Advertisment

Indian Journal of Nephrology About us |  Subscription |  e-Alerts  | Feedback | Login   
  Print this page Email this page   Small font sizeDefault font sizeIncrease font size
 Home | Current Issue | Archives| Ahead of print | Search |Instructions |  Editorial Board  

Users Online:220

Official publication of the Indian Society of Nephrology
  Search
 
  
 ~  Similar in PUBMED
 ~  Search Pubmed for
 ~  Search in Google Scholar for
 ~Related articles
 ~  Article in PDF (670 KB)
 ~  Citation Manager
 ~  Access Statistics
 ~  Reader Comments
 ~  Email Alert *
 ~  Add to My List *
* Registration required (free)  

 
   Abstract
  Introduction
   Materials and Me...
  Results
  Discussion
  Conclusion
   References
   Article Tables

 Article Access Statistics
    Viewed557    
    Printed22    
    Emailed0    
    PDF Downloaded76    
    Comments [Add]    

Recommend this journal

 


 
  Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 32  |  Issue : 3  |  Page : 206-215
 

Acute kidney injury in a tertiary care center of South India


Department of Nephrology, Government Stanley Medical College and Hospital, The Tamil Nadu Dr. M.G.R. Medical University, Old Jail Road, Chennai, Tamil Nadu, India

Date of Submission11-Oct-2020
Date of Acceptance03-Aug-2021
Date of Web Publication30-Dec-2021

Correspondence Address:
M Edwin Fernando
Professor and Head of Department of Nephrology, Government Stanley Medical College and Hospital, The Tamil Nadu Dr. M.G.R. Medical University, Old Jail Road, Chennai - 600 001, Tamil Nadu
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijn.IJN_481_20

Rights and Permissions

  Abstract 


Background and Objective: Data regarding the epidemiology and outcomes of acute kidney injury (AKI) from our part of the world are limited. The irking consequences of AKI, both on the patient and the health care system, are being increasingly recognized. We aimed to study the epidemiology and short-term outcomes of AKI and to analyze the factors associated with adverse renal outcomes. Materials and Methods: We retrospectively studied AKI patients stratified according to the Kidney Disease: Improving Global Outcomes (KDIGO) stage, regarding clinicodemographic data, renal replacement therapy (RRT), and 90-day outcomes. Those with preexisting CKD Stage 4 (defined by estimated glomerular filtration rate [eGFR] <30 mL/min/1.73 m2) and above, prior renal transplant (s), or acute glomerulonephritis were excluded. The primary outcome was a composite of de novo CKD (eGFR <60 mL/min/1.73 m2) or CKD progression (decline in eGFR category to any higher stage) in patients with baseline CKD at 90 days. The secondary outcome was a composite of de novo CKD, CKD progression, or death at 90 days. Results: Of the 358 patients, 52.5% had Stage 3 AKI. Eighty-eight patients (24.6%) had baseline CKD. Sepsis (51.4%) was the predominant etiology followed by nephrotoxins (42.5%). Renal replacement therapy (RRT) was required in 94 (26.3%) patients with hemodialysis being the most common modality. After excluding lost to follow-up, 66 patients (20.3%) had the primary outcome, and 195 patients (60%) had the secondary outcome. The 90-day mortality was observed in 39.7% of patients. AKI stage (P = 0.002), baseline CKD (P = 0.000) and RRT need (P = 0.005) were significantly associated with the primary outcome, while age >60 (P = 0.018), SOFA (Sequential Organ Failure Assessment) ≥9 (P = 0.000), hypoalbuminemia (P = 0.024), baseline CKD (P = 0.000) and RRT need (P = 0.001) were associated with the secondary outcome. Conclusion: Sepsis was the dominant precipitant of AKI and a major proportion had preventable etiology. AKI severity, baseline CKD status, and RRT need were found to predict the development or progression of CKD.


Keywords: AKI, epidemiology, outcomes, risk factors


How to cite this article:
Vairakkani R, Fernando M E, Sujith S, Harshavardhan T S, Raj T Y. Acute kidney injury in a tertiary care center of South India. Indian J Nephrol 2022;32:206-15

How to cite this URL:
Vairakkani R, Fernando M E, Sujith S, Harshavardhan T S, Raj T Y. Acute kidney injury in a tertiary care center of South India. Indian J Nephrol [serial online] 2022 [cited 2022 Jul 1];32:206-15. Available from: https://www.indianjnephrol.org/text.asp?2022/32/3/206/334441



