Abstract
Background
Hypertensive disorders of pregnancy (HDP) remain a major cause of maternal and perinatal morbidity and mortality globally. Quantifying the effects of HDP on complications during pregnancy is vital for enhancing risk prediction and improving pregnancy outcomes.
Methods
This study leveraged data from a cohort of 3652 women from a prior study investigating the prevalence of HDP at a tertiary maternity hospital in Kenya - between 1st January, 2018 and 31st December, 2019. Sociodemographic characteristics, pregnancy outcomes, and complications among women diagnosed with HDP compared with normotensive women were analysed. The maternal complications explored included acute renal injury, antepartum haemorrhage and postpartum haemorrhage. The perinatal complications included intrauterine foetal demise, intrauterine growth restriction, small-for-gestational-age neonates, preterm birth and low APGAR (7 or below). Log-binomial regression was used to estimate the risk ratios of maternal and perinatal complications between these groups. Both composite and individual complication analyses were done.
Results
The rate of maternal complications within the study was 1.3% (46/3652), whereas perinatal complications occurred in 13.0% (474/3652). After adjusting for maternal age ≥ 35 years and caesarean delivery, women with HDP had 3.34 times the risk of maternal composite complications compared to normotensive women (adjusted risk ratio 3.34; 95% CI 1.81– 6.16). These complications included acute renal injury and postpartum haemorrhage. Furthermore, there was a significant association between HDP and composite perinatal complications (adjusted risk ratio 1.38; 95% CI 1.07– 1.77). Specifically, the risk of intrauterine foetal demise and intrauterine growth restriction was elevated among the HDP group compared to normotensive women.
Conclusion
HDP continues to pose a significant burden on pregnancy and childbirth in Kenya. A strong association between pregnancy complications and HDP has been demonstrated. Regionally adapted pregnancy surveillance and optimised management approaches for acute kidney injury, post partum haemorrhage and perinatal morbidity prevention are urgently needed.
Supplementary Information
The online version contains supplementary material available at 10.1186/s12884-025-07941-1.
Keywords: Hypertension, Pregnancy-induced, Maternal morbidity, Perinatal morbidity, Acute kidney injury, Postpartum haemorrhage, Pregnancy outcome, Retrospective study, Kenya
Background
Pregnancy-related morbidity and mortality continue to reflect the alarming health disparities worldwide. In 2020, the World Health Organisation (WHO) noted that sub-Saharan Africa (SSA) alone accounted for 70% of global maternal deaths [1]. Major obstetric causes of maternal morbidity and mortality include haemorrhage, maternal sepsis, and hypertensive disorders of pregnancy (HDP). A multicounty survey across 29 countries in Asia, America and Africa found that HDPs contributed to more than 1 in 4 maternal deaths and near misses [2].HDPs are associated with a significant increase in expenditures, imposing a large financial burden on a country’s healthcare system [3].Despite scientific advances in understanding the mechanism of this disorder, the rates of HPD seem to be on a steady incline [4].
In addition to pregnancy complications such as foetal growth restriction, preterm birth, stillbirth, haemorrhage, and caesarean delivery, HDP also poses substantial risks for the development of future cardiovascular disease in mothers. These risks include stroke and heart failure [6, 7].
HDPs encompass a spectrum of pregnancy-specific hypertensive states. The National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy categorises HDPs as chronic hypertension, gestational hypertension, preeclampsia (PE) and related disorders, i.e., eclampsia and haemolysis, elevated liver enzymes, low platelet count (HELLP syndrome), and chronic hypertension superimposed on PE [5].
The precise causal pathway involved in HDP is unclear, making prevention and the prediction of complications challenging. In PE, placental antiangiogenic factors are upregulated, leading to disruption of the maternal endothelium and an antiangiogenic state, resulting in clinical signs of PE [6].HDPs are heterogeneous conditions, and it is necessary to quantify the risk profile and associated complications to better understand severity. This will ultimately enhance clinical surveillance, improve the management of these conditions, and in turn lead to better pregnancy outcomes.
