scholarly journals Kidney Injury Molecule-1 and Periostin Urinary Excretion and Tissue Expression Levels and Association with Glomerular Disease Outcomes

2021 ◽  
pp. 1-15
Author(s):  
Qiaoyan Wu ◽  
Jonathan P. Troost ◽  
Tiane Dai ◽  
Cynthia Nast ◽  
Sean Eddy ◽  
...  
Keyword(s):  
Interstitial Fibrosis ◽  
Kidney Injury ◽  
Distal Tubule ◽  
Tissue Expression ◽  
Diagnosis And Treatment ◽  
Tubular Atrophy ◽  
Expression Levels ◽  
Spot Urine ◽  
Histopathologic Diagnosis ◽  
Kidney Injury Molecule 1

<b><i>Introductions:</i></b> Kidney injury molecule-1 (KIM-1) and periostin (POSTN) are proximal and distal tubule injury biomarkers. We tested whether baseline urine KIM-1/Cr (uKIM-1/Cr) and/or uPOSTN/Cr correlated with disease severity or improved a remission prediction model. <b><i>Methods:</i></b> Baseline uKIM-1/Cr and uPOSTN/Cr were measured on spot urine samples from immunosuppression-free patients enrolled in Nephrotic Syndrome Study Network until December 15, 2014. Urine protein/Cr (UPCR) and albumin/Cr (UACR) were measured at baseline, 4 months, and until last follow-up. Glomerular and tubulointerstitial (TI) expression arrays were analyzed from a baseline research renal biopsy core collected during a clinically indicated biopsy. Renal diagnoses were centrally confirmed, sections scanned, and measured morphometrically. Correlations between baseline uKIM-1/Cr and uPOSTN/Cr and UPCR, UACR, histopathologic features, glomerular and TI KIM-1 and POSTN expression levels, and renal outcomes were assessed. <b><i>Results:</i></b> Baseline uKIM-1/cr correlated with UPCR and UACR and were associated with complete remission (CR) after adjustment for proteinuria, histopathologic diagnosis, and treatment. Baseline uKIM-1/Cr also correlated with degree of foot process effacement and acute tubular injury. Glomerular and TI KIM-1 expression levels correlated with UPCR and UACR. Higher TI KIM-1 expression levels correlated with interstitial fibrosis, tubular atrophy, and global glomerulosclerosis, while glomerular KIM-1 expression correlated with time to remission. Findings for POSTN were of lesser statistical strength. <b><i>Discussion/Conclusion:</i></b> Lower baseline uKIM-1/Cr values were associated with more rapid time to CR after adjusting for proteinuria, histopathologic diagnosis, and treatment. Increased TI KIM-1 expression levels in proteinuric states were associated with chronic morphological injury; lower glomerular expression levels were associated with a greater potential for proteinuria reversibility.

Abstract 19279: Rescue Of D2R Function in Mouse Kidney Using AAV9 Vector Abrogates the Renal Injury and High Blood Pressure Induced by D2R Silencing

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Prasad Konkalmatt ◽  
laureano D Asico ◽  
Yu Yang ◽  
Cinthia B Drachenberg ◽  
Pedro A Jose ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Injury ◽  
Dopamine D2 Receptor ◽  
Interstitial Fibrosis ◽  
D2 Receptor ◽  
Kidney Injury ◽  
Tubular Atrophy ◽  
Ki 67 ◽  
Downstream Target ◽  
Kidney Injury Molecule 1

