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Acute kidney injury in medical ICU-aetiology presentation and outcome.


Acute kidney injuiy (AKI) is a common clinical syndrome in intensive care units (ICUs) and is defined as "an abrupt (within 48 hours) reduction in kidney function that is an absolute increase in serum creatinine [greater than or equal to] 0.3 mg/dL, a percentage increase in serum creatinine of more than 50% (1.5 fold from baseline) or a reduction in urine output (documented oliguria of < 0.5 mL/kg/hr for more than 6 hours]. [1]" Although, acute kidney injuiy can occur as a single organ phenomenon, it is frequently seen in the critical care environment as a part of multiple organ failure syndrome. In this setting, multiple factors must be taken into account when considering precipitating cause and appropriate management. Acute kidney injuiy may complicate up to 5% of hospital admissions and 30% of emergency admissions to ICUs. [2] AKI exerts a negative effect on the course of the disease and its outcome. It is triggered by extremely diverse group of aetiologies and clinicians must understand the aetiologies of acute kidney injuiy to prevent occurrence and to start treatment early.

There have been few systematic studies in our state (Odisha) on the aetiology and clinical profile and changing trends and management on acute kidney injuiy, therefore the study was undertaken with following aims and objectives i.e. aetiology, presentation and outcome of acute kidney injuiy in medical ICU.


After clearance from Institutional Ethics Committee (IEC), we have designed a descriptive study in the medical ICU of SCB Medical College, Cuttack and consecutive 100 patients of age more than 15 years of AKI were included in the study for the period from Sep 2014 to Sep 2016. Informed consent from all patients was obtained.

Patient Selection Criteria

Patients with serum creatinine more than 2 times normal or decrease in glomerular filtration rate (GFR) of > 50% or urine output < 0.5 mg/kg/hr for more than 6 hrs. were taken for the study.

Exclusion Criteria

Patients of chronic renal failure, post renal AKI and patients with past histoiy of diabetes and hypertension were excluded from the study.

In every patient, detailed history and thorough clinical examination was done with special reference to history of fever, diarrhoea and snake bite. The following investigations were done: complete haemogram, erythrocyte sedimentation rate (ESR), malaria parasite (MP)-slide detection and immunochromatographic test (ICT) and IgM antibody for leptospira in case of fever. Renal function test (serum urea and creatinine) was done at the time of admission and subsequently daily. Liver function test and coagulation profile (bleeding time, clotting time, prothrombin time, activated partial thromboplastin time, serum FDP) were done in eveiy patient. Ultrasound of abdomen and pelvis was to be done in all patients to estimate the kidney size. Renal biopsy was done in selected patients, where there is unexplained acute kidney injuiy.

Glomerular filtration rate (GFR) was calculated at the time of admission and subsequently daily by using Cockroft-Gault equation:

Cr CI (ml/min) = {[(140-age) x weight(kg)/72 xserum Cr (mg/dl)]} (multiply factor 0.85 in case of female)


In our study, 66 patients were male and 34 patients were female. Majority of patients belonged to the age group of 30-40 yrs., i.e. 44 patients.

In our study, majority of patients presented with anaemia (74%) followed by fever (51%) and other symptoms such as hypotension (19%), jaundice (20%), acute gastroenteritis (21%), history of snake bite (19%), cerebral symptoms (15%), oedema (26%), haematuria (2%) and ARDS (4%).

In our study, out of 100 patients of acute kidney injuiy, 41 patients were of malaria, 21 patients were of acute gastroenteritis, 19 patients were of vasculotoxic snake bite, 10 patients were of unknown aetiology, sepsis patients were 4 and leptospirosis patients were 5 in number.

Out of 41 patients of malaria causing AKI 27 patients were positive for only Plasmodium falciparum, while 14 patients were found to be positive for both Plasmodium falciparum and vivax (mixed infection).

Out of 100 patients, 65 patients had oliguric acute kidney injury, while 35 patients had non-oliguric kidney injury.

