TY - JOUR
T1 - Renal structure and function in non-insulin dependent diabetic patients with microalbuminuria
AU - Brocco, E.
AU - Fioretto, P.
AU - Mauer, M.
AU - Saller, A.
AU - Carraro, A.
AU - Frigato, F.
AU - Chiesura- Corona, M.
AU - Bianchi, L.
AU - Baggio, B.
AU - Maioli, M.
AU - Abaterusso, C.
AU - Velussi, M.
AU - Sambataro, M.
AU - Virgili, F.
AU - Ossi, E.
AU - Nosadini, R.
PY - 1997
Y1 - 1997
N2 - We have recently described heterogeneity in renal structure in non- insulin-dependent diabetic patients (NIDDM) with microalbuminuria (MA; defined as albumin excretion rate from 20 to 200 μg/min). Thus, at variance with IDDM patients, 'typical' diabetic glomerulopathy by light microscopy is observed only in a third of NIDDM with MA (Category II, CII). Further, despite persistent MA, 30% of NIDDM have normal or near normal renal structure (Category I, CI). Another one-third shows 'atypical' patterns of renal injury with absent or mild diabetic glomerular changes, associated with disproportionately severe tubulointerstitial lesions and/or arteriolar hyalinosis and global glomerular sclerosis (Category III, CIII). The aims of this study were to evaluate whether similar patterns of renal lesions could be confirmed in a larger group of NIDDM with MA and to investigate tubular function in order to understand the mechanisms underlying MA in NIDDM patients. Renal biopsies were performed in 53 NIDDM with MA, Categories I, II and III were found in 41%, 26% and 33% of NIDDM with MA, respectively. All 8 patients with proliferative diabetic retinopathy were in CII. We also studied the urinary daily excretion rate of α1-microglobulin (α1m), a low molecular weight protein, which is a useful indicator of tubular function. α1m was markedly increased only in CII patients (CI vs. CII vs. CIII: 6.2 ± 1.2 vs. 13.7 ± 2.1 vs. 7.3 ± 0.9 mg/day, ANOVA, P < 0.01). In conclusion, we confirm that there is heterogeneity in renal structure in NIDDM patients with MA. This heterogeneity is not due to renal diseases other than diabetes. Increased α1m and proliferative retinopathy are useful indicators of the subgroup of MA NIDDM patients with typical diabetic glomerulopathy. It is suggested that diabetic microangiopathy explains the simultaneous occurrence of typical diabetic glomerulopathy, proliferative retinopathy and tubular dysfunction in a subgroup of NIDDM patients with MA.
AB - We have recently described heterogeneity in renal structure in non- insulin-dependent diabetic patients (NIDDM) with microalbuminuria (MA; defined as albumin excretion rate from 20 to 200 μg/min). Thus, at variance with IDDM patients, 'typical' diabetic glomerulopathy by light microscopy is observed only in a third of NIDDM with MA (Category II, CII). Further, despite persistent MA, 30% of NIDDM have normal or near normal renal structure (Category I, CI). Another one-third shows 'atypical' patterns of renal injury with absent or mild diabetic glomerular changes, associated with disproportionately severe tubulointerstitial lesions and/or arteriolar hyalinosis and global glomerular sclerosis (Category III, CIII). The aims of this study were to evaluate whether similar patterns of renal lesions could be confirmed in a larger group of NIDDM with MA and to investigate tubular function in order to understand the mechanisms underlying MA in NIDDM patients. Renal biopsies were performed in 53 NIDDM with MA, Categories I, II and III were found in 41%, 26% and 33% of NIDDM with MA, respectively. All 8 patients with proliferative diabetic retinopathy were in CII. We also studied the urinary daily excretion rate of α1-microglobulin (α1m), a low molecular weight protein, which is a useful indicator of tubular function. α1m was markedly increased only in CII patients (CI vs. CII vs. CIII: 6.2 ± 1.2 vs. 13.7 ± 2.1 vs. 7.3 ± 0.9 mg/day, ANOVA, P < 0.01). In conclusion, we confirm that there is heterogeneity in renal structure in NIDDM patients with MA. This heterogeneity is not due to renal diseases other than diabetes. Increased α1m and proliferative retinopathy are useful indicators of the subgroup of MA NIDDM patients with typical diabetic glomerulopathy. It is suggested that diabetic microangiopathy explains the simultaneous occurrence of typical diabetic glomerulopathy, proliferative retinopathy and tubular dysfunction in a subgroup of NIDDM patients with MA.
KW - Microalbuminuria
KW - Non-insulin dependent diabetes
KW - Proteinuria
KW - Renal structure
KW - Retinopathy
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M3 - Article
C2 - 9407419
AN - SCOPUS:0031475146
SN - 0098-6577
VL - 51
SP - S40-S44
JO - Kidney international. Supplement
JF - Kidney international. Supplement
IS - 63
ER -
