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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE Table of Contents   
Year : 2010  |  Volume : 21  |  Issue : 6  |  Page : 1088-1091
Malaria induced acute renal failure: A single center experience


1 Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, Dr. H. L. Trivedi Institute of Transplantation Sciences (ITS) - Smt Gulabben Rasiklal Doshi and Smt Kamlaben Mafatlal Mehta Institute of Kidney Diseases & Research Centre (IKDRC), Civil Hospital Campus, Asarwa, Ahmadabad, Gujarat, India
2 Department of Nephrology and Clinical Transplantation, Dr. H. L. Trivedi Institute of Transplantation Sciences (ITS) - Smt Gulabben Rasiklal Doshi and Smt Kamlaben Mafatlal Mehta Institute of Kidney Diseases & Research Centre (IKDRC), Civil Hospital Campus, Asarwa, Ahmadabad, Gujarat, India

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Date of Web Publication4-Nov-2010
 

   Abstract 

Malaria has protean clinical manifestations and renal complications, particularly acute renal failure that could be life threatening. To evaluate the incidence, clinical profile, out­come and predictors of mortality in patients with malarial acute renal failure, we retrospectively studied the last two years records of malaria induced acute renal failure in patients with peripheral smear positive for malarial parasites. One hundred (10.4%) (63 males, 37 females) malaria induced acute renal failure amongst 958 cases of acute renal failure were evaluated. Plasmodium (P). falciparum was reported in 85%, P. vivax in 2%, and both in 13% patients. The mean serum creatinine was 9.2 ± 4.2 mg%, and oligo/anuria was present in 82%; 78% of the patients required hemodialysis. Sixty four percent of the patients recovered completely, 10% incompletely, and 5% developed chronic kidney failure; mortality occurred in 21% of the patients. Low hemoglobin, oligo/anuria on admission, hyperbilirubinemia, cerebral malaria, disseminated intravascular coa­gulation, and high serum creatinine were the main predictors of mortality. We conclude that ma­laria is associated with acute renal failure, which occurs most commonly in plasmodium falci­parum infected patients. Early diagnosis and prompt dialysis with supportive management can reduce morality and enhance recovery of renal function.

How to cite this article:
Kanodia K V, Shah P R, Vanikar A V, Kasat P, Gumber M, Trivedi H L. Malaria induced acute renal failure: A single center experience. Saudi J Kidney Dis Transpl 2010;21:1088-91

How to cite this URL:
Kanodia K V, Shah P R, Vanikar A V, Kasat P, Gumber M, Trivedi H L. Malaria induced acute renal failure: A single center experience. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2019 Jul 22];21:1088-91. Available from: http://www.sjkdt.org/text.asp?2010/21/6/1088/72296

   Introduction Top


Malaria is endemic throughout south and south east Asia, south America and Africa and accounts for 1 to 3 million deaths per year. [1] Acute Renal Failure (ARF) occurs commonly in plasmodium (P) falciparum malaria infected patients, and rarely in P. vivax also infected ones. [2] The overall prevalence of ARF in falci­parum malaria varies between < 1% to 60%. [3]

This study was conducted to evaluate the in­cidence, clinico-pathological profile, outcome, and predictors of mortality of malarial ARF.


   Material and Method Top


We retrospectively studied the last two years ARF patients' records in our centre. Patients having ARF with peripheral smear displaying malarial parasites were included in the study. Clinical history and assessment were recorded in all the study patients and all other known etiological causes of fever and jaundice were excluded by relevant investigations. All the patients were subjected to complete hemogram with reticulocyte counts. Thick and thin peri­pheral smear examination using Geimsa stain was carried out for type and grading of para­sitemia. Urine samples were examined for rou­tine and microscopy examination. Serum was tested for sodium, potassium, alkaline phos­phatase, alanine aminotransaminase (ALT), bi­lirubin, lactic acid dehydrogenase and glucose 6-phosphate dehydrogenase. Serological tests for Human Immunodeficiency Virus (HIV) and hepatitis B and C were performed. Estimation of blood sugar, coagulation profile for disse­minated intravascular coagulation (DIC) and arterial blood gas analysis were carried out when indicated.

