Acute kidney injury (AKI) is a heterogeneous clinical syndrome characterized by an abrupt reduction in kidney excretory function, usually identified through a rise in serum creatinine, reduced urine output, or both [1,2]. The condition occurs across emergency, medical, surgical, and intensive care settings and reflects a complex interaction between patient vulnerability and acute insults. Although many episodes are reversible with timely treatment, AKI increases the risk of electrolyte imbalance, metabolic acidosis, fluid overload, dialysis requirement, prolonged hospitalization, and death [2,3].

The terminology and classification of AKI have evolved from older descriptions of acute renal failure to standardized definitions that improve case recognition and comparison across studies. The RIFLE and AKIN systems were important steps in harmonizing diagnostic thresholds, while KDIGO criteria further unified serum creatinine and urine output-based staging [4-6]. KDIGO staging is now widely used in clinical research because it allows stratification of AKI severity and provides a practical framework for monitoring disease progression, treatment response, and clinical outcomes [4].

The epidemiology of AKI varies by population, setting, socioeconomic environment, infection burden, comorbidity profile, and access to early care. Global estimates indicate that AKI is common among hospitalized adults, and the burden is particularly high in critically ill patients [7-9]. In low- and middle-income regions, infection, hypovolemia, obstetric complications, and delayed presentation remain important contributors, whereas hospital-acquired AKI is often linked to sepsis, surgery, hemodynamic instability, contrast exposure, and nephrotoxic medications [3,8,10]. The distinction between community-acquired and hospital-acquired AKI is clinically useful because these groups differ in risk factors, preventability, severity, and outcomes [11-13].

Indian tertiary care hospitals encounter a mixed spectrum of AKI, including sepsis-related AKI, dehydration-related prerenal AKI, drug-induced nephrotoxicity, obstructive uropathy, cardiorenal syndrome, and AKI superimposed on pre-existing chronic kidney disease [11,12]. This pattern underscores the need for institution-specific data, since local clinical profiles influence diagnostic priorities and resource planning. Short-term outcomes such as renal recovery, dialysis dependence at discharge, and in-hospital mortality are particularly relevant for clinicians and administrators because they reflect both disease severity and the effectiveness of early intervention.

The present study was conducted to describe the clinical profile, risk factors, etiological pattern, severity, treatment requirements, and short-term outcomes of adult patients with AKI admitted to a tertiary care hospital in routine clinical practice. The study also aimed to assess the distribution of community-acquired and hospital-acquired AKI and to document renal recovery, dialysis dependence, and mortality at discharge.

