The M. S. Ramaiah Hospital, attached to M. S Ramaiah Medical College, is a major tertiary care referral center, catering to patient population from North Bengaluru, State of Karnataka and adjacent states. Records were analyzed for demographic characteristics, obstetric history, and clinical profile on admission. Obstetric history included parity, history of antenatal follow-up, location, nature of delivery, pregnancy, and maternal and fetal outcomes.

Patients with preexisting diabetes mellitus, hypertension, chronic kidney disease defined as serum creatinine (SCr) > 1.5 mg/dL or presence of proteinuria >1+ on dipstick or renal transplant recipients, and presence of contracted kidneys on ultrasound were excluded from analysis.

Definitions

AKI was defined as SCr level >1.3 mg/dL. Preeclampsia was defined as blood pressure reading >140/90 mm Hg diagnosed for the first time after 20 weeks of gestation with 2+ proteinuria on dipstick. Severe preeclampsia was defined as the association of severe arterial hypertension (systolic arterial pressure exceeding 160 mm Hg and diastolic arterial pressure exceeding 110 mm Hg) or proteinuria >5 g/L or >3+ or signs of visceral involvement (headaches, visual disturbances, and epigastric or right upper-quadrant pain). Eclampsia was defined as the presence of new-onset grandmal seizures in a woman with preeclampsia.[1] The HELLP syndrome was defined by the combination of thrombocytopenia (<100 cells/L), elevated liver enzymes (aspartate amino-transferase >70 IU/L), and hemolysis. Sepsis was defined as per criteria laid down by American College of Chest Physicians.[6] Post-partum hemorrhage was defined as a blood loss of >500 mL after vaginal delivery or ≥1000 mL after cesarean delivery, or as noted in the medical record by a care provider.

Outcomes

Patient outcomes were noted for mortality, and renal outcomes were defined as recovery of renal function or requirement of renal replacement therapy (RRT), as well as presence or absence of proteinuria. Renal recovery was defined as a decline in SCr to ≤1.0 mg/dL and presence of 24 h urine protein of <150 mg within six weeks of diagnosis of AKI. Patients who did not satisfy the criteria for renal recovery were subjected to a renal biopsy. The biopsy sample was analyzed for light microscopy (H and E stain) and immunofluorescence to stain for immunoglobulin IgG, A, and M as well as complement factors C3 and C1q and kappa and lambda light chains. Pregnancy outcomes (preterm, term, miscarriages, and abortions) were also noted.


   Statistical Analysis Top


Data were analyzed using Statistical Package for the Social Sciences (SPSS) software version 18.0 (SPSS Inc, Chicago, IL, USA). Chi-square test was used to find the factors associated with the outcome. Statistical significance was tested at P <0.05. Risk estimate was calculated, and its 95% confidence interval was analyzed. Results are given as number, mean, median, and interquartile range for quantitative variables and percentages for nominal variables.


   Results Top


Three hundred and forty-seven patients satisfied the criteria for PIH with an overall incidence of 3.4% among all pregnancies. Severe preeclampsia as defined by blood pressure parameters was seen in 48 patients (14%) with systolic blood pressure >160 mm Hg, whereas 62 patients (18%) had high diastolic blood pressure >110 mm Hg. The HELLP syndrome was seen in 31 patients (9%). Median age of the patients and gestational age were 26 years and 36 weeks, respectively. Majority of the women were primiparous (54%). Pallor was noted in 247 patients (71%), whereas pedal edema was seen in 141 patients (40%). Sixty-eight patients (19%) presented with uterine bleeding, antepartum hemorrhage (APH), or postpartum hemorrhage (PPH). [Table 1] outlines the key epidemiologic features of this cohort.
Table 1: Demographics of patients with pregnancy-induced hypertension (n = 347).

