scholarly journals Identification of urinary metabolites that distinguish membranous lupus nephritis from proliferative lupus nephritis and focal segmental glomerulosclerosis

2011 ◽  
Vol 13 (6) ◽  
pp. R199 ◽  
Author(s):  
Lindsey E Romick-Rosendale ◽  
Hermine I Brunner ◽  
Michael R Bennett ◽  
Rina Mina ◽  
Shannen Nelson ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Focal Segmental Glomerulosclerosis ◽  
Urinary Metabolites ◽  
Segmental Glomerulosclerosis ◽  
Proliferative Lupus Nephritis ◽  
Membranous Lupus Nephritis

scholarly journals Urinary myo-inositol is associated with the clinical outcome in focal segmental glomerulosclerosis

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Jung Nam An ◽  
Jin Seong Hyeon ◽  
Youngae Jung ◽  
Young Wook Choi ◽  
Jin Hyuk Kim ◽  
...  
Keyword(s):  
Focal Segmental Glomerulosclerosis ◽  
Urinary Metabolites ◽  
Urine Samples ◽  
Resonance Spectroscopy ◽  
Important Indicator ◽  
Clinical Prognosis ◽  
Segmental Glomerulosclerosis ◽  
Healthy Control ◽  
Validation Set

Abstract Focal segmental glomerulosclerosis (FSGS) and minimal change disease (MCD) have similar initial histological findings; however, their prognoses are distinct. Therefore, it is of great importance to discriminate FSGS from MCD in the early phase of disease and predict clinical prognosis. A discovery set of 184 urine samples (61 healthy control, 80 MCD, and 43 FSGS) and a validation set of 61 urine samples (12 healthy control, 26 MCD, and 23 FSGS) were collected at the time of kidney biopsy. Metabolic profiles were examined using nuclear magnetic resonance spectroscopy. Of 70 urinary metabolites, myo-inositol was significantly higher in FSGS patients than in control patients (discovery set, 2.34-fold, P < 0.001; validation set, 2.35-fold, P = 0.008) and MCD patients (discovery set, 2.48-fold, P = 0.002; validation set, 1.69-fold, P = 0.042). Myo-inositol showed an inverse relationship with the initial estimated glomerular filtration rate (eGFR) and was associated with the plasma level of soluble urokinase-type plasminogen activator receptor in FSGS patients. Myo-inositol treatment ameliorated the decreased expression of ZO-1 and synaptopodin in an in vitro FSGS model, and as myo-inositol increased, myo-inositol oxygenase tissue expression decreased proportionally to eGFR. Furthermore, urinary myo-inositol exhibited an increase in the power to discriminate FSGS patients, and its addition could better predict the response to initial treatment. In conclusion, urinary myo-inositol may be an important indicator in the diagnosis and treatment of FSGS patients.

scholarly journals Non-histologic factors discriminating proliferative lupus nephritis from membranous lupus nephritis

2020 ◽  
Vol 22 (1) ◽  
Author(s):  
Oh Chan Kwon ◽  
Jung Hwan Park ◽  
Hyeong-Cheon Park ◽  
Seung Min Jung ◽  
Sang-Won Lee ◽  
...  
Keyword(s):  
Lupus Nephritis ◽  
Proliferative Lupus Nephritis ◽  
Membranous Lupus Nephritis

scholarly journals Th Subset Balance in Lupus Nephritis

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Katsuhisa Miyake ◽  
Mitsuteru Akahoshi ◽  
Hitoshi Nakashima
Keyword(s):  
Lupus Nephritis ◽  
Complex Disease ◽  
Lymphocyte Subsets ◽  
Clinical Manifestations ◽  
Pathogenetic Mechanism ◽  
Th2 Cytokine ◽  
Proliferative Lupus Nephritis ◽  
Th1 And Th2 Cytokines ◽  
Membranous Lupus Nephritis ◽  
Th1 And Th2

