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The messenger RNA-based vaccine for the coronavirus disease 2019 (COVID-19) may induce glomerulonephritis, including immunoglobulin A nephropathy (IgAN). New-onset IgAN triggered by vaccination against COVID-19 has been reported rarely, especially in children. Herein, we report a pediatric case of newly diagnosed IgAN after administration of the Pfizer vaccine for COVID-19. A 12-year-old girl was referred to our hospital for evaluation of gross hematuria after inoculation with the second dose of Pfizer’s COVID-19 vaccine; she had no adverse effects after the first dose. At the time of admission, she showed heavy proteinuria and persistent hematuria. Kidney biopsy revealed an IgAN, and she was treated with an oral steroid and an angiotensin-converting enzyme inhibitor. Four months after discharge, the proteinuria and hematuria resolved completely.
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Purpose@#We aimed to study the association of plasma neutrophil gelatinase-associated lipocalin (pNGAL) and leukocyte differential count in children with febrile urinary tract infection (UTI). @*Methods@#Medical records of 154 children aged 1 month to 13 years with febrile UTI who were hospitalized were retrospectively reviewed. Associations between pNGAL levels and blood leukocyte differential count at admission and after 48 hours of treatment were investigated in children with or without acute pyelonephritis (APN). @*Results@#The APN group (n=82) showed higher pNGAL levels, neutrophil count, monocyte count, and neutrophil-to-lymphocyte ratio (NLR), compared to the non-APN group (n=72) (all P<0.05). After adjustment for age and sex, pNGAL showed positive correlations with neutrophil count and NLR in both groups (all P<0.05). Additionally, it was correlated with the monocyte-to-lymphocyte ratio (MLR) only in the APN group (P<0.05). Before and after treatment, pNGAL was positively correlated with neutrophil count, NLR, and MLR in patients with APN while it was related with neutrophil count and NLR in those without APN (all P<0.05). Areas under the receiver operating curve of pNGAL, neutrophil count, NLR, and MLR for predicting APN were 0.804, 0.760, 0.730, and 0.636, respectively (all P<0.05). Only pNGAL was independently associated with the presence of APN in a multivariable logistic regression analysis (P<0.05). @*Conclusion@#In children with febrile UTIs, pNGAL might be associated with leukocyte differential count and the presence of APN.
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OBJECTIVES@#We aimed to evaluate the association between early-life weight status and urinary tract infection (UTI) risk in children. @*METHODS@#A nationwide study was conducted using Korean National Health Screening (NHS) data and National Health Insurance Service data. A sample cohort was selected using data from the 2014 and 2015 NHS for infants and children (4-71 months) and followed up until the end of 2017. Participants were divided into 4 groups (underweight, normal weight, overweight, and obese) based on the weight-for-age (< 2 years) or body mass index (≥ 2 years). Hazard ratios (HRs) with 95% confidence intervals (CIs) for developing UTIs, cystitis, and acute pyelonephritis (APN) were calculated using a Cox proportional hazard model. @*RESULTS@#Of 1,653,106 enrolled children, 120,142 (7.3%) developed UTIs, cystitis, and APN during follow-up. The underweight, overweight, and obese groups had higher risks of UTIs than the reference group after adjusting for age, sex, birth weight, and preterm birth. Between 2 years and 6 years of age, boys with underweight had a high risk of UTI and APN, while girls with overweight and obesity revealed elevated risks of UTIs, cystitis, and APN. The HRs for APN in boys with underweight and in girls with obesity were 1.46 (95% CI, 1.03 to 2.07) and 1.41 (95% CI, 1.13 to 1.75), respectively, after adjusting for age, sex, birth weight, and preterm birth. The incidence of APN did not decrease with age in underweight and obese children aged 2-6 years. @*CONCLUSIONS@#Children with underweight, overweight, and obesity may be at high risk for UTIs.
