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Marked increases in renal volume commonly occur in states of acute renal injury such as acute tubular necrosis or transplant rejection. This expansion appears to be due to a marked increase in compliance of the kidney. The present study examined whether compliance-mediated expansion of renal volume above normal impairs renal function. In each of 11 dogs, we compared the volume and function of a collagenase-treated kidney (CK) to the contralateral intact kidney (IK), first under control conditions, then when both kidneys were subjected to the same conditions to increase intrarenal pressure (raised ureteral or renal venous pressure) and then on return of intrarenal pressure toward control levels. The rationale is that since CK compliance exceeds IK compliance, the absolute difference between CK and IK volume is maximized at increased intrarenal pressure but minimized at normal intrarenal pressure. We found that CK and IK function were equal at normal intrarenal pressure. However, at increased intrarenal pressure there was suppression of GFR and sodium and water excretion in CK vs. IK. On return to normal intrarenal pressure, CK and IK function were, once again, equal. We also found that the difference in CK vs. IK volume correlated with the differences in CK vs. IK function. Thus, acute expansion of renal volume above normal impairs renal function.
Marked increases in renal volume commonly occur in states of acute renal injury such as acute tubular necrosis or transplant rejection. This expansion appears to be due to a marked increase in compliance of the kidney. The present study examined whether compliance-mediated expansion of renal volume above normal impairs renal function. In each of 11 dogs, we compared the volume and function of a collagenase-treated kidney (CK) to the contralateral intact kidney (IK), first under control conditions, then when both kidneys were subjected to the same conditions to increase intrarenal pressure (raised ureteral or renal venous pressure) and then on return of intrarenal pressure toward control levels. The rationale is that since CK compliance exceeds IK compliance, the absolute difference between CK and IK volume is maximized at increased intrarenal pressure but minimized at normal intrarenal pressure. We found that CK and IK function were equal at normal intrarenal pressure. However, at increased intrarenal pressure there was suppression of GFR and sodium and water excretion in CK vs. IK. On return to normal intrarenal pressure, CK and IK function were, once again, equal. We also found that the difference in CK vs. IK volume correlated with the differences in CK vs. IK function. Thus, acute expansion of renal volume above normal impairs renal function.
We measured changes in kidney volume and intrarenal pressure produced by step-wise, steady state increases and decreases in ureteral pressure (UP). The purpose of such maneuvers, termed exercises, was to examine the relationship between changes in kidney volume and the changes in intrarenal pressure responsible for those in kidney volume. Changes in kidney volume were assessed from directly measured changes in kidney weight. Changes in the intrarenal pressure distending the renal capsule (renal subcapsular pressure [RSCP]) were measured by a strain guage diaphragm-type microtransducer placed between cortex and capsule. We measured these whole kidney volume/pressure events before and after saline loading and examined their relationship to changes in renal function following saline loading. We found that after four "exercises", the kidney became more complaint, i.e., occupied a larger volume at any given UP or RSCP, and that the compliance of the kidney was further increased following saline loading. However, about one hour after saline loading, RSCP returned to or below pre-saline loading levels and renal volume returned to pre-saline loading levels; nevertheless, the natriuresis persisted. Thus, an increase in renal volume is not necessary to sustain increased sodium and water excretion in post-saline loading. Finally, we found evidence that the renal capsule provides the major force opposing expansion of outer cortex when intrarenal pressure is increased.
This study was undertaken to help clarify the relationship between capillary hemodynamic events and the tissue uptake of circulating immune complexes (IC). In each of 23 dogs, bovine serum albumin (BSA) and rabbit antiBSA soluble IC labeled with 125I were given by constant i.v. infusion, and IC uptake by a normally perfused kidney was compared to that of the contralateral kidney in which renal blood flow (RBF) was changed by renal artery constriction or raised ureteral pressure. In these same animals, IC uptake in 15 other major organ systems was also measured simultaneously. During IC infusion microspheres of 85Sr were injected to measure cardiac output and tissue blood flow, and red cells labeled with 51Cr were infused to mark tissue vascular volume. At completion of the IC infusion, tissue samples were taken from the kidneys and the 15 other major organs systems. From the isotope content of each tissue, we determined IC content, blood flow rate, vascular transit time, and fractional uptake of IC (FIC). In addition, glomeruli were isolated from renal cortex to assess IC uptake in glomerular versus renal nonglomerular tissue. We found that 1) for kidney, IC delivery rate, capillary hydrostatic pressure, and capillary ultrafiltration rate are less important than the plasma IC concentration in determining IC uptake; 2) for each organ studied, the principal determinant of IC uptake per gram of tissue, at any given PIC, is vascular volume per gram of tissue; 3) tissue vascular volume per gram of tissue may determine IC uptake per gram of tissue because tissue vascular volume determines the capillary surface area in contact with circulating IC or because tissue vascular volume determines tissue vascular transit time, at any given tissue blood flow rate.
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