While the adverse sequelae of HDPs are well-documented globally, data delineating their magnitude in low-resource contexts have received little systematic study. Delayed presentation and fragmented health services combined with constrained diagnostic capacity amplify the burden of HDP in SSA [7–9].Risk reduction strategies tailored to the region are therefore imperative.
This study aimed to analyse the risks of maternal and perinatal complications in HDP compared with normotensive women by examining data from a single-center patient cohort in the largest maternity hospital in Kenya.
Method
Study design and setting
The study employed a retrospective cohort design, leveraging data from a cohort of 3652 women included in a prior study investigating the prevalence of HDP at Pumwani Maternity Hospital between 1st January 2018 and 31st December 2019 [10].
Study population
The inclusion criteria for pregnant women were those who were diagnosed with HDP and who received pregnancy and postpartum care at the facility.
The exclusion criteria were as follows: pregnancies known to be complicated by major foetal anomalies, those with a gestational age of less than 20 weeks and those with multifoetal gestation.
Variables and data collection
Explanatory variable
HDP status. The definitions and categories of HDP were based on the Kenya National Guidelines for Quality Obstetric and Perinatal Care [11].The classifications used are similar to the diagnostic criteria established by the International Society for the Study of Hypertension in Pregnancy [12].Information on HPD status was extracted from clinical diagnoses, as recorded in medical files.
Data on maternal sociodemographic characteristics, pregnancy outcomes and perinatal complications were extracted from the medical files. Information on sociodemographic characteristics was collected for use in understanding the distribution of known risk factors that may confound or influence the outcome of interest (maternal and perinatal complications).
Outcome variables
Maternal complications included acute kidney injury (AKI), antepartum haemorrhage (APH) and postpartum haemorrhage (PPH).
The perinatal complications included intrauterine foetal demise (IUFD), intrauterine growth restriction (IUGR), small for gestational age (SGA), preterm birth and a low APGAR.
The definitions for each of the outcome variables are as follows:
Acute renal injury was identified by serum creatinine levels of > 70.72 µmol/l in pregnant women without any prior history of chronic kidney disease [13]. However, it is important to note that there is currently no consensus on the diagnostic criteria for pregnancy-related AKI [14].
The RIFLE criteria (Risk, Injury, Failure, Loss, End-stage Renal Disease), Acute Kidney Injury Network (AKIN), and the Kidney Disease Improving Outcomes (KDIGO) guidelines for diagnosing AKI in pregnant women have not been validated for use among the pregnant population [15].
APH refers to bleeding from or within the genital tract, at or after 24 + 0 weeks gestation (prior to delivery of the foetus) [16]. PPH is classically defined as blood loss greater than 500 ml after vaginal delivery and greater than 1000 ml after caesarean delivery within the initial 24 h postpartum [11, 17].Visual estimation is, however, subjective.
IUFD was defined as foetal death at or after 20 weeks of gestation or a birth weight equal to or above 350 g (clinically equivalent to stillbirth). Establishing a standard definition of stillbirth remains a priority [18].
Epidemiologically, a key indicator of IUGR is a birth weight falling below the third percentile (adjusted for sex and gestational age) or, alternatively, below the tenth percentile, often accompanied by abnormal umbilical blood flow on Doppler studies [19, 20].
The term prematurity included all neonates born prior to 37 weeks of gestation [21].
A low APGAR (specifically under 7) suggests asphyxia; however, confirmation of asphyxia requires further criteria to be met, such as an umbilical cord blood pH under 7, neurological signs (e.g., seizures, altered muscle tone), and multiorgan involvement. Consistently low APGAR scores over time nevertheless elevate the risk of poor neurologic outcomes [22].`.
Statistical analysis
Analyses were undertaken to quantify associations between HPD and pregnancy complications (maternal and perinatal).
Descriptive statistics were generated for the entire sample stratified by HDP status.
