Acute kidney injury (AKI), also referred to as acute renal failure, is a rapid and often reversible decline in kidney function that occurs over a short period, typically ranging from hours to days. It is characterized by elevated creatinine levels and/or reduced urine output. AKI disrupts the body’s electrolyte balance, fluid regulation, acid-base balance, and waste excretion, and if not detected and treated early, it can lead to life-threatening complications. AKI is commonly seen in hospitalized patients, affecting up to 7% of hospital admissions and 30% of ICU admissions.[1] It significantly contributes to prolonged hospital stays and increased patient morbidity.[2] According to the Kidney Disease: Improving Global Outcomes (KDIGO) criteria, AKI encompasses a broad spectrum of kidney dysfunction, from mild increases in blood creatinine to complete renal failure requiring renal replacement therapy (RRT).[3] In ICU settings, AKI is often caused by a combination of factors, including sepsis, ischemia-reperfusion injury, nephrotoxic medications, and pre- existing chronic conditions. The mortality rate among ICU patients with AKI ranges from 25% to 50%, with worse outcomes for those requiring RRT. Additionally, AKI survivors are at higher risk of developing chronic kidney disease (CKD) or progressing to end-stage renal disease (ESRD), underscoring the long-term effects of this acute condition.[4] Various renal replacement therapies (RRTs) are used to treat severe AKI, including intermittent hemodialysis (IHD), continuous renal replacement therapy (CRRT), and prolonged intermittent RRT.[5] There is a notable gap in the available data on AKI in Indian ICUs. Existing research from India largely consists of single-center studies on critically ill patients. The purpose of this current study is to assess the impact of renal replacement therapy on the clinical outcomes of AKI patients in medical ICUs undergoing RRT (IHD) and to identify the causes of AKI in these patients and correlate them with their outcomes.

The present study was conducted as a prospective observational study in patients presenting clinically with acute renal injury of any etiology and requiring RRT at medical ICU of Department of Medicine of Gandhi Medical College and associated Hamidia Hospital, Bhopal (M.P.), during the study period of 18 months from July 2023 to December 2024. All the patients aged 18 years and above with acute kidney injury (fulfilling criteria as per KDIGO guidelines[6]) admitted in medical ICU with indication for RRT for management of AKI were included whereas patient with chronic kidney disease, Patients with AKI with no indication for RRT and those not giving consent for the study were excluded. After Approval from institutional ethics committee, 200 patients who met the inclusion criteria were enrolled in the study. Written informed consent was obtained from each participant in either English or Hindi, as per their preference. Detailed history, physical examination and relevant investigations were recorded on Day of enrolment of the study, on day of discharge and on 90th day from date of admission on a Proforma. The diagnosis of Acute Kidney Injury (AKI) and staging of AKI in the enrolled patients was based on the KDIGO criteria.[6] Blood and urine samples were collected for following laboratory Investigation on day of enrolment, day of discharge and 90th day from date of admission: Day of enrolment Day of discharge 90th day from date of admission Complete blood picture (CBP) CBP CBP Renal function test Renal function test Renal function test Liver function test Urine output Sr. Calcium Urine Routine Microscopy Sr. phosphate C Reactive Protein (CRP) Urine output Erythrocyte sedimentation rate (ESR) Urine output All enrolled patients underwent an ultrasonogram of the kidney to record the size and struc¬tural abnormalities. Additional tests were conducted based on the clinical presentation. Baseline serum creatinine was recorded as the value obtained within 3 months prior to ICU admission, which served as the reference for baseline kidney function. If this value was unavailable, the lowest serum creatinine value at the time of ICU admission was used, or, for patients without chronic kidney disease (CKD), a calculated value using