Out of 65 patients of oliguric acute kidney injury 18 patients were due to malaria, 16 patients were due to acute gastroenteritis, 13 patients were due to vasculotoxic snake bite, 10 patients were due to unknown aetiology and 4 patients were each due to sepsis and leptospirosis.

Out of 35 patients of non-oliguric acute kidney injuiy 23 patients were due to malaria, 5 patients were due to acute gastroenteritis, 6 and 1 patients were due to vasculotoxic snake bite and leptospirosis respectively.

Maximum no. of patients at the time of admission had GFR between 20-30 mL/min with mean GFR of 23.19 mL/min.

Out of 100 patients of acute kidney injury; 41 patients were of malaria out of which 13 cases (31.7%) had GFR between 20-30 mL/min, 12 patients (29.2%) had GFR between 40-50 mL/min, 8 patients (19.5%) had between 10 - 20 mL/min, 6 patients (14.6%) had between 40-50

mL/min and 2 patients had GFR < 10 mL/min. Out of 21 patients of acute gastroenteritis, 12 patients (57%) had GFR between 20-30 mL/min and 9 patients (43%) had GFR between 10-20 mL/min. Out of 19 patients of vasculotoxic snake bite 11 patients (58%) had GFR between 20-30 mL/min, 7 patients (37%) between 10-20 mL/min and 1 patient (5%) between 30-40 mL/min. Out of 10 patients of unknown aetiology, 5 patients had GFR between 10-20 mL/min and other 5 between 20-30 mL/min. Out of 5 patients of leptospirosis 3 patients had GFR between 30-40 mL/min and one each between 10-20 and < 10 mL/min. All the 4 patients of sepsis had GFR between 10-20 mL/min.

Renal biopsy was done on 10 cases of acute kidney injury, where aetiology of acute kidney injury was uncertain. Out of 10 cases 2 cases had rapidly progressive glomerulonephritis, 2 had post infectious glomerulonephritis and 1 case had membranoproliferative glomerulonephritis.

In our study, out of 100 patients of AKI 46 patients needed renal replacement therapy in the form of haemodialysis.

All the patients survived and got discharged.


We have included 100 patients of acute kidney injury admitted to medical ICU in our study; 66 patients were males and 34 patients were females [Table 1]. Majority of patients were in the age group of 30-40 years. Similar findings were observed in the study done by Prakash et al in Patna, 1995 out of 426 patients of ARF, the majority of patients were males in the age group of 30-40 years. [3]

In our study majority of patients presented with anaemia 74%, fever 51% and jaundice 20%. Twenty-one patients (21%) presented with diarrhoea, history of snake bite 19% and 15% presented with cerebral symptoms [Table 2], while in the study by Mehta et al in Mumbai, 2001 on Malaria and ARF, the presenting clinical features were fever in 22 (91.6%) out of 24 patients, altered sensorium in 10 patients (41.6%) and diarrhoea in 3 patients (12.5%). [4] Therefore, the disparity in clinical presentation is due to difference in the aetiology of acute kidney injury.

In our study, out of 100 patients of acute kidney injury, majority of patients were due to malaria (41%) followed by acute gastroenteritis (21%), vasculotoxic snake bite (19%) [Table 3]. In the study done by Prakash et al in Patna 1995, out of 426 patients of acute renal failure the most common cause of AKI was found to be acute gastroenteritis (35.2%) followed by acute glomerulonephritis (10.3%), post abortai sepsis (10.5%) and falciparum malaria (4.2%). [3]

As Odisha is an endemic state for malaria, we found malaria is the commonest cause of AKI in contrary to sepsis in literature. [5] The second common cause of AKI in our study is acute gastroenteritis followed by vasculotoxic snake bite, as vast majority of people residing in rural and forest areas and lots of people are engaged in farming and agricultural activities.