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Bartter syndrome is an autosomal recessive hypokalemic salt-losing tubulopathy, and classic Bartter syndrome is associated with mutations in the CLCNKB gene. While chronic hypokalemia is known to induce renal cyst formation in different renal diseases, renal cyst formation in Bartter syndrome is rarely reported. Russian six-year-old identical male twins were referred to our hospital for the evaluation of renal cysts, which were incidentally detected on abdominal sonography due to diarrhea. Both twins had shown symptoms of polydipsia, polyuria, and nocturia since they were one year olds. Vital signs including blood pressure were normal in both twins. Renal sonography revealed nephromegaly, increased echogenicity of renal cortex, and various sized multiple cysts in both kidneys for both twins. Laboratory findings included hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis. Bartter syndrome with renal cysts were suspected. Genetic analysis for both twins confirmed a homozygous c.1614delC deletion on exon 15 of the CLCNKB gene, which was confirmed as a previously unreported variant to the best of our knowledge. They were managed with potassium chloride, nonsteroidal anti-inflammatory drugs, and angiotensin-converting-enzyme inhibitors. Metabolic alkalosis, hypokalemia, hypochloremia, and polyuria partially improved during the short course of treatment. This is the first report of a homozygous mutation in the CLCNKB gene in an identical twin, presenting with renal cysts.
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OBJECTIVES@#We aimed to evaluate the association between early-life weight status and urinary tract infection (UTI) risk in children. @*METHODS@#A nationwide study was conducted using Korean National Health Screening (NHS) data and National Health Insurance Service data. A sample cohort was selected using data from the 2014 and 2015 NHS for infants and children (4-71 months) and followed up until the end of 2017. Participants were divided into 4 groups (underweight, normal weight, overweight, and obese) based on the weight-for-age (< 2 years) or body mass index (≥ 2 years). Hazard ratios (HRs) with 95% confidence intervals (CIs) for developing UTIs, cystitis, and acute pyelonephritis (APN) were calculated using a Cox proportional hazard model. @*RESULTS@#Of 1,653,106 enrolled children, 120,142 (7.3%) developed UTIs, cystitis, and APN during follow-up. The underweight, overweight, and obese groups had higher risks of UTIs than the reference group after adjusting for age, sex, birth weight, and preterm birth. Between 2 years and 6 years of age, boys with underweight had a high risk of UTI and APN, while girls with overweight and obesity revealed elevated risks of UTIs, cystitis, and APN. The HRs for APN in boys with underweight and in girls with obesity were 1.46 (95% CI, 1.03 to 2.07) and 1.41 (95% CI, 1.13 to 1.75), respectively, after adjusting for age, sex, birth weight, and preterm birth. The incidence of APN did not decrease with age in underweight and obese children aged 2-6 years. @*CONCLUSIONS@#Children with underweight, overweight, and obesity may be at high risk for UTIs.
ABSTRACT
Bartter syndrome is an autosomal recessive hypokalemic salt-losing tubulopathy, and classic Bartter syndrome is associated with mutations in the CLCNKB gene. While chronic hypokalemia is known to induce renal cyst formation in different renal diseases, renal cyst formation in Bartter syndrome is rarely reported. Russian six-year-old identical male twins were referred to our hospital for the evaluation of renal cysts, which were incidentally detected on abdominal sonography due to diarrhea. Both twins had shown symptoms of polydipsia, polyuria, and nocturia since they were one year olds. Vital signs including blood pressure were normal in both twins. Renal sonography revealed nephromegaly, increased echogenicity of renal cortex, and various sized multiple cysts in both kidneys for both twins. Laboratory findings included hyponatremia, hypokalemia, hypochloremia, and metabolic alkalosis. Bartter syndrome with renal cysts were suspected. Genetic analysis for both twins confirmed a homozygous c.1614delC deletion on exon 15 of the CLCNKB gene, which was confirmed as a previously unreported variant to the best of our knowledge. They were managed with potassium chloride, nonsteroidal anti-inflammatory drugs, and angiotensin-converting-enzyme inhibitors. Metabolic alkalosis, hypokalemia, hypochloremia, and polyuria partially improved during the short course of treatment. This is the first report of a homozygous mutation in the CLCNKB gene in an identical twin, presenting with renal cysts.