the MDRD equation (as recommended by the Acute Dialysis Quality Initiative - ADQI) was used [3,4]. Indication for Renal replacement therapy (IHD) The following indications were considered for initiating hemodialysis as per KDIGO guidelines [6] in enrolled patients with AKI: • Severe metabolic acidosis unresponsive to medical therapy. • Severe refractory hyperkalemia • Fluid overload causing pulmonary edema and refractory to diuretics. • Uremia Symptoms – Symptoms of uremic encephalopathy, pericarditis, or bleeding. • Anuria not responding to medical therapy. Intermittent Hemodialysis (IHD) was the modality of RRT used in the enrolled patients with AKI as available in the institute. Patients were regularly followed up during hospital stay and on 90th day from date of admission. On the 90th day from date of admission, the estimated glomerular filtration rate (eGFR) of surviving patients was calculated using the CKD-EPI equation (2021). eGFRcr = 142 x min(Scr/κ, 1)α x max(Scr/κ, 1)-1.200 x 0.9938Age x 1.012 [if female] where: Scr = standardized serum creatinine in mg/dL κ = 0.7 (females) or 0.9 (males) α = -0.241 (female) or -0.302 (male) min(Scr/κ, 1) is the minimum of Scr/κ or 1.0 max(Scr/κ, 1) is the maximum of Scr/κ or 1.0 Age in years Patients were then assessed for CKD according to the KDIGO definition [7]. The staging of CKD was done according to the KDIGO guidelines.[7] Clinical Outcome was assessed on 90th day from date of admission as 1. Recovered from AKI. - Patients in whom serum creatinine decreased and reached baseline. If baseline value was not available serum creatinine cutoff of <1.4mg/dl was taken as baseline.[8] 2. AKI progressed to CKD (stage G1 to G5) with no further requirement of RRT and managed conservatively. 3. AKI progressed to CKD (stage G1 to G5) and dependent on RRT for further management. 4. Death STATISTICAL ANALYSIS: Data entry was carried out using Microsoft Excel, while statistical analysis was performed using the Statistical Package for the Social Sciences (SPSS), version 21.0, developed by IBM, Chicago, USA. Categorical variables were summarized using frequencies and percentages. To assess the relationship between in-hospital and final outcomes with different variables, the Chi-square test was utilized. A p-value less than 0.05 was considered statistically significant throughout the analysis.

The present study was conducted on a total of 200 cases presenting with acute kidney injury at the study area during the study period. Table 1- Distribution according to baseline variables Baseline variables No. of patients (n=200) Percentage Age (years) ≤30 48 24 31 – 40 29 14.5 41 – 50 45 22.5 51 – 60 50 25 >60 28 14 Gender Male 104 52 Female 96 48 Comorbidities Hypertension 61 30.5 Diabetes Mellitus 52 26 Coronary Artery Disease 27 13.5 Cerebrovascular Disease 17 8.5 Others 26 13.0 None 91 45.5 Blood urea nitrogen (mg/dl) <50 12 6.0 50-100 138 69.0 >100 50 25.0 Sr. Creatinine (mg/dl) <4 7 3.5 ≥4 193 96.5 Sr. Sodium (mEq/L) <135 99 49.5 135 – 145 85 42.5 >145 16 8 Sr. Potassium (mEq/L) <3.5 19 9.5 3.5 – 5 77 38.5 >5 104 52 Urine output (mL/kg/h) <0.5 100 50 0.5 – 1.0 81 40.5 1.1-1.5 19 9.5 We reported slight male predominance in our study, with males attributing to 52% of the study population. The mean age of patients with AKI was 44.63±15.32 years. The most common co-morbidity was hypertension (30.5%), followed by diabetes mellitus (26%) and coronary artery disease (13.5%). Other notable co-morbidities were hypothyroidism (5.5%), malignancy (4.5%), chronic liver disease (2%) and benign prostatic hyperplasia (1%). The majority of patients had blood urea nitrogen (BUN) levels between 50-100 mg/dl (69%) and serum creatinine levels in majority of patients were above 4 mg/dl (96.5%). About 49.5% cases with AKI had hyponatremia (<135 mEq/L), while more than half of the cases had hyperkalaemia (serum potassium>5 mEq/L). Half of the patients (50%) had a urine output of below 0.5 mL/kg/h, indicating severe oliguria (Table 1). Table 2- Distribution of patients with AKI according to clinical outcome. Clinical outcome No. of Patients (n=200) Percentage (%) During Hospital stay Discharged 141 70.5 Death 59 29.5 At 90th day from follow up Recovered from AKI 67 33.5 Progressed to CKD on conservative