INTRODUCTION
Acute kidney injury is a significant cause of morbidity and mortality worldwide and more so in developing countries. Community acquired AKI (CAAKI) develops outside of a hospital in home settings and has significantly different etiologies than hospital acquired AKI (HAAKI). AKI can also lead to CKD in significant group of patients which has further healthcare implications in developing countries like India. We aimed to evaluate the etiologies of CAAKI admitted to us over last 8 years (2016- 2024) with retrospective analysis of individual patients over 3 months.
Methods:
METHODS
This is a single centre retrospective observational study where we studied adults with AKI with follow up for 3 months post hospitalization. Data from all patients with AKI, who visited the center between June 2016 and May 2024 were included in the study.Baseline characteristics that included eGFR, hemogram, ultrasonography of KUB of each patient was noted. Specific etiologies of AKI were determined after a detailed history and physical examination. All patients received standard treatment as per the existing guideline including renal replacement therapy (RRT). All participants had assessments of kidney function (eGFR) at one and three months after the index hospitalization. This study was approved by the institutional ethics committee.
Inclusion and exclusion criteria
All patients >18 years of age with CA-AKI, defined as AKI occurring outside the hospital setting―typically in the community or home setting―and admitted to inpatient department of the institute were included in the study. Patients who had HA-AKI, developed AKI at any time after 48 h of hospitalization, Glomerulonephritis, preexisting CKD, renal transplant recipients, and those with incomplete records were excluded.
Data collection
The following data were collected: clinical; risk factors and etiology of AKI; comorbidities; laboratory investigation results; management; and patient outcomes. Patients with pre-existing diabetes mellitus, hypertension, or other cardiovascular diseases were also recorded. CKD was defined as kidney function and/or structural abnormalities persisting >3 months. Demographic and clinical data included age, sex, BMI, blood pressure, and general and systemic physical examinations. Laboratory parameters included baseline and follow-up hemoglobin levels and leukocyte counts, blood urea nitrogen (BUN), serum creatinine, proteinuria, serum uric acid, alkaline phosphatase, and any other special investigation(s) required for diagnosis at the discretion of the treating clinician.
Renal function assessment AKI was defined and classified using the KDIGO guidelines, which used serum creatinine (increase in serum creatinine by ≥0.3 mg/dl within 48 h or increase in serum creatinine to ≥1.5 × baseline) and urinary output <0.5ml/kg/hr.For patients with serum creatinine values before admission, the most recent value was considered the baseline level. For patients without baseline creatinine in the 7–365 days before admission, baseline creatinine was imputed by back calculation using the Modification of Diet in Renal Disease (MDRD) equation and glomerular filtration rate (GFR) of 75 ml/min/1.73 m2 , as suggested by Pickering et al. Staging of AKI was based on the following: an elevation of serum creatinine level 1.5–1.9 × baseline or ≥0.3 mg/dl elevation (stage 1); elevation of serum creatinine 2.0–2.9 × baseline (Stage 2); and 3.0 × baseline or increase in serum creatinine to ≥4.0 mg/dl or the initiation of renal replacement therapy (Stage 3).
Etiological assessment
The settings and specific etiologies of CAAKI were noted. When AKI was multifactorial, the factor attributed by the treating clinician as the most contributory factor was considered the etiology of AKI. If no clear single etiology was ascertained, it was considered undetermined. Sepsis was defined according to the Third International Consensus Definition as a documented source of infection with a quick Sequential Organ Failure Assessment (qSOFA) score ≥2.
Follow-up and outcome measures
Each patient data was noted for renal outcomes at discharge and at 1 and 3 months after the onset of AKI. Patient outcome (s) were classified as survivor or non-survivor. Among the survivors, complete recovery (CR) was defined as adequate urine output (>1 ml/kg/h) with serum creatinine < 1.4mg/dl without persistent proteinuria or microscopic hematuria. Partial recovery was defined as decrease in serum creatinine by >50% with improved urine output (>0.5ml/kg/h) and no further need of dialysis. Dialysis dependency was defined as need for any form of dialysis for >28 days. Proteinuria was defined as urine protein excretion of ≥1+ on urine dipstick examination. Microscopic hematuria was defined as >5 red blood cells/high-power field on spun urine evaluation.
