Acute Kidney Injury in Children with Severe Malaria Is Common and Associated with Adverse Hospital Outcomes.

BACKGROUND: The prevalence of acute kidney injury (AKI) in children with severe malaria in sub-Saharan African may have been underestimated. The study aimed to determine the prevalence of AKI in children with severe malaria and its association with adverse hospital outcomes. METHODS: At presentation, we measured complete blood count, serum bilirubin, and serum electrolytes, urea and creatinine in children with severe malaria. At 24 h after hospitalization, we repeated serum creatinine measurement. Urine passed in the first 24 h of hospitalization was also measured. We defined AKI and its severity using the Kidney Disease: Improving Global Outcome AKI guidelines. RESULTS: The study involved 244 children (53.3% males) with a median age of 3.5 (1.9-7.0) years. One hundred and forty-four (59%) children had AKI, and it reached maximum Stages 1, 2 and 3 in 56 (23%), 45 (18.4%) and 43 (17.6%) children, respectively. The majority (86.1%) with AKI had only elevated serum creatinine. Mortality increased with increasing severity of AKI on univariate analysis but weakened on multiple logistic regression. Mortality was also higher in those with both oliguria and elevated serum creatinine than in those with elevated serum creatinine only (50% vs. 4.8%, p < 0.001). Furthermore, children with AKI spent three days more in hospital than those without AKI (p < 0.001). CONCLUSIONS: Acute kidney injury complicates severe malaria in 6 out of every 10 children and is commonly identified using elevated serum creatinine. It is also associated with adverse hospital outcome.

Age-Related Clinical Spectrum of Plasmodium knowlesi Malaria and Predictors of Severity.

Background: Plasmodium knowlesi is increasingly reported in Southeast Asia, but prospective studies of its clinical spectrum in children and comparison with autochthonous human-only Plasmodium species are lacking. Methods: Over 3.5 years, we prospectively assessed patients of any age with molecularly-confirmed Plasmodium monoinfection presenting to 3 district hospitals in Sabah, Malaysia. Results: Of 481 knowlesi, 172 vivax, and 96 falciparum malaria cases enrolled, 44 (9%), 71 (41%), and 31 (32%) children aged ≤12 years. Median parasitemia was lower in knowlesi malaria (2480/µL [interquartile range, 538-8481/µL]) than in falciparum (9600/µL; P < .001) and vivax malaria. In P. knowlesi, World Health Organization-defined anemia was present in 82% (95% confidence interval [CI], 67%-92%) of children vs 36% (95% CI, 31%-41%) of adults. Severe knowlesi malaria occurred in 6.4% (95% CI, 3.9%-8.3%) of adults but not in children; the commenst severity criterion was acute kideny injury. No patient had coma. Age, parasitemia, schizont proportion, abdominal pain, and dyspnea were independently associated with severe knowlesi malaria, with parasitemia >15000/µL the best predictor (adjusted odds ratio, 16.1; negative predictive value, 98.5%; P < .001). Two knowlesi-related adult deaths occurred (fatality rate: 4.2/1000 adults). Conclusions: Age distribution and parasitemia differed markedly in knowlesi malaria compared to human-only species, with both uncomplicated and severe disease occurring at low parasitemia. Severe knowlesi malaria occurred only in adults; however, anemia was more common in children despite lower parasitemia. Parasitemia independently predicted knowlesi disease severity: Intravenous artesunate is warranted initially for those with parasitemia >15000/µL.

Visceral leishmaniasis-associated nephropathy in hospitalised Brazilian patients: new insights based on kidney injury biomarkers.

