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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2018  |  Volume : 29  |  Issue : 4  |  Page : 946-955
Clinical spectrum of hospital acquired acute kidney injury: A prospective study from Central India

Department of Nephrology, Sri Aurobindo Medical College and Postgraduate Institute, Indore, India

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Date of Submission28-Aug-2017
Date of Decision25-Oct-2017
Date of Acceptance06-Nov-2017
Date of Web Publication28-Aug-2018


Acute kidney injury (AKI) is a common disorder worldwide that is associated with severe morbidity, mortality and cost. If managed adequately and in a timely manner, the majority of these cases are preventable, treatable and often reversible with simple measures. We conducted a two years prospective study of patients admitted to medical and surgical units of a tertiary care center in Central India to identify the causes of Hospital Acquired AKI (HAAKI) and its impact on patient outcomes. HAAKI occurred in 215 of 9,800 patients (2.1%). Sepsis (75; 34.88%), volume depletion and hypo perfusion (62; 28.83%), drugs (50; 23.25%), multifactorial (18; 8.37%) and radiocontrast agents (9; 4.2%) were the causes of HAAKI. Thirty-nine percent of patients had complete recovery and 9.3% had partial recovery of renal function. The overall inhospital mortality due to HAAKI was 41.86%. On multivariate analysis, oliguria, multi-organ failure, metabolic acidosis, anemia, and sepsis showed significant association with in-hospital mortality. The mortality and morbidity associated with HAAKI mandates the need for active measures to decrease its incidence. Knowledge of incidence and risk factors is crucial because it drives local and international efforts on detection and treatment. To the best of our knowledge, no epidemiological study has been conducted or published on HAAKI from the Central India.

How to cite this article:
Goswami S, Pahwa N, Vohra R, Raju BM. Clinical spectrum of hospital acquired acute kidney injury: A prospective study from Central India. Saudi J Kidney Dis Transpl 2018;29:946-55

How to cite this URL:
Goswami S, Pahwa N, Vohra R, Raju BM. Clinical spectrum of hospital acquired acute kidney injury: A prospective study from Central India. Saudi J Kidney Dis Transpl [serial online] 2018 [cited 2020 May 26];29:946-55. Available from: http://www.sjkdt.org/text.asp?2018/29/4/946/239650

   Introduction Top

Acute Kidney Injury (AKI) is a syndrome characterized by rapid decline in glomerular filtration rate and retention of nitrogenous waste products such as blood urea nitrogen and creatinine. The incidence rate of AKI around the world is not well known.[1],[2],[3] Studies conducted in the United States have shown rising incidence of AKI with an annual increase of 11%.[4],[5] Ali et al reported a high incidence of 1811 cases of AKI per million population during 2003.[6] This disparity in reported incidence rates as well as the increasing frequency of occurrence of the condition, raise concerns as to the real magnitude of the problem. The epidemiology of AKI in developing countries differs from that of the developed world in many important ways.[7],[8],[9],[10],[11],[12],[13],[14],[15] Whereas in developed regions elderly patients predominate,[4],[5] in developing countries it is more common in young[13],[16],[17] and children[18],[19] with volume responsive prerenal mechanisms being more common.[20],[21],[22],[23] The difficulties of defining the incidence of AKI are especially notable when one searches for data on developing countries,[8],[12],[14],[15],[24],[25],[26] the place of residence of more than half of the world's population. No nationwide collection systems are available and data from isolated centers are not based on the current AKI definition. From South Africa, Seedat and Nathoo[24],[27] reported an incidence of 20 cases per year per million population; in Brazil, Noronha et al[9] reported an incidence of 7.9 cases per 1000 hospital admissions and in North India, Jha and Chugh[26] reported a yearly incidence of 6.4/1000 admissions. New definitions of AKI[28],[29],[30] make it necessary to again revisit this issue with unified criteria.