Results:
RESULTS
Total of 1340 patients data were registered . 343 patients had incomplete records or lacked proper follow-up. Thus data of 997 patients were analyzed.
Out of 997 patients, 605 patients (60.6%) were male. Approximately 50% patients had age more than 50yrs. Diabetes mellitus (DM) and Hypertension (HTN) were the most common comorbidities followed by chronic liver disease (CLD) and coronary artery disease (CAD) .
AKI evaluation and staging
Of 997 patients enrolled in the study. Majority of the patients belonged to AKI stage 3.Most patients ,irrespective of their AKI staging, had transaminitis [Mean- 79(AST), 56(ALT) ].
Total 997 patients with AKI were diagnosed and subdivided according to their etiology. Most common etiology was sepsis (N= 217, 21.8%) followed by Tropical fever (N=139, 13.9%). Malaria was the most common cause constituting about 41 % of all tropical fever. Other common causes were Leptospirosis(N=20), Dengue Fever (N=15) and Scrub typhus(N=08). Drug induced AKI was found in 105 patients (10.5%) with ACE inhibitors/ ARBs , NSAIDs and Rifampicin being the most common culprit. Other commonly encountered causes were Obstructive uropathy (N=109, 10.9%), Acute Gastroenteritis (N=85, 8.5%), Acute Pyelonephritis (N=72, 7.2%) and Nephrotic syndrome (N=21, 2.1%). (See Table 1)
Table 1 – Different AKI etiology and their percent contribution
CLINICAL OUTCOMES
Out of 997 patients, 240 patients (24.1%) had complete recovery at the time of discharge. Mortality at the index admission was 7.2% (N=72). Remaining patients (68.6%) had partial recovery at discharge. No patients were dialysis dependent at the time of discharge. At 1 months post discharge, additional 396 patients (39.7%) had completely recovered and another 17 patients died . At the follow up 3 months , complete recovery was noted in additional 83 patients. Total of 189 patients (18.9%) showed persistent renal dysfunction (Serum Cr >1.4mg/dl) out of which 23 patients(2.3%) were dialysis dependent.(table 2 and 3)
Table2
Table 3
Outcomes of patients in terms of mortality and recovery at discharge/ Follow-up
On analysis, In-hospital mortality was significantly associated with Diabetes mellitus and Hypertension (p<.05). 30.5% of In-hospital mortality belonged to Diabetes mellitus (DM) or conversely, 7.8% of all DM patients were non-survivors. Among patients who had persistent renal dysfunction at 3 months, 44.4% patients (N=84) had either DM or HTN. DM was the most common comorbidity in this group with about 24.8% patients of all DM patients having persistent renal dysfunction at 3 months. Presence of DM and Sepsis (as AKI etiology) was the single most important factor in predicting the progression of AKI to CKD.
Conclusions:
Sepsis (38.8%) was the most common cause of AKI followed by Obstructive Uropathy and Other related infective causes. Mortality at the index admission was 7.2% and Complete recovery at discharge was observed in 24.1% of patients. Remaining patients (69.7%) had partial recovery on discharge. On follow Up at 3 Months, 189 patients (18.9%) had persistent renal dysfunction of which 23 (2.3%) were on Renal replacement therapy.
Some patients had persistent renal dysfunction at 1 months and this group of patients (called as AKD, acute kidney disease) has been found to be of prognostic importance. In our study, AKD was noted in 27.2% patients. However, on further follow up, some patients showed complete recovery. At 3 months, 18.9% of the patients were labeled as CKD because of the persistent renal dysfunction.(Table 3)
In our study, presence of certain etiologies like Sepsis, Obstructive uropathy, pregnancy related AKI (Puerperal sepsis, APH/PPH) and Multiple myeloma were significantly associated with higher incidence of renal dysfunction at 3 months. Also Presence of Diabetes mellitus was associated with adverse renal outcome at 3 months. Better and closer follow-up protocols by nephrologists may help improve the short- and long-term outcomes of AKI.
Infective causes remain the common culprits of CAAKI with large contribution from Drug induced AKI. Significant number of patients progress to CKD and/or ESRD. Improving Socio-economic status is likely to lower the incidence of CAAKI.
I have no potential conflict of interest to disclose.
I did not use generative AI and AI-assisted technologies in the writing process.