management 29 14.5 Progressed to CKD requiring RRT 25 12.5 Death 79 39.5 During the course of hospital stay,70.5% of patients were discharged from the Hospital, while 29.5% of patients died during the hospital stay. At 90th day, 39.5% of patients died despite haemodialysis, while 33.5% recovered from AKI. 14.5% of patients progressed to chronic kidney disease (CKD) not requiring renal replacement therapy (RRT) and were managed conservatively, and 12.5% of patients progressed to CKD requiring RRT for management (Table 2). Table 3 - Correlation of cause of AKI with outcome in patients with Acute Kidney Injury (AKI) Outcome Cause of AKI P value Prerenal(n=49) Renal (n=122) Postrenal (n=29) During hospital stay Discharge 42 (85.7%) 79 (64.8%) 20 (69%) 0.025 Death 7 (14.3%) 43 (35.2%) 9 (31%) At 90th day from admission Recovered from AKI 24 (49%) 37 (30.3%) 6 (20.7%) 0.004 CKD on conservative management 10 (20.4%) 13 (10.7%) 5 (20.7%) CKD requiring RRT 6 (12.2%) 14 (11.5%) 5 (17.2%) Death 9 (18.4%) 58 (47.5%) 12 (41.4%) Out of 49 cases with prerenal AKI, 85.7% of patients were discharged from hospital while 14.3% patients died during hospital stay. On the other hand, out of 122 cases with renal AKI, we observed discharges and death during hospital stay in 64.8% and 35.2% cases respectively. However, out of 29 cases of post renal AKI, we observed discharges in 69% and mortality in 31% cases. The observed correlation of causes of AKI with outcome during hospital stay in patients with AKI was found to be statistically significant (p<0.05). Prerenal AKI was significantly associated with higher recovery (49%) and lower mortality rate (18.4%). Renal AKI was significantly linked to higher death (47.5%) and low rates of AKI progressed to CKD on conservative management (10.7%) and AKI progressed to CKD requiring RRT for management (11.5%) (P <0.05) (Table 3).

This study was a prospective observational study conducted on a total of 200 cases admitted in Medical ICU of department of medicine, Gandhi medical college, Bhopal among patients presenting with Acute Kidney Injury (AKI) of any cause undergoing renal replacement therapy (RRT). In the present study, during the course of hospital stay, 70.5% of patients were discharged from hospital, while 29.5% of patients died during hospital stay. While at 90th day from discharge, approximately one third of the patients recovered from AKI following RRT whereas remaining 27% patients progressed to CKD and among them, 14.5% were on conservative management and 12.5% were life long dependent on RRT for survival. While a greater percentage of stage G4 cases in our study were not dependent on RRT (86.4% vs. 13.6%;p<0.05) and a significantly higher percentage of patients with stage G5 were dependent on RRT following AKI (73.3% vs. 26.7%;p<0.05). Our study documented mortality in 39.5% cases of AKI overall at 90th day of admission. Out of 79 cases who succumbed to death, 59 cases died during the course of hospital stay and remaining 20 cases succumbed after being discharged from the hospital in whom the cause of death is not known. The findings of present study were also in line with the findings of Ibrahim et al, where the authors documented mortality in 29.1% cases with AKI on dialysis, 53% were discharged, and 7.3% progressed to ESRD.[9] Pawar et al observed recovery in 63% cases of AKI whereas mortality rate in AKI cases on dialysis was 24% and the authors observed progression of disease to CKD in 13% cases.[10] Bhargavi et al reported recovery in 60% cases following AKI whereas death was reported in 3.3% cases, 36% had partial recovery and 0.7% cases required lifelong renal replacement therapy (0.7%), and death occurred in 3.3% (n=5).[11] Jordan et al reported recovery following AKI in 41% of patients following dialysis, whereas 44% of patients progressed to chronic kidney failure, and 15% died.[12] Prasad et al reported that among the survivors at the time of hospital discharge, 22.1% achieved complete recovery (CR), 57.7% had partial recovery (PR), and 9.4% remained dependent on dialysis. At the three-month follow-up, the study observed a mortality rate of 11.4%, while 72.2% of patients showed complete recovery, 7.2% had partial recovery, and 1% continued to require dialysis.