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Background. Aristolochic acid nephropathy (AAN) is a worldwide problem and one of the common causes of chronic kidney disease (CKD) in China. Methods. Three hundred patients diagnosed as AAN from 1997 to 2006 were enrolled. Medical histories of Chinese herb ingestion, clinical–pathological features and risk factors for renal failure were recorded. Patients were followed up for 2–156 months. Factors involved in the prognosis of AAN were investigated. Results. The 300 patients with AAN manifested three clinical subtypes, including acute kidney injury (acute AAN) in 13 patients, abrupt tubular dysfunction with normal serum creatinine (Scr) levels in seven cases and chronic tubulointerstitial nephropathy with decreased estimated glomerular filtration rate (eGFR) (chronic AAN) in 280 cases. The acute AAN cases had the highest aristolochic acid (AA)-I intake per day and developed progressive kidney failure during 1–7 years follow-up. The tubular dysfunction AAN patients had the lowest cumulative AA-I intake and were able to keep normal Scr levels during 2–8 years follow-up. The chronic AAN patients took the lowest AA-I dose per day but with the longest period and the highest cumulative dosage and exhibited a very large range of eGFR changing rate (from −21.6 to 5.2, median −3.5 mL/min/year). The cumulative AA-I intake (r = 0.330, P = 0.045) and the time course from the termination of AA medication to the start of follow-up (r = −0.430, P = 0.009) were found to be independent factors correlated with the decrease rate of eGFR in the chronic AAN patients. AA and the metabolites could be detected in a high frequency in patients who had stopped herbal medication for 1 year, which indicates a rather long washout time for these chemicals. Conclusions. AAN has variant phenotypes with distinct prognosis, which is determined by the variable AA medications. With better understanding of toxic and environmental causes for kidney injury, there would be a better chance to uncover the causal factors of cases of ‘CKD without known causes’ which is crucial for improving the disease outcomes. [ABSTRACT FROM PUBLISHER]

Background. Massive proteinuria is often associated with hypoalbuminaemia in glomerulopathy. However, patients may have normal levels of serum albumin despite heavy proteinuria in many circumstances. This study analysed factors affecting serum levels of albumin in primary glomerulopathy patients with nephrotic-range proteinuria.Methods. The renal histopathological data of 780 consecutive adult patients (age ≥ 18 years old) with primary glomerulopathy and nephrotic-range proteinuria, who received native renal biopsies in Peking University First Hospital from 1998 to 2007, were retrospectively analysed.Results. Compared with patients with hypoalbuminaemia (serum albumin < 30 g/L), patients without hypoalbuminaemia were significantly younger (P < 0.001) and had significantly lower levels of proteinuria (P < 0.001). Patients without hypoalbuminaemia had a significantly higher proportion of IgA nephropathy (66.0% vs. 17.2%, P < 0.001). The independent predictors of hypoalbuminaemia in nephrotic-range proteinuria patients included age, gender, interval between onset of the disease and renal biopsy, proteinuria level, and pathological type of glomerulopathy. A serum level of albumin ≥ 35 g/L could predict IgA nephropathy with a specificity of 95.8%, and specificity increased with age.Conclusions. Among patients with primary glomerulopathy and nephrotic-range proteinuria, normoalbuminaemia is associated with IgA nephropathy. [ABSTRACT FROM AUTHOR]

Background. Although the clinical importance of demonstrating the presence of anti-glomerular basement membrane (anti-GBM) antibodies is well established, less is known concerning the clinical utility of measuring the levels of autoantibodies. Two conformational epitopes of anti-GBM antibodies have been defined at residues 17–31 and 127–141 of the α3(IV)NC1 domain of type IV collagen [α3(IV)NC1], which were named as EA and EB, respectively. In order to elucidate the importance of such antibodies, we studied the levels and the epitope specificities of anti-GBM antibodies in a large cohort of Chinese patients with anti-GBM disease. Methods. All patients, with anti-GBM disease and available clinical data, diagnosed at Peking University First Hospital from 1996 to 2005 were included in the present study. Recombinant chimeric proteins containing previously defined epitope regions designated as EA and EB were used to detect anti-GBM antibodies by ELISA. Results were compared and correlated with clinical data collected at the time of diagnosis, biopsy findings and outcome after 1 year of follow-up. Results. A retrospective diagnosis of anti-GBM disease was made in 147 patients. Haemoptysis was recorded for 47% of these cases while 53.5% cases had oliguria or anuria at the time of diagnosis. Among these patients, the levels of anti-GBM antibodies correlated with serum creatinine at diagnosis (P < 0.05 for anti EA, EB and α3(IV)NC1). Oliguric patients had higher levels of autoantibodies than non-oliguric patients, however, the difference being statistically significant only for EB (P < 0.05). Renal biopsies were performed in 66 patients, and it was found that 50 (75.8%) had cresent formation in >85% of the glomeruli. There was a correlation between the percentage of crescents and levels of antibodies, but it was significant only for anti-EA antibodies (P < 0.05). Clinical data regarding the follow-up were available for 102 patients; at the end of 1 year, 88 (86.3%) were either dead or dialysis dependent. The absorbance values of anti-GBM antibodies against both EA and EB were also associated with the subsequent development, death or terminal renal insufficiency (P < 0.05). Conclusion. In this study, patients with high levels of circulating antibodies against the specific epitopes EA and EB had a more severe renal disease at diagnosis as well as a worse prognosis. [ABSTRACT FROM AUTHOR]