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BACKGROUND: Neutrophil gelatinase-associated lipocalin (NGAL), a bacteriostatic agent, is known to inhibit erythropoiesis leading to anemia. We aimed to investigate the associations of NGAL, anemia, and renal scarring in children with febrile urinary tract infections (UTIs).METHODS: We retrospectively reviewed the medical records of 261 children with febrile UTIs. The relationship between the presence of anemia and plasma NGAL levels was investigated. NGAL performance in comparison with serum C-reactive protein (CRP) at admission and after 72 hours of treatment was also evaluated for the prediction of renal scarring as well as acute pyelonephritis (APN) and vesicoureteral reflux (VUR).RESULTS: Plasma NGAL levels were elevated in patients with anemia compared with those without anemia. Multiple linear regression analysis showed an inverse relationship between NGAL levels and erythrocyte counts (standard β = −0.397, P < 0.001). Increased NGAL, but not CRP, was independently associated with the presence of anemia (odds ratio [OR], 2.37; 95% confidence interval [CI], 1.07–5.27; P < 0.05). Receiver operating curve analyses showed good diagnostic profiles of pre- and post-treatment NGAL for identifying APN, VUR, and renal scarring (all P < 0.05). For detecting renal scars, the area under the curve of post-treatment NGAL (0.730; 95% CI, 0.591–0.843) was higher than that of post-treatment CRP (0.520; 95% CI, 0.395–0.643; P < 0.05). The presence of anemia and elevated NGAL at admission (> 150 ng/mL) were independent risk factors for renal scarring in children with febrile UTIs. With anemia, NGAL levels increased consecutively in children with febrile UTI without renal involvement, with APN without scar, and with APN with renal scarring.CONCLUSION: Increased plasma NGAL levels may be associated with the presence of anemia and renal scarring in children with febrile UTIs.
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Purpose@#To investigate the association between urinary neutrophil gelatinaseassociated lipocalin (uNGAL) and leukocyte differential count in children with urinary tract infections (UTIs). @*Methods@#A retrospective chart review was performed in children undergoing uNGAL measurements between June 2018 and September 2019. Patients with suspected or diagnosed UTIs were included. The relationship between uNGAL and blood leukocyte differential count was investigated in children. @*Results@#A total of 197 children were included in this study, 119 of whom (60%) had UTIs. The non-UTI patients (n=78) were diagnosed with pneumonia, acute gastroenteritis, viral upper respiratory infection, and others. After adjusting for age, gender, and fever duration, the leukocyte count, monocyte count, and uNGAL levels were higher in the UTI group than in the non-UTI group (P<0.05). uNGAL showed positive correlations with neutrophil counts, monocyte counts, the neutrophil-to-lymphocyte ratio, and the monocyte-to-lymphocyte ratio in the UTI group (P<0.05). uNGAL levels were only associated with the neutrophil-tolymphocyte ratio in the non-UTI group (P<0.05). In a multivariable logistic regression analysis, only uNGAL was associated with the presence of UTI (P<0.05). The area under the receiver operating characteristic curves for uNGAL and monocyte counts to identify UTI were 0.89 (95% confidence interval (CI): 0.824–0.939; P=0.025) and 0.7 (95% CI: 0.627–0.774; P=0.038), respectively. @*Conclusions@#In children with UTIs, uNGAL levels may be associated with blood leukocyte differential counts. uNGAL measurements and monocyte counts can be helpful in children with suspected UTIs.
