Reply from the Authors
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چکیده
To the Editor: In interesting paper, Fehr et al [1] showed relative erythropoietin deficiency in patients with GFR <40 mL/min, and concluded that it was the sequence of either altered set point for hormone production or due to renal tissue damage. On the other hand, Machiguchi et al’s paper [2] and our preliminary study led to extend Fehr’s explanation. Machiguchi et al [2] have shown that in patients with IgA nephropathy and relatively preserved renal function (sCr 0.5-2.5 mg/dL), urinary excretion of N-acetyl-b-D-glucosaminidase (NAG) inversely correlated with serum erythropoietin concentration. According to these results, our recent study by Sulikowska et al [3] showed that functional status of renal vasculature, estimated as dopamine-induced glomerular filtration response (DIR), strongly correlated with NAG excretion. Furthermore, our preliminary study conducted in 30 untreated IgA patients, with GFR 109 ± 27.5 mL/min, showed that DIR correlated with changes of serum erythropoietin concentration during dopamine infusion (serum erythropoietin, before dopamine mean: 10.9, range: from 1.3 to 10.4; after dopamine mean: 9.2, range: from 1.8 to 29.1 U/L) and 24-hour proteinuria (r = −48; P< 0.05), (r = 37; P< 0.05), respectively. In the same study, dopamine-induced changes of serum erythropoietin correlated with both 24-hour urinary NAG excretion and proteinuria (r = 0.56; P< 0.02), (r = 0.43; P< 0.03), respectively. Data from Machiguchi et al [2], together with our finding, suggest that proteinuria is a crucial factor disturbing the function of tubulointerstitial compartment (tubules, vessels, and interstitial cells) as a whole. Presented data, and comments of Fehr et al, suggest that serum erythropoietin concentration come into view as a marker of functional status of tubulointerstitial compartment in patients with various degrees of renal damage. Regarding these data, we have commenced the study to examine whether serum erythropoietin could be used as a marker to predict the progression of renal disease.
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تاریخ انتشار 2010