The chi-square test or Fisher’s exact test (as appropriate) was used to compare baseline categorical data between HDP and normotensive women. A t-test was used to compare means.
These tests identified differences in baseline characteristics by HDP status to inform the selection of covariates for the adjusted models.
Risk ratios (RRs) and the corresponding 95% CIs were used to estimate differences in maternal and perinatal complications between the two groups. Missing values were to be handled by no imputation method; however, data appeared missing at random and occurred in ≤ 5% of most of the variables, thus no imputation was employed. Analyses were performed with available data. Variance inflation factors (VIFs < 2.0) were applied to determine collinearity, and the Hosmer-Lemeshow test was used to check whether the model’s predicted probabilities matched the observed outcomes. A p > 0.05 was considered an adequate fit. Statistical analysis was performed via the Stata software package (Version 15.0; StataCorp).
Results
Among the 3652 hospital files analysed, 528 HDP cases were identified (14.5%). Approximately 3% of all women sampled experienced PE (109/3652). Eclamptic seizures occurred in 4.6% of women diagnosed with PE (5/109), accounting for 0.9% of all HDP cases. Haemolyses, elevated liver function tests, and low platelet count (HELLP) [23] syndrome were identified in about 2.8% of PE patients. There were four cases of chronic hypertension; however, the majority of HPD cases were uncategorised (n = 407).
A greater proportion of women aged 35 years or older at the time of delivery were in the HDP group than normotensive women were (20.8% vs. 16.2%, P = 0.023). Caesarean section (CS) as a mode of delivery was also notably more common in the HDP group. Despite the similarity in the distribution of gestational age at delivery (< 37 weeks’ gestation vs. ≥37 weeks gestation) among the HDP and normotensive groups, the proportion of infant birthweights under 2500 g was greater among women within the HDP than among normotensive women (Table 1).
Table 1.
Maternal demographic characteristics and pregnancy care among women receiving care at Pumwani maternity hospital
| Maternal characteristics | Normotensive (n = 3124) | Hypertensive disorder of pregnancy (n = 528) |
Total | p-value |
|---|---|---|---|---|
| Maternal age (weeks) | ||||
| < 20 | 279 (8.9) | 40 (7.6) | 319(8.7) | 0.023 |
| 20–34 | 2573 (82.4) | 423(80.1) | 2996(82.0) | |
| 35 and more | 272(8.7) | 65(12.3) | 337(9.2) | |
| Education | ||||
| None | 712(22.8) | 118(22.4) | 830(22.7) | |
| Primary | 294(9.4) | 61(11.6) | 355(9.7) | 0.117 |
| Secondary | 509(16.3) | 68 (12.9) | 577 (15.8) | |
| Tertiary | 197 (6.3) | 42 (7.9) | 239 (6.5) | |
| Missing | 1412(45.2) | 235(45.3) | 1651(45.2) | |
| Occupation | ||||
| Salaried employment | 145 (4.6) | 26(4.9) | 171 (4.7) | 0.803 |
| Casual labourer | 54 (1.7) | 11(2.1) | 65 (1.8) | |
| Unemployed | 2369 (75.8) | 407 (77.1) | 2776 (76.0) | |
| Self Employed | 493 (15.8) | 76 (14.4) | 569 (15.6) | |
| Missing | 63 (2.0) | 8 (1.5) | 71 (1.9) | |
| Marital status | ||||