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Purpose@#The aim of this study is to evaluate the clinical utility of late 6-month dimercapto-succinic acid (DMSA) renal scan in predicting vesicoureteral reflux (VUR) and long-lasting renal scars in children with first acute pyelonephritis (APN). @*Methods@#A retrospective case study of children admitted with APN from January 2010 to July 2017 was performed. The study included patients with voiding cystourethrography (VCUG) and acute and late 6-month DMSA scan. We analyzed the clinical, laboratory and imaging findings of patients with and without late cortical defects at 6 months and those with or without VUR. @*Results@#Among 145 children with APN, 50 (34.5%) had cortical defects on the late DMSA renal scan and 60 (41.4%) showed VUR. Thirteen of 38 (34.2%) children undergoing 18-month DMSA renal scan showed a long-lasting renal scars. Compared with children without late cortical defects, patients with late 6-month cortical defects had a higher incidence of VUR and long-lasting renal scars, and relapse of UTI (all P<0.05). In a multivariable analysis, both high-grade VUR and relapse of UTI were independently correlated with the presence of late 6-month cortical defects (P<0.05). Late cortical defects and relapse of UTI were also associated with the presence of VUR (P<0.05). Only the late 6-mo cortical defects was an independent predictor of long-lasting renal scars in children with APN (P<0.05). @*Conclusion@#An abnormal late 6-month DMSA renal scan may be useful in identifying VUR and long-lasting renal scars in children diagnosed with APN.
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Streptococcus agalactiae or group B streptococcus (GBS) is associated with infectionsin neonates and pregnant women. Herein, we describe a rare case of GBSrenal abscess with peritonitis and pleural effusion in a 17-year-old girl with type 1diabetes mellitus. The girl was admitted due to fever and right flank pain. Laboratoryfindings included leukocytosis and increased C-reactive protein level anderythrocyte sedimentation rate. Her serum glucose level was 484 mg/dL. Urinalysisshowed no pyuria. Renal sonography revealed parenchymal swelling in the rightkidney. The patient was administered intravenous cefotaxime. Urine and bloodcultures were negative. Fever seemed to improve, but the following day, she complainedof abdominal pain and fever. Antibiotic was switched to imipenem, andabdominal and pelvic CT revealed a ruptured right renal abscess, peritonitis, andbilateral pleural effusion with atelectasis. Pigtail catheter drainage of the abscesswas performed. Culture from the abscess was positive for GBS, and fever subsided2 days after the drainage. She was discharged with oral cefixime. The clinical courseof urinary tract infections (UTIs) can be atypical in patients with diabetes, and GBScan be a cause of UTIs. Prompt diagnosis and management are necessary to preventcomplications in patients showing atypical courses.
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BACKGROUND@#Neutrophil gelatinase-associated lipocalin (NGAL), a bacteriostatic agent, is known to inhibit erythropoiesis leading to anemia. We aimed to investigate the associations of NGAL, anemia, and renal scarring in children with febrile urinary tract infections (UTIs).@*METHODS@#We retrospectively reviewed the medical records of 261 children with febrile UTIs. The relationship between the presence of anemia and plasma NGAL levels was investigated. NGAL performance in comparison with serum C-reactive protein (CRP) at admission and after 72 hours of treatment was also evaluated for the prediction of renal scarring as well as acute pyelonephritis (APN) and vesicoureteral reflux (VUR).@*RESULTS@#Plasma NGAL levels were elevated in patients with anemia compared with those without anemia. Multiple linear regression analysis showed an inverse relationship between NGAL levels and erythrocyte counts (standard β = −0.397, P 150 ng/mL) were independent risk factors for renal scarring in children with febrile UTIs. With anemia, NGAL levels increased consecutively in children with febrile UTI without renal involvement, with APN without scar, and with APN with renal scarring.@*CONCLUSION@#Increased plasma NGAL levels may be associated with the presence of anemia and renal scarring in children with febrile UTIs.
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BACKGROUND@#Neutrophil gelatinase-associated lipocalin (NGAL), a bacteriostatic agent, is known to inhibit erythropoiesis leading to anemia. We aimed to investigate the associations of NGAL, anemia, and renal scarring in children with febrile urinary tract infections (UTIs).@*METHODS@#We retrospectively reviewed the medical records of 261 children with febrile UTIs. The relationship between the presence of anemia and plasma NGAL levels was investigated. NGAL performance in comparison with serum C-reactive protein (CRP) at admission and after 72 hours of treatment was also evaluated for the prediction of renal scarring as well as acute pyelonephritis (APN) and vesicoureteral reflux (VUR).@*RESULTS@#Plasma NGAL levels were elevated in patients with anemia compared with those without anemia. Multiple linear regression analysis showed an inverse relationship between NGAL levels and erythrocyte counts (standard β = −0.397, P 150 ng/mL) were independent risk factors for renal scarring in children with febrile UTIs. With anemia, NGAL levels increased consecutively in children with febrile UTI without renal involvement, with APN without scar, and with APN with renal scarring.@*CONCLUSION@#Increased plasma NGAL levels may be associated with the presence of anemia and renal scarring in children with febrile UTIs.