OBJECTIVE: To evaluate the usefulness of early acute kidney injury (AKI) biomarkers in clinical management of visceral leishmaniasis. METHODS: Prospective study with 50 hospitalised VL patients. AKI biomarkers, that is, serum and urinary neutrophil gelatinase-associated lipocalin (sNGAL, uNGAL, respectively), urinary kidney injury molecule-1 (uKIM-1) and urinary monocyte chemotactic protein-1 (uMCP-1), were quantified by immunoassay (ELISA). Also, interferon-gamma (INF-y) and C-reactive protein (CRP) were evaluated as inflammatory biomarkers possibly related to VL severity. RESULTS: VL patients had hyponatremia, hypoalbuminemia, hypergammaglobulinemia, haematologic and hepatic disorders. AKI was found in 46%, and one death (2%) occurred. The AKI group had significant longer hospital stay, lower levels of IFN-y and higher levels of CRP, more clinical renal abnormalities and higher levels of sNGAL, uNGAL, uKIM-1 and uMCP-1. Overall, sNGAL, uKIM-1 and uMCP-1 showed correlations with important clinical renal abnormalities, such as proteinuria, albuminuria, serum creatinine and glomerular filtration rate using adjusted correlations with CRP and IFN-y. Only sNGAL showed an early association with AKI development (OR = 2.78, 95% CI = 1.429-5.428, per each increase of 50 ng/ml), even after adjusting for clinical signals of VL severity and for immune biomarkers. Moreover, sNGAL showed a better performance in predicting AKI development (AUC-ROC = 0.81, 95% CI = 0.69-0.93; cut-off = 154 ng/ml, sensitivity = 82.6%, specificity = 74.1%, P < 0.001). CONCLUSIONS: Visceral leishmaniasis-associated nephropathy showed important proximal tubular injury and glomerular inflammation. Serum NGAL showed an early association with VL-associated nephropathy and may be used to improve clinical management strategies and decrease morbimortality in VL patients.

Diagnostic performance of salivary urea nitrogen dipstick to detect and monitor acute kidney disease in patients with malaria.

BACKGROUND: Acute kidney injury (AKI) is a common complication of malaria. In low resource settings, a lack of diagnostic tools and delayed treatment of malaria associated AKI lead to significant morbidity and mortality. The aim of this study was to assess the diagnostic performance of salivary urea nitrogen (SUN) dipstick to detect and monitor kidney disease [KD = AKI or acute kidney disease (AKD) without AKI] in malaria patients in Angola. METHODS: Patients 11-50 years old admitted with malaria at the Josina Machel (Maria-Pia) Hospital, Luanda, Angola, between 2nd March and 10th May 2016 were enrolled in this study. All participants had serum creatinine (sCr), blood urea nitrogen (BUN) and SUN dipstick tested at the time of recruitment and daily for up to 4 days. AKD without AKI refers to acute renal impairment which do not fulfilled the main criteria for AKI (increases in the baseline serum creatinine and/or decreases in urine output) according defined by the kidney disease improving global outcomes (KDIGO) guideline. RESULTS: Eight-six patients were admitted with malaria diagnosis (mean age 21.5 ± 9.4 years, 71% male) and 27 (32%) were diagnosed with KD. The mean (± SD) sCr and BUN of the KD group at admission (day 0) were 5.38 (± 5.42) and 99.4 (± 61.9) mg/dL, respectively. Three (3.5%) patients underwent haemodialysis and eight (9.3%) died within the first 4 days of hospital admission [5 (62.5%) with KD; 3 (37.5%) without kidney disease; p = 0.047]. The SUN threshold for KD diagnosis was tested pad #5 (SUN > 54 mg/dL). At this threshold, the SUN dipstick had a sensitivity of 67% and specificity of 98% to diagnose KD. The area under the receiver operating characteristics curve (ROC) for KD diagnosis on admission was 0.88 (95% CI 0.79-0.96). The SUN dipstick was most accurate at higher levels of BUN. CONCLUSION: The SUN dipstick had reasonable sensitivity and excellent specificity when used to diagnose KD in a cohort of patients with malaria in a resource-limited setting. Given the severity of presenting illness and kidney injury, the SUN dipstick diagnostic threshold was high (test pad #5). SUN may be used to detect AKI in patients with malaria in low resources settings, thus facilitating earlier access to adequate treatment, which may improve survival.

Acidosis and acute kidney injury in severe malaria.