| Married | 2617 (83.8) | 474 (89.8) | 3091(84.6) | 0.012 |
| Single | 490 (15.7) | 53 (10.0) | 543 (14.9) | |
| Divorced/Seperated | 14(0.5) | 1 (0.2) | 15(0.4) | |
| Widowed | 1(0.03) | 0(0.0) | 1(0.03) | |
| Missing | 2(0.1) | 0(0.0) | 2(0.1) | |
| Residence | ||||
| Non-slum | 1043 (33.4) | 169 (32.0) | 1212(33.2) | 0.749 |
| Slum | 2065 (66.1) | 357 (67.6) | 2422(66.3) | |
| Missing | 16 (0.5) | 2(0.38) | 18(0.49) | |
| Parity | ||||
| Primiparous | 1236 (39.6) | 197 (37.3) | 1433(39.2) | 0.398 |
| Multiparous | 1884 (60.3) | 330 (62.5) | 2214(60.6) | |
| Missing | 4(0.1) | 1(0.2) | 5(0.1) | |
|
Antenantal care current pregnancy |
||||
| No | 19 (0.6) | 4 (0.8) | 23 (0.6) | 0.779 |
| Yes | 3103 (99.3) | 524 (99.2) | 3627(99.3) | |
| Missing | 2(0.1) | 0(0.0) | 2(0.1) | |
| Gestational age | ||||
| 37 weeks or more | 2649 (84.8) | 439 (83.1) | 3088(84.6) | 0.332 |
| < 37 weeks | 475 (15.2) | 89 (16.7) | 2(0.05) | |
| Mode of delivery | ||||
| Vaginal | 2493 (79.8) | 368 (69.7) | 2861(78.3) | < 0.001 |
| Caesarean delivery | 628 (20.1) | 159 (30.11) | 787(21.55) | |
| Vacuum extraction | 2(0.06) | 1(0.19) | 3(0.08) | |
| Missing | 1(0.03) | 0(0.0) | 1(0.03) | |
| Infant birthweight (g) | ||||
| M ± SD | 3085.5 ± 538.8 | 3042.8 ± 641.2 | 3079.3 ± 554.9 | 0.102 |
| <2500 | 235 (7.52) | 77 (14.6) | 312 (8.5) | < 0.001 |
| 2500–4000 | 2824 (90.4) | 436 (82.6) | 3260 (89.3) | |
| >4000 | 65 (2.1) | 15 (2.8) | 80 (2.2) |
The data are presented as numbers (percentages). Tests: χ² for categorical, t-test for continuous, Fisher’s exact for small cell counts.. During the study period, the total rate of maternal complications within the sample was 1.3% (46/3652). Women diagnosed with HDP had 3.47 times the risk of maternal complications compared to normotensive women (RR 3.47, 95% CI 1.92– 6.27; P < 0.001). The maternal complications significantly associated with HDP were AKI (0.6% vs. 0%, p = 0.003) and PPH (RR 2.63, 95% CI 1.15–6.02; p = 0.018) (Table 2)
Table 2.
Maternal complications
| Normotensive (n = 3124) | HDP (n = 528) |
Total (n = 3652) |
p-value | RR | CI | |
|---|---|---|---|---|---|---|
| Maternal complications | ||||||
| Yes | 29 (0.9) | 17 (3.2) | 46(1.3) | < 0.001 | 3.55 | 1.94–6.51 |
| No | 3095(99.1) | 511(96.8) | 3606 (98.7) | |||
| Type of maternal complication | ||||||
| Acute renal injury | 0 (0.0) | 3(0.57) | 3(0.08) | 0.003 | - | - |
| Antepartum haemorrhage | 12(0.38) | 5(0.94) | 17(0.46) | 0.077 | 2.48 | 0.87 - 7.01 |
| Postpartum haemorrhage | 18(0.58) | 8 (1.52) | 26(0.71) | 0.018 | 2.63 | 1.15- 6.02 |
The data are presented as numbers (percentages). AKI was exclusive to women with PE, resulting in an AKI rate of 2.8% (3/109) within this group
RR: Risk ratio.
Perinatal complications occurred in 13% (474/3652) of the sample. There was a significant association between perinatal complications and HDP (RR 1.37, 95% CI 1.11–1.69; p = 0.004). The risk of intrauterine foetal demise (IUFD) (RR 2.82, 95% CI 1.69–4.71; p < 0.001) and intrauterine growth restriction (IUGR) (RR 8.88, 95% CI 1.49–52.99; p = 0.003) was also elevated among women diagnosed with HDP (Table 3).
