Is the urinary biomarkers assessment a non-invasive approach to tubular lesions of the solitary kidney?

Gădălean, Florica; Kaycsa, Adriana; Gluhovschi, Gheorghe; Velciov, Silvia; Gluhovschi, Cristina; Bob, Flaviu; Bozdog, Gheorghe; Petrică, Ligia

doi:10.3109/0886022x.2013.828367

Cited by 7 publications

(3 citation statements)

References 29 publications

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“…11 Gadalean et al also draw attention to high values of urinary NAG both in individuals with surgical SK and in persons with congenital SK. 12 Similar observations are reported by Stefanowicz et al 13 The SK undergoes hypertrophy and hyperfiltration adaptative phenomena, thus ensuring homeostasis under conditions of a limited number of nephrons. When the adaptative phenomena are surpassed there occur renal lesions manifested by proteinuria, hypertension and diminution of GFR.…”

Section: Urinary Elimination Of Nag and Alpha-1-microglobulin In Healsupporting

confidence: 76%

Urinary biomarkers in assessing the nephrotoxic potential of gentamicin in solitary kidney patients after 7 days of therapy

Gluhovschi¹,

Gădălean²,

Gluhovschi³

et al. 2014

Renal Failure

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Section: Urinary Elimination Of Nag and Alpha-1-microglobulin In Healsupporting

confidence: 76%

Urinary biomarkers in assessing the nephrotoxic potential of gentamicin in solitary kidney patients after 7 days of therapy

Gluhovschi¹,

Gădălean²,

Gluhovschi³

et al. 2014

Renal Failure

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“…In the CKD in Children (CKiD) multicenter cohort center, plasma concentrations of proximal tubular injury (kidney injury molecular-1, KIM-1), pro-inflammatory markers (monocyte chemoattractant protein-1, MCP-1) and receptors for proinflammatory markers (tumor necrosis factor alpha; TNFR1 and TNFR2) in the highest quartile identified children at greater risk of CKD progression compared with those with concentrations in the lowest quartile (Greenberg et al, 2020). Gadalean et al (2013) observed that in adult patients with an acquired and congenital SFK there was a ∼52-60% increase in urinary N-acetyl-beta-D-glucosaminidase, a marker of proximal tubule dysfunction. Similarly, in children with both a congenital SFK and acquired SFK, urinary N-acetyl-β-hexosaminidase (HEX), an indicator of proximal tubular damage, was elevated compared with age-matched healthy individuals (Taranta-Janusz et al, 2014).…”

Section: Tubular Injurymentioning

confidence: 99%

Physiology and Pathophysiology of Compensatory Adaptations of a Solitary Functioning Kidney

et al. 2020

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Children born with a solitary functioning kidney (SFK) have an increased risk of hypertension and kidney disease from early in adulthood. In response to a reduction in kidney mass, the remaining kidney undergoes compensatory kidney growth. This is associated with both an increase in size of the kidney tubules and the glomeruli and an increase in single nephron glomerular filtration rate (SNGFR). The compensatory hypertrophy and increase in filtration at the level of the individual nephron results in normalization of total glomerular filtration rate (GFR). However, over time these same compensatory mechanisms may contribute to kidney injury and hypertension. Indeed, approximately 50% of children born with a SFK develop hypertension by the age of 18 and 20–40% require dialysis by the age of 30. The mechanisms that result in kidney injury are only partly understood, and early biomarkers that distinguish those at an elevated risk of kidney injury are needed. This review will outline the compensatory adaptations to a SFK, and outline how these adaptations may contribute to kidney injury and hypertension later in life. These will be based largely on the mechanisms we have identified from our studies in an ovine model of SFK, that implicate the renal nitric oxide system, the renin angiotensin system and the renal nerves to kidney disease and hypertension associated with SFK. This discussion will also evaluate current, and speculate on next generation, prognostic factors that may predict those children at a higher risk of future kidney disease and hypertension.