  Introduction Top


The epidemiology and outcomes of acute kidney injury (AKI), the most common and perhaps the most serious renal event with short- and long-term repercussions, are determined to a large extent by the geographical, sociocultural, economic, genetic, and practice patterns in a country. Significant dissimilarities have been observed between countries, within different regions of a country, and even in a single center across different time periods.[1],[2] AKI, in low- to middle-income countries like ours, is frequently a community-acquired problem affecting relatively younger people with fewer comorbidities, precipitated by a single identifiable cause and associated with lower mortality, in comparison with developed nations, where older, hospitalized individuals with significant comorbidities are affected with excess mortality.[1],[3],[4] Globally, AKI is estimated to affect 13.3 million individuals in a year, 5% to 10% of hospitalized patients, and 60% of intensive care patients, and >85% of this burden is contributed by developing countries.[5],[6],[7] In-hospital mortality of AKI remains unacceptably high exceeding 50% in critically ill patients.[8] Since the central AKI registry in our country is in its infancy, a void exists regarding the epidemiology and outcomes of AKI. Existing literature from our country has inherent limitations including, but not limited to, single-center data, under reporting, under recognition, retrospective design, and varied definitions.[1],[4]

Although the short-term morbidity and mortality of AKI are better recognized, a critical knowledge gap exists regarding the long-term consequences in AKI survivors that have clinical and public health implications.[9] The conventional ideology of benign outcomes in AKI survivors has been recently challenged by observational studies. An episode of AKI elevates the risk of AKI recurrence, development of de novo CKD, or progression of existing CKD.[8],[9] AKI and CKD are now recognized as interconnected syndromes with either being the risk factor of the other.[8] AKI has also been linked to nonrenal consequences such as increased risk of cardiovascular events, hypertension, poor quality of life, and mortality.[9],[10],[11],[12],[13],[14] Even patients who had apparent complete recovery of renal function are at an increased risk of these adverse outcomes.[10],[15] Hence, AKI survivors represent a high-risk population predisposed to potential ominous complications imparting a significant burden on the patient and public health resources, calling for risk stratification and mitigation measures.[16]

This study aims to analyze the etiology and short-term (90-day) outcomes in patients with AKI in a tertiary care center. Furthermore, the study intends to identify the risk factors associated with CKD development or progression and mortality in these patients.


  Materials and Methods Top


This study was a retrospective study conducted in our tertiary care hospital between January 2018 and December 2019.

Patient selection and data collection

Adult patients (age ≥18 years) with AKI as defined by the Kidney Disease: Improving Global Outcomes (KDIGO) admitted either primarily in the nephrology unit or various other units seeking nephrology referral were included and staged as follows: Stage 1 (creatinine increase ≥0.3 mg/dL within past 48 hours or an increase of 1.5–1.9 times the baseline or a urine output <0.5 mL/kg/hour for 6–12 hours), Stage 2 (creatinine increase of 2.0–2.9 × baseline value or a urine output <0.5 mL/kg/hour for ≥12 hours), and Stage 3 (creatinine increase of 3 × baseline value or serum creatinine ≥4 mg/dL or RRT initiation or a urine output <0.3 mL/kg/hour for ≥24 hours or anuria for ≥12 hours). Those with preexisting CKD Stage 4 (defined by estimated glomerular filtration rate [eGFR] <30 mL/min/1.73 m2) and above, prior renal transplant (s), or acute glomerulonephritis were excluded from the study. Data on demographic characteristics, etiology, clinical features, comorbidities, biochemical parameters, histopathology, the treatment provided, vasopressor use, RRT, and outcomes were retrieved from patients' case records using a standardized data form. AKI at the time of admission or within 48 hours of admission was categorized as community-acquired AKI (CA-AKI) and that developing after 48 hours of hospitalization was categorized as hospital-acquired AKI (HA-AKI). Renal biopsy was performed when AKI did not improve by 14 days or earlier if there was a suspicion of a different disease process as per treating nephrologist's discretion. Baseline CKD was identified from serum creatinine measurement available within the preceding year from patients' records, finding of contracted kidneys on imaging, or chronicity (global glomerulosclerosis/moderate to severe interstitial fibrosis with tubular atrophy) on histology. Those with contracted kidneys or chronicity on biopsy without creatinine measurements were excluded as their CKD stage could not be ascertained. All eGFR measures were calculated using the Chronic Kidney Disease Epidemiology Collaboration 2009 creatinine equation.

Outcome

The data were analyzed regarding the demographic features, etiology, histopathology, RRT, and 90-day outcomes. The primary outcome was a composite of de novo CKD (defined by eGFR <60 mL/min/1.73 m2) or CKD progression (decline in eGFR category to any higher stage) in patients with baseline CKD at 90 days. The composite outcome of de novo CKD (defined by eGFR <60 mL/min/1.73 m2) or, CKD progression (decline in eGFR category to any higher stage) in patients with baseline CKD or death at 90 days was studied as the secondary outcome.

