“…However, a treatment strategy for IgAN has not yet been established. This may be because surrogate markers such as a reduction in proteinuria or percent change in renal function, expressed as the value of serum creatinine (sCr) or glomerular filtration rate (GFR), are frequently used to assess IgAN with a long clinical course, and the true outcomes of studies remain inadequate [14, 15]. …”
Background/Aims: Various treatment options for IgA nephropathy (IgAN) have been developed, particularly over the past decade. Nevertheless, whether such therapeutic interventions improve actual renal outcome as compared with previous therapies remains obscure. Methods: We examined data from 304 patients with IgAN whose serum creatinine value at renal biopsy was <2.0 mg/dl and who had been followed up for >12 months. We assigned the patients to groups according to the period of diagnosis (group E, between 1981 and 1995, n = 130; group L, between 1996 and 2006, n = 174). Results: Significantly more patients had received steroid therapy and renin-angiotensin system inhibitors (RAS-I) in group L than in group E (steroid 51.7 vs. 15.4%, p < 0.001; RAS-I 42.0 vs. 1.5%, p < 0.001). Forty patients overall reached end-stage renal disease (ESRD) within 81.9 ± 55.1 months of observation. Kaplan-Meier analysis showed that the 10-year renal survival rate of group L persisted and significantly differed from that of group E (95.7 vs. 75.2%, p = 0.005). The Cox proportional hazards model adjusted for known prognostic markers demonstrated that initial therapeutic interventions in group L prevented ESRD, with a hazard ratio of 0.29 (95% CI 0.11–0.76, p = 0.011). Conclusion: Although this study is not a prospective trial, our results indicate that aggressive therapeutic intervention for IgAN over the past decade has improved actual renal outcome.
“…However, a treatment strategy for IgAN has not yet been established. This may be because surrogate markers such as a reduction in proteinuria or percent change in renal function, expressed as the value of serum creatinine (sCr) or glomerular filtration rate (GFR), are frequently used to assess IgAN with a long clinical course, and the true outcomes of studies remain inadequate [14, 15]. …”
Background/Aims: Various treatment options for IgA nephropathy (IgAN) have been developed, particularly over the past decade. Nevertheless, whether such therapeutic interventions improve actual renal outcome as compared with previous therapies remains obscure. Methods: We examined data from 304 patients with IgAN whose serum creatinine value at renal biopsy was <2.0 mg/dl and who had been followed up for >12 months. We assigned the patients to groups according to the period of diagnosis (group E, between 1981 and 1995, n = 130; group L, between 1996 and 2006, n = 174). Results: Significantly more patients had received steroid therapy and renin-angiotensin system inhibitors (RAS-I) in group L than in group E (steroid 51.7 vs. 15.4%, p < 0.001; RAS-I 42.0 vs. 1.5%, p < 0.001). Forty patients overall reached end-stage renal disease (ESRD) within 81.9 ± 55.1 months of observation. Kaplan-Meier analysis showed that the 10-year renal survival rate of group L persisted and significantly differed from that of group E (95.7 vs. 75.2%, p = 0.005). The Cox proportional hazards model adjusted for known prognostic markers demonstrated that initial therapeutic interventions in group L prevented ESRD, with a hazard ratio of 0.29 (95% CI 0.11–0.76, p = 0.011). Conclusion: Although this study is not a prospective trial, our results indicate that aggressive therapeutic intervention for IgAN over the past decade has improved actual renal outcome.
“…A further implication of this work is that proteinuria change alone should not be relied upon to assess therapeutic efficacy of immunosuppression in clinical trials, as has been suggested [29,30,31]. Clearly, this requires further study [32].…”
Background: Relapse or worsening of nephrotic syndrome (NS) in idiopathic membranous nephropathy (IMN) is generally assumed to be due to recurrent disease. Here we document that often that may not be the case. Subjects and Methods: This is a prospective study of 7 consecutive IMN patients whose renal status improved, then worsened after completing a course of immunosuppressive therapy. Each underwent detailed testing and repeat kidney biopsy. Results: In 4 patients (group A), the biopsy showed recurrent IMN (fresh subepithelial deposits). Immunosuppressive therapy was begun. In the other 3 patients (group B), the biopsy showed that the deposits had been eradicated. However, the glomerular basement membrane (GBM) was thickened and vacuolated. Immunosuppressive therapy was withheld. Groups A and B were comparable except that group B had very high intakes of salt and protein, based on 24-hour urine testing. Reducing their high salt intake sharply lowered proteinuria to the subnephrotic range and serum creatinine stabilized. Conclusion: This work is the first to demonstrate that relapse/worsening of NS can occur in IMN even though the GBM deposits have been eradicated. High salt and protein intake in combination with thickened and vacuolated GBM appears to be the mechanism.
“…The worsening of albuminuria is associated with an increased risk of renal and cardiovascular disease progression 9 . In addition to the complicated clinical scenario of both acute and chronic renal injury, inflammatory cytokines, coordinated by innate cells and glomerular cells, including podocytes, tubular cells, and endothelial cells, play an important role in causing albuminuria and renal function deterioration 10 , 11 . Furthermore, albuminuria and the progression of renal disease are interwoven and mutually determined.…”
Activin A, a cytokine belonging to the transforming growth factor-β family, has been shown to play pivotal roles in tissue remodeling after renal injury and is present in elevated levels in diabetic patients. However, the association between activin A and albuminuria remains unclear. We aimed to evaluate their association by using cross-sectional data from community-dwelling middle-aged and older adults in Taiwan. We assessed 466 participants (67% male; mean age 71 ± 13 years) from the I-Lan Longitudinal Aging study for whom data pertaining to serum activin A level and urine albumin-to-creatinine ratio (UACR) were available. Of these, 323 (69%) had normal albuminuria, 123 (26%) had microalbuminuria, and 20 (4%) had overt albuminuria. Patients with overt albuminuria and microalbuminuria had significantly higher activin A concentrations than those in the normal albuminuria group (p < 0.001). Circulating activin A was significantly correlated with multiple risk factors, including higher systolic blood pressure and higher UACR. Univariate and multivariate results indicated that activin A level was an independent variable for albuminuria. The cutoff value of 602 pg/mL of activin A demonstrated a sensitivity of 70.6% and specificity of 75.7% (AUC 0.774) in diagnosing overt albuminuria. In conclusion, middle-aged and older adults with elevated activin A levels were associated with a higher incidence of albuminuria.
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