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Department of Nephrology, Postgraduate Institute of Medical Education and Research, Chandigarh, India. Received 20 October 2007. Revised 29 January 2008.
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Journal of Pediatric Infectious Diseases 3 (2008) 145–147 IOS Press

Case Report

Acute renal failure and severe thrombocytopenia in a young boy with vivax malaria Devidayala,∗, Zulfikar Jabbarb , Selva Kumara and Meenu Singh a a

Department of Pediatrics, Advanced Pediatric Center, Postgraduate Institute of Medical Education and Research, Chandigarh, India b Department of Nephrology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Received 20 October 2007 Revised 29 January 2008 Accepted 3 February 2008

Abstract. This 7-year-old boy presented with acute renal failure associated with Plasmodium vivax infection. In addition, he had severe thrombocytopenia. These apparently serious manifestations are rare in P. vivax malaria but respond favorably to antimalarials and supportive therapy.

Keywords: Vivax malaria, acute renal failure, thrombocytopenia

1. Introduction Malarial renal failure in children is commonly due to Plasmodium falciparum. Plasmodium vivax can occasionally cause severe renal failure requiring dialysis [1]. Severe thrombocytopenia, a common feature of P. falciparum infection, is sometimes seen in vivax malaria also [2]. However, a combination of these unusual manifestations is rare and prompted us to report this case with a view to highlight the good outcome with early supportive therapy combined with antimalarials.

∗ Correspondence: Dr. Devidayal, Assistant Professor, Department of Pediatrics, Advanced Pediatric Center, Postgraduate Institute of Medical Education and Research, Chandigarh-160012, India. Tel.: +91 172 2755657 (O); +91 172 2725781 (R); Fax: +91 172 274440; 2745078; E-mail: [email protected].

2. Case report A 7-year-old boy was referred to our hospital for acute renal failure. His illness began 10 days back with high-grade intermittent fever without rigors or chills. There was no history to suggest localization to any organ system. On day 5 of illness, urine output decreased and he became anuric from day 6. Investigations done at the referring clinic had shown hemoglobin of 7 g/dL, leukocyte count 6000/mm 3 and reduced platelets on smear. Trophozoites and ring forms of P. vivax were seen on peripheral smear without evidence of hemolysis. Serum urea and creatinine were 96.2 and 3.0 mg/dL respectively. A Widal test had been negative. Abdominal ultrasound revealed normal sized kidneys (right measuring 8.0 × 3.3 cm and left 8.3 × 3.8 cm). He had received a course of chloroquine before referral to our institute.

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Devidayal et al. / Vivax malaria in a boy

Examination showed both weight (15 kg) and height (108.5 cm) below 3rd centile. Both parents were short and mid-parental height was only 148.5 cm. He had marked pallor but no icterus, edema or lymphadenopathy. His vital parameters were normal except acidotic breathing pattern. Abdominal examination revealed hepatomegaly (liver span 11.5 cm) and splenomegaly (5 cm below left costal margin). Other systemic examination was unremarkable. A diagnosis of severe malaria with acute renal failure and thrombocytopenia was made at presentation. Investigations revealed hemoglobin of 4.5 g/dL, leukocyte count of 9400/mm 3 (neutrophils 63%, lymphocytes 30%, monocytes 4%, eosinophils 3%) and platelet count of 34,000/mm. 3 Serum urea was 105 mg/dL and creatinine 6.0 mg/dL. A rapid card test (QDx Malaria Pv/Pf, Nicholas Piramal India) which is based on detection of P. falciparum specific histidine rich protein-2 and P. vivax specific lactate dehydrogenase antigen was positive for P. vivax and negative for P. falciparum. Initial blood gas analysis showed metabolic acidosis (pH, 7.25). Coagulation profile and glucose-6-phosphate dehydrogenase levels were within normal limits. Plasma hemoglobin was not significantly elevated. Total serum bilirubin was 0.7 mg/dL with normal transaminase levels. Urine examination done on day 3 of admission did not reveal any casts, erythrocyte, albumin or hemoglobin. Cultures of urine grew Escherichia coli and Candida albicans during 2nd week of hospitalization. Blood and repeat urine cultures were sterile. In view of anuria, azotemia and acidosis, a peritoneal dialysis was initiated. Acidosis and anuria improved but azotemia persisted after 50 cycles. Dialysis was not repeated in absence of acute complications of renal failure. Renal functions showed a gradual return (maximum serum urea 280 mg/dL and creatinine 7.0 mg/dL on day 3 of hospitalization) to normal a month after admission. Fever became passive on day 6 of hospital stay and hepatosplenomegaly regressed completely over 3 weeks. Hemoglobin rose to 8.7 g/dL on day 7 without requiring a blood transfusion. The reticulocyte count was 10.7%. Platelet count improved to 72,000/mm 3 on day 3 and 200,000/mm 3 on day 7 of stay in the hospital. He was not noted to have hypotension, dehydration, icterus or dark urine during hospitalization. Specific antimalarial therapy was started with intravenous quinine hydrochloride given for 2 days and completed with oral quinine sulfate for a total of 7 days. In addition, he received primaquine, antibiotics and antifungals during hospital admission.