Chest x-ray and ultrasonography (USG) of abdomen were recorded in all the patients. ARF was defined as serum creatinine (SCr) of ≤ 3 mg% and urine output < 400 mL/day, with normal kidney size on USG.

The patients were managed using anti-mala­rial drugs, fluid replacement and hemodialysis. Renal biopsy was performed when oliguria/ heavy proteinuria (> 3 gm/day) persisted for three weeks. Exchange transfusion was per­formed with parasitemia grade + 4 (> 10 para­sites /high power field) or hyperbilirubinemia (serum bilirubin > 25 mg/dL).


   Results Top


A total of 100 (10.43%) (63 males, 37 females) patients with malaria induced ARF amongst 958 ARF patients were entered into the study. The mean age (± SD) was 32 ± 12.61 years. P. falciparum was reported in 85% patients, P. vivax in 2%, and mixed infection was reported in 13%.

The patients' presentations included fever (100 %), nausea-vomiting (89%), oligo/anuria (82%), abdominal pain/tenderness (55%), jaun­dice (55%), dyspnea (30%), altered sensorium (31%), convulsions (18%), diarrhea (17%), splenomegaly (69%) and hepatomegaly (39%) [Table 1].
Table 1 :Clinical presentation of malarial ARF.

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The mean of the hemoglobin levels was 8.52 ± 2.25 gm%, serum creatinine (SCr) 9.21 ± 4.18 mg%, D. dimer > 500ng/mL (measured by immuno-turbidimetric assay, STAGO, France) in 30% of the patients, ALT > 70 U/L (normal: 0-40 U/L) in 40%, hyperkalemia (s. potassium > 5.5 meq/L) in 26%, proteinuria (> 1 gm /24 hours) in 38%, and microscopic hematuria in 44% [Table 2].
Table 2 :Laboratory findings of malarial acute renal failure.

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Renal biopsies were performed in 10 patients of whom 70% had patchy cortical necrosis, 20% had mesangial proliferative glomerulo­nephritis (GN) without any immune deposits and acute tubular necrosis (ATN), and 10% had idiopathic membranous GN.

Artensunate was administered in 80% of the patients, Quinine in 18%, and combined treat­ment in 2%. Hemodialysis was performed in 78% of the patients and exchange transfusion was required in 16%. Sixty four percent of the patients had complete recovery with normal renal function (SCr < 1.2 mg%), 10% had in­complete recovery (SCr 1-3 mg/dL) and re­mained on conservative management, 5% ended up as chronic kidney failure and continued on maintenance hemodialysis, and 21% succumbed to ARF.


   Discussion Top


The incidence of malarial ARF was 10.43% in our study as compared with 5-15% in other Asian groups. [2],[4],[5] ARF is a serious complica­tion of falciparum malaria dreaded for its mor­tality commonly found in South East Asia. [6] Our study showed 21% mortality in malarial ARF, consistent with 15-45% mortality repor­ted by others. [7]

Several factors including various chemical mediators, catecholamine release, cytoadhe­rence of parasitized erythrocytes, dehydration, intravascular hemolysis, intravascular coagu­lation, sepsis, hyperbilirubinemia and hyper­parasitemia have been implicated in the patho­genesis of ARF in malaria. [8]

Men were more affected in our study as com­pared with women, similar to observations of other groups. [2],[4],[5] This could be explained by the fact that men are more mobile and moving about, including the swampy areas as com­pared with women in Asian countries, since women are more confined to their homes and near cooking fire, which offers them protec­tion from biting mosquitoes. P. falciparum was observed in 85% of our cases and only 15% had P. vivax or mixed infections. P. falciparum parasitemia is known to be associated with a significantly greater reduction in endogenous creatinine clearance. [9] ARF in P. falciparum can occur in three ways: ATN, the commonest presentation, acute tubulo-interstitial nephritis or less commonly acute GN. ATN may be mo­nitored in 1-4% of P. falciparum malarial ARF, but may reach up to 60% in severe malaria. [7],[10] ARF in falciparum malaria is usually oliguric and hyper-catabolic; oliguric phase lasts for a few days to several weeks, which was also found in our study.