AKI in hospitalized patients is associated with high rates of morbidity, mortality and consumption of health-care resources. Occurrence of renal failure in patients hospitalized for nonrenal problems complicates the hospital course with profound impact on patient outcome. An understanding of the etiology of HAAKI is important to establish its overall burden, risk factors and devising potential preventive strategies. In developing countries, the incidence varies seasonally; incidence peaks cause critical shortages in medical and nursing personnel. In addition, in developing countries, lack of systematic evaluation of the role of falciparum malaria, higher incidence of sepsis and lack of trained persons to deal with intensive care, hampers efforts to prevent AKI. In developing countries, the costs of renal replacement therapies are also prohibitively high.[16],[31],[32]

Prevention is often the only realistic way to decrease its severe impact on morbidity and mortality. Although inexpensive, such interventions will not be carried out until the problem reaches political visibility and achieves institutional and organizational support.[15] Limited data are available on the etiology and outcome of AKI in Indian population especially from Central India. The objectives of this prospective study were to identify the causes and assess the outcomes of HAAKI.

   Methods Top

We conducted a prospective study of all patients who were admitted in Sri Aurobindo Medical College and Postgraduate Institute, Indore from January 2014 to December 2015. The facility is a tertiary care referral center in Central India catering to the states of Madhya Pradesh, Uttar Pradesh, Rajasthan and Gujarat. Written informed consent was obtained from all the patients with HAAKI. The patients were subjected to detailed history and thorough clinical examination. Particulars such as name, age, sex, address, and telephone number were noted in a prestructured proforma. Details regarding past medical illness which can be a risk factor for AKI were obtained. Detailed history regarding drugs and other ayurvedic or native preparations were obtained. Immunological assays, such as hepatitis B surface antigen, anti-hepatitis C virus, anti-nuclear antibody, anti-double-stranded DNA, anti-neutrophil cyto-plasmic antibody, anti-glomerular basement membrane antibody were performed in selected cases. AKI was defined as per Kidney Disease: Improving Global Outcomes (KDIGO) guidelines.[30]

Using the KDIGO criteria, AKI was staged as follows:

Stage 1: 1.5-1.9 times baseline odds ratio (OR) ≥0.3 mg/dL (≥26.5 pmol/L) increase in the serum creatinine, OR urine output <0.5 mL/kg per hour for 6–12 h.

Stage 2: 2.0–2.9 times baseline increase in the serum creatinine OR urine output <0.5 mL/kg per hour for ≥12 h.

Stage 3: 3.0 times baseline increase in the serum creatinine OR increase in serum creatinine to ≥4.0 mg/dL (≥353.6 pmol/L) or urine output of <0.3 mL/kg/h for ≥24 h, or anuria for ≥12 h or the initiation of renal replacement therapy OR in patients <18 years, decrease in estimated GFR to <35 mL/min/1.73 m2.

Patients admitted with community acquired AKI, chronic kidney disease, pediatric patients, and obstetrics patients were excluded from the study.

Decreased renal perfusion was identified by one or more of the following:

  1. Decrease in blood pressure to less than 90/60 mm Hg
  2. Evidence of congestive heart failure
  3. Signs of volume depletion
  4. Improvement with the restoration of blood flow.

Drug was identified as the cause of HAAKI when there was a temporal relationship to the administration of the drug in the absence of other causative mechanisms.

Sepsis was defined when two or more of the following were present, as a result of proven or suspected infection

  1. Temperature >38°C or <36°C
  2. Heart rate >100/min
  3. Respiratory rate >24 /min
  4. White blood count >12,000/μL, <4000/ μL or >10% band forms.

Radiographic contrast nephropathy was defined as either a 25% increase in serum creatinine or an absolute increase in serum creatinine of 0.5 mg/dL within 24 hours of the procedure.[33]

Obstruction was attributed to cause HAAKI if there was radiological evidence and improvement in renal function after relief of obstruction.