Statistical methods

To describe the data, descriptive statistics, frequency analysis, and percentage analysis were used for categorical variables and mean with standard deviation (SD) or median with interquartile range (IQR) were used for continuous variables. Chi-square, Fisher exact, and Student t tests were used as appropriate. The risk factors with P < 0.1 for primary and secondary outcomes identified with univariate analysis using Chi-square test were further assessed using binary regression analysis. Collinearity was analyzed between the covariates. Statistical significance was considered at a P < 0.05, and odds ratios with 95% confidence interval were also calculated. Statistical analysis was done using IBM SPSS statistics software Version 26.0.


  Results Top


Of the 358 patients included in the study, 77 patients (21.5%) had Stage 1, 93 (26%) had Stage 2, and 188 (52.5%) had Stage 3 AKI. The mean age of the study population was 46.09 ± 17 years; 213 (59.5%) of the total cohort were male, with a male: female ratio of 1.47:1. Among the comorbidities, diabetes mellitus was the most common in 99 patients (27.7%) followed by hypertension (n = 95, 26.5%). Among the entire study cohort, 88 patients (24.6%) had baseline CKD, 63.6% (56 patients) of them were in Stage 3 AKI group. The demographic and clinical characteristics are summarized in [Table 1].
Table 1: Patient characteristics and outcomes

Click here to view


The etiology was multifactorial in most cases. Sepsis was the most common precipitating event (51.4%) with skin and soft tissue being the predominant source (n = 78/184, 42.4%). Next to sepsis, nephrotoxins contributed to AKI in 152 patients (42.5%) with drugs contributing to the majority (n = 53/152, 34.9%). Among poisons consumed, paraquat ingestion (44.7%) was the most common. [Table 2] provides a summary of the various AKI etiologies. Acute tubular injury was the most common histologic finding (23.9%) among patients who underwent renal biopsy (n = 46, 12.8%) [Table 3].
Table 2: Etiological risk factors

Click here to view
Table 3: Histopathology

Click here to view


Outcome

Of the 94 patients (26.3%) requiring RRT, hemodialysis was the most common modality employed (72.3%). Acute intermittent peritoneal dialysis was done in 27.7% of patients who had hemodynamic instability or other contraindications to hemodialysis [Table 1]. At 90 days, 33 patients (9.2%) were lost to follow-up. Of the remaining 325 patients, 66 patients (20.3%) and 195 patients (60%) met the primary and secondary composite outcomes, respectively. Eighteen (5.5%) AKI patients without baseline CKD developed de novo CKD at 90 days. Sixteen of the 18 patients had Stage 3 AKI, whereas the remaining two patients had Stage 2 AKI, and all these patients progressed to CKD without AKI recovery. At 90 days, 129 patients (39.7%) had mortality, of which 79 patients (61.2%) expired during their hospital stay. The 30-day and 60-day mortality were observed in 101 patients (31.1%) and 117 patients (36%), respectively. The outcomes according to stage are tabulated in [Table 4].
Table 4: The 90-day outcomes of the study population

Click here to view


Risk factors associated with primary and secondary outcomes

In multivariate analysis, stage of AKI (P = 0.002), presence of baseline CKD (P = 0.000) and need for RRT (P = 0.005) were significantly associated with the primary outcome, whereas age >60 (P = 0.018), Sequential Organ Failure Assessment (SOFA) ≥9 (P = 0.000), hypoalbuminemia (P = 0.024), baseline CKD (P = 0.000), and need for RRT (P = 0.001) were associated with the secondary outcome [Table 5].
Table 5: Analysis of risk factors associated with primary and secondary outcomes

Click here to view



  Discussion Top


Accumulating evidence on the adverse long-term consequences of AKI, both renal and nonrenal, has changed our perception of this syndrome, once considered to have a benign outcome. The development and validation of consensus definitions of AKI, apart from use in epidemiologic studies and trials, has increased our understanding of the short- and long-term outcomes of AKI.[7],[9],[17]

More than half of our study population belonged to the KDIGO Stage 3, reasons being delayed recognition, inadequate management of the precipitating cause, difficulty in health care access, resorting to alternative medicine, and delayed referral including in-hospital nephrology referral. The mean age of our cohort was 46 years, which was comparable with most of the Indian studies, although some studies have reported considerably lesser and greater mean age than ours.[2],[5],[18],[19],[20],[21] Compared with data from developed countries, our patients were about two decades younger.[22] Males were represented more than females (1.47:1) in our study, as has been observed in other studies, which may be related to more health care access for males or to the hormonal differences in susceptibility as shown in few animal studies.[1],[19],[23],[24] Majority of the AKI were related to medical causes (71.8%), followed by surgical (22.1%) and obstetric (6.1%) causes. This relative contribution has varied between 73% and 87% for medical causes, 3% and 9% for surgical causes, and 3% and 20% for obstetrical causes across various studies done in different regions of our country.[1],[18],[20] Two thirds of the AKI were community acquired during our study period, the proportion has varied between 53% and 92% among recent studies, which might be due to regional epidemiological variations.[5],[18],[23] One fourth of our study population had baseline CKD Stage 2 or 3, of which the majority had advanced AKI, which was one of our strengths as many studies excluded CKD patients.

