Abstract

Community acquired AKI is a frequent disease with a large subset of patients progressing to CKD with incomplete recovery. CA-AKI has unique clinical, demographic profile, short and long term outcomes when compared to hospital-acquired AKI. CA-AKI constitutes a unique population who were previously healthy and had an AKI from the community and presents to the hospital. This is the first prospective CA-AKI cohort established till date. This is a prospective observational cohort study coupled with a serial bio-banking. Our primary objective was to elucidate the risk factors for non-recovery in CA-AKI and assess the proportion of patients who progress to CKD. Secondary objective was to assess the causes of CA-AKI and follow them prospectively with serial bio-banking for one year. All patients of CA-AKI who visit our centre and fulfil the inclusion and exclusion criteria were enrolled in the cohort. We included all adult hospitalised patients with CA-AKI and excluded patients with pre-existing CKD or high likelihood of underlying CKD, obstructive uropathy, suspected glomerulonephritis, decompensated chronic liver disease, heart failure, malignancy and transplant recipients. A follow up visit was scheduled at 1, 4 and 12 months after discharge. Study consort diagram We enrolled total 573 patients of CA-AKI from April 2017 to April 2021 after screening. Average age of the cohort is 37.3 years (S.D. 14.5) with males constituting 56.7% of our cohort. Mean baseline serum creatinine at enrolment was 7.4 mg/dl (S.D 3.6 mg/dl) and 78% of the patients required dialysis requiring during admission. Etiology of CA-AKI in our cohort was Obstetric in majority (17.4%) followed by sepsis (15.5%), acute gastroenteritis (13.6%), miscellaneous/burns/rhabdomyolysis/suspected drug toxicity (13%), tropical illness (12.5%), snake/insect bite (11.8%), pancreatitis (8.2%) and poisoning (6.4%). 1 and 4 month follow up was available for 263 and 196 patients with mean serum creatinine 1.6 mg/dl (S.D 1.77) and 1.27 mg/dl (S.D. 1.5) respectively. 22.3% and 16.3% patients had non recovery (eGFR<60 ml/min) at 1 and 4 month respectively. Biopsy for non-resolving/cause unknown was done in 3.6% of the cohort. The most common histological diagnosis in patients with non resolving AKI was pigment cast nephropathy and AIN. Plasmapheresis was done in 12 patients in the cohort, maximum for obstetric AKI (7) followed by gastroenteritis associated with TMA (2) and snake bite patients (2). 105 (18.3%) of patients of CA-AKI cohort expired. The mortality was highest in the poisoning subgroup (54%) and lowest in the acute gastroenteritis subgroup (6.4%). The severity of AKI described by RRT dependency at discharge, discharge creatinine, and hospitalisation duration was associated with higher non-recovery at 4 months. Etiology of CA-AKI in our cohort The most common etiology of CA-AKI in our cohort is obstetric followed by septic. Of the total 196 pts for which follow up at 4 months was available, CKD progression was seen in 16.3% of patients. Mortality was 18.3%, highest in the poisoning AKI subgroup. The studies focusing on long term renal recovery of CA-AKI is limited. So the fact that 16.3% of our previously healthy population had renal nonrecovery at 4 months is alarming and highlights the importance of CA-AKI as a contributor to ESRD in our population

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