In humans decreased dopamine D2 receptor (D2R) expression and function is associated hypertension and inflammation and fibrosis in renal proximal tubule cells. In mice selective D2R silencing in the kidney results in renal inflammation, injury and hypertension. We hypothesized that these alterations are ameliorated by rescue of renal D2R function. To test this hypothesis we silenced renal D2R expression by sub-capsular infusion of D2R siRNA (D2RsiRNA) using osmotic mini pumps (3 μg/day, n=6 per group). Mice treated with non-silencing siRNA (NS siRNA) served as controls. Two weeks after starting siRNA treatment, mice were treated with control AAV (CAAV) or AAV carrying wild-type D2R (D2RAAV) (n=3 per group, 1e+11 vgp/mouse). Two weeks following AAV treatment, blood pressure was measured and organs were collected. D2R expression was decreased in D2RsiRNA-treated kidneys compared with NSsiRNA-treated kidneys (54 ± 0.8 vs 100± 22 %; P<0.05). D2RAAV treatment increased D2R expression (7.5-11-fold; P<0.01) in both D2RsiRNA and NS siRNA-treated mice. Mice with silenced D2R expression (D2RsiRNA+CAAV) had increased systolic blood pressure (121±3 mmHg; P<0.05) in comparison with the D2R rescued group ( D2RsiRNA+D2RAAV) (100±6 mm Hg), NSsiRNA+CAAV (101±4 mm Hg), or NS siRNA +D2RAAV (101±1 mm Hg). D2R silencing caused an increase in the expression of TNF-α, TGF-β1 and its downstream target fibronectin-1, as well as kidney injury molecule-1 and ki-67, a marker of cell proliferation. By contrast, the expression of these proteins was decreased or reversed to normal in the D2R-rescued group. Masson trichrome staining showed tubular atrophy, interstitial fibrosis and extensive areas of scaring in D2R silenced mice while these abnormalities were significantly reduced in the D2R rescued group. T cells infiltration was significantly higher in D2R silenced group compared to the D2R-rescued group (309 ± 38 vs 217± 17 %; P<0.05). These results show that D2R re-expression prevented the progression of the lesions and demonstrate that increased blood pressure and renal injury due to D2R silencing could be rescued by over expression of D2R in the kidney using AAV9 vector. Furthermore, these data provide the basis for designing novel therapies for kidney disease.

scholarly journals Circulating Plasma Biomarkers in Biopsy-Confirmed Kidney Disease: Results from the Boston Kidney Biopsy Cohort

2021 ◽  
Author(s):  
Insa M. Schmidt ◽  
Suraj Sarvode Mothi ◽  
Parker C. Wilson ◽  
Ragnar Palsson ◽  
Anand Srivastava ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Disease Progression ◽  
Multiple Testing ◽  
Interstitial Fibrosis ◽  
Kidney Diseases ◽  
Kidney Injury ◽  
Future Research ◽  
Tubular Atrophy ◽  
Kidney Disease Progression ◽  
Kidney Injury Molecule 1

AbstractBackgroundBiomarkers for non-invasive assessment of histopathology and prognosis are needed in patients with kidney disease.MethodsUsing a proteomics assay, we measured a multi-marker panel of 225 circulating plasma proteins in a prospective cohort study of 549 individuals with biopsy-confirmed kidney diseases and semi-quantitative assessment of histopathology. We tested the associations of each biomarker with histopathologic lesions and the risks of kidney disease progression (defined as ≥40% decline in eGFR or ESKD) and death.ResultsAfter multivariable adjustment and correction for multiple testing, 46 proteins associated with different histopathologic lesions. The top performing markers positively associated with acute tubular injury and interstitial fibrosis and tubular atrophy were kidney injury molecule-1 (KIM-1) and V-set and immunoglobulin domain-containing protein 2 (VSIG2). 30 proteins were significantly associated with kidney disease progression and 35 with death. The top performing markers for kidney disease progression were placental growth factor (PGF; HR 5.4, 95% CI 3.4 to 8.7) and BMP and Activin Membrane Bound Inhibitor (BAMBI; HR 3.0, 95% CI 2.1 to 4.2); the top performing markers for death were TRAIL-receptor-2 (TRAIL-R2; HR 2.9, 95% CI 2.0 to 4.0) and CUB Domain Containing Protein-1 (CDCP1; HR 2.4, 95% CI 1.8, 3.3).ConclusionWe identified several biomarkers associated with kidney disease histopathology and prognosis – many of which have not been reported previously and may represent important avenues for future research.