[13] In the present study, prerenal factors accounted for 24.5% of AKI patients, renal causes for 61%, and postrenal causes for 14.5%. The most frequent pre-renal aetiology was hypovolemia (13%), which was followed by ischemic heart disease (3.5%) and heart failure (4.5%). Sepsis (51%), specifically pneumonia (14%) and urinary tract infections (11.5%) were the common causes responsible for renal causes of AKI. Nephrotoxins (4.5%) and glomerulonephritis (3.5%) were other renal causes of AKI. Obstructive uropathy with malignancy accounted for 7% of postrenal causes, followed by calculi (4.5%). Vairakkani et al documented sepsis as the most common cause of AKI (51.4%), followed by nephrotoxins (42.5%).[14] Bhargavi et al documented acute tubular necrosis as the most common cause of AKI (56%), followed by volume loss/hypoperfusion (26%), acute interstitial nephritis (12%), urinary tract obstruction (4.7%), and glomerulonephritis (1.3%).[11] Tarachandani et al documented AKI due to pre-renal causes in 49.9% cases (volume loss-21.6%, evidence of shock- 19.1%, cardiorenal syndrome -6% and hepatorenal syndrome -3.2%), whereas renal causes attributed to more than 70% cases (sepsis associates- 55.8%), and post renal causes attributed to 3.2% cases.[15] We observed in hospital mortality in significantly higher proportions of patients with renal causes of AKI (35.2%) and post renal causes of AKI (31%) whereas significantly higher proportions of patients with pre-renal AKI were discharged from hospital (85.7%; p<0.05). On the other hand, significantly higher proportions of cases with pre-renal AKI recovered from AKI (49%) whereas 58% cases with renal AKI succumbed to death during the study period (47.5%; p<0.05). Ibrahim et al reported deaths to be associated with hypovolemia (22.7%), AGN (15.9%) and sepsis (15.9%) in patients with AKI despite RRT.[9] Tarachandani et al observed no significant association of outcome with single versus multiple aetiologies of AKI as well as with Cardiogenic shock, hypovolemic shock, septic shock, evidence of glomerulonephritis and sepsis (p>0.05).[15] In our study, most common primary indication of haemodialysis was refractory volume overload (36%), followed by anuria (21.5%), uraemia (16.5%), refractory hyperkalaemia (14%), and refractory severe metabolic acidosis (12%). Our study findings were supported by the findings of Ibrahim et al, in which the most common indication for dialysis was refractory fluid overload was the most common indication of haemodialysis in patients with AKI (89.4%), followed by uraemia (61.1%), hyperkalaemia (29.1%) and metabolic acidosis (9.3%).[9] The most common indication of dialysis in cases with AKI in a study of Mathew et al were metabolic acidosis and anuria (52.9%).[16] Patel et al observed oliguria in 56.5%, hyperkalaemia in 34.7%, fluid overload in 6.1%, and metabolic acidosis in 22.6% with AKI.[17] Similarly, Alam et al documented refractory fluid overload, metabolic acidosis, and hyperkalemia as common indications of RRT.[18] Our study had certain limitations. The study was conducted as a facility based study at a single centre, where the population seeking care may be homogeneous, and thus the findings could not be generalized. Being a prospective follow up study, some loss to follow up was inevitable. Staging of CKD according to albuminuria was not done as urinary albumin to creatinine ratio test was not available in the study institute. Impact of AKI on quality of life could not be assessed. Also, the association of timing of initiation of RRT with outcomes was not assessed.

Severe form of AKI of any etiology should be managed with renal replacement therapy at the earliest for favorable outcomes. Various underlying causes attribute to acute kidney injury and may have impact on short term as well as long term outcome of these patients. Simple measures like oral rehydration education, timely infection control, and caution while administering potentially nephrotoxic drugs may help in preventing the majority of AKI incidence. This study emphasizes that AKI is associated with high mortality and a high risk of progression to CKD in recovered patients. Therefore, it is crucial to focus on AKI prevention to reduce the morbidity and mortality related to this condition.