The etiology of AKI was multifactorial in the vast majority. In our study, sepsis was the most common precipitating cause (51.4%). In the epidemiological studies conducted after 2010 at various centers of our country, the major etiological factor was sepsis contributing variably between 22% and 53%.[2],[5],[18],[23] In the multicentric study by Bagshaw et al.,[22] 47.5% of AKI were attributable to sepsis, with chest and abdomen being the most involved sites. Among the different sites, skin and soft tissue was the most common sepsis source in our cohort, which could have been largely prevented had they been managed appropriately early. In the study by Priyamvada et al.,[5] skin and soft tissue was the most common foci, whereas other studies have cited urogenital, lung, or abdomen as the predominant site.[19],[25],[26] Scrub typhus was shown to be the major cause in a study from Shimla by Vikrant et al.,[18] probably related to the geographical terrain of the study location. Nephrotoxins including drugs, exogenous or endogenous toxins, and radiocontrast media contributed next to sepsis as the major cause. One third of the nephrotoxic AKI was drug induced, the major culprit being nonsteroidal anti-inflammatory drugs followed by mannitol, aminoglycoside, rifampicin, cisplatin, and other antimicrobials. Among different studies, nephrotoxic drugs were the precipitating agent in 1.5% to 13.4% of AKI compared with 14.8% in our study.[1],[2],[18],[20] It has been shown that the odds of developing AKI are 53% greater with each nephrotoxin administered, and the risk gets compounded with each additional agent added.[10],[27] Snake envenomation as a cause of AKI was observed in 4.2% of the cohort, with about three fourth of them presenting with Stage 3 AKI, mostly related to late referral or to use of local folk remedies instead of seeking health care. Tropical infections including malaria, leptospirosis, scrub typhus, and dengue contributed to 5.9% of cases, which was similar to that reported by Eswarappa et al.[23] (6.4%) and Umesh et al.[2] (7.6%), whereas tropical infections were the most common etiology in the studies by Vikrant et al.[18] and Bhadade et al.[19] In the study by Prakash et al.,[1] malaria contributed to 17% of cases, while they did not observe a single case of leptospiral AKI over 26 years. More than half of obstetrical causes were related to pre-eclampsia–eclampsia followed by puerperal sepsis and obstetric hemorrhage. However, puerperal sepsis was contributing most to obstetrical AKI in few studies.[2],[18] Acute pancreatitis contributed to about 5% of cases in our study. AKI in acute pancreatitis occurs due to increased vascular permeability, inflammation, intense renal vasoconstriction, abdominal compartment syndrome, thrombotic microangiopathy, and rhabdomyolysis, and is a poor prognostic factor.[28]

In our current study, 26.3% of patients needed RRT, which was preferably provided as intermittent hemodialysis in the majority. Few studies reported similar RRT rates, whereas few others have reported rates as high as 72% to 80%.[1],[2],[18],[19],[29] At 90 days, 9.2% of the cohort were lost to follow-up. Eighteen (5.5%) AKI patients without baseline CKD developed de novo CKD at 90 days. Eswarappa et al.[23] reported CKD as an outcome in 2.4% of patients. Lai et al.[30] in his study on nondialysis requiring AKI survivors of surgical intensive care unit patients observed CKD Stage 3 and above at 90 days in 38.5% of patients, which was quite high. In a study of U.S. veterans, Amdur et al.[31] observed that 20% of patients with acute tubular necrosis progressed to CKD Stage 4 within a period of 20 months. Heung et al.,[32] in his analysis of Veterans Health Administration data, showed that 18.2% AKI patients had CKD Stage 3 or higher at 1 year. Experimental models have shown maladaptive repair, disordered regeneration, or both, due to renin–angiotensin activation, tubular G2/M arrest, inflammation, epigenetic changes, and mitochondrial dysfunction among others, culminate in vascular dropout, glomerulosclerosis, and interstitial fibrosis with tubular atrophy, each of which contributes to progressive renal dysfunction by perpetuating injury and hampering repair.[8],[33] Different drivers of nephron damage have a differential incidence and rate of progression, where the relative mix alters according to time after injury but can operate simultaneously. In clinical context, AKI progresses to CKD through at least two trajectories, either non-recovering AKI progressing to CKD, which is well recognized or after an “apparent” recovery following AKI, the trajectory of normal renal function decline is hastened, which is being increasingly appreciated.[15] In our study, we have observed only the first pathway of non-recovering AKI progressing to CKD. Another problem with apparent “complete” recovery is that, factors such as muscle mass loss, changes in volume of distribution, and hyperfiltration may confound with creatinine used as surrogate for renal recovery.[7],[10] There is a need for better biomarkers to identify ongoing renal injury, which may help in risk stratifying patients for intervention.[10],[33]

