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Titolo:
Does circulating erythropoietin reflect progression of IgA nephropathy? Comparison with urinary N-acetyl-beta-D-glucosaminidase
Autore:
Machiguchi, T; Yoshida, H; Yonemoto, S; Minakata, T; Nomura, K; Muso, E; Tamura, T; Sasayama, S;
Indirizzi:
Kitano Hosp, Inst Med Res, Div Nephrol, Kita Ku, Osaka 5300026, Japan Kitano Hosp Osaka Japan 5300026 v Nephrol, Kita Ku, Osaka 5300026, Japan Himeji Natl Hosp, Dept Internal Med, Himeji, Hyogo, Japan Himeji Natl Hosp Himeji Hyogo Japan t Internal Med, Himeji, Hyogo, Japan Kyoto Univ, Dept Cardiovasc Med, Kyoto 606, Japan Kyoto Univ Kyoto Japan606 o Univ, Dept Cardiovasc Med, Kyoto 606, Japan
Titolo Testata:
NEPHROLOGY DIALYSIS TRANSPLANTATION
fascicolo: 3, volume: 14, anno: 1999,
pagine: 635 - 640
SICI:
0931-0509(199903)14:3<635:DCERPO>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
ENDOGENOUS ERYTHROPOIETIN; ESSENTIAL-HYPERTENSION; RENAL-FAILURE; CELLS; HYPOXIA; GLOMERULONEPHRITIS; DEFICIENCY; EXCRETION; NECROSIS; INJURY;
Keywords:
anaemia; erythropoietin; glomerulosclerosis; IgA nephropathy; N-acetyl-beta-D-glucosaminidase; tubulointerstitial damage;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Yoshida, H Kitano300026,Inst Med Res, Div Nephrol, Kita Ku, 13-3 Kamiyama Cho, Osaka 5 Kitano Hosp 13-3 Kamiyama Cho Osaka Japan 5300026 Cho, Osaka 5
Citazione:
T. Machiguchi et al., "Does circulating erythropoietin reflect progression of IgA nephropathy? Comparison with urinary N-acetyl-beta-D-glucosaminidase", NEPH DIAL T, 14(3), 1999, pp. 635-640

Abstract

Background. Recent reports describe that erythropoietin (Epo) is produced by peritubular interstitial fibroblast-like cells in response to a hypoxic stimulus. We studied serum Epo levels as a possible marker of tubulointerstitial damage in the progression of IgA nephropathy (IgAN), in comparison with urinary (u-) levels of N-acetyl-beta-D-glucosaminidase (NAG), which is mainly derived from proximal tubular cells and is used as a marker of tubular damage. Methods. Thirty-eight patients with IgA nephropathy (IgAN) with relativelypreserved renal function (serum creatinine: sCr, 0.5-2.2mg/dl) were examined. The severity of glomerulosclerosis and interstitial fibrosis of the renal biopsy tissue was expressed by semiquantitative grading scores. Clinicalparameters including serum creatinine (sCr), blood pressures, and 24-h proteinuria levels were obtained at the renal biopsy. Epo was measured by a radioimmunoassay (RIA) of sera obtained in the morning and u-NAG was measuredby colorimetric method of 24-h urine samples. Results. The mean Epo level of the patients ( 17.7 +/- 6.3 mU/ml) was not different from the control level (19.3 +/-3.7 mU/ml). There were no significant correlations between Epo levels and red blood cell (RBC) counts, haematocrit (Hct), or haemoglobin (Hb) levels. The mean u-NAG level of the patients (6.7 +/- 6.2 U/gCr) was significantly higher than the control level (1.9+/-0.5 U/gCr). There was an inverse quantitative correlation between Epo and u-NAG levels in the patients (P<0.02). The u-NAG levels showed quantitative positive correlations with sCr (P<0.001), u-proteins (P<0.001), systolic (SBP) (P<0.001), and diastolic blood pressures (DBP) (P<0.05). Conversely, Epo levels were inversely correlated with sCr, SEP and DBP (each P<0.05). The patients with higher u-proteins (> 2.0 g/day) showed significantly decreased Epo levels (P<0.05) than those with lower u-proteins (<2.0 g/day). The both scores of glomerulosclerosis and interstitial fibrosis were positively correlated with the u-NAG levels (each P<0.001), but were not correlated with the Epo levels. Conclusions, The significant correlation between u-NAG and serum Epo levels suggests that tubular damage and interstitial cell dysfunction are associated each other in the progression of IgAN. Serum Epo levels bearing inverse correlations with sCr, blood pressure levels and heavy proteinuria seem to reflect clinical severity of IgAN, whereas u-NAG can be more useful progression marker of IgAN bearing correlations with both clinical and histological findings.

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Documento generato il 03/04/20 alle ore 19:14:18