In our study, out of 41 patients of malaria causing AKI 27 (66%) were due to Plasmodium falciparum infection alone, while 14 cases (34%) were due to Plasmodium falciparum and vivax mixed infection [Table 4] and 32 (78%) of them needed haemodialysis. Similar findings were found by Mehta et al in their study on malaria and AKI in 2001, which showed that out of 24 patients 12 patients were Plasmodium falciparum positive and 4 showed mixed infection with both Plasmodium falciparum and vivax. [4] The incidence of acute kidney injury is less in mixed infection (Pf/Pv).

In our study, 65 patients had oliguric AKI and 35 patients had non-oliguric AKI [Table 5]. Malaria was found to be most common cause of non-oliguric AKI, while acute gastroenteritis was found to be most common cause of oliguric AKI. In the study on malaria and AKI in 1998 by Panda et al in Odisha showed that 18% had non-oliguric acute renal failure, while 75% patients had oliguric renal failure. [6]

In our study, the mean GFR at the time of admission was 23.19 mL/min. 41% of patients had their GFR within 20-30 mL/min followed by 34% of patients within 10-20 mL/min [Table 7],

Renal biopsy was done in 10 cases, where the aetiology of AKI could not be determined after doing all the basic investigations. Out of 10 biopsies 5 showed normal report, 2 cases showed rapidly progressive glomerulonephritis, 2 cases showed post infectious glomerulonephritis and 1 case showed membranoproliferative glomerulonephritis [Table 9].


AKI in the ICU results from multiple factors. The incidence of AKI reported in critically ill patients varies substantially. [7] Therefore, early identification and appropriate majors for the patients at the risk of developing AKI prevents subsequent renal failure and ultimately impact overall ICU morbidity and mortality. Among 100 cases of acute kidney injury, the most common aetiology was Malaria followed by acute gastroenteritis, vasculotoxic snake bite and leptospirosis. As these diseases are preventable by maintaining proper hygiene and vector control, the burden of acute kidney injury can be reduced. Whatever may be the aetiology, prompt diagnosis, specific therapy and proper fluid management and use of dialysis as and when required can reduce mortality and morbidity in patients with acute kidney injury.


[1] Mehta RL, Kellum JA, Shah SV, et al. Acute kidney injuiy network: report of an initiative to improve outcomes in acute kidney injury. Crit Care 2007;11(2):R31.

[2] Waikar SS, Bonventre JV. Acute kidney injury. 1[] edn. Harrison's principles of internal medicine 1799.

[3] Prakash J, Tripathy K, Malhotra V, et al. Acute renal failure in eastern India. Nephrol Dial Transplant 1995;10(11):2009-12.

[4] Mehta KS, Halankar AR, Makwana PD, et al. Severe acute renal failure in malaria. J Postgrad Med 2001;47(1):24-6.

[5] Dennen P, Douglas IS, Anderson R. Acute kidney injury in the intensive care unit: an update and primer for the intensivist. Criti Care Med 2010;38(1):261-75.

[6] Panda SK, Das MC, Meher LK, et al. Risk factors of acute renal failure in severe falciparum malaria. Indian J Nephrol 2003;13:55-8.

[7] Gammelager H, Christiansen CF, Johansen MB, et al. Oneyear mortality among Danish intensive care patients study with acute kidney injury: a cohort study. Crit Care 2012;16(4):R124.

Samarendra Nath Das (1), Pravat Kumar Thatoi (2), S. Sandeep Kumar (3), Ninnai Chandra Sahu (4), Sk. Maheboob Salim (5), Sagar Khadanga (6)

(1) Associate Professor, Department of Medicine, SCB Medical College, Cuttack.

(2) Assistant Professor, Department of Medicine, SCB Medical College, Cuttack.

(3) Postgraduate Student, Department of Medicine, SCB Medical College, Cuttack.

(4) Assistant Professor, Department of Medicine, SCB Medical College, Cuttack.

(5) Assistant Surgeon, SCB Medical College, Cuttack,

(6) Assistant Professor, Department of Medicine, AIIMS, Bhopal.

Financial or Other, Competing Interest: None. Submission 26-07-2017, Peer Review 20-08-2017, Acceptance 26-08-2017, Published 31 -08-2017.