Acute kidney disease (AKD), a relatively newer concept was introduced in KDIGO 2012 AKI guidelines to identify patients with kidney structure and/or function abnormalities that do not meet the criteria for AKI or CKD but need medical attention to reverse renal damage to prevent adverse outcomes.[34],[35] KDIGO defined AKD as either AKI or new or previously unrecognized decrease in glomerular filtration rate or increase in creatinine of less than 3 months duration. Both AKI and AKD without AKI can be superimposed on CKD.[34] The 16th Acute Dialysis Quality Initiative (ADQI) workgroup identified AKD as a vulnerable transition period for patients who have suffered AKI wherein critical interventions might be initiated to alter the natural history of kidney disease.[10] The National Kidney Foundation – Kidney Disease Outcomes Quality Initiative (NKF-KDOQI) and the Canadian Society of Nephrology in their commentaries on AKD concept cautioned against the confusion created by the introduction of new terminology and the risk of overlooking other nephrology syndromes when evaluating patients first presenting with kidney disease and mislabeling unique pathologies under the umbrella term of AKD.[34] Although the concept of AKD can be used in epidemiological research, important knowledge gaps need to be addressed before adoption into clinical practice, as AKD has not been systematically studied.[10],[34]

We observed 90-day mortality rate in 39.7% of the study population, of which 61% expired during the hospital stay. Indian studies from different centers have reported mortality rates varying between 8.7% and 90%.[18],[21],[23]

The epidemiologic change over time can be discerned by comparing our study results with the 10-year data of Jayakumar et al.[20] conducted at a tertiary care center catering to the same population as ours. The mean age was a decade less compared to our study. Hospital-acquired AKI saw a drastic increase from 7.9% to 35.2%, perhaps as a sequel of advances in medicine capable of providing advanced and prolonged life support, among others.[17] Although medical causes were contributing the most, acute diarrheal disease was the most common etiology in about 28.6% of patients compared with only 5% in the present study, which might be related to better personal and public health care measures. Surgical causes have increased from 3.4% to 22.1% owing to the progress made in the field resulting in more complicated cases being operated on. Sepsis contributed to only 8.8% in the previous study, whereas in ours, it was the major etiology in over half of the cases. The contribution of nephrotoxic drugs was similar to our study. Among the ingested toxins, copper sulfate was the most common in yesteryears, whereas paraquat, a mitochondrial poison with grave prognosis was predominant in our study (5.9%). Myoglobinuric AKI, a negligible entity in the previous study (0.62%), was contributing to 5.9% in the present study, which could be attributed to improved diagnostics. RRT requirement was about 2.5 times more in the previous study compared with ours. Mortality in the past cohort was only half of that observed in our study, which might be related to younger age, exclusion of patients with comorbidities, and majority being community-acquired AKI with an identifiable cause.[20]

On analyzing the risk factors associated with 90-day outcomes, advanced AKI stage, presence of baseline CKD, and need for RRT were associated with de novo CKD or progression. For the combined outcome of de novo CKD or progression or mortality, advanced age, SOFA ≥9, hypoalbuminemia, baseline CKD, and RRT need were the significant risk factors identified. Chawla et al.,[36] in his study of 5,351 U.S. war veterans who had AKI without CKD, showed that advanced age, hypoalbuminemia, diabetes mellitus, and severity of AKI by RIFLE (Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease) score were predictive of adverse renal outcomes, and RRT need was associated with over 500-fold increased risk of CKD progression. In the study by Lo et al.,[37] in a community-based cohort of more than 5.5 lakh adults, an episode of dialysis requiring ARF increased the risk of developing Stage 4 or 5 CKD by 28 times, and the mortality risk was twice as compared with patients not requiring dialysis. They also observed that ESRD did not develop in patients with a baseline eGFR of 45 mL/min or more over an 8-year follow-up unless ARF requiring dialysis supervened. Ishani et al.,[38] in their study of elderly Medicare beneficiaries, showed that the ESRD risk was 13 times more in patients who had an AKI compared with non-AKI patients and that the risk increased to 41 times if they had baseline CKD. In a Canadian study by Wald et al.,[39] the risk of chronic dialysis was almost three times in patients with dialysis requiring AKI compared with non-AKI patients; however, the mortality risk was similar between the two groups. Thakar et al.[40] showed that recurrent AKI was independently associated with a cumulative risk of developing advanced-stage CKD in their study of 4,082 diabetics over a 9-year period. Recurrent AKI, though significantly associated with the primary outcome of our study on univariate analysis, did not reach statistical significance on multivariate analysis. In Heung et al.'s[32] study, the timing of AKI recovery was found to predict the risk of developing CKD Stage 3 and above, even for Stage 1 AKI. In a systematic review and meta-analysis of 13 cohort studies, Coca et al.[41] showed that compared with non-AKI patients, AKI patients had 8.8 times the risk for ensuing CKD, thrice the risk for ESRD, and twice the risk for mortality. Most published studies on AKI outcomes suffer from methodological difficulties including retrospective study design, varying definitions, lack of comparator group, code creep, and ascertainment bias.[8],[42] These issues are likely to be addressed by the Assessment, Serial Evaluation, and Subsequent Sequelae of Acute Kidney Injury (ASSESS-AKI), a prospective study to characterize the short-term and long-term outcomes of AKI, including development and progression of CKD, cardiovascular outcomes, mortality and other patient-centered outcomes compared with non-AKI patients to evaluate the utility of biomarkers in predicting progression and risk stratification of AKI patients.[42]