BACKGROUND: In severe falciparum malaria metabolic acidosis and acute kidney injury (AKI) are independent predictors of a fatal outcome in all age groups. The relationship between plasma acids, urine acids and renal function was investigated in adult patients with acute falciparum malaria. METHODS: Plasma and urinary acids which previously showed increased concentrations in proportion to disease severity in patients with severe falciparum malaria were quantified. Patients with uncomplicated malaria, sepsis and healthy volunteers served as comparator groups. Multiple regression and multivariate analysis were used to assess the relationship between organic acid concentrations and clinical syndromes, in particular AKI. RESULTS: Patients with severe malaria (n = 90), uncomplicated malaria (n = 94), non-malaria sepsis (n = 19), and healthy volunteers (n = 61) were included. Univariate analysis showed that both plasma and creatinine-adjusted urine concentrations of p-hydroxyphenyllactic acid (pHPLA) were higher in severe malaria patients with AKI (p < 0.001). Multiple regression analysis, including plasma or creatinine-adjusted urinary acids, and PfHRP2 as parasite biomass marker as independent variables, showed that pHPLA was independently associated with plasma creatinine (ß = 0.827) and urine creatinine (ß = 0.226). Principal component analysis, including four plasma acids and seven urinary acids separated a group of patients with AKI, which was mainly driven by pHPLA concentrations. CONCLUSIONS: Both plasma and urine concentrations of pHPLA closely correlate with AKI in patients with severe falciparum malaria. Further studies will need to assess the potential nephrotoxic properties of pHPLA.

Chitinase-3-like 1 is a biomarker of acute kidney injury and mortality in paediatric severe malaria.

BACKGROUND: Chitinase-3-like 1 (CHI3L1) is a glycoprotein elevated in paediatric severe malaria, and an emerging urinary biomarker of acute kidney injury (AKI). Based on the hypothesis that elevated CHI3L1 levels in malaria are associated with disease severity, the relationship between plasma CHI3L1 levels, AKI and mortality was investigated in Ugandan children enrolled in a clinical trial evaluating inhaled nitric oxide (iNO) as an adjunctive therapy for severe malaria. METHODS: Plasma CHI3L1 levels were measured daily for 4 days in children admitted to hospital with severe malaria and at day 14 follow up. AKI was defined using the Kidney Disease: Improving Global Outcomes consensus criteria. This is a secondary analysis of a randomized double-blind placebo-controlled trial of iNO versus placebo as an adjunctive therapy for severe malaria. Inclusion criteria were: age 1-10 years, and selected criteria for severe malaria. Exclusion criteria included suspected bacterial meningitis, known chronic illness including renal disease, haemoglobinopathy, or severe malnutrition. iNO was administered by non-rebreather mask for up to 72 h at 80 ppm. RESULTS: CHI3L1 was elevated in patients with AKI and remained higher over hospitalization (p < 0.0001). Admission CHI3L1 levels were elevated in children who died. By multivariable analysis logCHI3L1 levels were associated with increased risk of in-hospital death (relative risk, 95% CI 4.10, 1.32-12.75, p = 0.015) and all-cause 6 month mortality (3.21, 1.47-6.98, p = 0.003) following correction for iNO and AKI. Treatment with iNO was associated with delayed CHI3L1 recovery with a daily decline of 34% in the placebo group versus 29% in the iNO group (p = 0.012). CHI3L1 levels correlated with markers of inflammation (CRP, sTREM-1, CXCL10), endothelial activation (Ang-2, sICAM-1) and intravascular haemolysis (LDH, haem, haemopexin). CONCLUSIONS: CHI3L1 is a novel biomarker of malaria-associated AKI and an independent risk factor for mortality that is associated with well-established pathways of severe malaria pathogenesis including inflammation, endothelial activation, and haemolysis. Trial registration Clinicaltrials.gov, NCT01255215. Registered December 7th 2010.

Expression of cleaved caspase-3 in renal tubular cells in Plasmodium falciparum malaria patients.

