Acute Kidney Injury in Children With Visceral Leishmaniasis

Libório, Alexandre Braga; Rocha, Natália A.; Oliveira, Michelle Jacintha Cavalcante; Franco, Luiz F. L. G.; Aguiar, Graziela B. R.; Pimentel, Rodrigo; Abreu, Krasnalhia Lívia S.; Silva, Geraldo Bezerra da; Daher, Elizabeth De Francesco

doi:10.1097/inf.0b013e318247f533

Cited by 33 publications

(27 citation statements)

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“…The main difference is a lower cutoff SCr to achieve the F category, requiring a GFR lower than 35 mL/min instead of a SCr of 4.0 mg/dL. Several studies have also validated pRIFLE in children, mainly in critically ill patients or after cardiac surgery [11–16]. After that, it was mathematically demonstrated that it is not necessary to calculate the GFR and that, by using only the SCr increment, it was possible to diagnose and to assess AKI severity [17].…”

Section: Acute Kidney Injury Definitionmentioning

confidence: 99%

Acute Kidney Injury in Neonates: From Urine Output to New Biomarkers

Libório

Branco

Bezerra

2014

BioMed Research International

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In the past 10 years, great effort has been made to define and classify a common syndrome previously known as acute renal failure and now renamed “acute kidney injury (AKI).” Initially suggested and validated in adult populations, AKI classification was adapted to the pediatric population and recently has been modified for the neonatal population. Several studies have been performed in adults and older children using this consensus definition, leading to improvement in the knowledge of AKI incidence and epidemiology. In spite of these advances, the peculiar renal pathophysiology of critically ill newborn patients makes it difficult to interpret urine output (UO) and serum creatinine (SCr) levels in these patients to diagnose AKI. Also, new urine biomarkers have emerged as a possible alternative to diagnose early AKI in the neonatal population. In this review, we describe recent advances in neonatal AKI epidemiology, discuss difficulties in diagnosing AKI in newborns, and show recent advances in new AKI biomarkers and possible long-term consequences after AKI episode.

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Section: Acute Kidney Injury Definitionmentioning

confidence: 99%

Acute Kidney Injury in Neonates: From Urine Output to New Biomarkers

Libório

Branco

Bezerra

2014

BioMed Research International

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“…In Brazil, VL is endemic with 3298 cases in 2015, being responsible for 272 deaths, with a lethality rate of almost 8% . VL‐associated nephropathy has been related with higher mortality in these patients .…”

Section: Introductionmentioning

confidence: 99%

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

Meneses

Daher

Silva

et al. 2018

Tropical Med Int Health

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“…5,6 However, VLassociated kidney disease is progressive and, without therapy, can result in end-stage renal disease (ESRD; approximately 1.5% of human cases). 4 Previous reports regarding the pathophysiology of VL-associated renal disease are conflicting, showing either presence or absence of IgG Q16 and complement protein C3. 1,7 Accurate assessment of VL-associated glomerular lesions early in their progression is essential to determining an efficacious treatment regimen and aid in determining prognosis.…”

Section: Q15mentioning

confidence: 99%

Activation of Autophagy and Nucleotide-Binding Domain Leucine-Rich Repeat–Containing-Like Receptor Family, Pyrin Domain–Containing 3 Inflammasome during Leishmania infantum–Associated Glomerulonephritis

Esch

Schaut

Lamb

et al. 2015

The American Journal of Pathology

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Chronic kidney disease is a major contributor to human and companion animal morbidity and mortality. Renal complications are sequelae of canine and human visceral leishmaniasis (VL). Despite the high incidence of infection-mediated glomerulonephritis, little is known about pathogenesis of VL-associated renal disease. Leishmania infantum-infected dogs are a naturally occurring model of VL-associated glomerulonephritis. Membranoproliferative glomerulonephritis type I [24 of 25 (96%)], with interstitial lymphoplasmacytic nephritis [23 of 25 (92%)], and glomerular and interstitial fibrosis [12 of 25 (48%)] were predominant lesions. An ultrastructural evaluation of glomeruli from animals with VL identified mesangial cell proliferation and interposition. Immunohistochemistry demonstrated significant Leishmania antigen, IgG, and C3b deposition in VL dog glomeruli. Asymptomatic and symptomatic dogs had increased glomerular nucleotide-binding domain leucine-rich repeat-containing-like receptor family, pyrin domain containing 3 and autophagosome-associated microtubule-associated protein 1 light chain 3 associated with glomerular lesion severity. Transcriptional analyses from symptomatic dogs confirmed induction of autophagy and inflammasome genes within glomeruli and tubules. On the basis of temporal VL staging, glomerulonephritis was initiated by IgG and complement deposition. This deposition preceded presence of nucleotide-binding domain leucine-rich repeat-containing-like receptor family, pyrin domain containing 3-associated inflammasomes and increased light chain 3 puncta indicative of autophagosomes in glomeruli from dogs with clinical VL and renal failure. These findings indicate potential roles for inflammasome complexes in glomerular damage during VL and autophagy in ensuing cellular responses.

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Acute Kidney Injury in Children With Visceral Leishmaniasis

Abstract: AKI is a frequent complication in children with VL. The risk factors for AKI were secondary infections, high serum globulin and low serum albumin.

Cited by 33 publications

References 1 publication

Acute Kidney Injury in Neonates: From Urine Output to New Biomarkers

Acute Kidney Injury in Neonates: From Urine Output to New Biomarkers

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

Activation of Autophagy and Nucleotide-Binding Domain Leucine-Rich Repeat–Containing-Like Receptor Family, Pyrin Domain–Containing 3 Inflammasome during Leishmania infantum–Associated Glomerulonephritis

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