Functional response of healthy and diseased glomeruli to a large, protein-rich meal.

Abstract

Differential solute clearances and hormone assays were used to characterize the effect of a large, protein-rich meal (1.5 g/kg) on glomerular function in 12 healthy volunteers (group I) and 12 patients with chronic glomerular disease (group II). Changes from baseline during 3 h after the meal included an elevation of plasma osmolality, progressive urinary concentration, and increasingly positive fluid balance. Plasma renin activity and arginine vasopressin levels (measured in group II only) increased significantly. Nevertheless, the rate of peak postmeal renal plasma flow became elevated by 13 and 33% in groups I and II, respectively. Corresponding peak increases in postmeal glomerular filtration rate exceeded baseline by 10 and 16%. In the proteinuric subjects of group II the fractional clearances of albumin, IgG and uncharged dextrans in the radius interval 36-54 A, declined significantly after the meal. A similar depression of the fractional dextran-clearance profile was observed also in group I. Applying the fractional clearances of relatively permeant dextrans (radii < 44 A) to a model of hindered solute transport through an isoporous membrane, we estimate that transmembrane hydraulic pressure difference increased by 12% in group I and by between 0 to 12% in group II after protein ingestion. We conclude (i) that oral protein ingestion increases glomerular ultrafiltration pressure and rate in both normal and diseased glomeruli, (ii) that this hemodynamic response may be mediated in part by the glomerulopressor hormones angiotensin II and arginine vasopressin, and (iii) that the foregoing hemodynamic changes exert no acute adverse effect on glomerular barrier size-selectivity.

Outcome of the acute glomerular injury in proliferative lupus nephritis.

“…It seems likely therefore, that Kf was depressed profoundly during the active episode of DPLN, as has been found to be the case in experimental animals with glomerulonephritis (25)(26)(27). Previous estimates of this quantity in subjects with healthy kidneys in our laboratory have varied between 12 and 16 ml/(min* mmHg) compared to the mean pre-TLI estimate of only 2.1-2.8 ml/(min * mmHg) in the actively nephritic patients of the present study (10,17,23). The computed two-to threefold increase of Kf at both study times post-TLI (Table IV) (Table V).…”

“…3). Thus, diminishing urinary protein (22), we estimated the approximate value of AP by using a curve fitting technique that has been described in detail previously (23,24). In brief, possible values for AP over a 25-45-mmHg range were examined at l-mmHg intervals.…”

“…The results of this analysis are summarized in Table IV Table IV are likely to be imprecise (23,24). However, the model is useful in identifying relative changes in the direction of Kf (22).…”

Creatinine-Based Definitions: From Baseline Creatinine to Serum Creatinine Adjustment in Intensive Care

“…Glomerular hyperfiltration, which may be considered another potential mechanism, is still controversial. Indeed, in most studies, the filtration fraction appears to be unaltered [34,35], although some authors found an increase in the transcapillary hydraulic pressure gradient [36,37]. However, whether we consider the hypothetical recruitment of dormant cortical nephrons or the increase in net glomerular ultrafiltration pressure, these factors are both related to afferent vasodilation [34][35][36]38], a mechanism which all authors agree on.…”

“…Indeed, in most studies, the filtration fraction appears to be unaltered [34,35], although some authors found an increase in the transcapillary hydraulic pressure gradient [36,37]. However, whether we consider the hypothetical recruitment of dormant cortical nephrons or the increase in net glomerular ultrafiltration pressure, these factors are both related to afferent vasodilation [34][35][36]38], a mechanism which all authors agree on. Because pre-surgical kidney function is one of the most important determinants of both mortality and AKI outcomes [20,39], it is reasonable to assume that the RFR plays a role in a patient's susceptibility to develop AKI.…”