Introduction:
Pregnancy related acute kidney injury (PRAKI) contributes to 3-7% of overall AKI in India with most AKI studies focussing mainly on hospital acquired AKI. Many reports have highlighted the dysregulation of alternate complement pathway in pregnancy related aHUS and Preeclampsia. There is a strong unmet need of a prospective study to look into the outcomes and basic pathophysiology (alternate pathway system activation) in PRAKI patients.
Methods:
This was a prospective observational study aimed to study the clinic-epidemiological profile and outcomes of PRAKI from a tertiary care centre in Northern India. We also studied the association and contribution of activated ACP with the severity and outcomes of PRAKI (by assessing serum complement factor C3, C4, ACP functional assay, anti- factor H autoantibody quantitative Enzyme Linked Immunosorbent Assay (ELISA) levels. All cases with incident AKI in the setting of pregnancy and postpartum state (6 weeks post-delivery) were included. All patients were followed up at 3 months with serum creatinine to assess the proportion of patients who have incomplete renal recovery and progressed to chronic kidney disease.
Results:
A total of 44 patients were studied with a mean age of 26.45 years (SD ± 4.68).Oliguria was common, affecting 41 (93.2%) patients. The requirement for Renal Replacement Therapy (RRT) was high, with 40 (90.9%) needing Intermittent Hemodialysis (IHD). With respect to fetal outcomes, around 2/3rd (65.9%) of the pregnancies resulted in a live birth, while 6.8% ended in abortion, 13.6% in stillbirth and 2.3% in intrauterine fetal demise (IUFD).Sepsis was the most common cause of PRAKI in 25 (56.7%) patients followed by PPH in 11 (25%) patients. Severe PE/HELLP syndrome, SLE flare and AFI were identified in 5 (11.4%), 1(2.3%) and 1(2.3%) patient respectively. Acute cortical necrosis was noted in 17 (38.6%) patients, indicating severe renal injury. At discharge, 35 (79.5%) patients were stable, 8 (18.2%) improved and 1 (2.3%) patient expired , probably secondary to sepsis. Renal biopsy was done in 4 patients (9.1%), 3 of which revealed cortical necrosis and 1 revealed lupus nephritis. Out of 43 patients of PRAKI, 20 (46.5%) had complete renal recovery with a mean creatinine of 0.84±0.23 mg/dl at 3 months. Interestingly, 23/43 (53.4%) had incomplete renal recovery and progressed to CKD at the end of 3 months. Out of these, 9 patients i.e. 20.9% of total were dialysis dependent at the end of 3 months. Whereas, 14 patients (32.5%) had progressed to CKD but did not require RRT by the end of 3 months with a mean serum creatinine of 6.5±3.66 mg/dl A total of 8 (18.2%) patients showed low complement C3 levels and 5 patients had low level of alternate pathway functional assay, suggesting activation of the alternative pathway of the complement system. However, there was no significant difference between the recovered and non-recovered (who progressed to CKD) group. Anti-factor H autoantibody levels were similar in both recovered and non-recovered groups (p=0.9). High serum urea, peak serum creatinine, higher average post partum days and development of cortical necrosis predicted progression to CKD in our cohort.
Conclusions:
Our study indicates a disturbingly high incidence of CKD and ACN among women with PRAKI. In our study the mortality was 2.3 % with 81.8% being dialysis dependent at discharge. 23 (52.3%) patients progressed to CKD at 3 months out of which 14 (60.8%) were dialysis dependent at 3 months. The testing of complement levels along with alternate complement pathway functional assay and antibodies against complement factors was unique as it tried to correlate the development of PRAKI and its progression to CKD with complement pathway abnormalities.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.