Abstract
Background: The efficacy of ACE-inhibitors in decreasing microalbuminuria and proteinuria has been reported in a few patients with glycogen storage disease type 1 (GSD1); however, no case-control study has ever been published. Aim: The aim of the current study was to evaluate the efficacy of ACE-inhibitors in reducing glomerular hyperfiltration, microalbuminuria and proteinuria, and in delaying the progression of renal damage. Patients and methods: Ninety-five patients (median age at the time of the study: 14.5 years) were enrolled from nine Italian referral centres for metabolic diseases. A retrospective study of a 10-year follow-up was conducted in order to compare the evolution of these parameters in treated patients with those who were not treated with ACE-inhibitors. Results: A significant and progressive decrease of glomerular filtration rate was observed in treated patients vs. those who were not treated with ACE-inhibitors (P <0.05). No difference was observed for microalbuminuria and proteinuria between the two groups of patients. Moreover, the ACE-inhibitors significantly delayed the progression from glomerular hyperfiltration to microalbuminuria, but not that from microalbuminuria to proteinuria. Conclusions: The results of the present study underline the importance of a strict follow-up of renal function in GSD1 patients. The detection of glomerular hyperfiltration suggests precocious initiation of ACE-inhibitor treatment to delay the progression of renal damage. A randomized prospective study is needed to establish for certain the real effectiveness of this treatment in GSD1 patients.
| Original language | English |
|---|---|
| Pages (from-to) | 19-25 |
| Number of pages | 7 |
| Journal | Clinical Endocrinology |
| Volume | 63 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jul 2005 |
Fingerprint
ASJC Scopus subject areas
- Endocrinology
Cite this
Efficacy of ACE-inhibitor therapy on renal disease in glycogen storage disease type 1 : A multicentre retrospective study. / Melis, Daniela; Parenti, G.; Gatti, R.; Della Casa, R.; Parini, R.; Riva, E.; Burlina, A. B.; Vici, C. Dionisi; Di Rocco, M.; Furlan, F.; Torcoletti, M.; Papadia, F.; Donati, A.; Benigno, V.; Andria, G.
In: Clinical Endocrinology, Vol. 63, No. 1, 07.2005, p. 19-25.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Efficacy of ACE-inhibitor therapy on renal disease in glycogen storage disease type 1
T2 - A multicentre retrospective study
AU - Melis, Daniela
AU - Parenti, G.
AU - Gatti, R.
AU - Della Casa, R.
AU - Parini, R.
AU - Riva, E.
AU - Burlina, A. B.
AU - Vici, C. Dionisi
AU - Di Rocco, M.
AU - Furlan, F.
AU - Torcoletti, M.
AU - Papadia, F.
AU - Donati, A.
AU - Benigno, V.
AU - Andria, G.
PY - 2005/7
Y1 - 2005/7
N2 - Background: The efficacy of ACE-inhibitors in decreasing microalbuminuria and proteinuria has been reported in a few patients with glycogen storage disease type 1 (GSD1); however, no case-control study has ever been published. Aim: The aim of the current study was to evaluate the efficacy of ACE-inhibitors in reducing glomerular hyperfiltration, microalbuminuria and proteinuria, and in delaying the progression of renal damage. Patients and methods: Ninety-five patients (median age at the time of the study: 14.5 years) were enrolled from nine Italian referral centres for metabolic diseases. A retrospective study of a 10-year follow-up was conducted in order to compare the evolution of these parameters in treated patients with those who were not treated with ACE-inhibitors. Results: A significant and progressive decrease of glomerular filtration rate was observed in treated patients vs. those who were not treated with ACE-inhibitors (P <0.05). No difference was observed for microalbuminuria and proteinuria between the two groups of patients. Moreover, the ACE-inhibitors significantly delayed the progression from glomerular hyperfiltration to microalbuminuria, but not that from microalbuminuria to proteinuria. Conclusions: The results of the present study underline the importance of a strict follow-up of renal function in GSD1 patients. The detection of glomerular hyperfiltration suggests precocious initiation of ACE-inhibitor treatment to delay the progression of renal damage. A randomized prospective study is needed to establish for certain the real effectiveness of this treatment in GSD1 patients.
AB - Background: The efficacy of ACE-inhibitors in decreasing microalbuminuria and proteinuria has been reported in a few patients with glycogen storage disease type 1 (GSD1); however, no case-control study has ever been published. Aim: The aim of the current study was to evaluate the efficacy of ACE-inhibitors in reducing glomerular hyperfiltration, microalbuminuria and proteinuria, and in delaying the progression of renal damage. Patients and methods: Ninety-five patients (median age at the time of the study: 14.5 years) were enrolled from nine Italian referral centres for metabolic diseases. A retrospective study of a 10-year follow-up was conducted in order to compare the evolution of these parameters in treated patients with those who were not treated with ACE-inhibitors. Results: A significant and progressive decrease of glomerular filtration rate was observed in treated patients vs. those who were not treated with ACE-inhibitors (P <0.05). No difference was observed for microalbuminuria and proteinuria between the two groups of patients. Moreover, the ACE-inhibitors significantly delayed the progression from glomerular hyperfiltration to microalbuminuria, but not that from microalbuminuria to proteinuria. Conclusions: The results of the present study underline the importance of a strict follow-up of renal function in GSD1 patients. The detection of glomerular hyperfiltration suggests precocious initiation of ACE-inhibitor treatment to delay the progression of renal damage. A randomized prospective study is needed to establish for certain the real effectiveness of this treatment in GSD1 patients.
UR - http://www.scopus.com/inward/record.url?scp=22044453413&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=22044453413&partnerID=8YFLogxK
U2 - 10.1111/j.1365-2265.2005.02292.x
DO - 10.1111/j.1365-2265.2005.02292.x
M3 - Article
C2 - 15963056
AN - SCOPUS:22044453413
VL - 63
SP - 19
EP - 25
JO - Clinical Endocrinology
JF - Clinical Endocrinology
SN - 0300-0664
IS - 1
ER -