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“…24-hour urine protein excretion was similar between all stages of CKD (Table II). increased in 52.6% and 60.6% of the patients respectively (17). They showed an inverse correlation between urinary NAG and estimated glomerular filtration rate (eGFR).…”

Section: Discussionmentioning

confidence: 98%

Urinary N-Acetyl-Beta-D Glucosaminidase Activity is Associated with Inflammation and Proteinuria in Diabetic and Non-Diabetic Patients with Different Stages of Chronic Kidney Disease

Gençtoy¹,

Arikan²

2015

Turk Neph Dial Transpl

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OBJECTIVE:Clinical studies have demonstrated that tubulointerstitial rather than glomerular pathology correlates with the degree and progression of renal impairment. Urinary n-acetyl-beta-D-glucosaminidase (NAG) is a biomarker of tubular damage, shown to be elevated in patients with glomerulonephritis and acute kidney injury. However, it has not been assessed longitudinally in chronic kidney disease (CKD). The aim of the present study was to determine urinary NAG activity and its possible associations with metabolic and inflammatory parameters in CKD. MATERIAL and METHODS:A total of 72 patients (mean age: 64.5±15.7) with stage 1-5 CKD were included. Of the 72 patients 23 (32%) had diabetic nephropathy and 49 (68%) had different types of primary glomerular diseases. Fasting blood samples were collected to analyse complete blood count, urea, creatinine, albumin, lipid parameters, C-reactive protein, uric acid and parathyroid hormone. 24-hour urine was collected to determine protein excretion. Urinary NAG and creatinine levels were analysed from the first morning urine samples. The NAG index (urinary NAG/ creatinine) was used to exclude dilutional errors. RESULTS:Mean eGFR was 38.3±21.7 ml/min. The urinary NAG index was significantly higher in stage 3 compared to stage 2 (32.1±23.5 vs. 7.5±3.3 U/gr-creatinine; p=0.002) and lower in stage 5 compared to stage 3 CKD (8.2±7.6 vs. 32.1±23.5; p=0.017). The urinary NAG index was positively correlated with 24-hour urine protein excretion (r=0.43; p=0.0001) and serum CRP (r=0.549; p=0.04) and negatively correlated with hemoglobin levels (r-0.394; p=0.004). CONCLUSION:The present study demonstrated that urinary NAG correlates with systemic inflammation and proteinuria and may be associated with progression of CKD. KEY WORDS:Chronic kidney disease, Proteinuria, Inflammation, N-acetyl-beta-D-glucosaminidase ÖZ AMAÇ: Klinik çalışmalar glomerüler patolojiden ziyade tubulointerstisyel hasarın böbrek yetmezliği derecesi ve ilerlemesi ile ilişkili olduğunu göstermiştir. İdrarda saptanan n-asetil-beta-D-glukosaminidaz (NAG) enzimi glomerülonefrit ve akut böbrek hasarında yükselen bir tübüler hasar biyomarkeridir ancak NAG düzeyi, kronik böbrek hastalığının (KBH) değişen aşamalarında değerlendirilmemiştir. Çalışmada, farklı evrelerdeki kronik böbrek hastalarında idrar NAG aktivitesi, NAG aktivitesi ile metabolik ve inflamatuvar parametreler arasında olası ilişki araştırılmıştır. GEREÇ ve YÖNTEMLER:Evre 1-5 KBH tanılı toplam 72 hasta (ortalama yaş:64,5 ± 15,7) çalışmaya alındı. Hastaların 23'ünde (% 32) diyabetik nefropati ve 49'una (% 68) farklı türde primer glomerüler hastalıklar mevcuttu. Açlık kan örneklerinde C-reaktif protein, ürik asit ve paratiroid hormon, hemogram, üre, kreatinin, albümin, lipid parametreleri çalışıldı. Kantitatif protein analizi için 24 saatlik idrar örnekleri kullanıldı. İdrar NAG ve kreatinin seviyeleri sabah ilk idrar örneklerinden analiz edildi. Dilüsyonel hataları dışlamak için NAG indeksi (idrar NAG / kreatinin:mg/gr) hesaplanarak değerlendiri...

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Is the urinary biomarkers assessment a non-invasive approach to tubular lesions of the solitary kidney?

Abstract: Urinary biomarkers allow a non-invasive, sensitive, early assessment of the tubular lesions of the SK. Urinary biomarkers of PT injury parallel renal function decline, thus complementing the estimation of GFR. Monitoring of PT dysfunction is mandatory in patients with SK.

Cited by 7 publications

References 29 publications

Urinary biomarkers in assessing the nephrotoxic potential of gentamicin in solitary kidney patients after 7 days of therapy

Urinary biomarkers in assessing the nephrotoxic potential of gentamicin in solitary kidney patients after 7 days of therapy

Physiology and Pathophysiology of Compensatory Adaptations of a Solitary Functioning Kidney

Urinary N-Acetyl-Beta-D Glucosaminidase Activity is Associated with Inflammation and Proteinuria in Diabetic and Non-Diabetic Patients with Different Stages of Chronic Kidney Disease

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