MALARIA

1. ACUTE CORTICAL NECROSIS – A RARE PRESENTATION IN COMPLICATED
VIVAX MALARIA – CASE REPORT
INTRODUCTION
Malaria is a vector borne disease transmitted by female
anopheles mosquito. Malaria is caused by parasite
Plasmodium species. In india malaria is caused mainly by P.
falciparum and P.vivax rarely by P. ovale and P.malariae. The
2023 World Malaria Report reveals a global surge with an
estimated 249 million cases in 2022. In
2022, India accounted for 66% of malaria cases in the
WHO South-East Asia Region.
CASE PRESENTATION
15 year female, resident of Ludhiana, student, presented to ER with c/o fever since 3-4 days, abdominal pain for 2 days(pain
score 3/10) and black colored stools since 1 day. H/o hospital admission for sibling in another hospital for similar complaints.
On examination BP-100/60, pr-136, T- N, Spo2- 94%. RS - B/L basal crackles +, P/A – soft, non tender. Patient was shifted to
ICU. Patient was started on with O2 support, inotropes was started in view of hypotension. RT aspirate showed blood. CT
Abdomen showed moderate ascites, mild pleural effusion and reactive GB wall edema. Patient developed anuria and ABG was
suggestive of metabolic acidosis. Nephrology consultation was taken and SLED was done urgently. NAC infusion was started
after gastro consult in view of severely deranged liver enzymes. NIV was started. Daily SLED was done for 3 consecutive days. In
view of persistent anuria CRRT was done for 2 days. Patient improved clinically and was shifted to ward. Multiple PRBC, SDP
and FFP was transfused during the hospital stay. Alternate day dialysis continued. Patient started pouring urine after 15 days of
hospital stay. Patient was discharged and dialysis continued on OPD basis. RFT of the patient improved and maintenance HD
was also stopped. Bone marrow biopsy was done in view of persistent thrombocytopenia –s/o Normocellular marrow with
decreased erythropoiesis. USG Guided Renal Biopsy was done. Now the patient is on regular follow up on OPD basis.
Unfortunately the sibling who was admitted in outside hospital could not be saved.
REFERENCES
1. Nair RK, Rao KA, Mukherjee D, Datt B, Sharma S, Prakash
S. Acute kidney injury due to acute cortical necrosis
following vivax malaria. Saudi Journal of Kidney Diseases
and Transplantation. 2019 Jul 1;30(4):960-3.
2. Patel MP, Ugale PP, Jagtap AB, Chaudhari ST, Dighore
PN. Novel presentation of Plasmodium vivax malaria
with acute kidney injury and hemolytic uremic
syndrome. Clinical Queries: Nephrology. 2015 Oct 1;4(3-
4):34-7.
3. Kute VB, Trivedi HL, Vanikar AV, Shah PR, Gumber MR,
Patel HV, Goswami JG, Kanodia KV. Plasmodium vivax
malaria–associated acute kidney injury, India, 2010–
2011. Emerging infectious diseases. 2012 May;18(5):842.
HB- 10.5
TLC-4800
PLT- <10000
CREAT 0.51
VIRAL MARKERS-NR
DENGUE- NON REACTIVE
PBF- P. VIVAX
WIDAL- NON REACTIVE
INR -1.3
ABG – METABOLIC ACIDOSIS
AMYLASE – 15
LIPASE -10
CRP-39.75
BILIRUBIN – 3.3 (2.6+0.7)
OT/PT -40/41
URINE C/S – KLEBSIELLA
LDH- 4680
TIBC – 216
VIT B12 >2000
G6PD – NORMAL
URINE R/E- PROTEIN 3+
RBC FULL FIELD
PUS 8-10
RENAL BIOPSY - Focal cortical
necrosis
INVESTIGATIONS DISCUSSION
AKI is a known complication of malaria and can occur in around
40% of patients with severe disease by P. falciparum. AKI is a
rare in P. vivax malaria. Cytoadherence of parasitized RBC to
vascular endothelium and obstruction of small vessels are most
common reason followed by immune complex deposition for
AKI in malaria. Renal replacement therapy is life saving in these
patients. Primaquine must be added after initial treatment
using Artemisinin to prevent relapse of malaria.