Circulating Plasma Biomarkers in Biopsy-Confirmed Kidney Disease

2021 ◽  
pp. CJN.09380721
Author(s):  
Insa Schmidt ◽  
Suraj Sarvode Mothi ◽  
Parker Wilson ◽  
Ragnar Palsson ◽  
Anand Srivastava ◽  
...  
Keyword(s):  
Kidney Disease ◽  
Disease Progression ◽  
Multiple Testing ◽  
Interstitial Fibrosis ◽  
Kidney Diseases ◽  
Kidney Injury ◽  
Protein Biomarkers ◽  
Tubular Atrophy ◽  
Kidney Disease Progression ◽  
Kidney Injury Molecule 1

Background: Biomarkers for non-invasive assessment of histopathology and prognosis are needed in patients with kidney disease. Methods: Using a proteomics assay, we measured a multi-marker panel of 225 circulating plasma proteins in a prospective cohort study of 549 individuals with biopsy-confirmed kidney diseases and semi-quantitative assessment of histopathology. We tested the associations of each biomarker with histopathologic lesions and the risks of kidney disease progression (defined as ≥40% decline in eGFR or initiation of kidney replacement therapy) and death. Results: After multivariable adjustment and correction for multiple testing, 57 proteins were associated with different histopathologic lesions. The top performing markers positively associated with acute tubular injury and interstitial fibrosis and tubular atrophy were kidney injury molecule-1 (KIM-1) and V-set and immunoglobulin domain-containing protein 2 (VSIG2), respectively. 30 proteins were significantly associated with kidney disease progression and 35 with death. The top performing markers for kidney disease progression were placental growth factor (HR per doubling 5.4, 95% CI 3.4 to 8.7) and BMP and Activin Membrane Bound Inhibitor (HR 3.0, 95% CI 2.1 to 4.2); the top performing markers for death were TRAIL-receptor-2 (HR 2.9, 95% CI 2.0 to 4.0) and CUB Domain Containing Protein-1 (HR 2.4, 95% CI 1.8 to 3.3). Conclusion: We identified several plasma protein biomarkers associated with kidney disease histopathology and adverse clinical outcomes in individuals with a diverse set of kidney diseases.

scholarly journals Kidney injury molecule-1 expression in human kidney transplants with interstitial fibrosis and tubular atrophy

2015 ◽  
Vol 16 (1) ◽  
Author(s):  
Aline Lima Nogare ◽  
Francisco Veríssimo Veronese ◽  
Virna Nowotny Carpio ◽  
Rosangela Munhoz Montenegro ◽  
José Alberto Pedroso ◽  
...  
Keyword(s):  
Interstitial Fibrosis ◽  
Kidney Injury ◽  
Human Kidney ◽  
Kidney Transplants ◽  
Tubular Atrophy ◽  
Kidney Injury Molecule 1

scholarly journals Cellular Mechanisms of Tissue Fibrosis. 3. Novel mechanisms of kidney fibrosis

2013 ◽  
Vol 304 (7) ◽  
pp. C591-C603 ◽  
Author(s):  
Gabriela Campanholle ◽  
Giovanni Ligresti ◽  
Sina A. Gharib ◽  
Jeremy S. Duffield
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Interstitial Fibrosis ◽  
Kidney Injury ◽  
Innate Immune ◽  
Cellular Mechanisms ◽  
Tubular Atrophy ◽  
Kidney Fibrosis ◽  
Capillary Rarefaction ◽  
Peritubular Capillaries

Chronic kidney disease, defined as loss of kidney function for more than three months, is characterized pathologically by glomerulosclerosis, interstitial fibrosis, tubular atrophy, peritubular capillary rarefaction, and inflammation. Recent studies have identified a previously poorly appreciated, yet extensive population of mesenchymal cells, called either pericytes when attached to peritubular capillaries or resident fibroblasts when embedded in matrix, as the progenitors of scar-forming cells known as myofibroblasts. In response to sustained kidney injury, pericytes detach from the vasculature and differentiate into myofibroblasts, a process not only causing fibrosis, but also directly contributing to capillary rarefaction and inflammation. The interrelationship of these three detrimental processes makes myofibroblasts and their pericyte progenitors an attractive target in chronic kidney disease. In this review, we describe current understanding of the mechanisms of pericyte-to-myofibroblast differentiation during chronic kidney disease, draw parallels with disease processes in the glomerulus, and highlight promising new therapeutic strategies that target pericytes or myofibroblasts. In addition, we describe the critical paracrine roles of epithelial, endothelial, and innate immune cells in the fibrogenic process.