Click here to view


Laboratory parameters were suggestive of AKI in 56 patients (16%). Oligo-anuria was seen in 42 patients (12%) and microscopic hematuria was seen in 32 patients (9%). The mean 24 h proteinuria was 2.8 g. Other significant laboratory parameters pertaining to PIH are mentioned in [Table 2].
Table 2: Clinical and laboratory parameters in patients with pregnancy-induced hypertension (n = 347)

Click here to view


In the 56 patients with AKI, 19 (34% of AKI cohort) required RRT. Persistent renal failure, either in the form of elevated SCr or persistent proteinuria was seen in nine patients (2.5%). Patients with persistent proteinuria were found to have various glomerulonephritides, whereas the incidence of cortical necrosis in this cohort was 1.1% [Table 3]. In terms of other maternal outcomes, 164 patients (47%) required lower abdominal cesarean section. Fetal outcomes were characterized by 12 intrauterine deaths (3.4%). Maternal mortality was 2.5% (9 patients), of which majority was attributable to sepsis.
Table 3: Patient and renal outcomes of pregnancy-induced hypertension (n = 347).

Click here to view


[Table 4] outlines the prevalence of risk factors for PIH in our cohort. Primiparity was identified as the biggest risk factor in our series.
Table 4: Prevalence of risk factors for pregnancy-induced hypertension in the study cohort.

Click here to view



   Discussion Top


Preeclampsia is a clinical syndrome that embraces a wide spectrum of signs and symptoms, either singly or in combination. Elevated blood pressure is the most important sign for the diagnosis of the disease. However, recent evidence suggests that in some patients, the disease may manifest itself in the form of either capillary leak (edema and proteinuria) or a spectrum of abnormal hemostasis with multiple organ dysfunction.[10] Severity of the preeclampsia depends on the blood pressure measurements. However, other important features such as edema, proteinuria, epigastric pain, and neurological symptoms should also be taken into consideration.[11] The diagnosis of severe preeclampsia based only on dipstick measurements in urine sample (>3+) is not adequate.[12] In our series, we noted a low prevalence of preeclampsia-eclampsia in our cohort. This low rate can be explained by exclusion from our study of certain high-risk populations such as patients with preexisting hypertension or chronic kidney disease. In a study involving 1802 patients, 5.8% had preeclampsia of which 8.5% had chronic hypertension.[13],[14] In the Third National Family Health Survey, it was published that 28.7% of women in their cohort of 124,385 women reported symptoms consistent with preeclampsia, a percentage much higher than reported elsewhere in literature for a mixed risk obstetric population. The reason for this discrepancy lies in their utilization of “symptoms” to define preeclampsia rather than using strict definitions, which may have resulted in over-estimation of its prevalence.[15] The prevalence of gestational hypertension ranges between 6%–17% in primiparous women and 2%–4% in multiparous women.[16],[17],[18],[19] Gestational hypertension may often become chronic hypertension, and this may occur one or two decades before it manifests.[20] Walters and Walters studied the pattern of normalization of hypertension in gestational hypertension.[21] These patients recover from hypertension faster than patients with preeclampsia.[22] The rate is substantially higher in women with twin gestation (14%),[15] and in those with previous preeclampsia.[18],[23] Similar risk factors for preeclampsia were identified in their case–control study of 200 obstetric patients from South India.[24]

We observed AKI in 16% of our cohort. Earlier studies have reported AKI in 1% of patients with preeclampsia, which increases to 3%–15% in patients with HELLP syndrome. A higher rate of AKI in our study could be attributed to the presence of concomitant sepsis and uterine hemorrhage. Blood loss secondary to abruptio placenta, APH, PPH, associated HELLP syndrome, and disseminated intravascular coagulation is responsible for causing renal injury at a microlevel through a combination of hypercoagulable state, vasoconstriction, impaired release of nitrous oxide, and intravascular thrombosis.[23] Our results were similar to Aggarwal et al, where the incidence of all cause sepsis was as high as 42%.[1] The high incidence of puerperal sepsis is mainly due to cesarean section and obstructed labor deliveries performed by unskilled professionals at primary health-care centers in rural areas and late referral to tertiary care centers.[24] Sepsis was more common in pregnancy with retained placenta in the uterus.[25] In a hospital-based study of 97 patients with PIH, it was noted that the incidence of AKI was 7.2%. However, in this paper, the authors defined AKI as SCr >3 mg/dL, hence leading to underestimation of the incidence of AKI in their cohort. While there is no standardized definition for pregnancy-related AKI, it is well established that a SCr value >0.8 mg/dL or urinary protein/creatinine ratio >300 mg is considered as renal dysfunction.[1],[21],[26]