Patients were followed-up with daily creatinine values till the date of discharge and then every week in the outpatient department. KDIGO stage was assigned as per elevated creatinine value or decrease in urine output, which ever was more severe. We classified patients according to the maximum stage (stage 1, stage 2, or stage 3) reached during their hospital stay. Outcomes were classified as complete recovery of renal function, partial recovery, dialysis dependant, and in-hospital mortality. Complete recovery was defined as decrease in the serum creatinine to <1.2 mg/dL along with improvement in urine output during the hospital stay. Partial recovery of renal function was defined as improvement in renal function but serum creatinine level remaining >1.2 mg/dL.

Statistical study

The data for the study were collected in predesigned format. The data were edited for completeness and consistency. A descriptive analysis was performed; continuous data were presented as mean and standard deviation and categorical data as a percentage. On univariate analysis, proportions were compared between groups using a Pearson chi-squared test. Factors which had significant association with mortality on univariate analysis were included in a multivariate logistic regression analysis. P <0.05 was considered significant. All statistical analysis was performed with the Statistical Package for Social Sciences (SPSS) software version 20.0 (SPSS Inc., Chicago, IL, USA).

   Results Top

During the study period from January 2014 to December 2015, 9800 patients were admitted to our medical and surgical services. 2.1% of patients experienced renal injury during the hospital stay. The mean age of the population was 44 ± 17.3 years. A total of 128 patients (59.5%) were male while 87 patients (40.5%) were female.

Just under half of the patients (49, 45.4%) had medical comorbidities. Of the comorbidities, hypertension was the commonest (28, 57.1%), with diabetes and ischemic heart disease present in 27 (55.1%) and 17 patients (34.7%), respectively.

The most common cause of HAAKI was sepsis in 75 patients (34.88%) as depicted in [Figure 1]. The most common causes of sepsis were pneumonia in 32 patients (42.7%), urinary tract infection in 23 patients (30.66%), and postoperative wound infection in 15 patients (20%). Volume depletion and hypo-perfusion was the second most common cause seen in 62 patients (28.83%). Volume depletion occurred due to blood or fluid loss and inadequate fluid resuscitation in 41 patients (66.12%). Congestive heart failure in eight patients, decompensated liver disease in eight patients and third space loss in five patients were the other causes of decreased renal perfusion. Other common causes of HAAKI were drug-induced in 50 patients (23.25%), contrast induced nephropathy in nine patients (4.2%) and multi factorial in 18 patients (8.34%) [Table 1].
Figure 1: Causes of hospital acquired acute kidney injury.

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Table 1: Etiology and management of hospital-acquired acute kidney injury.

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Drugs were the second most common precipitating agents [Table 2]. Of the 50 episodes caused by drugs, 20 were due to non-steroidal anti-inflammatory agents (NSAID), 10 due to aminoglycosides, eight due to chemotherapy drugs, four due to mannitol and amphotericin B and, co-trimoxazole and acyclovir accounted for one episode each. In five episodes, multiple nephrotoxic drugs (2 or more) were identified.
Table 2: Drugs causing hospital acquired acute kidney injury.

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Radiographic contrast media was responsible for nine episodes (4.1%). Coronary artery angiogram and angioplasty was the most common cause (six episodes). Computerized tomography with contrast was the cause in other three patients.

Eighteen episodes (8.34%) occurred due to multiple factors, 10 patients had sepsis with nephrotoxic drugs and eight patients had renal hypo-perfusion, sepsis, and contrast-induced nephropathy. Patients with HAAKI due to multiple factors developed more severe renal injury and needed renal replacement therapy more often than other patients. Out of 18 patients, all reached KDIGO stage III, 16 patients (88.8%) required renal replacement therapy and 14 patients (77.78%) died.

The mean duration of hospital stay was 30.8 ± 19.3 days. One hundred and fifteen patients (53%) required intensive care; 80 patients (37%) needed mechanical ventilation during their hospital stay.