P0661DIAGNOSTIC VALUE OF FULL AGE SPECTRUM EQUATION AS A PREDICTOR OF MORPHOLOGICAL LESIONS IN PATIENTS WITH GLOMERULONEPHRITIS

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Saganova Elena ◽  
Olga Galkina ◽  
Vasiliy Sipovskii ◽  
Ivan Kayukov, ◽  
Alexei Smirnov
Keyword(s):  
Serum Creatinine ◽  
Interstitial Fibrosis ◽  
Severe Heart Failure ◽  
Kidney Injury ◽  
Roc Curves ◽  
Diagnostic Value ◽  
Tubular Atrophy ◽  
Mild Degree ◽  
Severe Group ◽  
Global Glomerulosclerosis

Abstract Background and Aims Glomerular filtration rate (GFR) is generally accepted as a best overall index of kidney function. However, it remains controversial to choose the optimal equation to estimate GFR in patients with glomerulonephritis (GN). Recent studies have reported that newly developed full age spectrum equation based on normalized serum creatinine (FASsCr) showed improved validity and was less biased, more accurate than currently recommended sCr-based eGFR equations. Our aim was to assess FASsCr equation as a predictor of various morphological lesions in patients with GN. Method 100 patients [48 female, age Me 39 (27; 54) years] with biopsy proven primary GN and without acute kidney injury, infectious diseases, severe heart failure, respiratory insufficiency, cancer were included in the study. Minimal change disease was diagnosed in 9% of cases based on the results of kidney biopsy, in 28% – focal segmental glomerulosclerosis, in 26% – membranous nephropathy and in 37% – IgA-nephropathy. Serum creatinine (sCr) level was measured by enzymatic method (Uni Cel DxC 800 PRO, «Beckman Coulter»,USA). eGFR was calculated using FASsCr equation. The extent of global glomerulosclerosis (GS) was assessed quantitatively as a sum of full and focal sclerotic glomeruli. Tubulo-interstitial fibrosis (TIF) and tubular atrophy (TA) were assessed semi-quantitatively (0-lesions absent; 1-mild focal tubular and interstitial lesions; 2-moderate tubular and interstitial lesions; 3 - diffuse tubular and interstitial lesions). All patients consistently were separated into 2 groups according to the degree of each morphological lesion (GS, TIF or TA): “mild” (GS&lt;25% or TIF/TA grade 0 or 1) and “severe” (GS ≥ than 25% or TIF/TA grade 2-3). Results eGFR using FASsCr equation positively correlated (p&lt;0,001 in all cases) with GS (r=0,44), TIF (r=0,64) and TA (r=0,61) and was significantly higher in patients with “mild” GS, TIF and TA (p&lt;0,001) in comparison with “severe” group. Using ROC-analysis all patients were separated (p&lt;0.001) in 2 groups using FASsCr equation according to the degree of morphological lesions (“mild” or “severe”): GS (Sn – 48.8%, Sp – 88.1%, ACC – 72.0%, AUC – 0.696, cut-off value – 47 ml/min/1.73m2), TIF (Sn - 75.4%, Sp – 76.9%, ACC – 76.0%, AUC – 0.815, cut-off value – 72 ml/min/1.73m2), TA (Sn – 65.9%, Sp – 88.8%, ACC – 70.0%, AUC – 0.798, cut-off value – 74 ml/min/1.73m2), (Figure). Conclusion Our results show that FASsCr equation is a significant marker of various morphological lesions in patients with GN. FASsCr equation predominantly can be used as a predictor of mild degree of interstitial sclerosis and tubular atrophy with high diagnostic value. Figure: ROC curves with 95% CI of BM panel for A – GS; B – TIF; C – TA

scholarly journals Cisplatin-induced renal toxicity in elderly people

2020 ◽  
Vol 12 ◽  
pp. 175883592092343 ◽  
Author(s):  
ZhiYu Duan ◽  
GuangYan Cai ◽  
JiJun Li ◽  
XiangMei Chen
Keyword(s):  
Elderly Patients ◽  
Elderly People ◽  
Renal Toxicity ◽  
Enzyme Inhibitor ◽  
Interstitial Fibrosis ◽  
Angiotensin Receptor Blockers ◽  
Young Patients ◽  
Kidney Injury ◽  
The Elderly ◽  
Tubular Atrophy

