Home About us Current issue Back issues Submission Instructions Advertise Contact Login   

Search Article 
  
Advanced search 
 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 615 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 
 


 
Table of Contents   
RENAL DATA FROM ASIA-AFRICA  
Year : 2012  |  Volume : 23  |  Issue : 3  |  Page : 619-628
Spectrum of community-acquired acute kidney injury in India: A retrospective study


1 Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttarpradesh, India
2 Department of Surgery, Era's Lucknow Medical College, Lucknow, Uttarpradesh, India

Click here for correspondence address and email

Date of Web Publication7-May-2012
 

   Abstract 

An understanding of the epidemiology of community-acquired acute kidney injury (CAAKI) is necessary to establish its overall burden and plan potential preventive strategies. This study was done in an urban tertiary care center in northern India with the aim to identify the etiology and outcomes as well as the factors associated with in-hospital mortality of CAAKI patients. A five year retrospective analysis of all patients with CAAKI admitted to the Nephrology Department from January 2005 to December 2009 was done. From 5499 consecutive patients, 240 patients (2.5%), with a mean age of 39.8 ± 14.48 years, were diagnosed to have CAAKI as per our specified criteria. The most common cause of CAAKI was medical (77.5%), followed by obstetrical (14.2%) and surgical (8.3%) causes. Among the medical causes, acute diarrheal disease was the most common cause (29%), followed by malaria (18.8%) and sepsis (13.9%). Sepsis had the highest in-hospital mortality (46%). Nephrolithiasis was the most common surgical cause. Puerperal sepsis (44.1%), pre-eclampsia (23.5%), intrauterine death (11.8%), antenatal hemorrhage (11.8%) and post-partal hemorrhage (8.8%) were the obstetric causes of CAAKI. Among 45 patients who underwent a renal biopsy, acute tubulointerstitial nephritis (33.3%) was the most common, followed by acute tubular necrosis (22.2%), glomerulonephritis (17.7%), thrombotic microangiopathy (17.7%) and acute cortical necrosis (8.89%). Of the 83% patients who underwent dialytic therapy, 44.5% underwent hemodialysis, 22.5% continuous veno-venous hemodiafiltration, 21.6% sustained low efficiency dialysis and 11.4% peritoneal dialysis. The overall in-hospital mortality among patients with CAAKI was 26.20%. CAAKI remains a common problem affecting nearly 2.5% of patients attending nephrology units.

How to cite this article:
Kaul A, Sharma RK, Tripathi R, Suresh KJ, Bhatt S, Prasad N. Spectrum of community-acquired acute kidney injury in India: A retrospective study. Saudi J Kidney Dis Transpl 2012;23:619-28

How to cite this URL:
Kaul A, Sharma RK, Tripathi R, Suresh KJ, Bhatt S, Prasad N. Spectrum of community-acquired acute kidney injury in India: A retrospective study. Saudi J Kidney Dis Transpl [serial online] 2012 [cited 2019 Mar 25];23:619-28. Available from: http://www.sjkdt.org/text.asp?2012/23/3/619/95859

   Introduction Top


In the past few decades, nephrology care in India has seen impressive advancements. [1] Des­pite improvements in preventive and diagnos­tic facilities, community acquired acute kidney injury (CAAKI) still remains a major reason for admissions to nephrology units. Acute kidney injury (AKI) is the most common renal emergency in India, and as many as 1.5% of hospital admissions are referred to nephrology service for acute renal failure. [2],[3],[4]

The etiology of CAAKI in tropics is different from that seen in other countries. Trauma, surgery and sepsis contribute to a majority of the cases of AKI in developed countries. [5] In contrast, AKI in tropical countries occur in the younger age group and usually follows infec­tions and obstetric complications. Poor hygiene, warm climate, low socioeconomic status, wide­spread availability of over-the-counter drugs and high incidence of infections like malaria and leptospirosis contribute to the varied etio­logy of CAAKI seen in India. [6] It is important to understand that epidemiology of CAAKI will be influenced by the changes in the epide­miology of infections causing it. For example, malarial AKI, which was seen predominantly in Plasmodium falciparum infections, is being increasingly seen in Plasmodium vivax infections. [7],[8] Sethi et al have demonstrated an in­creasing incidence of leptospirosis in northern India from 11.5% in 2004 to 20.5% in 2008. Sixty percent of the 86 cases included in their study had AKI. [9]