Dialysis was required in 125 patients (58%). Out of these 125, 50 patients (40%) underwent conventional hemodialysis, 71 patients (56.8%) underwent sustained low efficiency daily dialysis (SLEDD) while four patients (3.2%) underwent went peritoneal dialysis. The vascular access used was femoral venous catheter in 12 patients (9.99%) and internal jugular access in 109 patients (90%).

All patients were classified as per KDIGO and depicted in [Table 3]; 30 patients (13.85%) were in stage 1, 35 patients (16.27%) were in stage 2 and 150 patients (69.76%) were in stage 3. The outcome was good in KDIGO stages 1 and 2. There was complete recovery in 28 patients (93.33%) of stage 1 and 24 patients (68.57%) of stage 2; highest mortality was seen in stage 3. Eighty-one patients (54%) out of 150 died.
Table 3: KDIGO classification and its association with outcome.

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Only 84 patients (39 %) had complete recovery of renal function, 20 patients (9.3%) had partial recovery of renal function and 21 (9.76%) were discharged on long-term renal replacement therapy. The overall in-hospital mortality among patients with HAAKI was in 90 patients (41.86%) as depicted in [Figure 2]. In comparison with survivors, factors associated with increased in-hospital mortality (P <0.05) are depicted in [Table 4].
Figure 2: Outcome of hospital acquired acute kidney injury.

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Table 4: Factors associated with in-hospital mortality in HAAKI.

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Forty-four patients were oliguric at presentation. On univariate analysis, oliguria, metabolic acidosis, comorbid conditions, male sex, anemia, need for renal replacement therapy, and sepsis related kidney injury had significant association with in-hospital mortality. On multivariate analysis, oliguria, metabolic acidosis, anemia, multi-organ failure, and sepsis showed significant association with in-hospital mortality.

   Discussion Top

The aim of this paper was to study the clinical profile and outcome of HAAKI from central India; this is the first data on acute kidney injury from central India. The incidence and etiology of HAAKI varies depending on the definition used, variations in methods of patient accrual and populations analyzed. The incidence varies from 0.6% to 7.2%.[8],[34] KDIGO in 2012 has defined AKI as an absolute increase of serum creatinine of >0.3 mg/dL.[30] The same definition has been used by us to diagnose HAAKI in our study population. Even small increase in serum creatinine by 10 to 24% can produce a relative risk of death of 1.9.[35] Hospitalized patients with acute kidney injury had 14 times higher mortality rate when compared with hospitalized patients without AKI.[36] Pre-existing chronic kidney disease[37] and co-morbid conditions[38] increases the risk of acute renal injury.[38] In our study, 127 patients had co-morbid conditions, diabetes was the most common. The leading cause of HAAKI is dynamically changing in our country from drug-induced[8],[39] to volume depletion[40] to sepsis.

Sepsis was the leading cause of AKI in our study, sepsis associated AKI had the highest in-hospital mortality. In a hospital-based study,[41] ARF developed in 19% with sepsis, 23% with severe sepsis, and 51% with septic shock, in culture positive individuals. Despite advances in the understanding of the patho-genesis and pathophysiology, the mortality rate of severe sepsis has remained unacceptably high. Occurrence of AKI represents an independent risk factor for in-hospital mortality in these patients.[42] Decreased renal perfusion has remained the most common cause of HAAKI in the Western world.[43],[44] In our study, 62 patients (28.83%) had AKI due to decreased renal perfusion with volume loss being the most common precipitating factor. Volume depletion was seen in 41 patients and most of them were managed conservatively. Odds ratios for development of HAAKI increases by 9.4-fold and 9.2-fold in the presence of the prerenal insults such as volume depletion and congestive heart failure.[45]

Drug induced HAAKI accounts for 18%–29%[34] of the episodes. Fifty patients (23.25%) in our study were due to medications, with NSAIDs being the most common agents. NSAID-induced HAAKI was particularly common in patients with co-morbid conditions (8 of 20, P = NS), and patients on diuretic therapy. Only 10 patients were due to amino-glycosides, probably due to use of alternative antibiotics which are less nephrotoxic. Optimal selection, dosing and monitoring can prevent the occurrence of drug-induced HAAKI. Eighteen patients (8.37%) had multiple etiological factors and the prognosis was poor in this group.[40],[46] The incidence of post-operative renal failure in India is increasing[22] and various studies have established acute renal failure as a poor prognostic factor in these[47] patients.