Despite burgeoning evidence accumulating on poor long-term outcomes of AKI, barriers and knowledge gap exist about interventions to improve outcomes.[16] The strategies include avoiding preventable factors pre-AKI, mitigating the severity during AKI, and post-AKI care in survivors [Table 6].[3] AKI survivors are a high-risk population, but unfortunately the care provided during AKI does not extend to the follow-up period, which is amenable to interventions to forestall the development of CKD and other adverse consequences.[10],[16] Even in developed countries, the follow-up care is lacking.[9],[16] Documentation of the AKI episode in the patient's record to alert future caregivers, patient/primary care physician education on AKI and its consequences, post-AKI risk stratification, improved processes of care including regular monitoring of blood pressure, glycemic control, proteinuria and renal function, and medication reconciliation are strategies to improve the quality of outcomes in AKI survivors as echoed in the consensus statements of the 18th ADQI workgroup.[3],[6],[9],[10],[16],[36] The KDIGO 2012 AKI guidelines endorse this view by advising to evaluate AKI patients at 3 months, and even if CKD is not detected, these individuals are to be considered at risk for CKD and receive appropriate care. Novel strategies such as nephrology specialty ambulatory clinics are being studied in developed countries.[9] Two randomized control trials, FUSION and AFTER AKI trials, are underway to assess the impact of specialized nephrology follow-up and care bundles on major adverse kidney events.[9]
Table 6: Strategies to prevent the development/progression of chronic kidney disease after acute kidney injury

Click here to view


Our study did have few limitations, including retrospective study design, single-center study, small sample size, and being a tertiary care center, and a study population that may not be representative of the general population.


  Conclusion Top


The present study has thrown light on the epidemiological differences compared with other studies and across time periods in the same population. Sepsis leads the etiology list, necessitating attention to prevention, early recognition, and aggressive management of the same. In the current study, a significant proportion had preventable precipitating events. The severity of AKI, baseline CKD status, and the need for RRT were found to predict the development or progression of CKD in our study. Longer follow-up of “apparently” recovered patients is needed to better characterize the impact of AKI. Knowledge of epidemiology and outcomes is essential to frame policies to overcome the barriers and care gaps to improve outcomes.

Acknowledgements

We would like to acknowledge Dr. Deepak Balakumar, Dr. Archana Chiniwalar, and Dr. Subashri Mohan for helping us with data collection.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Prakash J, Singh TB, Ghosh B, Malhotra V, Rathore SS, Vohra R, et al. Changing epidemiology of community-acquired acute kidney injury in developing countries: Analysis of 2405 cases in 26 years from eastern India. Clin Kidney J 2013;6:150-5.  Back to cited text no. 1
    
2.
Umesh L, Shivaprasad SM, Niranjan MR, Leelavathi V, Sreedhara CG, Rajiv EN. Acute kidney injury: Experience from a state run tertiary care centre in southern India. Int J Med Res Health Sci 2016;5:83-7.  Back to cited text no. 2
    
3.
Kashani K, Macedo E, Burdmann EA, Hooi LS, Khullar D, Bagga A, et al. Acute kidney injury risk assessment: Differences and similarities between resource- limited and resource- rich countries. Kidney Int Rep 2017;2:519-29.  Back to cited text no. 3
    
4.
Cerdá J, Bagga A, Kher V, Chakravarthi RM. The contrasting characteristics of acute kidney injury in developed and developing countries. Nat Clin Pract Nephrol 2008;4:138-53.  Back to cited text no. 4
    
5.
Priyamvada PS, Jayasurya R, Shankar V, Parameswaran S. Epidemiology and outcomes of acute kidney injury in critically ill: Experience from a tertiary care center. Indian J Nephrol 2018;28:413-20.  Back to cited text no. 5
[PUBMED]  [Full text]  
6.
Mehta R, Bagga A, Patibandla R, Chakravarthi R. Detection and management of AKI in the developing world: The 18th Acute Disease Quality Initiative (ADQI) international consensus conference. Kidney Int Rep 2017;2:515–8.  Back to cited text no. 6
    