A significant trend changes in the epidemio­logy of CAAKI are being observed in the past few years. Incidence of diarrheal disease, intravascular hemolysis, copper sulfate poisoning and obstetric CAAKI are decreasing. [10],[11] A single-center study from eastern India has shown a reduction in the incidence of acute cortical necrosis from 6.7% in 1994 to 1.6% in 2005. [12] In contrast, there is an increase in the incidence of surgical and sepsis-related AKI. [13],[14]

These dynamic trend changes mandate the need for frequent epidemiological studies to devise preventive and therapeutic strategies. The aim of the present study is to identify the etiology and outcomes of CAAKI and analyze the risk factors for in-hospital mortality in patients admitted with CAAKI.


   Materials and Methods Top


We conducted a retrospective analysis of all patients who were admitted to the Nephrology department from January 2005 to December 2009. The facility is a tertiary care referral center in Northern India catering to the states of Uttarpradesh, Bihar, Madyapradesh and Jharkhand. The majority of the population belongs to Indo-Aryan subraces in the low-and middle-socioeconomic status. Patient data were recovered from the computerized hospital information system. All patients with the diag­nosis of "acute renal failure" or "acute kidney injury" as their hospital admission diagnosis were included in the study. The term AKI is followed in this article to represent both "acute renal failure" and "acute kidney injury." Community-acquired AKI was defined as a serum creatinine of ≥2 mg/dL at the time of admis­sion in a patient with normal-sized kidneys and prior normal renal function. All records of patient's history, physical examination, labora­tory investigations and discharge reports were examined by two nephrologists. A clinical and histopathological diagnosis was made after scrutinizing all the details. Patients who had diabetes mellitus, pre-existing renal insufficiency or referred following a hospital-acquired renal insufficiency were excluded from the study. A total of 339 case records were examined and, of these, 240 patients who satisfied the inclu­sion criteria were analyzed. Patients who did not have their previous renal function records or prior history of renal disease were presumed to have normal renal function in the past. The first serum creatinine obtained after admission to the hospital was taken as baseline value. Oliguria was defined as urine output <400 mL/24 h. Decreased renal perfusion was identified by one or more of: (a) decrease in blood pressure to less than 90/60 mmHg, (b) evidence of congestive heart failure, (c) signs of volume depletion or (d) improvement with restoration of blood flow. Drugs were identified as cause of AKI when there was a temporal relationship to administration of the drug in the absence of other pathogenetic mechanisms. Sepsis was defined as two or more of the following as a result of proven or suspected infection: (a) temperature >38°C or <36°C, (b) heart rate >90/min, (c) respiratory rate >24/min and (d) white blood count >12,000/μL, <4000/μL or >10% band forms. Obstruction was considered to be responsible if there was evidence of obstruction on imaging studies and improve­ment in renal function with relief of obstruc­tion. Hepato-renal syndrome was the cause of renal failure if a patient with liver failure has renal failure with urine sodium less than 15 meq/L in the absence of other identifiable cause of renal failure. Acute tubular necrosis was considered when renal functions did not improve after correc­tion of possible pre-renal causes and when hepato-renal syndrome and vascular, interstitial, glomerular and obstructive etiologies were ruled out. Acute glomerulonephritis was con­sidered in a case with histological confirma­tion except for acute post-infectious state with clinical and biochemical markers substan­tiating the diagnosis. Acute tubulointerstitial nephritis was considered in state of high grade of clinical suspicion or a histological demons­tration. Patients were evaluated on the follo­wing outcomes: complete recovery, partial re­covery not requiring renal replacement therapy (RRT), discharged on RRT or in-hospital mortality.