Approximately one-third of our cohort with AKI and 5% of the overall cohort required RRT, consistent with reports by Prakash et al and Drakeley et al who reported short-term RRT requirement in 4% and 10% of their cohort with preeclampsia, respectively.[5],[8] While majority of the patients showed complete recovery of renal function, cortical necrosis was noted in 1% of the overall cohort, again consistent with the declining trend of cortical necrosis.[27] AKI in pregnancy is associated with a high risk for maternal mortality (9%–55%).[29] Maternal mortality secondary to preeclampsia or HELLP is reportedly low ranging from 0% to 5.5%.[4],[8],[27] However, perinatal mortality continues to be high in literature (37%–38%).[28],[29] In our case, maternal mortality was low and was mostly related to sepsis.


   Conclusion Top


PIH remains an important cause of maternal morbidity and mortality. Identification of high-risk population, close follow-up, and an integrated management between obstetricians and nephrologists are important for improving maternal and fetal outcomes.

Conflict of interest:

None declared.

 
   References Top

1.
Aggarwal RS, Mishra VV, Jasani AF, Gumber M. Acute renal failure in pregnancy: Our experience. Saudi J Kidney Dis Transpl 2014; 25:450-5.  Back to cited text no. 1
[PUBMED]  [Full text]  
2.
ACOG Committee on Practice Bulletins – Obstetrics. ACOG practice bulletin. diagnosis and management of preeclampsia and eclampsia. Number 33, January 2002. Obstet Gynecol 2002;99:159-67.  Back to cited text no. 2
    
3.
Audibert F, Friedman SA, Frangieh AY, Sibai BM. Clinical utility of strict diagnostic criteria for the HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome. Am J Obstet Gynecol 1996;175:460-4.  Back to cited text no. 3
    
4.
Killam AP, Dillard SH, Patton RC, Pederson PR. Pregnancy-induced hypertension complicated by acute liver disease and disseminated intravascular coagulation. Five case reports. Am J Obstet Gynecol 1975;123:823-8.  Back to cited text no. 4
    
5.
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.  Back to cited text no. 5
    
6.
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.  Back to cited text no. 6
    
7.
Goplani KR, Shah PR, Gera DN, et al. Pregnancy-related acute renal failure: A single-center experience. Indian J Nephrol 2008;18: 17-21.  Back to cited text no. 7
[PUBMED]  [Full text]  
8.
Prakash J, Tripathi K, Malhotra V, Kumar O, Srivastava PK. Acute renal failure in Eastern India. Nephrol Dial Transplant 1995;10:2009-12.  Back to cited text no. 8
    
9.
Levy MM, Fink MP, Marshall JC, et al. 2001 SCCM/ESICM/ACCP/ATS/SIS international sepsis definitions conference. Crit Care Med 2003;31:1250-6.  Back to cited text no. 9
    
10.
Prakash J. The kidney in pregnancy: A journey of three decades. Indian J Nephrol 2012;22: 159-67.  Back to cited text no. 10
[PUBMED]  [Full text]  
11.
Prakash J, Pandey LK, Singh AK, Kar B. Hypertension in pregnancy: Hospital based study. J Assoc Physicians India 2006;54:273-8.  Back to cited text no. 11
    
12.
Agrawal S, Walia GK. Prevalence and Risk Factors for Symptoms Suggestive of Preeclampsia in Indian Women. J Womens Health Issues Care 2014;3:6.  Back to cited text no. 12
    
13.
Ferrazzani S. Hypertension in pregnancy. Saudi J Kidney Dis Transpl 1999;10:298-312.  Back to cited text no. 13
[PUBMED]  [Full text]  
14.
Hauth JC, Ewell MG, Levine RJ, et al. Pregnancy outcomes in healthy nulliparas who developed hypertension. Calcium for preeclampsia prevention study group. Obstet Gynecol 2000;95:24-8.  Back to cited text no. 14
    