AIM: In Plasmodium falciparum malaria, the clinical manifestation of acute kidney injury (AKI) is commonly associated with acute tubular necrosis (ATN) in the kidney tissues. Renal tubular cells often exhibit various degrees of cloudy swelling, cell degeneration, and frank necrosis. To study individual cell death, this study evaluates the degree of renal tubular necrosis in association with apoptosis in malarial kidneys. METHODS: Kidney tissues from P. falciparum malaria with AKI (10 cases), and without AKI (10 cases) were evaluated for tubular pathology. Normal kidney tissues from 10 cases served as controls. Tubular necrosis was assessed quantitatively in kidney tissues infected with P. falciparum malaria, based on histopathological evaluation. In addition, the occurrence of apoptosis was investigated using cleaved caspase-3 marker. Correlation between tubular necrosis and apoptosis was analyzed. RESULTS: Tubular necrosis was found to be highest in P. falciparum malaria patients with AKI (36.44% ± 3.21), compared to non-AKI (15.88% ± 1.63) and control groups (2.58% ± 0.39) (all p < 0.001). In the AKI group, the distal tubules showed a significantly higher degree of tubular necrosis than the proximal tubules (p = 0.021) and collecting tubules (p = 0.033). Tubular necrosis was significantly correlated with the level of serum creatinine (r = 0.596, p = 0.006), and the occurrence of apoptosis (r = 0.681, p = 0.001). CONCLUSION: In malarial AKI, the process of apoptosis occurs in ATN.

P. vivax Malaria presenting as Thrombotic Microangiopathy.

INTRODUCTION: Acute kidney injury (AKI) is reported to occur in patients with falciparum malaria but not uncommon with vivax malaria. AKI, anemia, thrombocytopenia and jaundice is a recurrent finding in severe malaria and can mimic as thrombotic microangiopathy (TMA). Relationship of malaria with TMA is unclear till date however evidences suggest their association. METHODS & MATERIAL: We reviewed our electronic database to evaluate relationship of malaria with TMA, of cases of malaria, jaundice and AKI. RESULTS: 4 patients found to have P. vivax malaria and histopathologically confirmed TMA. All had fever, oliguria, jaundice at presentation. The time between onset of symptoms and admission ranged from 7 to 14 days. All had parasitemia at presentation so were treated with Artesuanate. Hemodialysis and Plasmapheresis was done in all patients. On follow-up all patients recovered and asymptomatic urinary abnormality persisting in one patient. CONCLUSION: High index of suspicion should be kept for TMA in a patient who has nonrecovering AKI with persistent anemia and thrombocytopenia even after clinical and laboratory evidences of recovery from malaria, as response to plasmapheresis seems excellent in this subset of malarial AKI. There could be a pathogenetic link between P.vivax and TMA though yet to be confirmed in larger studies.

Ruling out nosocomial transmission of Cryptosporidium in a renal transplantation unit: case report.

BACKGROUND: Cryptosporidium spp. is a ubiquitous parasite affecting humans as well as domestic and wild vertebrates, causing diarrhea in both immunocompetent and immunocompromised hosts worldwide. Its transmission occurs primarily by the fecal-oral route. In humans, C. parvum and C. hominis are the most prevalent species, whereas immunocompetent and immunocompromised individuals can also be infected by other zoonotic species. Renal transplant patients are prone to develop cryptosporidiosis, which can induce severe and life-threatening diarrhea. CASE PRESENTATION: We report here a series of nearly concomitant cases of acute symptomatic cryptosporidiosis in three renal transplant patients attending the Strasbourg University Hospital Nephrology Unit. The clinical presentation was persistent diarrhea and acute renal failure. The diagnosis was confirmed by microscopic stool examination using a modified Ziehl-Neelsen staining method and species identification by molecular tools. All patients were treated with nitazoxanide and recovered from diarrhea after 14 days of therapy. CONCLUSION: Genotypic species identification was not consistent with an epidemic context, thus underlining the need for genotyping to monitor at risk patients.

