No abstract

No abstract

No abstract

Focal segmental glomerular hyalinosis and/or sclerosis (FSHS) was observed in five Wistar‐Imamichi rats with congenital unilateral hydronephrosis (CUH rats). Marked proteinuria (164.9+138.4mg/day) was observed in the CUH rats. Immunoperoxidase staining for IgM, C3 and IgG was positive in the glomerull, showing in a focal, segmental pattern that corresponded to the areas of FSHS seen by light microscopy. These glomerular findings were extremely similar to those of human focal glomerular sclerosis (FGS). FSHS was found to be common to both the hydronephrotic kidney and the contralateral kidney without hydronephrosis. Morphometry revealed that the glomerular area of the juxtamedullary glomeruli was greater than that of superficial glomeruli in control rats (11,037 μm2 vs. 6,847 μm2). On the other hand, glomerular hypertrophy was observed in non‐sclerotic glomeruli of CUH rats (superficial glomeruli; 12,477–16,123 μm2, juxtamedullary glomeruli; 14,635–18,418 μm2). Also, a decreased in the number of glomeruli within the range 1.8‐4.1 per unit area (1 mm2) was seen in CUH rats compared with control rats (mean 4.4). These results suggest that the increased rate of development of FSHS is based on hyperfiltration in the remaining functional nephrons. Acta Pathol Jpn 41: 653–660, 1991.

We examined the responses on blood pressure when the renal vasoactive system such as renin-angiotensin-aldosterone system (RAAS) and kallikrein-kinin system (KKS) was activated by dietary salt restriction in the congenitally bilateral hydronephrotic rat (BHN). In a low salt diet (LS)-normotensive and normal kidney control rats after 8 weeks from initiating dietary salt restriction, the plasma sodium concentration (PNa) was retained at a level similar to that in the normal diet (ND)-control rats, and plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urinary kallikrein activity (UKA) were about 1.8-, 9.4- and 1.7-fold higher, respectively, than those in the ND-control rats. In addition, LS-control rats had a significantly (p < 0.001) high systolic blood pressure (163 ± 2.0 mm Hg) compared with that (136 ± 5.8) of ND-control rats. These results suggest that the activated renal vasoactive system acted for not only sodium retention but also for elevation of blood pressure in LS-control rats. In LS-BHN at week 8, PNa was also retained at a nearly normal level. However, the renal vasoactive system activation for sodium retention was higher than that of LS-control rats; that is, increase of PRA, PAC and UKA were about 3.8-, 24.7- and 10.0-fold, respectively, than in ND-BHN. The higher activation of RAAS, nevertheless, does not affect blood pressure in BHN; that is, both hypertension of BHN fed LS and ND developed similarly. These findings suggest that dietary salt restriction could markedly activate the renal vasoactive system for sodium retention without elevating blood pressure in BHN different from control rats.

No abstract

No abstract

No abstract