Despite available prevention and treatment measures, such as hydration, diuresis, magnesium supplementation, and amifostine, renal toxicity is still one of the major dose-limiting side effects of cisplatin. The aim of this review is to discuss the issue of cisplatin-induced nephrotoxicity in the elderly. Compared with young patients, the incidences of cisplatin-induced nephrotoxicity and acute kidney injury (AKI) in elderly patients are significantly increased, and survival time may be decreased. Following cisplatin treatment of elderly patients, tubulointerstitial injuries will be significantly aggravated based on their original age, both for acute injuries due to cell necrosis and exfoliation and chronic injuries due to interstitial fibrosis, tubular atrophy, and dilatation. The high incidence of cisplatin-induced nephrotoxicity in elderly patients may be associated with renal hypoperfusion; increased comorbidities, such as chronic kidney disease (CKD), cardiovascular disease, and diabetes mellitus; increased use of combined drugs [especially non-steroidal anti-inflammatory drugs, angiotensin-converting enzyme inhibitor and angiotensin receptor blockers (ACEI/ARB), and antibiotics]; decreased clearance of cisplatin; and high plasma ultrafilterable cisplatin. Considering hemodynamic stability and water balance, short duration and low volume hydration may be more suitable for treating elderly people. With the increasing popularity of low-dose daily/weekly regimens, we do not recommend routine diuretic treatment for elderly patients. We recommend using a less nephrotoxic platinum if large doses of cisplatin (100mg/m2) are needed.

scholarly journals Comparative Histological Subtyping of Immune Cell Infiltrates in MPO-ANCA and PR3-ANCA Glomerulonephritis

2021 ◽  
Vol 12 ◽  
Author(s):  
Samy Hakroush ◽  
Désirée Tampe ◽  
Philipp Ströbel ◽  
Peter Korsten ◽  
Björn Tampe
Keyword(s):  
Mononuclear Cell ◽  
Plasma Cells ◽  
Immune Cell ◽  
Interstitial Fibrosis ◽  
Kidney Injury ◽  
Tubular Atrophy ◽  
Interstitial Inflammation ◽  
Tubulointerstitial Lesions ◽  
Mononuclear Cell Infiltrates ◽  
Immune Cell Infiltrates

BackgroundAcute kidney injury (AKI) is a common and severe complication of anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV), potentially leading to chronic kidney disease (CKD), end-stage renal disease (ESRD), or death. Pathogenic ANCAs, in particular proteinase 3 (PR3) and myeloperoxidase (MPO), trigger a deleterious immune response with intrarenal immune cell infiltration resulting in a pauci-immune necrotizing and crescentic glomerulonephritis (GN). However, a systematic analysis of intrarenal immune cell subtypes concerning neutrophils, eosinophils, plasma cells, and mononuclear cell infiltrates (macrophages, lymphocytes) in ANCA GN remains elusive. Therefore, we aimed to compare distinct immune cell infiltrates in association with clinicopathological findings in ANCA GN.MethodsA total of 53 kidney biopsies with ANCA GN at the University Medical Center Göttingen were retrospectively analyzed. Histological infiltrates of neutrophils, eosinophils, plasma cells, and mononucleated cells (macrophages, lymphocytes) were quantified as a fraction of the total area of inflammation.ResultsNeutrophilic infiltrates were associated with glomerular necrosis and severe kidney injury in ANCA GN. Among tubulointerstitial lesions, intrarenal neutrophils correlated with interstitial inflammation, tubulitis, and inflammation in areas of interstitial fibrosis/tubular atrophy (IFTA), representing active inflammatory lesions. Concerning eosinophils, infiltrates were associated with severe kidney injury, interstitial inflammation, and cellular casts independent of glomerular lesions, implicating a distinct role in inflammation and damage in ANCA GN. Plasma cell infiltrates correlated with tubulitis and interstitial fibrosis and were associated with renal replacement therapy during the short-term disease course. Finally, mononuclear cell infiltrates correlated with severe kidney injury and active histopathological lesions (glomerular crescents, interstitial inflammation, tubulitis, inflammation, and tubulitis in areas of IFTA) besides chronic lesions (interstitial fibrosis and tubular atrophy) in ANCA GN. Interestingly, intrarenal subtypes of immune cell infiltrates differed in MPO-ANCA versus PR3-ANCA GN and were associated with distinct glomerular and tubulointerstitial lesions, implicating different pathogenic mechanisms of kidney injury in ANCA subtypes.ConclusionOur observations imply distinct pathomechanisms contributing to inflammation and renal injury in MPO vs. PR3-associated ANCA GN and potentially contribute to new therapeutic targets in specific ANCA subtypes.