7.
Moore PK, Hsu RK, Liu KD. Management of acute kidney injury: Core curriculum 2018. Am J Kidney Dis 2018;72:136-48.  Back to cited text no. 7
    
8.
Chawla LS, Eggers PW, Star RA, Kimmel PL. Acute kidney injury and chronic kidney disease as interconnected syndromes. N Engl J Med 2014;371:58-66.  Back to cited text no. 8
    
9.
James MT, Bhatt M, Pannu N, Tonelli M. Long-term outcomes of acute kidney injury and strategies for improved care. Nat Rev Nephrol 2020;16:193-205.  Back to cited text no. 9
    
10.
Chawla LS, Bellomo R, Bihorac A, Goldstein SL, Siew ED, Bagshaw SM, et al. Acute kidney disease and renal recovery: Consensus report of the Acute Disease Quality Initiative (ADQI) 16 Workgroup. Nat Rev Nephrol 2017;13:241-57.  Back to cited text no. 10
    
11.
Bucaloiu ID, Kirchner HL, Norfolk ER, Hartle JE, Perkins RM. Increased risk of death and de novo CKD following reversible AKI. Kidney Int 2012;81:477-85.  Back to cited text no. 11
    
12.
Hsu CY, Hsu RK, Yang J, Ordonez JD, Zheng S, Go AS. Elevated BP after AKI. J Am Soc Nephrol 2016;27:914-23.  Back to cited text no. 12
    
13.
Odutayo A, Wong CX, Farkouh M, Altman DG, Hopewell S, Emdin CA, et al. AKI and long-term risk for cardiovascular events and mortality. J Am Soc Nephrol 2017;28:377-87.  Back to cited text no. 13
    
14.
Parr SK, Siew ED. Delayed consequences of AKI. Adv Chronic Kidney Dis 2016;23:186-94.  Back to cited text no. 14
    
15.
Sawhney S, Marks A, Fluck N, Levin A, McLernon D, Prescott G, et al. Post-discharge kidney function is associated with subsequent ten-year renal progression risk among survivors of acute kidney injury. Kidney Int 2017;92:440-52.  Back to cited text no. 15
    
16.
Silver SA, Adu D, Agarwal S, Gupta KL, Lewington AJP, Pannu N, et al. Strategies to enhance rehabilitation after acute kidney injury in the developing world. Kidney Int Rep 2017;2:579-93.  Back to cited text no. 16
    
17.
Bagshaw SM. Short- and long-term survival after acute kidney injury. Nephrol Dial Transplant 2008;23:2126-8.  Back to cited text no. 17
    
18.
Vikrant S, Gupta D, Singh M. Epidemiology and outcome of acute kidney injury from a tertiary care hospital in India. Saudi J Kidney Dis Transpl 2018;29:956-66.  Back to cited text no. 18
[PUBMED]  [Full text]  
19.
Bhadade R, De'Souza R, Harde MJ, Mehta KS, Bhargava P. A prospective study of acute kidney injury according to KDIGO definition and its mortality predictors. J Assoc Physicians India 2016;64:22-8.  Back to cited text no. 19
    
20.
Jayakumar M, Prabahar MR, Fernando EM, Manorajan R, Venkatraman R, Balaraman V. Epidemiologic trend changes in acute renal failure--A tertiary center experience from South India. Ren Fail 2006;28:405-10.  Back to cited text no. 20
    
21.
Sural S, Sharma RK, Singhal MK, Kher V, Gupta A, Arora P, et al. Acute renal failure in an Intensive Care Unit in India – Prognostic factors and outcome. J Nephrol 1999;12:390-4.  Back to cited text no. 21
    
22.
Bagshaw SM, Uchino S, Bellomo R, Morimatsu H, Morgera S, Schetz M, et al. Septic acute kidney injury in critically ill patients: Clinical characteristics and outcomes. Clin J Am Soc Nephrol 2007;2:431-9.  Back to cited text no. 22
    
23.
Eswarappa M, Gireesh MS, Ravi V, Kumar D, Dev G. Spectrum of acute kidney injury in critically ill patients: A single center study from south India. Indian J Nephrol 2014;24:280-5.  Back to cited text no. 23
[PUBMED]  [Full text]  
24.
Kim J, Kil IS, Seok YM, Yang ES, Kim DK, Lim DG, et al. Orchiectomy attenuates post-ischemic oxidative stress and ischemia/reperfusion injury in mice. A role for manganese superoxide dismutase. J Biol Chem 2006;281:20349–56.  Back to cited text no. 24
    