   Statistical Analysis Top


Values were expressed as mean ± standard deviation. Univariate analysis to identify risk factors was performed using chi-square test or Fisher's exact test for discrete variables and Student's "t " test for continuous variables. Thirty-six variables including age, need for Intensive Care Unit care, hypotension at ad­mission, jaundice, oliguria, icterus and encephalopathy were compared in survivors and non-survivors. Statistical analysis was done with SPSS 15 software for windows. A P-value less than 0.05 was considered significant.


   Results Top


Of the 5499 consecutive patients admitted during a five-year period between January 2005 and December 2009, 240 patients (2.5%) were diagnosed to have CAAKI. The mean age of the population was 39.8 ± 14.48 years. One hundred and forty-one (58.9%) were males while 99 (41.2%) patients of the 240 were females. The mean age of males was 39.23 ± 14.64 years and mean age among females was 40.63 ± 14.28 years.

The most common cause of CAAKI was me­dical (77.5%), followed by obstetrical (14.2%) and surgical causes (8.3%). Among the medical causes, acute diarrheal disease was the most common cause (29%), followed by mala­ria and sepsis [Table 1]. Fifteen percent (36 episodes) of the CAAKI followed diarrheal episodes. Eleven had positive bacterial stool ana­lysis, which included  Salmonella More Details (four), Shigella (three), E. coli (two) and V. cholerae (two). Eighteen patients required emergency dialytic therapy at the time of admission. Severe meta­bolic acidosis (six patients), hyperkalemia (four patients) and volume overload (four patients) were the most common indications for emer­gency dialysis.
Table 1: Etiology and management of CAAKI.

Click here to view


Puerperal sepsis was the most common cause of obstetric CAAKI (44.1%), followed by pre-eclampsia (23.5%), intrauterine death (11.8%), antenatal hemorrhage (11.8%) and post-partum hemorrhage (8.8%). Among the surgical cau­ses of CAAKI, nephrolithisis was the most common etiology presenting with obstruction and acute renal failure. Twelve of the 20 patients with surgical CAAKI had nephrolithiasis as the cause of obstruction. In four patients, carcinoma cervix was the cause of obstructive AKI.

The "histological diagnosis" of all 240 pa­tients was analyzed. Forty-five patients under­went renal biopsy during their hospital stay [Table 2]. The most common indication for renal biopsy in our population was persistent renal failure of more than three weeks dura­tion. Absence of an obvious cause for CAAKI and extrarenal manifestation suggestion of a systemic disease were the other common indi­cations of renal biopsy. In those patients who did not undergo renal biopsy, a "probable" histological diagnosis was assigned based on patient's history, clinical findings, laboratory investigations and hospital course.
Table 2: Renal histology in CAAKI.

Click here to view


When the histological diagnosis (biopsy diag­nosis or "probable" histological diagnosis) was analyzed, acute tubular necrosis (ATN) was the most frequent cause of CAAKI. Hypovolemia was the most common precipitating factor for ATN (54 patients). However, in those patients who underwent a renal biopsy, acute inters­titial nephritis was the most common diag­nosis. Drugs were the most common etiological agents of AIN, causing 14 of the 25 episodes. Analgesics (seven episodes), antibiotics (ampicillin - three, cotrimoxazole - two), acyclovir (one episode) and aminoglycoside (one episode) were the drugs causing AIN.