Fever, thrombocytopenia, and AKI-A profile of malaria, dengue, and leptospirosis with renal failure in a South Indian tertiary-care hospital.

INTRODUCTION: In the tropics, the triad of fever, thrombocytopenia, and AKI portends a grim prognosis with high mortality and a severe strain on already-stretched resources. Malaria, dengue, and leptospirosis account for most cases. We undertook a review of cases to determine factors accounting for adverse prognosis. METHODS: All patients presenting to the emergency room (ER) with a history of fever, thrombocytopenia, and renal failure were included in the study. Patients were followed until discharge or death, and end points looked at were 1-week and 30-day mortality, and renal function upon discharge. Parameters like liver function test (LFT), renal function, and platelet count upon discharge were also documented. RESULTS: A total of 43 patients was included in the study. Mean age was 42.5 years with 86% males. Mean APACHE and SOFA scores on admission were 23.89 and 15.42, respectively. Mean admission platelet counts were 41,000. Mean serum creatinine was 4.1, and bilirubin was 9.94. A platelet count of < 34,000, serum creatinine of > 4, albumin of > 2.3, SOFA score of > 20, and APACHE score of > 32.2 were significantly predictive of 1 week mortality. Need for mechanical ventilation, oliguria on admission, and need for dialysis all were highly predictive of 30-day mortality. In addition, a serum bicarbonate of < 12, INR of > 1.5, hemoglobin of < 9.5 were highly predictive of higher 30 day mortality. Overall, 1-week mortality was 16.3%, of which 48% was accounted for by patients with leptospirosis. CONCLUSIONS: Factors like low platelet count, oliguria, need for dialysis, high APACHE and SOFA scores on admission, need for mechanical ventilation, and low serum albumin portend a grave prognosis. There is need for randomized control trials (RCT) to further determine adverse prognostic factors in this subsect of patients.

AN IMPORTED CASE OF COMPLICATED FALCIPARUM MALARIA.

The paper describes a clinical case of imported severe Pfalciparum malaria in a French citizen treated at the clinic of the Research Institute of Epidemiology, Microbiology, and Infectious Disdases, Ministry of the Republic of Uzbekistan. Due to the fact that the patient with tropical malaria sought medical advice too late, the disease was complicated by grade I malaria-induced coma, acute renal failure- in an oliguric phase, severe anemia, and disseminated intravascular coagulation syndrome. Thanks to effective etiopathogenetic and pathogenetic therapy, the patient recovered and returned to his motherland.

Severe falciparum malaria treated with artesunate complicated by delayed onset haemolysis and acute kidney injury.

BACKGROUND: Severe falciparum malaria may be complicated by haemolysis after parasite clearance, however the mechanisms remain unclear. Recent reports describe a pattern of delayed onset haemolysis among non-immune travellers with hyperparasitaemia treated with intravenous artesunate, termed post-artesunate delayed haemolysis (PADH). The occurrence and clinical impact of PADH following severe malaria infections in areas of unstable transmission are unknown. CASE: A 45-year-old Bangladeshi male was initially admitted to a local hospital with severe falciparum malaria complicated by hyperparasitaemia and treated with intravenous artesunate. Twenty days from his first presentation he was readmitted with delayed onset haemolytic anaemia and acute kidney injury. Multiple blood transfusions and haemodialysis were required. Renal biopsy revealed acute tubular injury and haem pigment nephropathy. His haemoglobin and renal function recovered to baseline after 62 days from his second admission. DISCUSSION: This case highlights the differential diagnosis of post-malaria delayed onset haemolysis, including the recently described syndrome of post-artemisinin delayed haemolysis. The pathophysiology contributing to acute kidney injury in this patient and the limited treatment options are discussed. CONCLUSIONS: This report describes PADH complicated by acute kidney injury in an adult patient living in a malaria hypoendemic region who subsequently required blood transfusions and haemodialysis. This case emphasizes the importance of routine follow up of haemoglobin and renal function in artesunate-treated patients who have recovered from severe malaria.

Acute kidney injury in imported Plasmodium falciparum malaria.