Table 3.
Perinatal complications
| Normotensive (n = 3124) | HDP (n = 528) |
Total (n = 3652) |
p-value | RR | CI | |
|---|---|---|---|---|---|---|
| Perinatal complications | ||||||
| Yes | 385 (12.3) | 89 (16.9) | 474(13.0) | 0.004 | 1.44 | 1.12–1.85 |
| No | 2739 (87.7) | 439 (83.1) | 3606 (98.7) | |||
| Type of perinatal complication | ||||||
| Intrauterine foetal demise | 44 (1.4) | 21(3.8) | 65(1.8) | < 0.001 | 2.82 | 1.69- 4.71 |
| Intrauterine growth restriction | 2(0.1) | 3(0.6) | 5(0.1) | 0.003 | 8.88 | 1.49- 52.99 |
| Small for gestation-age neonates | 3(0.1) | 2(0.4) | 5(0.1) | 0.104 | 3.95 | 0.66–23.55 |
| Preterm birth | 109(3.5) | 22(4.2) | 131(3.6) | 0.439 | 1.19 | 0.76–1.87 |
| Low APGAR | 242(7.6) | 48(9.1) | 290(7.9) | 0.291 | 1.17 | 0.87 - 1.57 |
The data are presented as numbers (percentages)
RR: Risk ratio
After controlling for age ≥ 35 years, and caesarean section (based on significant differences in Table 1), the risk of experiencing maternal and perinatal complications remained significantly associated with HDP diagnosis (3.34-times the risk of maternal complications and a 1.38-times the risk of perinatal complications) (Table 4).
Table 4.
Risk ratios for maternal and perinatal complications
| RR | P -value | 95% Confidence Interval | |
|---|---|---|---|
| Maternal complications | |||
| Unadjusted | 3.55 | < 0.001 | 1.94–6.51 |
| Adjusted | 3.34 | < 0.001 | 1.81–6.16 |
| Perinatal complications | |||
| Unadjusted | 1.44 | 0.004 | 1.12–1.85 |
| Adjusted | 1.38 | 0.014 | 1.07–1.77 |
*Adjusted for maternal age ≥ 35 years and cesarean section. Covariates were chosen on the basis of significant baseline differences and clinical relevance
The variance inflation factors (VIFs) for the adjusted covariates were < 2.0, indicating no significant collinearity (Supplementary file 3. Table A).
When excluding uncategorized HDP, the adjusted risk ratio (aRR) for maternal complications increased to 5.12 (95% CI: 2.63–9.95). In subtype analysis, PE was associated with 5.41-fold risk of maternal complications (95% CI: 2.78–10.52), while uncategorized HDP showed no significant risk (aRR 2.07; 95% CI: 0.91–4.72). Similar trends occurred for PE risk of perinatal complications (aRR 2.01; 95% CI:1.45–2.79) (Supplementary file 3. Table B). Additional adjustment for parity, gestational age, and residence minimally altered HDP-associated risks. Maternal complications (adjusted risk ratio) aRR changed from 3.34 to 3.28 (-1.8%); perinatal complications RR changed from 1.38 to 1.41 (+ 2.2%) (Supplementary file 3. Table C).
Sparse outcomes (AKI, IUGR) were analyzed using Poisson regression with robust standard errors due to log-binomial non-convergence. Sensitivity analyses showed minimal changes. Maternal complications aRR ranged 3.29–3.34 across methods; perinatal complications aRR ranged 1.38–1.41. All changes were < 1.5%. Full results are exploratory (Supplementary file 3. Table D).
After Benjamini-Hochberg FDR adjustment for 6 secondary outcomes, HDP remained significantly associated with IUFD (FDR-p = 0.006), IUGR (FDR-p = 0.009), and PPH (FDR-p = 0.018). Other associations remained non-significant (Supplementary file 3. Table E).
