Studies on the Mechanism of Experimental Proteinuria Induced by Renin

Abstract

In recent years, especially since the advent of the electron microscope, there has been a renewed interest in the morphologic and functional aspects of a variety of experimental and human renal diseases associated with proteinuria. An excellent experimental model for such studies has been the renin-induced proteinuria in the rabbit and the rat. In 1940, Pickering and Prinzmetal (1) reported that parenteral administration of renin, the renal enzyme implicated in experimental renal hypertension, induced a marked diuresis in the rabbit, accompanied by increased rate of sodium and chloride excretion and a significant degree of proteinuria. Brandt and Gruhn (2) confirmed this observation, and by studying the simultaneous excretion of injected hemoglobin, concluded that the proteinuria was caused by diminished tubular reabsorption of protein from the glomerular filtrate and not by altered glomerular permeability. Shortly afterwards, Addis et al. (3) discovered that renin produced an intense proteinuria in the rat also and, from a combination of morphological and functional data obtained by these workers and by others, it was concluded that renin produced this effect mainly by increasing glomerular permeability. Thus, conflicting views have been expressed concerning the mechanism by which renin produces an increased excretion of protein in the urine.Previous studies on the relationship between the pressor and proteinuric activities of renin have also led to similar conflicting results. Thus, Addis et al. (3) suggested that the proteinuria was dependent on the pressor activity of renin, since inhibition of this activity by heat also abolished the proteinuric effect. On the other hand, Sellers et al. (4) concluded that "the proteinuric property of renin is not related to the ability of this compound to elevate

Studies on the Mechanism of Oliguria in a Model of Unilateral Acute Renal Failure

“…In addition, the epithelial changes after angiotensin also occurred after a nonpressor dose and were invariably associated with proteinuria. Since these changes are quite like those reported in lipoid nephrosis (41), it is possible that this may be related to the proteinuria seen after the administration of renin (42,43) or angiotensin II (40). The infusion of norepinephrine has not been reported to cause proteinuria.…”

IMephrotic-Range Proteinuria in a Patient with High Renin Hypertension: Effect of Treatment with an ACE-lnhibitor

“…The association between renal artery stenosis and ne phrotic syndrome has been described in several anecdotal reports [1][2][3][4][5][6][7][8], probably mediated by the increased activity of the renin-angiotensin system [9][10][11]. Either nephrec tomy [5,7] or surgical repair of the affected vessel [1] has been proposed as the treatment of choice.…”

Glomerular permeability of macromolecules. Effect of molecular configuration on the fractional clearance of uncharged dextran and neutral horseradish peroxidase in the rat.

“…The filtration of macromolecules across the glomerular capillary wall is determined by the structural characteristics of the filter (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12), glomerular hemodynamics (13)(14)(15)(16)(17)(18)(19)(20)(21), and molecular parameters of the solute. Molecular determinants include the molecular radius (22)(23)(24)(25) and the net molecular charge (26)(27)(28)(29)(30).…”

“…We conclude that other molecular parameters such as shape, flexibility, and deformability play important roles in the transport of macromolecules across the extracellular matrix that constitutes the glomerular filter. INTRODUCTION The filtration of macromolecules across the glomerular capillary wall is determined by the structural characteristics of the filter (1-12), glomerular hemodynamics (13)(14)(15)(16)(17)(18)(19)(20)(21), and molecular parameters of the solute. Molecular determinants include the molecular radius (22)(23)(24)(25) and the net molecular charge (26-30).…”