Thrombotic microangiopathy needs a special mention as it presents interesting diagnostic challenges in adults with AKI [Table 3]. These disorders at presentation are often misdiagnosed as sepsis, complicated malaria, HELLP syndrome or antiphospholipid antibody syn­drome (APLA) syndrome. In India, compli­cated malaria often presents with fever, thrombocytopenia, renal failure and neurological symptoms mimicking hemolytic uremic syn­drome (HUS) and thrombotic thrombocytopenic purpura (TTP). Often, renal biopsy is needed to confirm the diagnosis when other laboratory parameters are equivocal. The di­sease needs to be identified because of its favorable response to early initiation of plasma exchange. Of the eight patients who had a diagnosis of thrombotic microangiopathy in renal biopsy, five had a clinical diagnosis of HUS, two had a diagnosis of TTP and one patient had primary APLA syndrome. Eighteen percent had icterus, 23.7% had encephalopathy and 65% were oliguric at pre­sentation. 14.6% patients required less than 14 days of hospital stay. The mean duration of hospital stay was 44.8 ± 29.3 days. 32.9% (79 patients) needed mechanical ventilation during their hospital stay. Dialysis was indicated in 83%. 44.5% (89 patients) underwent conven­tional hemodialysis, 22.5% (45 patients) under­went continuous venovenous hemodiafiltration (CVVHDF), 21.6% (43 patients) sustained low efficiency dialysis (SLED) while 11.4 % underwent peritoneal dialysis (PD) [Figure 1]. The vascular access used was femoral venous ca­theter in 39% and internal jugular access in 61% of the dialysis sessions. One hundred and six patients (44%) had com­plete recovery of renal function and 33 pa­tients had partial recovery of renal function. Thirty-eight patients (15%) were discharged on long-term RRT. The overall in-hospital morta­lity among patients with CAAKI was 26.20% [Figure 2]. In comparison with survivors, fac­tors associated with increased in-hospital mor­tality (P <0.05) are depicted in [Table 4].
Figure 1: Treatment of CAAKI.

Click here to view
Figure 2: Outcomes of CAAKI.

Click here to view
Table 3: Treatment and outcomes of thrombotic microangiopathies.

Click here to view
Table 4: Factors associated with in-hospital mortality in CAAKI.

Click here to view



   Discussion Top


Ever since the introduction of the term "acute renal failure" by Homer W. Smith in 1951, at least 35 different definitions have been used to identify the syndrome. [15] The incidence varies from 1% to 31%, and mortality ranges from 28% to 82% depending on the definition used. [16],[17],[18] Hoste et al in a recent review on the epidemiology of AKI identified the most spe­cific definition of AKI as an absolute increase of serum creatinine of ≥2.0 mg/dL. The same definition has been used by us to diagnose CAAKI in our patients. [19]

2.5% of the patients admitted to the nephrology department of our hospital had a diag­nosis of CAAKI. The mean age of the popu­lation admitted with CAAKI was 39.8 years. Only 9.1% were more than 60 years of age. Although this may be reasoned by the shorter life expectancy in Indian population, it also implies to the occurrence of CAAKI in the younger age group as compared with developed countries. In a country like India, where access to health care insurance is limited, CAAKI in the middle-aged population creates a huge economical burden on families.

Medical causes accounted for about three-fourth of CAAKI. Diarrheal diseases, malaria and sepsis contribute to 47.9% of CAAKI. Diarrheal diseases still continue to be the most common cause of CAAKI in our population. Shigella, E. coli and Salmonella are the most common etiological agents in this region, with seasonal occurrences of V. cholerae. [20] Although the incidence of diarrheal disease-related acute renal failure has decreased from 23% in the 1960s to <10%, diarrheal diseases still continue to be a major cause of CAAKI necessitating emergency dialytic therapy. [21]

India contributes 80% of all the cases of ma­laria in Southeast Asia. The prevalence of AKI in malaria is less than 1%, but increases to 60% in severe infections. [22] Although falciparum infections remain the most common cause of complicated malaria, various Indian investigators have documended the increasing incidence of complicated malaria in Plasmo­dium vivax infections. [7],[8],[23] Twenty percent (seven out of 35) of our patients with malaria AKI had P. vivax infection; in contrast, 6.25% of malarial AKI follows P. vivax infections in southern India. This could indicate an increa­sing incidence of vivax malaria in our popu­lation or a rising rate of AKI in P. vivax infections.