Discussion
This study identified a HDP proportion of 14.5%, which is notably higher than the global average (5.2–8.2%) [24]. Although this figure may be partially influenced by the hospital-based setting, it reflects a greater trend toward increased HDP prevalence throughout the African continent. Variations in factors, such as diet and health-seeking behaviours (the timing of the first ANC visit), may influence the variations in rates [25].
There was a substantial risk of maternal complications with HDP, including AKI.
Notably, very few cases of AKI were identified in this study (2.8% among PE), this difference may reflect under-detection, especially considering existing literature which globally estimates that 15–20% of pregnancies are related to AKI among PE [14]. As the data were collected retrospectively, the discrepancy may also be influenced by the study design, which relied on documented serum creatinine measurements rather than prospective, standardised protocol-driven screening.
Renal injury in HDP results from placental release of antiangiogenic factors such as endothelin and thromboxane (vasoconstrictors), stimulation of proinflammatory cytokines, and reduced production of vasodilators (nitric oxide and prostacyclin), collectively driving microvascular injury and endothelial damage which impair renal perfusion [26]. In Africa, pregnancy-related AKI ranks second among the most prevalent causes of acute kidney injury, aggravated by late detection of high-risk cases and restricted access to quality obstetric care. Despite its significance, the problem remains under-researched and underreported [27].The need for AKI screening and frequent assessment of renal function in HDP is emphasised by these findings. This could help alleviate strain on healthcare systems by minimising the demand for intensive treatments (such as dialysis) to prevent progression of disease.
Consistent with previous studies [28, 29], a significant association between HDP and PPH was found in this analysis. Impaired vascular integrity due to insufficient extravillous trophoblast infiltration is observed in PE. In combination with oxidative stress, placental damage is exacerbated, vascular endothelial dysfunction and uterine smooth muscle oedema disrupt uterine contraction [30]. This potentially contributes to a greater risk of atony.
Moreover, coagulation abnormalities such as thrombocytopenia are often characteristic of severe PE and HELLP syndrome [31].
Intrapartum magnesium sulphate (a common anticonvulsant used in the management of PE with severe features) administration has also been independently linked to increased odds of PPH [32]. Close postpartum surveillance (for early detection of haemorrhage) may be particularly crucial in this cohort of women, especially as PPH remains a top contributor to mortality in SSA [33].
There was a significantly increased risk of perinatal complications with HDP, including IUFD, which is in concordance with studies from India and Kazakhstan [34, 35]. Placental insufficiency and hypoxia can result in foetal compromise and ultimately IUFD. PE and HELLP syndrome have been linked to IUGR, where the foetus fails to attain its genetic development potential [36, 37], reflecting impaired nutrient and oxygen transfer from placental dysfunction.
Uncategorised HDP cases (77.1%) attenuated original risk estimates. When isolated, PE drove most complications, aligning with its known pathophysiology.
While the study centers on biological risk associations, healthcare system influence, including human resource and infrastructure challenges, may influence outcomes in this setting [38, 39]. Kenya, similar to other SSA settings, faces structural deficiencies. In 2020, only 30.1 skilled health workers per 10 000 population are reported in the country, a figure below the Sustainable Development Goals (SDGs) index threshold of 44.5 [40]. In an assessment of 746 Kenyan health facilities, Ahmed et al. found an overall healthcare professional availability index score of 17.2% [41].This raises concerns about healthcare workforce adequacy as well as the quality of healthcare services. Workforce shortages are compounded by chronic underfunding, weakening overall maternal and neonatal health systems [42].Supply chain gaps further undermine healthcare quality. Public health facilities– especially at lower levels– often face chronic stock-outs and stringent budgetary constraints [43].Referral pathways exhibit severe fragmentation. Heavy staff workloads non-availability of ambulances limit referral guideline application [44].These delays particularly impact pregnancies at risk of IUFD due to placental insufficiency, for which timely intervention is necessary.