Hyperbilirubinemia in falciparum malaria po­ssibly predisposes to ARF, which may be only revealed by laboratory investigations. [11] All patients of ARF and jaundice had conjugated hyperbilirubinemia with cholestasis. This well described association may contribute to the reduction of glomerular filtration rate or deve­lopment of ATN. [5],[8] ARF associated with jaun­dice had high mortality in comparison with non jaundiced ARF patients. [12]

The major factors associated with mortality in our study were increased SCr, low hemo­globin, severe oligo/anuria, CNS involvement, DIC, sepsis, and hyperbilirubinemia whereas age had no role in survival [Table 3] and [Table 4]. We believe that since our hospital is a tertiary care center, the patients were referred for treatment, when they were already in a morbid condition. We be-lieve that survival can be improved by edu-cation and early transfer to a tertiary care center, where prompt dialysis and supportive ma-nagement can be instituted.
Table 3 :Indicators of mortality in malaria associated with acute renal failure.

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Table 4 :Significance of age, hemoglobin, s. creatinine and jaundice on mortality.

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We conclude that malaria is an important cause of ARF in Asia and particularly in tro­pical areas. ARF occurs most commonly in association with P. falciparum malaria. Early diagnosis and prompt management including dialysis can reduce mortality and expedite re­covery of renal function.

 
   References Top

1.Breman JG, White NJ. Malaria, Babesiosis. In: Isselbacher KJ, Eugene B. Wilson JD, eds. Harrison's Principles of Internal Medicine, 13th edn. McGraw-Hill, New York, 1994:887-96  Back to cited text no. 1
    
2.Prakash J, Singh AK, Gujrati S, Maheshwari A. Acute renal failure in Malaria: Changing trends. Indian J Nephrol 2002;12:113-7.  Back to cited text no. 2
  Medknow Journal  
3.Sheehy TW, Reba RC. Complications of falci­parum malaria and their treatment. Ann Inter Med 1967;66:807-9.  Back to cited text no. 3
    
4.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. 4
[PUBMED]  Medknow Journal  
5.Naqvi R, Ahmad E, Akhtar F, Naqvi A, Rizvi A. Outcome in severe acute renal failure asso­ciated with malaria. Nephrol Dial Transplant 2003;18:1820-3.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.Boonpucking V, Sitprija V. Renal disease in acute plasmodium falciparum infection in man. Kidney Int 1979;16:44-52.  Back to cited text no. 6
    
7.Eiam-Ong S, Sitprija V. Falciparum malaria and the kidney: a model of inflammation. AM J Kidney Dis 1998;32:361-75.  Back to cited text no. 7
    
8.Barsoum RS. Malarial acute renal failure. J Am Soc Nephrol 2000;11:2147-54.  Back to cited text no. 8
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9.Ahmad SH, Danish T, Faridi MM, Ahmad AJ. Fakhir S, Khan AS. Renal function in acute malaria in children. J Trop Pediatr 1989;35(6): 291-4.  Back to cited text no. 9
    
10.Sitprija V. Nephropathy in falciparum malaria. Kidney Int 1988;34:966-77.  Back to cited text no. 10
    
11.Sural S, Sharma RK, Gupta A, Sharma AP, Gulati S. Acute renal failure associated with liver disease in India. Etiology and outcome. Ren Fail 2000;22:623-34.  Back to cited text no. 11
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12.Pati SS, Mishra SK, Mohanty S, Patnaik JK, Das BS. Influence of renal impairment on plasma concentrations of conjugated bilirubin in cases of plasmodium falciparum malaria. Ann Trop Med Parasitol 2003;97:581-6.  Back to cited text no. 12
    

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Correspondence Address:
K V Kanodia
Department of Pathology, Laboratory Medicine, Transfusion Services and Immunohematology, Dr. H.L. Trivedi Institute of Transplantation Sciences (ITS)- Smt Gulabben Rasiklal Doshi and Smt Kamlaben Mafatlal Mehta Institute of Kidney Diseases & Research Centre (IKDRC), Civil Hospital Campus, Asarwa, Ahmadabad-380 016, Gujarat
India
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    Tables

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

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    Abstract
    Introduction
    Material and Method
    Results
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