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The ketogenic diet (KD) has been used as an effective antiepileptic therapy for intractable childhood epilepsy. However, various adverse effects have been reported with use of the KD. We report a case of a child who developed acute tubular necrosis subsequent to therapy with KD. A 5-year-old girl had myoclonic epilepsy with developmental delay. She was under the treatment with antiepileptic drugs since the age of 3 months and on the KD during the past 18 months. Proteinuria persisted intermittently with the initiation of the KD and subsequently increased in the past 2 months. She was admitted with intermittent mild fever, vomiting, and lethargy for the past 3–4 weeks. At the time of admission, she presented with hypertriglyceridemia, heavy proteinuria, renal Fanconi syndrome, and acute kidney injury. Renal sonography showed a marked increase in the size and parenchymal echogenicity of both kidneys. A renal biopsy revealed acute tubular necrosis accompanied by early interstitial fibrosis. After the withdrawal of the KD and supportive therapy, without changing other anticonvulsants and their dosages, improvement of renal function was observed. Proteinuria had disappeared after 1 month and kidney size returned to normal after 8 months. It is hypothesized that the KD can induce and/or aggravate the renal tubulointerstitial injury in some patients who are under the treatment with anticonvulsants.
Subject(s)
Child , Child, Preschool , Female , Humans , Acute Kidney Injury , Anticonvulsants , Biopsy , Drug Resistant Epilepsy , Epilepsies, Myoclonic , Epilepsy , Fanconi Syndrome , Fever , Fibrosis , Hypertriglyceridemia , Diet, Ketogenic , Kidney , Lethargy , Necrosis , Proteinuria , VomitingABSTRACT
Renal cortical necrosis (RCN) is patchy or diffuse ischemic destruction of the renal cortex caused by significantly reduced renal arterial perfusion. It is a rare cause of acute kidney injury (AKI) and is associated with high mortality. Here, we review the case of RCN in a 15-year-old boy who developed AKI. A 15-year-old boy was referred to our hospital from a local hospital due to a sharp decrease in his renal function. He presented with acute flank pain, nausea with vomiting, and oliguria for the past two days. He had taken a single dose of antihistamine for nasal congestion. At our hospital, his peak blood pressure was 148/83 mmHg and he had a high body mass index of 32.9 kg/m². The laboratory data showed a blood urea nitrogen (BUN) of 28.4 mg/dL, a creatinine of 4.26 mg/dL, and a glomerular filtration rate estimated from the serum cystatin C of 20.2 mL/min/1.73m². Proteinuria (spot urine protein to creatinine ratio 1.66) with pyuria was observed. Kidney sonography showed parenchymal swelling and increased renal echogenicity. Due to rapidly progressing nephritis, steroid pulse therapy (750 mg/IV) was done on the second day of his admission and the patient showed complete recovery with normal renal function. However, the kidney biopsy findings revealed renal cortical hemorrhagic necrosis. Multifocal, relatively well-circumscribed, hemorrhagic necrotic areas (about 25%) were detected in the tubulointerstitium. Although RCN is an unusual cause of AKI, especially in children, pediatricians should consider the possibility of RCN when evaluating patients with rapidly decreasing renal function.