scholarly journals Automated Computational Detection of Interstitial Fibrosis, Tubular Atrophy, and Glomerulosclerosis

2021 ◽  
Vol 32 (4) ◽  
pp. 837-850 ◽  
Author(s):  
Brandon Ginley ◽  
Kuang-Yu Jen ◽  
Seung Seok Han ◽  
Luís Rodrigues ◽  
Sanjay Jain ◽  
...  
Keyword(s):  
Patient Outcome ◽  
Interstitial Fibrosis ◽  
Kidney Injury ◽  
Automated Identification ◽  
Statistical Tools ◽  
Tubular Atrophy ◽  
Biopsy Specimens ◽  
Chronic Kidney Injury ◽  
Modern Machine ◽  
Whole Slide Images

BackgroundInterstitial fibrosis, tubular atrophy (IFTA), and glomerulosclerosis are indicators of irrecoverable kidney injury. Modern machine learning (ML) tools have enabled robust, automated identification of image structures that can be comparable with analysis by human experts. ML algorithms were developed and tested for the ability to replicate the detection and quantification of IFTA and glomerulosclerosis that renal pathologists perform.MethodsA renal pathologist annotated renal biopsy specimens from 116 whole-slide images (WSIs) for IFTA and glomerulosclerosis. A total of 79 WSIs were used for training different configurations of a convolutional neural network (CNN), and 17 and 20 WSIs were used as internal and external testing cases, respectively. The best model was compared against the input of four renal pathologists on 20 new testing slides. Further, for 87 testing biopsy specimens, IFTA and glomerulosclerosis measurements made by pathologists and the CNN were correlated to patient outcome using classic statistical tools.ResultsThe best average performance across all image classes came from a DeepLab version 2 network trained at 40× magnification. IFTA and glomerulosclerosis percentages derived from this CNN achieved high levels of agreement with four renal pathologists. The pathologist- and CNN-based analyses of IFTA and glomerulosclerosis showed statistically significant and equivalent correlation with all patient-outcome variables.ConclusionsML algorithms can be trained to replicate the IFTA and glomerulosclerosis assessment performed by renal pathologists. This suggests computational methods may be able to provide a standardized approach to evaluate the extent of chronic kidney injury in situations in which renal-pathologist time is restricted or unavailable.

scholarly journals Roles Played by Biomarkers of Kidney Injury in Patients with Upper Urinary Tract Obstruction

2020 ◽  
Vol 21 (15) ◽  
pp. 5490 ◽  
Author(s):  
Satoshi Washino ◽  
Keiko Hosohata ◽  
Tomoaki Miyagawa
Keyword(s):  
Renal Function ◽  
Urinary Tract ◽  
Interstitial Fibrosis ◽  
Urinary Tract Obstruction ◽  
Kidney Injury ◽  
Upper Urinary Tract ◽  
Obstructive Nephropathy ◽  
Ureteral Stricture ◽  
Kidney Injury Molecule 1 ◽  
Upper Urinary Tract Obstruction

Partial or complete obstruction of the urinary tract is a common and challenging urological condition caused by a variety of conditions, including ureteral calculi, ureteral pelvic junction obstruction, ureteral stricture, and malignant ureteral obstruction. The condition, which may develop in patients of any age, induces tubular and interstitial injury followed by inflammatory cell infiltration and interstitial fibrosis, eventually impairing renal function. The serum creatinine level is commonly used to evaluate global renal function but is not sensitive to early changes in the glomerular filtration rate and unilateral renal damage. Biomarkers of acute kidney injury are useful for the early detection and monitoring of kidney injury induced by upper urinary tract obstruction. These markers include levels of neutrophil gelatinase-associated lipocalin (NGAL), monocyte chemotactic protein-1, kidney injury molecule 1, N-acetyl-b-D-glucosaminidase, and vanin-1 in the urine and serum NGAL and cystatin C concentrations. This review summarizes the pathophysiology of kidney injury caused by upper urinary tract obstruction, the roles played by emerging biomarkers of obstructive nephropathy, the mechanisms involved, and the clinical utility and limitations of the biomarkers.

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