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Prevention of diabetic glomerulopathy by pharmacological amelioration of glomerular capillary hypertension.
- R. Zatz, B. R. Dunn, T. Meyer, S. Anderson, H. Rennke, B. Brenner
- Medicine, BiologyThe Journal of clinical investigation
- 1 June 1986
Prevention of glomerular capillary hypertension in rats with diabetes mellitus effectively protects against the subsequent development ofglomerular structural injury and proteinuria, further supporting the view that hemodynamic rather than metabolic factors predominate in the pathogenesis of diabetic glomerulopathy.
Chronic inhibition of nitric oxide synthesis. A new model of arterial hypertension.
- M. O. Ribeiro, E. Antunes, G. De Nucci, S. M. Lovisolo, R. Zatz
- Medicine, BiologyHypertension
- 1 September 1992
It is concluded that chronic nitric oxide blockade may constitute a new model of severe arterial hypertension.
Predominance of hemodynamic rather than metabolic factors in the pathogenesis of diabetic glomerulopathy.
- R. Zatz, T. Meyer, H. Rennke, B. Brenner
- Medicine, BiologyProceedings of the National Academy of Sciences…
- 1 September 1985
The findings indicate that the metabolic disorder seen in stable, moderately hyperglycemic diabetic rats does not lead to glomerulopathy as long as elevations in glomerular pressures and flows are prevented.
Chronic inhibition of nuclear factor-kappaB attenuates renal injury in the 5/6 renal ablation model.
- C. Fujihara, G. Antunes, A. L. Mattar, D. Malheiros, J. Vieira, R. Zatz
- BiologyAmerican journal of physiology. Renal physiology
Activation of the NF-kappaB system plays an important role in the pathogenesis of renal injury in the Nx model and inhibition of this system may represent a new strategy to prevent the progression of chronic kidney disease.
Mycophenolate mofetil prevents the development of glomerular injury in experimental diabetes.
- R. Utimura, C. Fujihara, A. L. Mattar, D. Malheiros, I. Noronha, R. Zatz
- Medicine, BiologyKidney international
Treatment with mycophenolate mofetil had no effect on blood pressure, glomerular dynamics or blood glucose levels, but did prevent albuminuria, glomersular macrophage infiltration and glomerulosclerosis, consistent with the notion that inflammatory events are central to the pathogenesis of diabetic nephropathy.
Effects of acute nitric oxide inhibition on rat glomerular microcirculation.
It is suggested that EDRF exerts a basal relaxing effect on the glomerular microcirculation, as shown in rats the renal effect of acute administration of L-NMMA, a specific inhibitor of NO synthesis.
Chronic nitric oxide inhibition model six years on.
This review is centered on the cardiovascular and particularly the renal functional and structural consequences of chronic pharmacologic NO inhibition by l-arginine analogues, and devoted special attention to the mechanisms of hypertension and organ injury that occur under these circumstances.
Sodium excess aggravates hypertension and renal parenchymal injury in rats with chronic NO inhibition.
- C. Fujihara, S. M. Michellazzo, G. De Nucci, R. Zatz
- Medicine, BiologyThe American journal of physiology
- 1 May 1994
Sodium overload aggravates the renal and systemic consequences of chronic NO inhibition by mechanisms that may include paradoxical activation of renin secretion, and interstitial expansion and glomerular ischemia constitute the chief modalities of renal injury in this model.
Urinary MCP-1 and RBP: independent predictors of renal outcome in macroalbuminuric diabetic nephropathy.
End-stage renal disease in Brazil: epidemiology, prevention, and treatment.
Much effort is needed to limit the prevalence of renal disease, to detain or retard the progression of chronic nephropathies, and to ensure that high-quality RRT will remain available to all those who need it.