Subject(s)
Adolescent , Child , Humans , Male , Acute Kidney Injury , Biopsy , Blood Pressure , Blood Urea Nitrogen , Body Mass Index , Creatinine , Cystatin C , Estrogens, Conjugated (USP) , Flank Pain , Glomerular Filtration Rate , Kidney , Kidney Cortex Necrosis , Mortality , Nausea , Necrosis , Nephritis , Obesity , Oliguria , Perfusion , Proteinuria , Pyuria , VomitingABSTRACT
Acute idiopathic scrotal edema (AISE) is a self-limiting condition that is characterized by acute scrotal swelling and erythema. AISE is a very rare cause of acute scrotum, especially in neonates. We report a case of AISE in a 26-day-old infant who was admitted to the outpatient clinic with swelling and erythema of the penis and scrotum for a week. His vital signs were stable, and laboratory findings were non-specific. A diagnosis of AISE was made using scrotal ultrasonography with color Doppler. His symptoms resolved within four days after the onset of supportive treatment, and he was discharged from the hospital. In neonates with an acute scrotum, AISE should be considered to prevent unnecessary surgical exploration.
Subject(s)
Humans , Infant , Infant, Newborn , Male , Ambulatory Care Facilities , Diagnosis , Edema , Erythema , Penis , Scrotum , Ultrasonography , Urologic Diseases , Vital SignsABSTRACT
This study was aimed to investigate the association of candidate gene polymorphisms and obesity or overweight in young Korean children. A total of 190 Korean preschool children (96 control, 48 overweight, and 46 obese children) were genotyped for the angiotensin converting enzyme (ACE) insertion (I)/deletion (D), angiotensin II type 2 receptor (AT2) C3123A, transforming growth factor (TGF)-β1 T869C, vascular endothelial growth factor (VEGF) T460C, and tumor necrosis factor (TNF)-α G308A polymorphisms. No differences were found among the groups with respect to age, sex, birth weight, blood pressure levels, and serum concentrations of glucose and total cholesterol. Obese children showed a higher incidence of ACE DD genotype and D allelic frequency compared to the controls (odds ratio [OR], 2.7, 95% confidence interval [CI], 1.01–7.21; OR, 2.5, 95% CI, 1.49–4.19; all P < 0.05). The frequency of TC genotype and C allele in the TGF-β1 T869C polymorphism (OR, 2.08, 95% CI, 1.01–4.27; OR, 1.93, 95% CI, 1.15–3.21) and that in the VEGF T460C polymorphism (OR, 2.5, 95% CI, 1.19–5.28; OR, 2.15, 95% CI, 1.26–3.68) was also higher in obese children than in control subjects (all P < 0.05). Overweight children exhibited a higher frequency of the A allele in the AT2 C3123A polymorphism compared to the controls (OR, 1.72, 95% CI, 1.03–2.88, P < 0.05). There were no differences in the TNF-α G308A polymorphism among the groups. The ACE I/D, AT2 C3123A, TGF-β1 T869C, and VEGF T460C polymorphisms can affect susceptibility to obesity or overweight in Korean children.
Subject(s)
Child , Child, Preschool , Humans , Alleles , Angiogenic Proteins , Birth Weight , Blood Pressure , Cholesterol , Genetic Variation , Genotype , Glucose , Incidence , Obesity , Overweight , Pediatric Obesity , Peptidyl-Dipeptidase A , Receptor, Angiotensin, Type 2 , Renin-Angiotensin System , Transforming Growth Factors , Tumor Necrosis Factor-alpha , Vascular Endothelial Growth Factor AABSTRACT
PURPOSE: Neutrophil gelatinase-associated lipocalin (NGAL) has been identified as an early marker of acute kidney injury (AKI). This study was designed to evaluate the clinical utility of the rapid plasma NGAL assay for diagnosing AKI in critically ill newborn infants in the neonatal intensive care unit (NICU). METHODS: The medical records of 178 critically ill newborn infants >34 weeks of gestational age who underwent plasma NGAL measurement during the first week of life in the Korea University Ansan Hospital NICU from February 2011 to August 2015 were retrospectively reviewed. Plasma NGAL levels were measured at bedside by using a commercial competitive immunoassay kit simultaneously with serum creatinine (Cr) level determination. RESULTS: Of 178 newborn infants enrolled in this study (study group), 25 infants had AKI (AKI group) while 153 infants had no AKI (control group). The plasma NGAL level in the AKI group (114.0 [76.5–281.5] ng/mL) was significantly higher than that in the control group (74.0 [52.5–122.5] ng/mL, P=0.001). Moreover, plasma NGAL levels were found to be correlated with serum Cr levels in the study group (r=0.208, P=0.005). Plasma NGAL achieved an area under the receiver operating characteristic curve of 0.705 for detecting AKI (95% confidence interval: 0.593–0.817). The best cutoff plasma NGAL level for AKI diagnosis was 100 ng/mL. CONCLUSION: The rapid plasma NGAL assay has diagnostic value for AKI in critically ill newborn infants >34 weeks of gestational age. Further investigations with a larger population are needed to confirm the potential use of plasma NGAL levels for diagnosing AKI in newborn infants.