BACKGROUND: Acute kidney injury (AKI) is a known complication of malaria, and is reported to occur in up to 40% of adult patients with a severe Plasmodium falciparum infection in endemic regions. To gain insight in the incidence and risk factors of AKI in imported P. falciparum malaria, a retrospective analysis was performed on a large cohort of mostly non-immune patients with imported P. falciparum malaria. Aiming to include not only severe but also milder forms of renal failure, the KDIGO criteria were used to define AKI. METHODS: Clinical and laboratory data from 485 consecutive cases of imported P. falciparum malaria were extracted from the Rotterdam Malaria Cohort database. Acute kidney injury (AKI) was defined using the KDIGO criteria. Univariate and multivariate logistic regression analyses were used to identify risk factors for AKI. RESULTS: AKI was seen in 39 (8%) of all patients and in 23 (38%) of the 61 patients with severe malaria. Eight patients eventually needed renal replacement therapy (RRT); seven of them already had AKI at presentation. Higher age, higher leucocyte count and thrombocytopaenia were independently-associated with AKI but their positive predictive values were relatively poor. CONCLUSION: AKI was found to be a common complication in adults with imported P. falciparum necessitating RRT in only a small minority of patients. The use of the KDIGO staging allows early recognition of a decline in renal function.

A link between circulating immune complexes and acute kidney injury in human visceral leishmaniasis.

Visceral leishmaniasis (VL) is an infectious disease caused by Leishmania infantum. Clinically, VL evolves with systemic impairment, immunosuppression and hyperactivation with hypergammaglobulinemia. Although renal involvement has been recognized, a dearth of understanding about the underlying mechanisms driving acute kidney injury (AKI) in VL remains. We aimed to evaluate the involvement of immunoglobulins (Igs) and immune complexes (CIC) in the occurrence of AKI in VL patients. Fourteen VL patients were evaluated between early treatment and 12 months post-treatment (mpt). Anti-Leishmania Igs, CIC, cystatin C, C3a and C5a were assessed and correlated with AKI markers. Interestingly, high levels of CIC were observed in VL patients up to 6 mpt. Concomitantly, twelve patients met the criteria for AKI, while high levels of cystatin C were observed up to 6 mpt. Plasmatic cystatin C was positively correlated with CIC and Igs. Moreover, C5a was correlated with cystatin C, CIC and Igs. We did not identify any correlation between amphotericin B use and kidney function markers in VL patients, although this association needs to be further explored in subsequent studies. Our data reinforce the presence of an important renal function impairment during VL, suggesting the involvement of Igs, CIC, and C5a in this clinical condition.

Babesiosis-induced acute kidney injury with prominent urinary macrophages.

Babesia is an obligate intracellular erythrocyte parasite that can infect humans. Severe symptomatic disease from massive hemolysis and multiorgan system failure, including acute kidney injury (AKI), occurs. Acute tubular injury from a combination of volume depletion and heme pigment toxicity from profound hemolysis is the most common cause of AKI. We present a case of severe babesiosis complicated by dialysis-requiring AKI with the unique finding of large macrophages containing engulfed erythrocyte fragments in urine sediment. This urinary finding raised the possibility of another diagnosis distinct from acute tubular injury. Subsequent kidney biopsy demonstrated infection-associated acute interstitial nephritis.

Outcome of malaria-associated acute kidney injury: a prospective study from a single center.