Sepsis had the highest in-hospital mortality of 46%, which is similar to data from other Indian centers. Worldwide, the incidence of sepsis-related AKI is increasing [14] and occurrence of AKI represents an independent risk factor for in-hospital mortality in these patients. [24]

Pregnancy-related AKI comprise 9-25% of nephrology referrals in developing countries as compared with 1-2.8% in the developed world. In northern India, the incidence of obstetric AKI decreased from 22% in the 1960s to 10% in the 1980s. [10] Since then, the incidence of obstetric AKI has remained fairly constant, between 10% and 15%. However, significant improvement in maternal mortality has been achieved. Maternal mortality has decreased from 20% in the 1980s to 6.4% in the 1990s. [11] Obstetric AKI contributed to 14% of CAAKI in our population and had 36% mortality. This higher mortality may be due to the higher percentage of patients with puerperal sepsis (35%), improper delivery techniques and de­layed referral.

8.3% of CAAKI was due to surgical causes. Nephrolithiasis was the most common cause. Urinary stone disease in the Indian population is different from that in the Western countries, with a larger percentage of patients having cal­cium oxalate stones. Previous studies in our center have found calcium oxalate monohy­drate as the major component of stones, with hyperoxaluria and hypocitraturia being the most common urinary abnormalities. [25] Dietary factors, inherited metabolic disorders and fluid losses contribute to the increased incidence of nephrolithiasis in the Asian population. [6] Four of the 20 patients with surgical AKI had obs­tructive uropathy due to carcinoma cervix pre­senting as AKI. Such complications are not uncommon in the Indian population, and indi­cate the need for improved screening covering the widest possible population and also regular follow-up of women with pre-cancerous lesions. [26],[27]

In southern India, snake bite causes 7.8% of AKI and copper sulfate poisoning contributes to 4.7% of AKI. [13] In contrast, none of our pa­tients with CAAKI had snake bite or copper sulfate poisoning. Another significant trend is the increasing incidence of leptospirosis-related AKI in north India. 6.25% of the AKI in our population was due to leptospirosis, which is similar to data from southern India. Histology helps in diagnosis, predicting di­sease course and outcomes. Around one-fifth of our patients with CAAKI underwent a renal biopsy, 33.3% had AIN, followed by ATN -22.2%. In comparison, Liano et al biopsied 6.15% of patients with AKI observed AIN in 8.6%, ATN in 8.6% and glomerular diseases in 39%. [28] The higher percentage of AIN seen in our study may be due to easy availability of over-the-counter medications and frequent use of drugs from alternate systems of medicine. In AKI, the most useful role of kidney biopsy is in early detection of glomerular diseases, as it helps to plan therapy and to estimate prog­nosis. The percentage of glomerular disease and thrombotic microangiopathy were equal in our series. This is because patients with clas­sical post-infectious glomerulonephritis were not biopsied. TTP and HUS are disorders characterized by fever, Coomb's-negative microangiopathic hemolytic anemia, thrombocytopenia and systemic ischemia and multiple organ failure. [29]-[32] In Asia, HUS is responsible for 25-55% of pediatric AKIs. [33],[34],[35] Although E. coli O157:H7 is the most common cause in many parts of the world, Shigella is the pri­mary etiological agent in the Indian population and has poor outcomes with a mortality rate of 60%. [6]

Literature on the choice of dialytic modality is conflicting and no study has conclusively demonstrated the appropriate type and dose of RRT in AKI. [36] In India, use of continuous renal replacement therapy (CRRT) as a dialytic modality is increasing with the availa­bility of advanced equipments and bicarbonate replacement solutions. When the choice of dialytic modality in our center was analyzed, decreasing anticoagulation, reducing cost and improving patient mobility were the major rea­sons to choose SLED over CRRT. Continuous therapies were preferred in those who are hemodynamically unstable, patients requiring large volume infusions and septic shock.