Study design and setting This hospital-based observational study was conducted in the Department of General Medicine and allied inpatient units of Konaseema Institute of Medical Sciences & Research Foundation, Amalapuram, Andhra Pradesh, India. The institution is a tertiary care teaching hospital serving urban, semi-urban, and rural populations, with emergency, inpatient, intensive care, laboratory, imaging, nephrology referral, and renal replacement therapy facilities. The study was carried out from August 2025 to January 2026. Study population and sample size A total of 100 adult patients admitted with AKI during the study period were included. Patients were enrolled consecutively after applying eligibility criteria. Adults aged 18 years and above were eligible when they fulfilled KDIGO-based AKI criteria using serum creatinine change, reduced urine output, or laboratory-supported clinical diagnosis [4]. Both community-acquired and hospital-acquired AKI cases were included. Community-acquired AKI was defined as AKI present at admission or during initial evaluation, whereas hospital-acquired AKI was defined as AKI developing after hospitalization in a patient without AKI at admission. Inclusion and exclusion criteria The study included adult inpatients with AKI due to sepsis, hypovolemia, nephrotoxic exposure, obstructive uropathy, cardiorenal syndrome, or glomerular disease. Patients with end-stage renal disease on maintenance dialysis, renal transplant recipients, incomplete clinical or laboratory records, and refusal of consent were excluded. Chronic kidney disease cases were included only when the course indicated acute deterioration suggestive of superimposed AKI. Data collection and study variables Data were recorded using a structured proforma. Demographic variables included age and sex. Clinical variables included fever or infective symptoms, oliguria, vomiting or dehydration, pedal edema, breathlessness, and altered sensorium. Risk factors and comorbidities included diabetes mellitus, hypertension, sepsis, hypovolemia, nephrotoxic exposure, pre-existing chronic kidney disease, cardiac failure, and chronic liver disease. Etiology was categorized using clinical assessment, laboratory evaluation, imaging where required, and treating physician diagnosis. Laboratory variables included serum creatinine at admission, peak serum creatinine, blood urea, hyperkalemia, metabolic acidosis, and hyponatremia. AKI severity was staged according to KDIGO criteria [4]. Treatment and outcome assessment Management was individualized according to etiology and clinical status. Conservative treatment included fluid optimization, correction of electrolyte and acid-base abnormalities, infection control, withdrawal or dose adjustment of nephrotoxic drugs, relief of obstruction where indicated, and supportive care. Renal replacement therapy was initiated for refractory hyperkalemia, severe metabolic acidosis, fluid overload, uremic complications, or progressive azotemia despite conservative care [2,4]. Short-term outcomes were assessed at discharge or death as complete recovery, partial recovery, dialysis dependence, or mortality. Intensive care, mechanical ventilation, renal replacement therapy, and hospital stay were also documented. Statistical analysis and ethical considerations Data were entered into a spreadsheet and analyzed descriptively. Continuous variables were expressed as mean and standard deviation, and categorical variables as frequency and percentage. The analysis described clinical patterns and short-term outcomes rather than testing a prespecified hypothesis. The study protocol was approved by the Institutional Ethics Committee of Konaseema Institute of Medical Sciences & Research Foundation before initiation. Written informed consent was obtained from participants. Confidentiality was maintained throughout the study.

A total of 100 adult patients with AKI were included in the study. The mean age of the study population was 56.4 ± 15.2 years. Most patients belonged to the 51-70 years age group. Male predominance was observed, with 62 males and 38 females. Community-acquired AKI was more frequent than hospital-acquired AKI, as shown in Table 1.

Table 1. Baseline demographic and clinical profile of patients with acute kidney injury

The most common presenting features were fever or infective symptoms, reduced urine output, pedal edema, vomiting or dehydration, breathlessness, and altered sensorium. Fever or infective symptoms were documented in 52% of patients, and oliguria was documented in 41% of patients. The distribution of presenting clinical features is summarized in Table 2.

Table 2. Clinical presentation among patients with acute kidney injury

Diabetes mellitus and hypertension were the most frequent comorbidities. Sepsis was the leading clinical risk factor and etiological contributor, followed by hypovolemia, nephrotoxic drug exposure, pre-existing chronic kidney disease, and cardiac failure. Sepsis-associated AKI accounted for 38% of cases, followed by hypovolemia-related AKI in 24% and drug-induced AKI in 18%. The risk factor, comorbidity, and etiological profile is presented in Table 3.

Table 3. Risk factors, comorbidities, and etiological profile of acute kidney injury

According to KDIGO staging, Stage 1 AKI was observed in 36%, Stage 2 in 34%, and Stage 3 in 30% of patients. The mean serum creatinine at admission was 3.1 ± 1.4 mg/dL, and the mean peak serum creatinine was 4.0 ± 1.7 mg/dL. Conservative management was sufficient in most cases, while 23% required renal replacement therapy. Complete renal recovery was observed in 58% of patients, whereas mortality was 17%. Severity, treatment profile, hospital course, and short-term outcomes are shown in Table 4.

Table 4. Severity, treatment profile, and short-term outcomes

Overall, AKI was more frequent among middle-aged and elderly adults, with male predominance. Sepsis, diabetes mellitus, hypertension, hypovolemia, and nephrotoxic drug exposure were the major associated factors. Most patients improved with conservative management; however, advanced AKI stage, sepsis, ICU admission, and requirement for mechanical ventilation were linked with poorer short-term outcomes.