1. Palevsky PM. Endpoints for clinical trials of acute kidney injury. Nephron. 2018 Sep 28;140(2):111-5. 2. Zuber K, Davis J. The ABCs of chronic kidney disease. JAAPA. 2018 Oct 1;31(10):17-25. 3. Pereira M, Rodrigues N, Godinho I, Gameiro J, Neves M, Gouveia J, Costa e Silva Z, Lopes JA. Acute kidney injury in patients with severe sepsis or septic shock: a comparison between the ‘Risk, Injury, Failure, Loss of kidney function, End-stage kidney disease’(RIFLE), Acute Kidney Injury Network (AKIN) and Kidney Disease: Improving Global Outcomes (KDIGO) classifications. Clinical kidney journal. 2017 Jun 1;10(3):332- 40. 4. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P, ADQI workgroup. Acute renal failure–definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Critical care. 2004 Aug;8:1-9. 5. Sancho-Martínez SM, Casanova AG, Düwel AG, Rivero-García K, García- Garrido T, Morales AI, Martínez-Salgado C, López-Hernández FJ, Fraile P. Identification of pre-renal and intrinsic acute kidney injury by anamnestic and biochemical criteria: distinct association with urinary injury biomarkers. International Journal of Molecular Sciences. 2023 Jan 17;24(3):1826. 6. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney inter., Suppl. 2012; 2:1–138. 7. Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease. Kidney Int. 2024;105(4S): S117–S314. 8. Pickering J.W., Endre Z.H. Back-calculating baseline creatinine with MDRD misclassifies acute kidney injury in the intensive care unit. Clin J Am Soc Nephrol. 2010;5(7):1165–1173. doi: 10.2215/CJN.08531109. 9. Ibrahim A, Ahmed MM, Kedir S, Bekele D. Clinical profile and outcome of patients with acute kidney injury requiring dialysis—an experience from a haemodialysis unit in a developing country. BMC Nephrol. 2016 Dec;17(1):1–5. 10. Pawar SG, Thoppalan B, Sezhian AS, Ramadoss K. OUTCOME AND CLINICO-ETIOLOGICAL PROFILE OF PATIENTS WITH ACUTE KIDNEY INJURY REQUIRING DIALYSIS. Ind. J. of Applied Res. 2023. Nov. 13 (11); 24-6. 11. Bhargavi KS, Mani R, Sathyamurthy P. Clinical spectrum and outcomes of acute kidney injury: A prospective study from an intensive care unit of South India. Critical Care & Shock. 2023 Sep 1;26(5). 12. Jordan M, Ortiz-Soriano V, Pruitt A, Chism L, Liu LJ, Chaaban N, Elias M, Sawaya BP, Chen J, Neyra JA. Kidney recovery in patients with acute kidney injury treated in outpatient hemodialysis or rehabilitation facilities. Kidney Medicine. 2021 Nov 1;3(6):916-24. 13. Prasad N, Jaiswal A, Meyyappan J, Gopalakrishnan N, Chaudhary AR, Fernando E, Rathi M, Singh S, Rajapurkar M, Jeloka T, Kishun J, Lobo V. Community-acquired acute kidney injury in India: data from ISN-acute kidney injury registry. Lancet Reg Health Southeast Asia. 2024 Jan 25;21:100359. 14. Vairakkani R, Sujith S, Harshavardhan TS, Yashwanth Raj T. Acute kidney injury in a tertiary care center of South India. Indian Journal of Nephrology. 2022 May 1;32(3):206-15. 15. Tarachandani R, Pursnani L, Balakrishnan M, Mahapatra HS, Bhattacharyya S, Chaudhary P. Clinical Profile and Predictors Affecting Outcome in Community-Acquired Acute Kidney Injury: A 3 Months Follow-Up Study. Indian J Nephrol. 2024;34(5):475–81. 16. Mathew DM, Radha DT. Etiological Factors and Clinical Profile of Acute Kidney Injury in MICU. Journal of Medical Biomedical and Applied Sciences. 2019 Nov 29;2(11). 17. Patel ML, Sachan R, Kumar R. A Comparative Study of Community- acquired Acute Kidney Injury and Hospital-acquired Acute Kidney Injury from a Tertiary Care Hospital in North India. Annals of African Medicine. 2024 Sep;23(3):420. 18. Alam M, Mahapatra HS, Kaur R, Pursnani LK, Balakrishnan M, Binoy R. Short-Term Renal Replacement Therapy Outcomes of Critically Ill Patients of Acute Kidney Injury and Acute on Chronic Kidney Disease. Cureus. 2025 Jan;17(1):e78183.