Coronary angiographic procedures are the most common events resulting in the usually reversible AKI seen with contrast agents. Dialysis is necessary in only a small percentage (0.4%–0.8%) of patients undergoing percutaneous coronary intervention.[48] However, even in those patients who had complete recovery of AKI, increased 5-year mortality has been demonstrated.[49]

The incidence of contrast nephropathy can reach up to 25% in patients with predisposing factors such as chronic kidney disease, volume depletion, multiple myeloma and diabetes mellitus.[50] Peri-procedural hydration, avoiding concomitant use of NSAIDs and diuretics can reduce the incidence of contrast nephropathy.

Oliguria, metabolic acidosis, anemia, multiorgan failure and sepsis were associated with increased mortality in our study as depicted in [Table 4]. Patients who develop oliguric AKI have longer hospital stay and require more frequent dialysis sessions. Oliguria has been established as a bad prognostic indicator in AKI.[51]

The RIFLE criteria have been evaluated in AKI and have displayed a graded association with adverse outcomes.[52],[53]

There is increasing linear trend in mortality with worsening KDIGO stage when compared with other groups with worsening RIFLE class.[54]

Mortality in patients with HAAKI varies from 19%—59%. Mortality of 41.86% in our study was comparable to mortality seen in other studies from India.[39],[40] Even in patients who do not require dialysis, AKI is associated with increased long-term mortality risk, independent of their residual kidney function.[55] Among survivors of AKI at long-term follow-up (1-10 years), approximately 12.5% are dialysis dependent and 19%–31% had chronic kidney disease.[56] A recent study has shown that survivors of HAAKI experience higher odds of early hospital readmission.[57] Transition of care services may be warranted for such patients to prevent readmissions and reduce health-care costs.

Sustained low efficiency dialysis was used in 71 patients and continuous renal replacement therapy (CRRT) was not used in our study group because of financial constrain of our patients. Previous studies have shown that CRRT has an advantage over intermittent HD in that it provides greater hemodynamic stability and greater flexibility in providing paren-teral nutrition.[58] Current evidence however, does not demonstrate a significant advantage of CRRT over SLEDD in terms of mortality or renal recovery.[59]

   Conclusions Top

AKI is an increasingly common and potentially catastrophic complication in hospitalized patients. An understanding of the incidence and consequences of AKI has grown considerably, yet mortality rates remain unacceptably high despite significant advances in the care of the critically ill. In contrast to community acquired AKI which has changing etiological factors and prognosis in India[60] the etiology of HAAKI in India is similar to those reported in other countries and outcomes are comparable. Sepsis has emerged as the leading cause of AKI and in-hospital mortality and needs further attention. With the emerging multi-drug resistant organisms and limited researches in the field of antibiotics, the situation is not encouraging. Drug-induced AKI is still responsible to a substantial number of patients even though it is known since decades. Early nephrology consultation in hospitalized patient can reduce the burden of AKI.[61]

   Disclosure Top

The authors have not received reimbursements, fees, funding, or salary from any organization that may in any way gain or lose financially from the publication of this paper in the past five years.

Conflict of interest: None declared.

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Prakash J, Singh TB, Ghosh B, 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. 60
Balasubramanian G, Al-Aly Z, Moiz A, et al. Early nephrologist involvement in hospital-acquired acute kidney injury: A pilot study. Am J Kidney Dis 2011;57:228-34.  Back to cited text no. 61

Correspondence Address:
Dr. Shraddha Goswami
Department of Nephrology, Sri Aurobindo Medical College and Postgraduate Institute, Indore
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DOI: 10.4103/1319-2442.239650

PMID: 30152434

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


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