IgA nephropathy: prognostic classification of end-stage renal failure

Firmat, L.; Briançon, Serge; Hestin, D.; Aymard, B.; Renoult, E.; Huu, T. Cao; Kessler, Michèle; l'Est, L. des Nephrologues de

doi:10.1093/ndt/12.12.2569

Cited by 80 publications

(70 citation statements)

References 8 publications

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“…IgAN progression was observed significantly more often in patients with the baseline eGFR of less Renal impairment at diagnosis is a well-documented predictor for progression of IgAN. 10,11 In the present study, baseline eGFR of less than 60 ml/min/1.73 m 2 was the strongest marker for progression, associated with an almost 8-fold increase in the risk of reaching the endpoint.…”

Section: Survival Analysissupporting

confidence: 48%

Stratifying risk for progression in IgA nephropathy: how to predict the future?

Rafalska¹,

Franczuk²,

Franczuk³

et al. 2014

Polish Archives of Internal Medicine

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Section: Survival Analysissupporting

confidence: 48%

Stratifying risk for progression in IgA nephropathy: how to predict the future?

Rafalska¹,

Franczuk²,

Franczuk³

et al. 2014

Polish Archives of Internal Medicine

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“…Of note, despite the severity of glomerular lesions, serum creatinine returned to baseline values in most other patients. It is interesting that, although the presence or intensity of microscopic hematuria has been associated with worse kidney function prognosis in IgA nephropathy (14), a history of macroscopic hematuria bouts has even been associated with a better kidney outcome (15)(16)(17)(18)(19). However, this association was frequently lost on multivariate analysis, probably because macroscopic hematuria was frequently observed in cases with earlier (characterized by less fibrosis) or milder glomerular injury (17).…”

Section: Macroscopic Glomerular Hematuria and Akimentioning

confidence: 99%

AKI Associated with Macroscopic Glomerular Hematuria

Moreno

Martín-Cleary

Gutiérrez

et al. 2012

Clinical Journal of the American Society of Nephrology

117

110

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SummaryHematuria is a common finding in various glomerular diseases. This article reviews the clinical data on glomerular hematuria and kidney injury, as well as the pathophysiology of hematuria-associated renal damage. Although glomerular hematuria has been considered a clinical manifestation of glomerular diseases without real consequences on renal function and long-term prognosis, many studies performed have shown a relationship between macroscopic glomerular hematuria and AKI and have suggested that macroscopic hematuria-associated AKI is related to adverse long-term outcomes. Thus, up to 25% of patients with macroscopic hematuriaassociated AKI do not recover baseline renal function. Oral anticoagulation has been associated with glomerular macrohematuria-related kidney injury. Several pathophysiologic mechanisms may account for the tubular injury found on renal biopsy specimens. Mechanical obstruction by red blood cell casts was thought to play a role. More recent evidence points to cytotoxic effects of oxidative stress induced by hemoglobin, heme, or iron released from red blood cells. These mechanisms of injury may be shared with hemoglobinuria or myoglobinuria-induced AKI. Heme oxygenase catalyzes the conversion of heme to biliverdin and is protective in animal models of heme toxicity. CD163, the recently identified scavenger receptor for extracellular hemoglobin, promotes the activation of anti-inflammatory pathways, opening the gates for novel therapeutic approaches.

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“…This is seen in multiple sclerosis and in several types of glomerulonephritis. Examples of the latter are IgA nephropathy, where an upper respiratory tract infection commonly precedes disease presentation (1), and antiglomerular basement membrane disease, where exacerbations during treatment are often related to infection (2). Relapses of anti-neutrophil cytoplasmic Ab-associated vasculitis are also associated with nasal carriage of Staphylococcus aureus (3) and prevented by antimicrobial therapy (4).…”

Section: Tlr2 Stimulation Of Intrinsic Renal Cells In the Inductionmentioning

confidence: 99%

TLR2 Stimulation of Intrinsic Renal Cells in the Induction of Immune-Mediated Glomerulonephritis

Brown

Lock

Sacks

et al. 2006

The Journal of Immunology

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Infection may exacerbate organ-specific autoimmune disease such as glomerulonephritis. This may occur in the absence of a measurable effect on the adaptive immune response, and the mechanisms responsible are not fully understood. To investigate this, we have studied the effect of TLR2 ligation by the synthetic ligand Pam3CysSK4 on the development of glomerulonephritis in mice. We demonstrated that glomerular inflammation induced by passive administration of nephrotoxic Ab does not occur in the absence of TLR2 stimulation, with a strong synergy when Ab deposition and TLR2 stimulation occur together. Parameters of glomerular inflammation were neutrophil influx, thrombosis, and albuminuria. To investigate the relative contribution of TLR2 on bone marrow-derived cells and intrinsic renal cells, we constructed bone marrow chimeras. Nephrotoxic Ab and TLR2 ligation caused a neutrophil influx in both types of chimera at a similar level to that seen in sham chimeras totally TLR2 sufficient. Albuminuria was seen in both types of chimera above that seen in sham chimeras that were totally TLR2 deficient. This was greater in chimeras with TLR2 present on bone marrow-derived cells. To find a potential mechanism by which intrinsic renal cells may contribute toward disease exacerbation, mesangial cells were studied and shown to express TLR2 and MyD88. Wild-type but not TLR2-deficient mesangial cells produced CXC chemokines in response to stimulation with Pam3CysSK4. These results demonstrate that TLR2 stimulation on both bone marrow-derived and resident tissue cells plays a role in amplifying the inflammatory effects of Ab deposition in the glomerulus.

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IgA nephropathy: prognostic classification of end-stage renal failure

Abstract: These classifications identify groups at high risk of ESRF. Therapeutic studies should focus on these groups.

Cited by 80 publications

References 8 publications

Stratifying risk for progression in IgA nephropathy: how to predict the future?

Stratifying risk for progression in IgA nephropathy: how to predict the future?

AKI Associated with Macroscopic Glomerular Hematuria

TLR2 Stimulation of Intrinsic Renal Cells in the Induction of Immune-Mediated Glomerulonephritis

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