25.
Gurjar M, Baronia AK, Azim A, Prasad N, Jain S, Singh RK, et al. Septic acute kidney injury in critically ill Indian patients. Indian J Crit Care Med 2013;17:49-52.  Back to cited text no. 25
[PUBMED]  [Full text]  
26.
Avasthi G, Sandhu JS, Mohindra K. Acute renal failure in medical and surgical Intensive Care Units – A one year prospective study. Ren Fail 2003;25:105-13.  Back to cited text no. 26
    
27.
Cartin-Ceba R, Kashiouris M, Plataki M, Kor DJ, Gajic O, Casey ET. Risk factors for development of acute kidney injury in critically ill patients: A systematic review and meta-analysis of observational studies. Crit Care Res Pract 2012;2012:691013.  Back to cited text no. 27
    
28.
Nassar TI, Qunibi WY. AKI associated with acute pancreatitis. Clin J Am Soc Nephrol 2019;14:1106–15.  Back to cited text no. 28
    
29.
Mahajan S, Tiwari S, Bharani R, Bhowmik D, Ravi S, Agarwal SK, et al. Spectrum of acute renal failure and factors predicting its outcome in an intensive care unit in India. Ren Fail 2006;28:119-24.  Back to cited text no. 29
    
30.
Lai CF, Wu VC, Huang TM, Yeh YC, Wang KC, Han YY, et al. Kidney function decline after a non-dialysis-requiring acute kidney injury is associated with higher long-term mortality in critically ill survivors. Crit Care 2012;16:R123.  Back to cited text no. 30
    
31.
Amdur RL, Chawla LS, Amodeo S, Kimmel PL, Palant CE. Outcomes following diagnosis of acute renal failure in U.S. veterans: Focus on acute tubular necrosis. Kidney Int 2009;76:1089-97.  Back to cited text no. 31
    
32.
Heung M, Steffick DE, Zivin K, Gillespie BW, Banerjee T, Hsu CY, et al. Acute kidney injury recovery pattern and subsequent risk of CKD: An analysis of veterans health administration data. Am J Kidney Dis 2016;67:742-52.  Back to cited text no. 32
    
33.
Chou YH, Huang TM, Chu TS. Novel insights into acute kidney injury-chronic kidney disease continuum and the role of renin-angiotensin system. J Formos Med Assoc 2017;116:652-9.  Back to cited text no. 33
    
34.
Barry R, James MT. Guidelines for classification of acute kidney diseases and disorders. Nephron 2015;131:221-6.  Back to cited text no. 34
    
35.
James MT, Levey AS, Tonelli M, Tan Z, Barry R, Pannu N, et al. Incidence and prognosis of acute kidney diseases and disorders using an integrated approach to laboratory measurements in a universal health care system. JAMA Netw Open 2019;2:e191795.  Back to cited text no. 35
    
36.
Chawla LS, Amdur RL, Amodeo S, Kimmel PL, Palant CE. The severity of acute kidney injury predicts progression to chronic kidney disease. Kidney Int 2011;79:1361-9.  Back to cited text no. 36
    
37.
Lo LJ, Go AS, Chertow GM, McCulloch CE, Fan D, Ordoñez JD, et al. Dialysis-requiring acute renal failure increases the risk of progressive chronic kidney disease. Kidney Int 2009;76:893-9.  Back to cited text no. 37
    
38.
Ishani A, Xue JL, Himmelfarb J, Eggers PW, Kimmel PL, Molitoris BA, et al. Acute kidney injury increases risk of ESRD among elderly. J Am Soc Nephrol 2009;20:223-8.  Back to cited text no. 38
    
39.
Wald R, Quinn RR, Luo J, Li P, Scales DC, Mamdani MM, et al. Chronic dialysis and death among survivors of acute kidney injury requiring dialysis. JAMA 2009;302:1179-85.  Back to cited text no. 39
    
40.
Thakar CV, Christianson A, Himmelfarb J, Leonard AC. Acute kidney injury episodes and chronic kidney disease risk in diabetes mellitus. Clin J Am Soc Nephrol 2011;6:2567-72.  Back to cited text no. 40
    
41.
Coca SG, Singanamala S, Parikh CR. Chronic kidney disease after acute kidney injury: A systematic review and meta-analysis. Kidney Int 2012;81:442-8.  Back to cited text no. 41
    
42.
Go AS, Parikh CR, Ikizler TA, Coca S, Siew ED, Chinchilli VM, et al. The assessment, serial evaluation, and subsequent sequelae of acute kidney injury (ASSESS-AKI) study: Design and methods. BMC Nephrol 2010;11:22.  Back to cited text no. 42
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]



 

Top
Print this article  Email this article
 

    

Indian Journal of Nephrology
Published by Wolters Kluwer - Medknow
Online since 20th Sept '07