Risk Stratification of Patients With IgA Nephropathy

Department of Medicine, Division of Nephrology, University of British Columbia, Vancouver, British Columbia, Canada.
American Journal of Kidney Diseases (Impact Factor: 5.9). 04/2012; 59(6):865-73. DOI: 10.1053/j.ajkd.2012.02.326
Source: PubMed


In this review, we summarize recent advances in the risk stratification of patients with immunoglobulin A (IgA) nephropathy. Several clinical variables have consistent and independent associations with worse kidney prognosis, including blood pressure, proteinuria, and baseline kidney function. Although one-time cross-sectional assessments of blood pressure and proteinuria are important, a more thorough understanding of risk can be achieved when these variables are considered over a follow-up period. IgA nephropathy is unique compared with other glomerular diseases in that a much lower threshold of proteinuria (protein excretion, 1 g/d) is associated with glomerular filtration rate (GFR) loss. Controlling proteinuria and blood pressure over time is important to reduce the risk of future loss of kidney function. The recently described Oxford classification has helped standardize the pathologic characterization of IgA nephropathy using a scoring system that is readily reproducible and associated with increased risk of GFR loss independent of clinical variables. We suggest an approach to risk stratification in IgA nephropathy when considering potential treatment with immunosuppression. Despite our current understanding of risk stratification in IgA nephropathy, the ability to accurately predict individual patient-level risk currently is limited, and further research into additional biomarkers or risk prediction tools is needed to improve the care of patients with IgA nephropathy.

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Available from: Heather N Reich, Sep 02, 2015
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    • "24-h proteinuria might thus be not completely attributable to IgAN in these particular cases. The importance of proteinuria as a predictor of decreasing estimated glomerular filtration rate (eGFR) was highlighted by previous studies (Moriyama et al. 2014; Bartosik et al. 2001; Barbour and Reich 2012). Thus maintenance of 24-h proteinuria levels below 1 g/24 h is one of the targets in the management of IgAN. "
    SpringerPlus 12/2015; 4(1). DOI:10.1186/s40064-015-1323-x
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    • "The initial manifestation of disease is frequently synpharyngitic hematuria, that is, macroscopic hematuria concurrent with upper respiratory tract infection [1, 2]. Progressive renal damage often culminates in end-stage renal disease (ESRD) that requires dialysis or transplantation as renal replacement therapy [3, 4]. In patients undergoing renal transplantation, the high rate of recurrence, up to 50–60%, suggests that the disease is of extrarenal origin [5]. "
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    ABSTRACT: Immunoglobulin A (IgA) nephropathy (IgAN), the leading cause of primary glomerulonephritis, is characterized by IgA1-containing immunodeposits in the glomeruli. IgAN is a chronic disease, with up to 40% of patients progressing to end-stage renal disease, with no disease-specific treatment. Multiple studies of the origin of the glomerular immunodeposits have linked elevated circulating levels of aberrantly glycosylated IgA1 (galactose-deficient in some O-glycans; Gd-IgA1) with formation of nephritogenic Gd-IgA1-containing immune complexes. Gd-IgA1 is recognized as an autoantigen in susceptible individuals by anti-glycan autoantibodies, resulting in immune complexes that may ultimately deposit in the kidney and induce glomerular injury. Genetic studies have revealed that an elevated level of Gd-IgA1 in the circulation of IgAN patients is a hereditable trait. Moreover, recent genome-wide association studies have identified several immunity-related loci that associated with IgAN. Production of Gd-IgA1 by IgA1-secreting cells of IgAN patients has been attributed to abnormal expression and activity of several key glycosyltransferases. Substantial evidence is emerging that abnormal signaling in IgA1-producing cells is related to the production of Gd-IgA1. As Gd-IgA1 is the key autoantigen in IgAN, understanding the genetic, biochemical, and environmental aspects of the abnormal signaling in IgA1-producing cells will provide insight into possible targets for future disease-specific therapy.
    Research Journal of Immunology 07/2014; 2014:197548. DOI:10.1155/2014/197548
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    • "Although dominant mesangial IgA deposits represent the diagnostic hallmark of IgAN, its clinical features are highly variable, ranging from simple hematuria with or without proteinuria to a rapidly progressive loss of renal function. Therefore, the renal survival and risk factors of long-term IgAN patients have been studied extensively over the last 30 years [2]. Previous studies indicate that the likelihood of dialysis or death can be estimated using three clinical risk factors: urinary protein excretion of more than 1 g/day, high blood pressure exceeding 140/90 mmHg, and a decreased estimated glomerular filtration rate (eGFR) of less than 60 mL/min/1.73 "
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    ABSTRACT: Background The long-term prognosis of clinically early IgA nephropathy (IgAN) patients remains to be clarified. We investigated the long-term outcomes of IgAN patients with an apparently benign presentation and evaluated prognostic factors for renal survival. Methods We included patients with biopsy-proven IgAN who had estimated glomerular filtration rates (eGFR) ≥60 mL/min/1.73 m2, normal blood pressure, and proteinuria <0.5 g/day at the time of biopsy. The primary outcome was progression to end-stage renal disease (ESRD). The secondary outcome was a 50% increase in serum creatinine level or an increase in proteinuria to >1 g/day. Results The analysis included 153 patients who met the inclusion criteria. At diagnosis, their median systolic blood pressure was 120 (110–130) mmHg, eGFR was 85.9 (74.9–100.1) mL/min/1.73 m2, and proteinuria was 0.25 (0.13–0.38) g/day. Of these, 4 patients died and 6 reached ESRD. The 30-year renal survival rate was 85.5%. Three patients had increased serum creatinine levels and 11 developed proteinuria. Remission was observed in 35 (22.9%) patients. A moderate or severe degree of interstitial fibrosis (adjusted odd ratio [OR] 5.93, 95% confidence interval [CI] 1.44–24.45, P = 0.014) and hypoalbuminemia (adjusted OR 6.18, 95% CI 1.20–31.79, P = 0.029) were independent predictors of the secondary outcome. Conclusions This study showed that the prognosis of early IgAN was not always favorable, even resulting in progression to ESRD in some cases. Hypoalbuminemia and interstitial fibrosis should also be considered important prognostic factors in clinically early IgAN patients.
    BMC Nephrology 06/2014; 15(1):94. DOI:10.1186/1471-2369-15-94 · 1.69 Impact Factor
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