3. Discussion Renal involvement in malaria varies widely from abnormal urinary sediment to acute renal failure. While P. falciparum accounts for majority of cases of malarial acute renal failure, P. vivax has been variously reported to range from 2.4–14% [1,3,4]. The authors of the paper that reported high percentage of vivax renal failure, acknowledged in a subsequent communication that possibility of a mixed infection could not be completely ruled out [5]. In children also, malarial renal failure is predominantly due to falciparum species. Although some impairment of renal function in the form of decreased endogenous creatinine clearance is demonstrable in vivax infections also, the progression to severe renal failure is rare [6]. The diagnosis of vivax malaria in the index patient was based on smear positivity and card test positive for P . vivax and negative for P. falciparum thereby ruling out the possibility of a mixed infection. The rapid card test has a high accuracy to exclude P. falciparum infection [7]. None of the possible etiological factors [1,3,8] observed previously viz. hypotension, hyperbilirubinemia, disseminated intravascular coagulation and sepsis was seen in our patient. We presumed that marked azotemia was possibly due to renal ischemia related to endothelial cytoadherence, sequestration and capillary lumen obstruction by sticky cell aggregates; a mechanism proposed by some previous authors also [3,9]. Since the index patient was anuric at presentation, the possibility that volume depletion had caused or contributed to the renal failure can not be excluded. Our patient also showed severe thrombocytopenia at admission, which improved over a week of hospitalization without requiring platelet transfusions. Previously thought to be a rare manifestation of vivax malaria [10,11] a few recent reports suggest this to be more commonly associated and may even be taken as an early indicator of acute infection [2,12,13]. A variety of immunological and non-immunological mechanisms have been suggested to cause thrombocytopenia in malaria [12,13]. In our patient, hypersplenism could have accounted for thrombocytopenia as spleen had shown moderate enlargement over initial few days of illness. A combination of severe thrombocytopenia and renal failure similar to the index patient has also been reported recently [14]. The prognosis of acute renal failure in vivax malaria is said to be favorable with majority of patients recovering after antimalarials and peritoneal dialysis and mortality is low [3]. Our patient also demonstrated a

Devidayal et al. / Vivax malaria in a boy

relatively benign course. Despite being anuric for 4 days at presentation, the dialysis requirement was minimal and subsequent recovery of renal function was spontaneous. It is extremely important to highlight the favorable prognosis despite presence of seemingly serious manifestations so that attending physicians don’t get deterred in offering timely and aggressive therapy. Although chloroquine resistant vivax malaria is rare in India [15], we used quinine keeping in view the severity of illness at presentation and prior treatment with chloroquine.

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