Acute PD was used in 11% of the patients. Although hemodialysis has become the pre­ferred dialysis modality in many centers, PD, because of easy availability and cost benefits, remains the major dialytic modality in many Indian hospitals. Hayat et al [37] reported a sur­vival rate of 90% in adult AKI patients of northern India who underwent PD. Gabriel et al [38] have recently suggested that PD was associated with more rapid renal recovery in AKI. PD can also be used as a "bridge," there­by avoiding the use of central venous cathe­ters, which can be associated with infectious complications such as bacterial endocarditis. [39]

The overall in-hospital mortality among pa­tients with CAAKI was 26.2%. Sepsis had the highest in-hospital mortality. Indian studies on CAAKI report a mortality of 16-26%. [40] As compared with hospital-acquired AKI, the lower mortality rate in CAAKI is probably due to the higher percentage of diarrheal disease and younger age group of our population. Instead, this could also imply a trend toward better survival in AKI.

Fifteen percent of the patients were dis­charged on RRT. Among survivors of AKI, at long-term follow-up (1-10 years), approxi­mately 12.5% are dialysis dependent and 19-31% have chronic kidney disease. [41] Even in patients who do not require dialysis, AKI is associated with increased long-term mortality risk, independent of their residual kidney function. [42]

When survivors and non-survivors were com­pared, need for assisted ventilation, encephalopathy at presentation, hypotension at presenta­tion, oliguria at presentation, hemoglobin levels <10 gm/dL at admission, serum creatinine >4 mg/dL, serum albumin <3.5 mg/dL and co­existing liver disease were associated with increased in-hospital mortality. In compa­rison, Liano et al [28] in the largest epidemiological study of 748 acute renal failure patients identified presence of oliguria, sustained hypo­tension, assisted respiration, jaundice, sedation or coma as risk factors of mortality.

In conclusion, CAAKI remains a common problem affecting 2.5% of patients in nephrology unit. Infections and obstetric causes lead to majority of CAAKI episodes. Hemodialysis is the preferred treatment modality. In India, use of SLED and CRRT in the management of CAAKI is increasing.


   Acknowledgment Top


The authors thank Dr. Mandal SN. PhD, for assistance in preparing the manuscript.

 
   References Top

1.Chugh KS. Five Decades of Indian Nephrology: A Personal Journey. Am J Kidney Dis 2009; 54:753-63.  Back to cited text no. 1
    
2.Muthusethupathi MA, Shivakumar S. Acute renal failure in south India. Our experience with 187 patients. J Assoc Physicians India 1987;35:504-7.  Back to cited text no. 2
    
3.Chugh KS, Singhal PC, Nath IV. Spectrum of acute renal failure in North India. J Assoc Physicians India 1978;26:147-54.  Back to cited text no. 3
    
4.Jha V, Malhotra HS, Sakhuja V, Chugh KS. Spectrum of hospital-acquired acute renal fai­lure in the developing countries--Chandigarh study. Q J Med 1992;83:497-505.  Back to cited text no. 4
    
5.Waikar SS, Liu KD, Chertow GM. Diagnosis, epidemiology and outcomes of acute kidney injury. Clin J Am Soc Nephrol 2008;3:844-61.  Back to cited text no. 5
    
6.Jha V, Chugh KS. Community-Acquired Acute Kidney Injury in Asia. Seminars in Nephrology 2008;28:330-47.  Back to cited text no. 6
    
7.Prakash J, Singh AK, Kumar NS, Saxena RK. Acute renal failure in Plasmodium vivax mala­ria. J Assoc Physicians India 2003;51:265-7.  Back to cited text no. 7
    
8.Mehta KS, Halankar AR, Makwana PD, Torane PP, Satija PS, Shah VB. Severe acute renal failure in malaria. J Postgrad Med 2001; 47:24-6.  Back to cited text no. 8
[PUBMED]  Medknow Journal  
9.Sethi S, Sharma N, Kakkar N, et al. Increasing trends of leptospirosis in northern India: a clinico-epidemiological study. PLoS Negl Trop Dis 2010;4:e579.  Back to cited text no. 9
    
10.Chugh KS, Sakhuja V, Malhotra HS, Pereira BJ. Changing trends in acute renal failure in third-world countries-Chandigarh study. Q J Med 1989;73:1117-23.  Back to cited text no. 10
    