15.
Roberts JM, Taylor RN, Musci TJ, Rodgers GM, Hubel CA, McLaughlin MK. preeclampsia: An endothelial cell disorder. Am J Obstet Gynecol 1989;161:1200-4.  Back to cited text no. 15
    
16.
Meyer NL, Mercer BM, Friedman SA, Sibai BM. Urinary dipstick protein: A poor predictor of absent or severe proteinuria. Am J Obstet Gynecol 1994;170:137-41.  Back to cited text no. 16
    
17.
Knuist M, Bonsel GJ, Zondervan HA, Treffers PE. Risk factors for preeclampsia in nulliparous women in distinct ethnic groups: A prospective cohort study. Obstet Gynecol 1998;92:174-8.  Back to cited text no. 17
    
18.
Buchbinder A, Sibai BM, Caritis S, et al. Adverse perinatal outcomes are significantly higher in severe gestational hypertension than in mild preeclampsia. Am J Obstet Gynecol 2002;186:66-71.  Back to cited text no. 18
    
19.
Hnat MD, Sibai BM, Caritis S, et al. Perinatal outcome in women with recurrent preeclampsia compared with women who develop preeclampsia as nulliparas. Am J Obstet Gynecol 2002;186:422-6.  Back to cited text no. 19
    
20.
Sibai BM, Hauth J, Caritis S, et al. Hypertensive disorders in twin versus singleton gestations. National Institute of Child Health and Human Development Network of Maternal-Fetal Medicine Units. Am J Obstet Gynecol 2000; 182:938-42.  Back to cited text no. 20
    
21.
Walters BN, Walters T. Hypertension in the puerperium. Lancet 1987;2:330.  Back to cited text no. 21
    
22.
Ganesh KS, Unnikrishnan B, Nagaraj K, Jayaram S. Determinants of preeclampsia: A case-control study in a district hospital in South India. Indian J Community Med 2010; 35:502-5  Back to cited text no. 22
    
23.
Krane NK, Hamrahian M. Pregnancy: Kidney diseases and hypertension. Am J Kidney Dis 2007;49:336-45.  Back to cited text no. 23
    
24.
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.  Back to cited text no. 24
    
25.
Yücesoy G, Ozkan S, Bodur H, et al. Maternal and perinatal outcome in pregnancies complicated with hypertensive disorder of pregnancy: A seven year experience of a tertiary care center. Arch Gynecol Obstet 2005;273:43-9.  Back to cited text no. 25
    
26.
Ferrazzani S, De Carolis S, Pomini F, Testa AC, Mastromarino C, Caruso A. The duration of hypertension in the puerperium of preeclamptic women: Relationship with renal impairment and week of delivery. Am J Obstet Gynecol 1994;171:506-12.  Back to cited text no. 26
    
27.
Nisescrt S, Dribusch E, Bellmann O, Kauhausen H. Disorders of liver function, thrombopenia and hemodialysis in a special clinical form of hypertension in pregnancy (the so-called HELLP syndrome) [Article in German]. Geburtshilfe Frauenheilkd 1988; 48(9):637-40.  Back to cited text no. 27
    
28.
Pahwa N, Bharani R, Kumar R. Post-partum acute kidney injury. Saudi J Kidney Dis Transpl 2014;25:1244-7.  Back to cited text no. 28
[PUBMED]  [Full text]  
29.
Silva Júnior GB, Daher Ede F, Mota RM, Menezes FA. Risk factors for death among critically ill patients with acute renal failure. Sao Paulo Med J 2006;124:257-63.  Back to cited text no. 29
    

Top
Correspondence Address:
Mahesh Eswarappa
Department of Nephrology, M.S. Ramaiah Medical College, Bengaluru - 560 054, Karnataka
India
Login to access the Email id


DOI: 10.4103/1319-2442.202790

PMID: 28352008

Rights and Permissions



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

Top
   
 
 
    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  
 


 
    Abstract
   Introduction
    Materials and Me...
   Statistical Analysis
   Results
   Discussion
   Conclusion
    References
    Article Tables
 

 Article Access Statistics
    Viewed1215    
    Printed6    
    Emailed0    
    PDF Downloaded324    
    Comments [Add]    

Recommend this journal