MECHANISMS INVOLVED IN THE PROGRESSION TO GLOMERULAR SCLEROSIS INDUCED BY SYSTEMIC HYPERTENSION DURING MILD PUROMYCIN AMINONUCLEOSIDE NEPHROSIS

被引:7
作者
AMATO, D [1 ]
TAPIA, E [1 ]
BOBADILLA, NA [1 ]
FRANCO, M [1 ]
CALLEJA, C [1 ]
GARCIATORRES, R [1 ]
LOPEZ, P [1 ]
ALVARADO, JA [1 ]
HERRERAACOSTA, J [1 ]
机构
[1] INST NACL CARDIOL IGNACIO CHAVEZ,DEPT NEPHROL,JUAN BADIANO 1,MEXICO CITY 14080,DF,MEXICO
关键词
HYPERTENSION; PUROMYCIN AMINONUCLEOSIDE NEPHROSIS; PROTEINURIA; GLOMERULAR SCLEROSIS;
D O I
10.1093/ajh/5.9.629
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
To evaluate the contribution of systemic hypertension in the progression of nephropathies to glomerular sclerosis, a mild form of puromycin aminonucleoside (PAN) nephrosis was associated with Goldblatt hypertension and studied after 18 weeks. We studied four groups: Group I, controls; Group II, Goldblatt hypertension; Group III, PAN nephrosis; and Group IV, both conditions. Systolic blood pressure, 24-h proteinuria, serum cholesterol, triglycerides, glomerular hemodynamics, and histological studies were compared among the groups. Rats in groups II and IV developed systemic hyper tension, but only group IV rats showed persistent proteinuria. No alterations in lipid metabolism were present in any of the groups. The most striking findings in the micropuncture studies were a significant increase of glomerular capillary pressure in group IV rats (63.15 +/- 1.34 mm Hg) as compared to controls (48.74 +/- 0.97 mm Hg) and to groups II and III (55.31 +/- 2.11 and 48.17 +/- 1.23 mm Hg, respectively), and a marked fall in K(f) in groups III and IV. Only group IV showed significant histological alterations such as glomerular sclerosis, interstitial damage, and increased glomerular area. These results suggest that, in the presence of an underlying nephropathy, a greater fraction of systemic pressure is transmitted to the glomerular capillaries when systemic hypertension is present, the resulting elevation in glomerular pressure and proteinuria seems to be responsible for the progression to glomerular sclerosis.
引用
收藏
页码:629 / 636
页数:8
相关论文
共 33 条
[1]  
Whelton P.K., Klag M.J., Hypertension as a, Hypertension, 13, pp. 119-127, (1989)
[2]  
Mauer M.S., Steffes M.W., Azar S., Et al., The effects of Goldblatt hypertension on the development of the glomerular lesions of diabetes mellitus in the rat, Diabetes, 27, pp. 738-744, (1978)
[3]  
Neugarten J., Feiner H.D., Schacht R.G., Et al., Aggravation of experimental glomerulonephritis by superimposed clip hypertension, Kidney Int, 22, pp. 257-263, (1982)
[4]  
Baldwin D.S., Neugarten J., Treatment of hypertension in renal disease, Am J Kidney Dis, 5, pp. A57-A70, (1985)
[5]  
Hostetter T.H., Olson J.L., Rennke H.G., Et al., Hyperfiltrationin remnant nephrons: A potentially adverse response to renal ablation, Am J Physiol, 241, pp. F85-F93, (1981)
[6]  
Dworkin, Feiner L., Glomerular injury in unin- ephrectomized spontaneously hypertensive rats: A consequence of glomerular capillary hypertension, J Clin Invest, 77, pp. 797-809, (1986)
[7]  
Raij L., Azar S., Keane W., Mesangial immune injury, hypertension, and progressive glomerular damage in Dahl rats, Kidney Int, 26, pp. 137-143, (1984)
[8]  
Blantz R.C., Gabbai F., Gushwa L.C., Wilson C.B., The influence of concomitant experimental hypertension and glomerulonephritis, Kidney Int, 32, pp. 652-663, (1987)
[9]  
Anderson S., Diamond J.R., Karnovsky M.J., Brenner B.M., Mechanisms underlying transition from acute glomerular injury to late glomerular sclerosis in a rat model of nephrotic syndrome, J Clin Invest, 82, pp. 1757-1768, (1988)
[10]  
Herrera-Acosta J., Franco M., Tapia E., Et al., Mechanism of glomerular permeability reduction in nonclipped kidney of rats with Goldblatt hypertension, Hypertension, 8, pp. I105-I109, (1986)