Corresponding Author:

Pravat Kumar Thatoi, Flat-104, Aryabhatta Complex, College Square, Cuttack-753003, Odisha, India.


DOI: 10.14260/jemds/2017/1081
Table 1. Age and Sex (n=100)

Age       Male   Female   Total   Percentage

10-20     8      5        13      13%
20-30     9      11       20      20%
30-40     34     10       44      44%
40-50     12     5        17      17%
50-60     2      2        4       4%
60-70     1      1        2       2%
Total     66     34       100

Table 2. Clinical Presentation (n=100)

Clinical Feature        Number of Patients   Percentage

Anaemia                 74                   74%
Fever                   51                   51%
Hypotension             19                   19%
Jaundice                20                   20%
Acute gastroenteritis   21                   21%
Histoiy of snake bite   19                   19%
Cerebral symptoms       15                   15%
Oedema                  26                   26%
Haematuria              2                    2%
ARDS                    4                    4%

Table 3. Aetiology (n=100)

                          No. of Cases   Percentage

Malaria                   41             41%
Acute gastroenteritis     21             21%
Vasculotoxic snake bite   19             19%
Sepsis                    4              4%
Leptospirosis             5              5%
Unknown                   10             10%

Table 4. Malaria and AKI (n= 41)

                                   Number   Percentage

Plasmodium falciparum (pf +ve)     27       66%
Plasmodium falciparum and vivax    14       34%
(pf/pv +ve)

Table 5. Oliguric and Non-oliguric AKI (n=100)

Oliguric AKI             Non-oliguric AKI
65 patients              35 patients
65%                      35%

Table 6. Aetiology of Oliguric and Non-oliguric AKI

Aetiology                Oliguric (n=65)   Non-oliguric (n=35)

Malaria                  18 (27%)          23 (66%)
Acute gastroenteritis    16 (24%)          5(14%)
Vasculotoxic snake bite  13 (20%)          6(17%)
Unknown                  10 (15%)
Leptospirosis            4 (6%)            1(3%)
Sepsis                   4 (6%)

Table 7. GFR (Glomerular Filtration Rate) (n=100)

Total Cases     No. of Cases with        No. of Cases with
                increased Serum FDP      decreased Platelet Count

100 cases       32                       32
                32%                      32%

GFR (mL/min)       No. of Cases

< 10               3
10-20              34
20-30              41
30-40              16
40-50              6

Table 8. Correlation of GFR (mL/min) with Aetiology of AKI (n=100)

GFR (mL/min)   Malaria      Acute Gastro.   Snake Bite

< 10           2 (4.8%)
10-20          8 (19.5%)    9 (43%)         7 (37%)
20-30          13 (31.7%)   12 (57%)        11 (58%)
30-40          12 (29.2%)                   1 (5%)
40-50          6 (14.6%)
               41           21              19

GFR (mL/min)    Unknown Aetiology   Leptospirosis   Sepsis

< 10                                1 (20%)
10-20           5 (50%)             1 (20%)         4 (100%)
20-30           5 (50%)
30-40                               3(60%)
                10                  5               4

Table 9. Renal Biopsy (n= 10)

No. of Cases      Biopsy Report

5 cases           Normal
2 cases           Rapidly progressive glomerulonephritis (RPGN)
2 cases           Post infectious glomerulonephritis
1 case            Membranoproliferative glomerulonephritis (MPGN)

Table 10. Patients Undergone Haemodialysis (n= 46)

                             No. of Patients   Haemodialysis   %

Malaria                      41                32              78%
Acute gastroenteritis        21                8               38%
Vasculotoxic snake bite      19                6               31%
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Article Details
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Title Annotation:Original Research Article
Author:Das, Samarendra Nath; Thatoi, Pravat Kumar; Kumar, S. Sandeep; Sahu, Ninnai Chandra; Salim, Sk. Mahe
Publication:Journal of Evolution of Medical and Dental Sciences
Article Type:Report
Date:Aug 31, 2017
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