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Background. Although the clinical importance of immunoglobulin-A nephropathy (IgAN) is widely recognized, the characteristics of intrarenal arterial lesions in this disease and the main factors associated with them have not been studied extensively, and a large-scale analysis of intrarenal arterial lesions in IgAN has not been performed.Methods. To clarify these issues, we investigated the prevalence, underlying factors and significance of intrarenal arterial lesions in 1005 patients with IgAN. We distinguished different degrees of severity of small artery and arteriolar lesions (mild, moderate and severe), using a semi-quantitative scoring system. We compared the arterial lesions of IgAN patients with those of 627 non-IgAN patients, who had mesangial proliferating glomerulonephritis without IgA deposits, and of 221 patients with membranous nephropathy (MN).Results. The IgAN patients with arterial lesions were significantly younger than the non-IgAN and MN patients (mean ages 34.6 vs 40.4 and 47.7 years, respectively). The prevalence of intrarenal small artery and arteriolar lesions was 54.6% in IgAN patients, compared with 26.6 and 47.1% in non-IgAN and MN patients, respectively; the percentages of moderate/severe arterial lesions were 37.0 vs 21.6 and 23.1%, respectively; and the percentages of hyaline changes were 43.7 vs 16.8 and 21.2%, respectively. The differences in the prevalence of lesions between IgAN patients and the two other groups were statistically significant for all three parameters. Our search for possible relationships between arterialarteriolar lesions and various indirect outcome markers disclosed significant associations with hypertension, higher serum creatinine and uric acid, high urinary protein excretion, glomerulosclerosis, tubular atrophy and interstitial fibrosis. Furthermore, these parameters were changed more markedly in IgAN patients with moderate/severe arterial lesions and hyaline changes than in IgAN patients who had mild arterial lesions and wall thickening alone.Conclusions. The prevalence of small intrarenal arterialarteriolar lesions was higher in IgAN patients than in non-IgAN and MN patients; moreover, the lesions in IgAN patients were associated with younger age, were more severe and exhibited a higher degree of hyaline changes. Finally, the severity of small arterial arteriolar lesions was linked to several markers of adverse outcome. [ABSTRACT FROM AUTHOR]

Background. Renal diseases in diabetes include diabetic nephropathies (DN) and non-diabetic renal diseases (NDRD). The clinical differentiation between these two categories is usually not so clear and effective. This study aims to develop a quantified differential diagnostic model. Methods. We consecutively screened the diabetic patients with overt proteinuria but no severe renal failure for kidney biopsy from 1993 to 2003. The finally enrolled 110 patients were divided into two groups according to pathological features (60 in DN group and 50 in NDRD group). Clinical and laboratory data were compared between two groups. Then a diagnostic model was developed based on the logistic regression analysis. Results. Forty-six percent of patients were NDRD including a variety of pathological types. Many differences between DN and NDRD were found by comparison of the clinical indices. In the final logistic regression analysis, only diabetes duration (Dm), systolic blood pressure (Bp), HbA1c (Gh), haematuria (Hu) and diabetic retinopathy (Dr) showed statistical significance. Based on the logistic regression model: π = ez/(1 + ez), a diagnostic model was constructed as follows: PDN = exp(−13.5922 + 0.0371Dm + 0.0395Bp + 0.3224Gh − 4.4552Hu + 2.9613Dr)/ [1 + exp(−13.5922 + 0.0371Dm + 0.0395Bp + 0.3224Gh − 4.4552Hu + 2.9613Dr)]. PDN was the probability of DN diagnosis (PDN ≥ 0.5 as DN, PDN Conclusions. This diagnostic model may be helpful to clinical differentiation of DN and NDRD in type 2 diabetic patients with overt proteinuria. [ABSTRACT FROM AUTHOR]

Hepatocyte growth factor (HGF) is one of the major growth factors that stimulate the growth and the migration of vascular endothelial cells. In this study, we examined the beneficial effects of HGF for glomerular repair in an experimental progressive glomerulonephritis (GN) model prepared by injecting both anti-Thy-1.1 antibody (day 0) and habu-snake venom (day 1) in rats. The rats received continuous intraperitoneal administration of recombinant human HGF (80 μg/100 g/day) or vehicle control at an early stage (day 2 to day 9), after severe glomerular injury. The vehicle-infused control rats initially showed severe mesangiolysis with large ballooning (day 2), followed by the prominent proliferation of mesangial cells with minimal capillary regeneration (day 5 to week 2), and global sclerosis with chronic renal failure (week 4 to week 8). Although mesangiolysis with large ballooning and mesangial cell proliferation were also observed in the HGF-infused rats, glomerular capillary regeneration with marked endothelial cell proliferation occurred during HGF administration from day 2 to day 9. Subsequently, the glomerulus was repaired with the development of the capillary network and the reduction of mesangial hypercellularity from week 2 to week 4, and almost all of the glomeruli showed a normal structure by week 8. The HGF-treated rats showed significantly better renal functions (Cr: 0.3 ± 0.1 vs. 3.5 ± 1.1 mg/dl in control, p < 0.001), less proteinuria (21.2 ± 8.0 mg/day vs. 421.4 ± 45.1 mg/day in control, p < 0.001) and less glomerular sclerosis at week 8 than the vehicle-infused rats. We conclude that HGF accelerated glomerular repair through the growth of capillary endothelial cells and capillary regeneration in experimental progressive GN. Administering HGF is a logical and efficient strategy for treating progressive GN with severe capillary destruction.Copyright © 2003 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]