Pediatric acute kidney injury: prevalence, impact and management challenges

Ciccia, Eileen; Devarajan, Prasad

doi:10.2147/ijnrd.s103785

Cited by 41 publications

(35 citation statements)

References 46 publications

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“…[3] Majority of neonates in this study had AKI stage I (78.2%). The diagnosis of AKI was established by measuring serum creatinine at baseline and 48 hours after admission, despite the caveats of using creatinine, it is important for clinicians to consider measuring serum creatinine at baseline and repeat after 48 hours for all critically ill neonates based on high rate of AKI noted in this study [13,15]. This will facilitate timely diagnosis of AKI and in early stages, which is relatively easy to manage and requiring minimal resources.…”

Section: Discussionmentioning

confidence: 99%

Acute kidney injury among critically ill neonates in a tertiary hospital in Tanzania; Prevalence, risk factors and outcome

2020

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Background Neonatal acute kidney injury contributes to high mortality in developing countries. The burden of neonatal AKI is not known in Tanzania despite having high neonatal mortality. This study was conducted to determine the burden of AKI among critically ill neonates admitted at Muhimbili National Hospital. Methods This was a cross-sectional study conducted in the neonatal ward at the MNH. Eligible critically ill neonates were recruited consecutively between October 2017 and March 2018. Data was collected using a standardized structured questionnaire. Blood specimen was drawn to measure baseline creatinine at admission, 48 th hour, 72 nd hour and 14 th day. Data was analysed using SPSS version 20.0 Univariate analysis was done using chi-square to determine the association between categorical variables and multivariate logistic regression was performed to determine predictors of AKI. Results A total of 378 critically ill neonates were recruited, 31.5% had AKI and independent predictors of AKI were noted to be neonatal sepsis (aOR 2.237, 95%CI 1.3-3.6, P = 0.001), severe pneumonia (aOR3.0, 95%CI 1.0-9.3, P = 0.047) and use of gentamycin (aOR6.8, 95%CI 1.3-9.3, P = 0.02). Complete resolution of renal dysfunction at the fourteenth day was seen in 83.1% of the neonates while 16.9% had persistence of renal dysfunction. Ultrasound scan were performed among 105 participants with AKI revealed increased echogenicity, mild hydronephrosis and ectopic kidneys in 25 (23.8%), 4 (3.8%) and 2 (1.9%) respectively. In-hospital mortality was significantly higher among neonates with AKI (70.6%) as compared to those without (29.4%) p< 0.001.

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Section: Discussionmentioning

confidence: 99%

Acute kidney injury among critically ill neonates in a tertiary hospital in Tanzania; Prevalence, risk factors and outcome

2020

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“…Acute kidney injury is a group of clinical syndromes that manifest as a sudden (from 1 to 7 days) and sustained (>24 hours) decreased in renal function, defined as an elevation of the Scr level by at least 0.5 mg/d (<400 mL/24 h or 17 mL/h) or anuria (<100 mL/24 h). (Quote the international guidelines KDIGO, [ 4 , 5 ] ). According to the lesion and cause, acute kidney injury can be divided into 3 categories: prerenal, renal, and postrenal, and each has a different etiology and pathophysiology.…”

Section: Discussionmentioning

confidence: 99%

Nitrite-induced acute kidney injury with secondary hyperparathyroidism

Peng

Yang

et al. 2018

Medicine

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Rationale:Acute kidney injury (AKI) with hyperparathyroidism caused by nitrite was rare, and renal function and parathyroid hormone (PTH) decreased to normal range after therapy.Patient concerns:Acute kidney injury was diagnosed in a 40-year-old male with hyperparathyroidism and cyanosis of his hands and both forearms.Diagnoses:The patient ate some recently pickled vegetables, and he experienced nausea, vomiting and diarrhoea without oliguria or anuria; Additionally, his hands and both forearms had a typical blue ash appearance. After admission, the laboratory findings indicated theincreasing serum creatinine (Scr) and parathyroid hormone (PTH). He was diagnosed as acute kidney injury with hyperparathyroidism caused by nitrite.Interventions:The patient stopped eating the pickled vegetables and was given rehydration, added calories and other supportive therapy without any glucocorticoids.Outcomes:According to his clinical manifestations, laboratory findings and imaging results, the patient was diagnosed with acute kidney injury with secondary hyperparathyroidism. He was given symptomatic supportive care therapy. After one week, the serum creatinine, parathyroid hormone (PTH), hypercalcemia, hyperphosphatemia, proteinuria, and urine red blood cell values decreased to normal range.Lessons:Nitrite-induced acute kidney injury with secondary hyperparathyroidism was relatively rare. After therapy, the function of the kidney and parathyroid returned to normal. This case suggests that detailed collection of medical history, physical examination and correct symptomatic treatment is very important.

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“…It has been reported in children undergoing cardiopulmonary bypass (CPB), the increase in urinary L-FABP maybe occur within 4 h of initiating CPB [125]. However, there are conflicting data about L-FABP, such as a prospective multi-center study of 311 children undergoing cardiac surgery did not show similar increase in L-FABP [106]. In SCD patients, Sundaram et al [57] reported that urine L-FABP level was highest in the youngest group (6-12 years old) even with little evidence of renal injury.…”

Section: Serum Liver-type Fatty Acid-binding Proteinmentioning

confidence: 99%

Sickle Cell Nephropathy: Current Understanding of the Presentation, Diagnostic and Therapeutic Challenges

Inusa¹,

Lodi²,

Palazzi³

et al. 2018

Hematology - Latest Research and Clinical Advances

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Sickle cell nephopathy (SCN) begins early in childhood from failure of urinary concentration (hyposthenuria), albuminuria to hyperfiltration, hematuria and progression to falling glomerular filtration to end-stage renal disease and increased mortality. Renal involvement is more severe in homozygous individuals (HbSS) than in compound heterozygous patients (HbSC). The pathogenesis of SCN is multifactorial from hypoxia, acidosis, hemolysis, ischemia-reperfusion injury and albuminuria. The clinical manifestations depend on whether the main pathology is tubular, glomerular or a mixture of both abnormalities. This chapter offers a critical review of the recent literature and will highlight the pathophysiology, epidemiology, clinical manifestations and management of sickle cell nephropathy with particular focus on the major advance in the early diagnosis. Learning points: For SCN, the onset of hyperfiltration and albuminuria in infants and childhood is an opportunity to intervene early. There is no diagnostic markertest capable of detecting the onset of these changes. Moreover there is no reliable therapeutic agent to prevent or halt early changes due to SCN. The development of a marker of renal impairment in SCD such as such as Cystatin C assay if validated may be appropriate for wider clinical application.

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Pediatric acute kidney injury: prevalence, impact and management challenges

Cited by 41 publications

References 46 publications

Acute kidney injury among critically ill neonates in a tertiary hospital in Tanzania; Prevalence, risk factors and outcome

Acute kidney injury among critically ill neonates in a tertiary hospital in Tanzania; Prevalence, risk factors and outcome

Nitrite-induced acute kidney injury with secondary hyperparathyroidism

Sickle Cell Nephropathy: Current Understanding of the Presentation, Diagnostic and Therapeutic Challenges

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