The present observational study describes the clinical spectrum, risk factors, severity, management profile, and short-term outcomes of AKI among 100 adults admitted to a tertiary care hospital in coastal Andhra Pradesh. The mean age was 56.4 years, and most patients were in the 51-70 years age group. This pattern is clinically relevant because older adults often have reduced renal reserve, greater comorbidity burden, polypharmacy, and higher susceptibility to hemodynamic and infective insults [1,8]. Male predominance was observed, as reported in several hospital-based AKI cohorts [11,12].

Community-acquired AKI accounted for 61% of cases. This indicates that many patients reached the hospital with renal dysfunction already established. Indian and international studies have emphasized that community-acquired AKI often reflects delayed presentation, infection, dehydration, drug exposure, or obstructive pathology [11,13]. In contrast, hospital-acquired AKI is commonly associated with severe illness, sepsis, invasive procedures, nephrotoxic medications, and intensive care exposure [9,10]. Recognizing the setting of onset is useful because community-acquired AKI requires early triage and referral, whereas hospital-acquired AKI requires inpatient surveillance.

Fever or infective symptoms and oliguria were the leading clinical presentations. Sepsis was the most frequent risk factor and the leading etiology, accounting for 38% of cases. Sepsis-related AKI arises through systemic inflammation, microcirculatory dysfunction, endothelial injury, altered renal perfusion, and tubular stress [2,3]. Diabetes mellitus and hypertension were also common. These conditions predispose patients to vascular disease, chronic kidney impairment, and reduced renal adaptive capacity during acute illness [1,14]. Hypovolemia and nephrotoxic exposure were additional modifiable contributors, highlighting the need for fluid assessment, rational antimicrobial use, careful analgesic prescribing, and dose adjustment of renally cleared drugs.

KDIGO Stage 3 AKI was present in 30% of patients, and renal replacement therapy was required in 23%. These findings reflect a clinically significant burden of moderate-to-severe AKI. Dialysis requirement depends not only on creatinine level but also on metabolic acidosis, hyperkalemia, fluid overload, uremic symptoms, and clinical deterioration [4]. ICU admission and mechanical ventilation were required in 21% and 14% of patients, respectively. These markers represent systemic illness severity and are associated with worse AKI outcomes in critical care cohorts [9,10,12].

Complete renal recovery was observed in 58%, partial recovery in 20%, dialysis dependence at discharge in 5%, and mortality in 17%. This mortality is consistent with the concept that AKI is not merely a biochemical abnormality but a multisystem risk marker linked to adverse short-term outcomes [7-10]. Incomplete renal recovery has implications beyond discharge because AKI survivors have higher risk of chronic kidney disease progression and recurrent hospitalization [14]. Discharge planning should include renal function reassessment, blood pressure and glycemic control, medication review, avoidance of unnecessary nephrotoxins, and nephrology follow-up for residual renal dysfunction.

Limitations

This was a single-centre observational study with a limited sample size of 100 patients. Long-term follow-up after discharge was not included, so delayed renal recovery, recurrent AKI, and progression to chronic kidney disease were not evaluated. Etiological classification depended on clinical records and routine investigations. Biomarkers, urine microscopy grading, and detailed nephrology follow-up data were not available for all participants, which restricts mechanistic interpretation.

This study showed that AKI among adults admitted to a tertiary care hospital was most frequent in middle-aged and elderly patients, with male predominance and a higher proportion of community-acquired cases. Sepsis, diabetes mellitus, hypertension, hypovolemia, and nephrotoxic drug exposure were the major associated factors. Sepsis-associated AKI was the leading etiology. Although most patients improved with conservative management, nearly one-fourth required renal replacement therapy. Complete renal recovery was achieved in more than half of the patients, while mortality remained clinically significant. Early recognition, infection control, fluid optimization, avoidance of nephrotoxins, renal dose adjustment of drugs, and close monitoring of high-risk patients are essential to improve short-term outcomes in tertiary care practice.

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