Subject(s)
Humans , Infant , Infant, Newborn , Acute Kidney Injury , Creatinine , Critical Illness , Diagnosis , Gestational Age , Immunoassay , Intensive Care, Neonatal , Korea , Lipocalins , Medical Records , Neutrophils , Plasma , Retrospective Studies , ROC CurveABSTRACT
Eosinophilic gastroenteritis is a rare disease characterized by prominent eosinophilic tissue infiltration of the gastrointestinal tract. Here, we report a case of eosinophilic gastroenteritis in an 18-year-old patient with prolonged nephrotic syndrome who presented with abdominal pain and peripheral hypereosinophilia. During the previous 2 years, he had visited local Emergency Department several times because of epigastric pain and nausea. He had been treated with steroid-dependent nephrotic syndrome since 3 years of age. Tests ruled out allergic and parasitic disease etiologies. Gastroduodenoscopy with biopsy revealed marked eosinophilic infiltration in the duodenum. Renal biopsy findings indicated minimal change disease spectrum without eosinophilic infiltration. The oral deflazacort dosage was increased, and the patient was discharged after abdominal pain resolved. To our knowledge, this is the first report of eosinophilic gastroenteritis in a patient with minimal change disease.
Subject(s)
Adolescent , Humans , Male , Abdominal Pain , Biopsy , Duodenum , Emergency Service, Hospital , Eosinophilia , Eosinophils , Gastroenteritis , Gastrointestinal Tract , Nausea , Nephrosis, Lipoid , Nephrotic Syndrome , Parasitic Diseases , Rare DiseasesABSTRACT
PURPOSE: Nephrogenesis is normally accompanied by a tightly regulated and efficient vascularization. We investigated the effect of angiotensin II inhibition on angiogenesis in the developing rat kidney. METHODS: Newborn rat pups were treated with enalapril (30 mg/kg/day) or vehicle (control) for 7 days after birth. Renal histological changes were checked using Hematoxylin & Eosin staining. We also investigated the intrarenal expression of vascular endothelial growth factor (VEGF)-A, VEGF receptor 1 (VEGFR1), VEGFR2, platelet-derived growth factor (PDGF)-B, and PDGF receptor-beta with Western blotting and immunohistochemical staining at postnatal day 8. Expression of the endothelial cell marker CD31 was examined to determine glomerular and peritubular capillary density. RESULTS: Enalapril-treated rat kidneys showed disrupted tubules and vessels when compared with the control rat kidneys. In the enalapril-treated group, intrarenal VEGF-A protein expression was significantly higher, whereas VEGFR1 protein expression was lower than that in the control group (P<0.05). The expression of VEGFR2, PDGF-B, and PDGF receptor-beta was not different between the 2 groups. The increased capillary CD31 expression on the western blots of enalapril-treated rat kidneys indicated that the total endothelial cell protein level was increased, while the cortical capillary density, assessed using CD31 immunohistochemical staining, was decreased. CONCLUSION: Impaired VEGF-VEGFR signaling and altered capillary repair may play a role in the deterioration of the kidney vasculature after blocking of angiotensin II during renal development.