Lupus nephritis, which has various histological patterns and variable clinical outcomes, is one of the most important complications of systemic lupus nephritis (SLE). This pathogenetic mechanism in each histologically different type of lupus nephritis (LN) remains unclear. Although SLE is suggested to be a Th2-driven disease, elevation of both Th1 and Th2 cytokines occurs in both humans and mice, suggesting that SLE is a complex disease driven by different lymphocyte subsets with high heterogeneity of clinical manifestations and organ involvement. Recent findings in LN elucidate an essential role for the Th1, IL-17 producing T cells and Th17 cells in the development of diffuse proliferative lupus nephritis (DPLN), and Th2 cytokine in that of membranous lupus nephritis (MLN). These data support the hypothesis that individual Th1/Th2 balance is one of the critical determinants for histopathology of LN.

scholarly journals Expression of Advanced Glycation End Products and Their Cellular Receptor RAGE in Diabetic Nephropathy and Nondiabetic Renal Disease

2000 ◽  
Vol 11 (9) ◽  
pp. 1656-1666 ◽  
Author(s):  
NOZOMU TANJI ◽  
GLEN S. MARKOWITZ ◽  
CAIFENG FU ◽  
THOMAS KISLINGER ◽  
AKIHIKO TAGUCHI ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Lupus Nephritis ◽  
Focal Segmental Glomerulosclerosis ◽  
Advanced Glycation End Products ◽  
Basement Membranes ◽  
Advanced Glycation ◽  
Hypertensive Nephrosclerosis ◽  
Segmental Glomerulosclerosis ◽  
Glycation End Products ◽  
End Products

Abstract.Advanced glycation end products (AGE) contribute to diabetic tissue injury by two major mechanisms,i.e., the alteration of extracellular matrix architecture through nonenzymatic glycation, with formation of protein crosslinks, and the modulation of cellular functions through interactions with specific cell surface receptors, the best characterized of which is the receptor for AGE (RAGE). Recent evidence suggests that the AGE-RAGE interaction may also be promoted by inflammatory processes and oxidative cellular injury. To characterize the distributions of AGE and RAGE in diabetic kidneys and to determine their specificity for diabetic nephropathy, an immunohistochemical analysis of renal biopsies from patients with diabetic nephropathy (n= 26), hypertensive nephrosclerosis (n= 7), idiopathic focal segmental glomerulosclerosis (n= 11), focal sclerosis secondary to obesity (n= 7), and lupus nephritis (n= 11) and from normal control subjects (n= 2) was performed, using affinity-purified antibodies raised to RAGE and two subclasses of AGE,i.e., Nϵ-(carboxymethyl)-lysine (CML) and pentosidine (PENT). AGE were detected equally in diffuse and nodular diabetic nephropathy. CML was the major AGE detected in diabetic mesangium (96%), glomerular basement membranes (GBM) (42%), tubular basement membranes (85%), and vessel walls (96%). In diabetic nephropathy, PENT was preferentially located in interstitial collagen (90%) and was less consistently observed in vessel walls (54%), mesangium (77%), GBM (4%), and tubular basement membranes (31%). RAGE was expressed on normal podocytes and was upregulated in diabetic nephropathy. The restriction of RAGE mRNA expression to glomeruli was confirmed by reverse transcription-PCR analysis of microdissected renal tissue compartments. The extent of mesangial and GBM immunoreactivity for CML, but not PENT, was correlated with the severity of diabetic glomerulosclerosis, as assessed pathologically. CML and PENT were also identified in areas of glomerulosclerosis and arteriosclerosis in idiopathic and secondary focal segmental glomerulosclerosis, hypertensive nephrosclerosis, and lupus nephritis. In active lupus nephritis, CML and PENT were detected in the proliferative glomerular tufts and crescents. In conclusion, CML is a major AGE in renal basement membranes in diabetic nephropathy, and its accumulation involves upregulation of RAGE on podocytes. AGE are also accumulated in acute inflammatory glomerulonephritis secondary to systemic lupus erythematosus, possibly via enzymatic oxidation of glomerular matrix proteins.

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