ArticleBMC nephrology2017
Unique proximal tubular cell injury and the development of acute kidney injury in adult patients with minimal change nephrotic syndrome.
Article in BMC nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Immunoglobulin A nephropathy with superimposed minimal change disease complicated by acute kidney injury requiring temporary hemodialysis.CEN case reports · 2026Article
- Urine-to-blood urea nitrogen ratio predicts proteinuria remission in nephrotic syndrome.Clinical and experimental nephrology · 2026Article
- Development and external validation of a machine learning-based predictive model for acute kidney injury in hospitalized children with idiopathic nephrotic syndrome.BMC medical informatics and decision making · 2025Article
- Urinary matrix metalloproteinase-7 is a sensitive biomarker to evaluate renal tubular injury in patients with minimal change disease and focal segmental glomerulosclerosis.Clinical kidney journal · 2024Article
- An Elderly Case of Minimal Change Nephrotic Syndrome: Correlation between Renal Tubular Dysfunction and the Onset of Oliguric Acute Kidney Injury Requiring Hemodialysis.Case reports in nephrology · 2024Article
- Intermittent thoracic resuscitative endovascular balloon occlusion of the aorta improves renal function compared to 60 min continuous application after porcine class III hemorrhage.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2023Article
- Revisiting the Role of NAG across the Continuum of Kidney Disease.Bioengineering (Basel, Switzerland) · 2023Review
- A Patient with Acute Kidney Injury Associated with Massive Proteinuria and Acute Hyperuricemia after Epileptic Seizures.Internal medicine (Tokyo, Japan) · 2022Article
- Hyperuricemia is a risk factor for the progression to end-stage renal disease in minimal change disease.Kidney research and clinical practice · 2021Article
- Sub-chronic microcystin-LR renal toxicity in rats fed a high fat/high cholesterol diet.Chemosphere · 2021Article
- Clinical and histopathological features of acute kidney injury in adult-onset minimal change nephrotic syndrome.Clinical and experimental nephrology · 2021Article
- A National Registry Study of Patient and Renal Survival in Adult Nephrotic Syndrome.Kidney international reports · 2021Article
- Glycyrrhetinic Acid Protects Renal Tubular Cells against Oxidative Injury via Reciprocal Regulation of JNK-Connexin 43-Thioredoxin 1 Signaling.Frontiers in pharmacology · 2021Article
- Functionally Essential Tubular Proteins Are Lost to Urine-Excreted, Large Extracellular Vesicles during Chronic Renal Insufficiency.Kidney360 · 2020Article
- Glomerulonephritis in AKI: From Pathogenesis to Therapeutic Intervention.Frontiers in medicine · 2020Review
- Adult minimal change disease with acute kidney injury: a case report and literature review.Journal of community hospital internal medicine perspectives · 2019Article
- Case of human immunodeficiency virus infection presenting as a tip variant of focal segmental glomerulosclerosis: A case report and review of the literature.World journal of nephrology · 2018Article
- Acute Kidney Injury in Nephrotic Syndrome.Frontiers in pediatrics · 2018Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAdult patients with minimal change nephrotic syndrome (MCNS) are often associated with acute kidney injury (AKI). To assess the mechanisms of AKI, we examined whether tubular cell injuries unique to MCNS patients exist.
methodsWe performed a retrospective analysis of clinical data and tubular cell changes using the immunohistochemical expression of vimentin as a marker of tubular injury and dedifferentiation at kidney biopsy in 37 adult MCNS patients. AKI was defined by the criteria of the Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guidelines for AKI.
resultsThirteen patients (35.1%) were designated with AKI at kidney biopsy. No significant differences in age, history of hypertension, chronic kidney disease, diuretics use, proteinuria, and serum albumin were noted between the AKI and non-AKI groups. Urinary N-acetyl-β-D-glucosaminidase (uNAG) and urinary alpha1-microglobulin (uA1MG) as markers of tubular injury were increased in both groups, but the levels were significantly increased in the AKI group compared with the non-AKI group. The incidence of vimentin-positive tubules was comparable between AKI (84.6%) and non-AKI (58.3%) groups, but vimentin-positive tubular area per interstitial area was significantly increased in the AKI group (19.8%) compared with the non-AKI group (6.8%) (p = 0.011). Vimentin-positive injured tubules with tubular simplification (loss of brush-border of the proximal tubule/dilated tubule with flattening of tubular epithelium) were observed in the vicinity of glomeruli in both groups, suggesting that the proximal convoluted tubules were specifically injured. Two patients exhibited relatively severe tubular injuries with vimentin positivity and required dialysis within 2 weeks after kidney biopsy. The percentage of the vimentin-positive tubular area was positively correlated with uNAG but not with uA1MG in the non-AKI group.
conclusionsProximal tubular injuries with increased uNAG exist in MCNS patients without renal dysfunction and were more severe in the AKI group than they were in the non-AKI group. The unique tubular injuries probably due to massive proteinuria might be a predisposing factor for the development of severe AKI in adult MCNS patients.
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