plasmodium vivax malaria is usually an uncomplicated disease , which runs a benign course . in the last few years , changing trends with severe and life - threatening complications due to p. vivax has been reported from different endemic regions such as india , indonesia , and brazil . complications similar to falciparum malaria such as hypotension , cerebral malaria , multiorgan dysfunction , hypoglycemia , thrombocytopenia , renal impairment , and hepatic dysfunction have been published . these manifestations may be due to the change in the clinical spectrum of disease , increase in resistance , indiscriminate use of anti - malarial drugs , delayed treatment , or missing the primaquine therapy . here , we present a case of acute cortical necrosis ( acn ) caused by p. vivax monoinfection in a young female from endemic zone of malaria which subsequently progressed to chronic kidney disease ( ckd ) . a 17-year - old female was referred from a primary health center in an endemic zone of malaria . she had a history of fever with chills , rigor , nausea , and headache . she developed reddish discoloration of urine 3 - 4 days following the onset of fever with progressive decrease in urine output and became anuric . there was no history of petechial hemorrhage , rash , loose stool , vomiting , cough , burning micturition , altered sensorium , or seizures . on examination , she was conscious , oriented , dyspneic at rest and had pallor , icterus , and anasarca . she was afebrile . she had pulse rate of 112/min , respiratory rate of 32/min and blood pressure was 170/100 mmhg . abdominal examination showed mildly enlarged liver with free fluid in the abdomen and had palpable spleen . her investigations at the time of admission and at discharge mentioned in detail in table 1 . diagnosis of p. vivax malaria was confirmed by rapid diagnosis test ( negative histidine - rich protein 2 of p. falciparum and positive p. vivax specific lactate dehydrogenase ) and peripheral blood smear examination . she was managed with who regimen of malaria and broad - spectrum intravenous antibiotic therapy . in next 2 days , patient 's respiratory parameters improved and she was weaned - off from the mechanical ventilation . her urine examination showed 2 + proteinuria , red blood cells ( rbcs ) and white blood cells per high power field . coomb 's test , c - reactive protein , d - dimer and fibrin degradation product level , antinuclear antibody , antidouble stranded dna , antineutrophil cytoplasmic antibody ( anca ) cytoplasmic - anca and perinuclear - anca , complement 3 and 4 , antiglomerular basement membrane antibody were normal . she had progressive decrease in hemoglobin level , platelet count , and increasing levels of serum urea and creatinine . diagnosis was kept as severe complicated malaria due to p. vivax with acute kidney injury , pulmonary edema , metabolic acidosis , hemolytic anemia , thrombocytopenia , and hyperbilirubinemia . she was kept on hemodialysis , and received six units of packed rbcs and five unit of platelet concentrates . kidney biopsy was done as renal function remained abnormal even after 3 weeks [ figures 13 ] kidney biopsy had 15 glomeruli which showed coagulative necrosis involving 9 glomeruli . coagulative necrosis of glomeruli ( arrow ) ; mild mesangial hypercellularity ( asterix ) ; tubules show presence of red blood cells and red blood cell casts ( arrow head ) and coagulative necrosis ( yellow arrow ) ( h and e , 100 ) presence of brown pigment in glomerular portion ( blue arrow ) ; coagulative necrosis of glomeruli ( black arrow ) ; red blood cell casts in tubule ( yellow arrow ) ; coagulative necrosis in tubules ( green arrow ) ; interstitium show edema and infiltration by lymphoplasmacytoid cells ( black star ) ( h and e , 100 ) silver stain shows features of coagulative necrosis of tubule and tubular red blood cell casts with interstitial infiltration of mononuclear cells ( 100 ) during hospital stay her urine output started increasing and she became dialysis independent . she was discharged on day 43 at serum creatinine of 2.6 mg / dl ( modification of diet in renal disease [ mdrd ] glomerular filtration rate [ gfr ] of 25.8 ml / min/1.73 m ) . she was on follow - up every month , at 3 months after discharge her serum creatinine was 2.4 mg / dl ( mdrd gfr of 28.3 ml / min/1.73 m ) ; in stage 4 ckd . p. falciparum infection causes severe and potentially fatal malaria and might present with severe complications like thrombocytopenia , acute tubular necrosis ( atn ) , acute respiratory distress syndrome ( ards ) , cerebral malaria , hypoglycemia , hypotension , and shock . p. vivax malaria ( benign tertian malaria ) is usually uncomplicated and is rarely fatal . in recent times , trends may be changing and there are reports of severe malaria due to p. vivax infection . severe malaria results from a combination of parasite - specific factors , such as adhesion and sequestration in the vasculature and the release of bio - active molecules , together with host inflammatory responses . p. vivax preferentially infects young rbcs , parasitemia rarely exceed 2% of circulating rbcs , and high parasite burdens are not a feature of severe disease . however , cytokine production during p. vivax infections is higher than p. falciparum infections of similar parasite biomass . in their study andrade et al . , found a strong linear trend between increased levels of c - reactive protein , tumor necrosis factor alpha ( tnf- ) , interferon gamma ( ifn- ) , ifn-/interleukin-10 ratio and the disease severity of p. vivax malaria . price et al . , reported that the plasma concentrations of tnf- are higher in p. vivax when compared to p. falciparum malaria with similar degree of parasitemia . several hypotheses have been described including mechanical obstruction caused by cytoadherence and sequestration of infected erythrocytes , immune - mediated glomerular pathology , and release of cytokines . p. vivax can cause both sequestration - related complications such as cerebral malaria , renal dysfunction , hepatic dysfunction , and ards and non sequestration - related complications such as anemia and thrombocytopenia . here , we reported a case of acn , an unusual complication of p. vivax monoinfection . this case illustrates that this parasite , which was supposed to be benign , can lead to serious complication like ckd . this region is the part of thar desert with hot and dry climate , which may exaggerate the clinical spectrum of the infectious diseases . a careful consideration of acn is required in patients who have prolonged oligo - anuria . p. vivax malaria can lead to ckd if such an adverse and rare complication develops . an integrated multidisciplinary approach is needed to study the changing spectrum of p. vivax infection . field studies , laboratory , molecular , and genomic methods can provide the way for better understanding of disease pathogenesis , prevention , control and treatment of malaria in endemic countries . epidemiologic studies , clinical description , and comparison of p. vivax with p. falciparum are needed to understand the dynamics and its interaction with the immune system . our case report highlights the fact that p. vivax monoinfection malaria can have wide range of presentation similar to p. falciparum and lead to serious , potentially life - threatening complications .
a young female with plasmodium vivax malaria presented with anemia , hyperbilirubinemia , thrombocytopenia , and advanced renal failure . 
 she remained anuric for more than 3 weeks . 
 kidney biopsy confirmed the diagnosis of acute cortical necrosis . during follow - up , she became dialysis independent , but remained in stage 4 chronic kidney disease ( ckd ) at 3 month . 
 p. vivax is supposed to be benign in nature , but can lead to rare and severe complication like renal cortical necrosis and progress to ckd .