11.Prakash J, Kumar H, Sinha DK, et al. Acute renal failure in pregnancy in a developing country: twenty years of experience. Ren Fail 2006;28:309-13.  Back to cited text no. 11
    
12.Prakash J, Vohra R, Wani IA, et al. Decreasing incidence of renal cortical necrosis in patients with acute renal failure in developing coun­tries: a single-centre experience of 22 years from Eastern India. Nephrol Dial Transplant 2007;22:1213-7.  Back to cited text no. 12
    
13.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. 13
    
14.Anandh U, Renuka S, Somiah S, Vincent L. Acute renal failure in the tropics: emerging trends from a tertiary care hospital in South India. Clin Nephrol 2003;59:341-4.  Back to cited text no. 14
    
15.Kellum JA, Levin N, Bouman C, Lameire N. Developing a consensus classification system for acute renal failure. Curr Opin Crit Care 2002;8:509-14.  Back to cited text no. 15
    
16.Chertow GM, Lazarus JM, Christiansen CL, et al. Preoperative renal risk stratification. Circulation 1997;95:878-84.  Back to cited text no. 16
    
17.Vivino G, Antonelli M, Moro ML, et al. Risk factors for acute renal failure in trauma patients. Intensive Care Med 1998;24:808-14.  Back to cited text no. 17
    
18.Schiffl H, Lang SM, Fischer R. Daily hemodialysis and the outcome of acute renal failure. N Engl J Med 2002;346:305-10.  Back to cited text no. 18
    
19.Hoste EA, Schurgers M. Epidemiology of acute kidney injury: how big is the problem?. Crit Care Med 2008;36:S146-51.  Back to cited text no. 19
    
20.Das S, Saha R, Singhal S. Enteric pathogens in north Indian patients with diarrhoea. Indian J Community Med 2007;32:27-31.  Back to cited text no. 20
  Medknow Journal  
21.Chugh KS, Narang A, Kumar L, et al. Acute renal failure amongst children in a tropical environment. Int J Artif Organs 1987;10:97-101.  Back to cited text no. 21
    
22.Boonpucknavig S, Srichaikul T, Punyagupta S. Clinical pathology of malaria. In: Peters W, Richards WH, (eds). Antimalarial drugs: biolo­gical background, experimental methods and drug resistance. Berlin: Springer-Verlag., 1984; 127-76.  Back to cited text no. 22
    
23.Sharma A, Khanduri U. How benign is benign tertian malaria? J Vector Borne Dis 2009;46: 141-4.  Back to cited text no. 23
    
24.Oppert M, Engel C, Brunkhorst FM, et al. German Competence Network Sepsis (Sepnet). Acute renal failure in patients with severe sepsis and septic shock--a significant indepen­dent risk factor for mortality: results from the German Prevalence Study. Nephrol Dial Transplant 2008;23:904-9.  Back to cited text no. 24
    
25.Mittal RD, Kumar R, Mittal B, Prasad R, Bandari M. Stone Composition, Metabolic Profile and the Presence of the Gut-Inhabiting Bacterium Oxalobacter formigenes as Risk Factors for Renal Stone Formation. Med Princ Pract 2003; 12:208-13.  Back to cited text no. 25
    
26.Singh I. Spontaneous renal forniceal rupture due to advanced cervical carcinoma with obs­tructive uropathy, Arch Gynecol Obstet 2009; 279:915-8.  Back to cited text no. 26
    
27.Mougin C, Dalstein V, Prétet JL, Gay C, Schaal JP, Riethmuller D. Epidemiology of cervical papillomavirus infections. Recent knowledge. Presse Med 2001;30:1017-23.  Back to cited text no. 27
    
28.Liaño F, Pascual J. Epidemiology of acute renal failure: A prospective, multicenter, community-based study. Madrid Acute Renal Failure Study Group. Kidney Int 1996;50:811-8.  Back to cited text no. 28
    