Recommendations
Enhanced surveillance
Personalised counselling on the risk of perinatal complications should remain a priority [45].This cohort could benefit from paired surveillance packages that are tiered at every ANC visit, including point-of-care creatinine testing and foetal Doppler studies or referrals. The study results suggest the necessity of improved foetal monitoring strategies and technologies to enhance antepartum and intrapartum foetal surveillance. This would ensure timely detection of perinatal complications.
PPH prevention and preparedness
Given the greater risk of PPH, targeted prophylactic measures and vigilance in postpartum surveillance in women with HDPs could be crucial in mitigating PPH morbidity and mortality. Delivery-room preparedness is essential. Resource-tailored prevention bundles that prioritise feasibility are key in aligning interventions with local realities. This could include advanced cross-matching, uterotonic combination prophylaxis, and rapid-response drills.
Longitudinal research
To clarify the broader impact of HDPs, longitudinal studies tracking maternal cardiovascular health post-pregnancy-related hypertensive disorders and long-term child neurodevelopmental outcomes are also recommended.
Improving clinical Documentation
At the health institution level in low-to-middle-income countries (LMICs), obstetric data are poorly captured [46]. We recommend an institutionally tiered documentation framework to tighten standardised diagnostic criteria with quality assurance checks. This could involve the adoption of electronic health record templates that prompt entries of key diagnostic criteria, coupled with relevant audits to ensure best practices.
Study limitations
These findings are drawn from a single tertiary center in Kenya, limiting the generalisability of the findings to other settings. HDP categories were largely uncategorised, limiting the analysis of results by HDP subtypes. Nonetheless, the use of a large sample enables valuable insights into HDP and pregnancy complications.
While our regression adjustments were based on variables differing in HDP status (i.e., mode of delivery and age), residual confounding due to unmeasured factors such as pre-pregnancy BMI & HIV status cannot be ruled out. Nonetheless, the comparable distributions of other characteristics (gestation, ANC attendance, and residence) reduce concerns about significant confounding factors in this research.
Only 5 cases of IUGR were observed, resulting in a wide confidence interval. This suggests low precision; and generalisation would require confirmation in expanded cohorts.
We used a fixed creatinine threshold to define AKI due to lack of baseline values. Though sensitivity analyses supported our findings, implementing the KDIGO criteria (0.3 mg/dL rise over 48 h) is advised for future studies.
Missing data for variables such as education precluded subgroup analyses. The missing-at-random assumption, despite being statistically supported, cannot be confirmed in retrospective data.
Conclusion
HDP continues to pose a significant burden on pregnancy and childbirth. A strong association between pregnancy complications and HDP has been demonstrated. Regionally adapted pregnancy surveillance and optimised management approaches for AKI, PPH and perinatal morbidity prevention are essential.
Supplementary Information
Below is the link to the electronic supplementary material.
Author contributions
Conceptualization of the study - MCM, OO, AP, RJK, GGN, EJC, PMN, DKO, AN, SM, CMW and AOO. Data curation - MCM and GGNData analysis - MCM, KAO and GGN Data visualisation - MCM, AOO, KAO and GGNWriting draft- MCM and KAO Review and editing - MCM, AOO, KAO and OO Supervision of the project - AOO and OO.
Funding
The authors did not receive support from any organisation for the submitted work. No funding was received to assist with the preparation of this manuscript. No funding was received for conducting this study.
Data availability
Data is available upon reasonable request from the corresponding authors: kinynki@gmail.com or kimbleyomwodo@alumni.harvard.edu.
Declarations
Ethics approval and consent to participate
The study protocol received review and approval by the Kenyatta National Hospital and the University of Nairobi Ethics and Research Committee (KNH/UON ERC) before the commencement of the study. Approval number: P65B/11/2020. Institutional permission to conduct the study was obtained from Kenyatta National Hospital. Informed consent was waived as anonymized data were collected from medical records. Confidentiality was maintained throughout the study.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
Data is available upon reasonable request from the corresponding authors: kinynki@gmail.com or kimbleyomwodo@alumni.harvard.edu.