OBJECTIVE: The aim of this prospective study was to determine the outcome of patients suffering from malaria with acute renal dysfunction. METHODS: All adult patients of laboratory-proven malaria with acute kidney injury (AKI) admitted during the period of May 2010 to June 2011 were included. Patient characteristics, physical examination findings, and laboratory parameters were recorded. Patient outcome was assessed in terms of peak serum creatinine level, duration of hospital stay, need for dialysis, and in-hospital mortality rate. Surviving patients were followed up for 3 months to determine progression to chronic kidney disease. RESULTS: This study enrolled 101 patients of malarial AKI. Mean age was 33.70 ± 15.39 years. Oliguric AKI was observed in 44.6% cases. Mean duration of hospital stay was 8.75 ± 7.60 days. Renal replacement therapy was required in 36.6% patients. Ten (9.9%) patients succumbed to illness during hospital stay. Majority of deaths occurred shortly after admission. Mortality risk was significantly associated with raised LDH (p = 0.019), lower hemoglobin level (p = 0.015), raised aspartate transaminases (p < 0.001), and elevated alanine transaminases (p = 0.016). Cerebral malaria was an important determinant of mortality (p = 0.002). Renal parameters, including severity of renal dysfunction and need for dialysis, were not associated with mortality risk. Among 91 survivors, 79 patients completed a 3-month follow-up and all of them had normalization of renal function. CONCLUSION: We observed 9.9% in-hospital mortality rate in the study cohort. Cerebral malaria was an important risk factor for mortality in malarial AKI patients. Severity of renal dysfunction did not correlate with the mortality risk in our study.

A case of imported severe plasmodium falciparum malaria in the emergency department and the current role of exchange transfusion treatment.

BACKGROUND: The role of exchange transfusion in the management of severe malaria is not well documented in Emergency Medicine literature. OBJECTIVES: The goal of this article is to review the importance of considering malaria in the differential diagnosis of the febrile returned traveler and to discuss the role of exchange transfusion in the management of severe Plasmodium falciparum malaria. CASE REPORT: A 59-year-old woman presented to the Emergency Department (ED) with severe P. falciparum malaria. Her physical examination was remarkable for scleral icterus, dry mucous membranes, and tachycardia. Her complete blood count revealed a white blood cell count of 6.9 k/uL, with 71% segmented neutrophils, 19% bands, a hemoglobin level of 11.9 g/dL, hematocrit of 37.2%, and a platelet count of 9 k/uL. Hepatorenal impairment was present and malaria parasites with ring form were seen on malaria prep in 18% of red blood cells. The patient was treated with fluids, platelets, quinidine gluconate, doxycycline, and exchange transfusion with significant improvement in the patient's clinical condition. CONCLUSIONS: The high level of parasitemia presenting with acute kidney injury, hyperbilirubinemia, and thrombocytopenia supported the use of exchange transfusion as adjunct therapy. Exchange transfusion was a reasonable consideration in this case and was well tolerated by our patient. Institutions that are equipped with apheresis units should evaluate each case individually in concert with Centers for Disease Control experts and local consultants and weigh the risks and benefits of the use of exchange transfusion as an adjunct in the treatment of severe P. falciparum malaria.

Intestinal infestation with Fasciolopsis buski leading to acute kidney injury.

Fasciolopsis buski is the largest intestinal fluke infecting human beings. This trematode is endemic in certain parts of the country. Migration poses the risk of spread of the worm to other parts of the country. We report fasciolopsis buski in a migrant from Bihar working in Coimbatore, Tamil Nadu. Acute kidney injury following intestinal obstruction occurred in this case which was never described before.

Unrecognized malaria and its consequences--a case report of severe malaria with acute renal failure.

Severe malaria is a medical emergency that requires urgent recognition and treatment, because it may rapidly progress to serious complications and death. We report a case of imported severe malaria tropica in an adult traveller, with a parasitemia of 20%, complicated by acute renal failure. Patient was initially misdiagnosed by a physician unaware of the importance of patients travel history, as having a viral infection. Despite the treatment delay, the patient was successfully cured with parenteral artemether combined with peroral mefloquine and vigorous supportive measures including renal replacement therapy.

Plasmodium vivax malaria-associated acute kidney injury, India, 2010-2011.

Plasmodium vivax is causing increasingly more cases of severe malaria worldwide. Among 25 cases in India during 2010-2011, associated conditions were renal failure, thrombocytopenia, jaundice, severe anemia, acute respiratory distress syndrome, shock, cerebral malaria, hypoglycemia, and death. Further studies are needed to determine why P. vivax malaria is becoming more severe.