29.Esplin MS, Branch DW. Diagnosis and management of thrombotic microangiopathies during pregnancy. Clin Obstet Gynecol Ambul Gynecol 1999;42:360-7.  Back to cited text no. 29
    
30.Elliott MA, Nichols WL. Thrombotic throm-bocytopenic purpura and hemolytic uremic syndrome. Mayo Clin Proc 2001;76:1154-62.  Back to cited text no. 30
    
31.Kilpatrick S, Laros R. Maternal hematologic disorders. In: Creasy RK, Resnik R, Iams JD (Eds). Maternal Fetal Medicine:Principles and Practice. Philadelphia: Saunders; 2004. p. 975-1004.  Back to cited text no. 31
    
32.Rock GA, Shumak KH, Buskard NA, et al. Comparison of plasma exchange with plasma infusion in the treatment of thrombotic throm-bocytopenic purpura. Canadian Apheresis Study Group. N Engl J Med 1991;325:393-7.  Back to cited text no. 32
    
33.Srivastava RN, Bagga A, Moudgil A. Acute renal failure in north Indian children. Indian J Med Res 1990;92:404-8.  Back to cited text no. 33
    
34.Arora P, Kher V, Gupta A, et al. Pattern of acute renal failure at a referral hospital. Indian Pediatr 1994;31:1047-53.  Back to cited text no. 34
    
35.Jamal A, Ramzan A. Renal and post-renal causes of acute renal failure in children. J Coll Physicians Surg Pak 2004;14:411-5.  Back to cited text no. 35
    
36.Ricci Z, Ronco C. Dose and efficiency of renal replacement therapy: Continuous renal replace­ment therapy versus intermittent hemodialysis versus slow extended daily dialysis. Crit Care Med 2008;36:S229-37.  Back to cited text no. 36
    
37.Hayat A, Kamili MA, Samia R, et al. Perito­neal dialysis for adults with acute renal failure: An underutilized modality. Saudi J Kidney Dis Transpl 2007;18:195-9.  Back to cited text no. 37
[PUBMED]  Medknow Journal  
38.Gabriel DP, Caramori JT, Martim LC, Barretti P, Balbi AL. High volume peritoneal dialysis vs daily hemodialysis: A randomized, con­trolled trial in patients with acute kidney injury. Kidney Int 2008;108:S87-93.  Back to cited text no. 38
    
39.Gabriel DP, Fernández-Cean J, Balbi AL. Uti­lization of peritoneal dialysis in the acute setting. Perit Dial Int 2007;27:328-31.   Back to cited text no. 39
    
40.Renuka S, Pais P. Clin­ical spectrum of hospital acquired renal failure: a study from tertiary care hospital. Indian J Nephrol 2004;14:93.  Back to cited text no. 40
  Medknow Journal  
41.Goldberg R, Dennen P. Long-term outcomes of acute kidney injury. Adv Chronic Kidney Dis 2008;15:297-307.  Back to cited text no. 41
    
42.Lafrance JP, Miller DR. Acute kidney injury associates with increased long-term mortality. J Am Soc Nephrol 2010;21:345-52.  Back to cited text no. 42
    

Top
Correspondence Address:
Anupma Kaul
Assistant Professor, Department of Nephrology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttarpradesh
India
Login to access the Email id


Rights and Permissions


    Figures

  [Figure 1], [Figure 2]
 
 
    Tables

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

This article has been cited by
1 Community-acquired acute kidney injury in tropical countries
Jha, V. and Parameswaran, S.
Nature Reviews Nephrology. 2013; 9(5): 278-290
[Pubmed]



 

Top
   
 
 
    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  
 


 
    Abstract
   Introduction
    Materials and Me...
   Statistical Analysis
   Results
   Discussion
   Acknowledgment
    References
    Article Figures
    Article Tables
 

 Article Access Statistics
    Viewed3778    
    Printed83    
    Emailed0    
    PDF Downloaded839    
    Comments [Add]    
    Cited by others 1    

Recommend this journal