A model of glomerular ultrafiltration in the rat

Deen, WM; Robertson, C R; Brenner, B M

doi:10.1152/ajplegacy.1972.223.5.1178

Cited by 332 publications

(195 citation statements)

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“…However, we have repeatedly shown GFR to remain constant during hypervolemia-induced elevations of Q A by 15-25% (16,19,29). Such independence of GFR from Q A is typical of filtration pressure dysequilibrium (6), from which we can infer that ⌬P is substantially higher than E and thus consistent with an estimate of 40 mmHg. We accordingly selected a ⌬P of 40 mmHg as the best-guess value for ⌬P in our gravid day 1 and our nongravid week 4 control subjects.…”

Section: Discussionsupporting

confidence: 87%

“…Instead we used physiological techniques to determine GFR and its hemodynamic determinants and then computed two-kidney K f with a modification of the mathematical model of glomerular ultrafiltration of Deen et al (6). Whereas A and renal plasma flow (Q A ) can be determined with reasonable precision in the human kidney (3, 4), ⌬P cannot be measured because of the inaccessibility of human glomeruli.…”

Section: Discussionmentioning

confidence: 99%

“…We then used the measured values of GFR, Q A, and A and the aforementioned assumed values for ⌬P to compute a corresponding range of values for whole kidney K f with a modification of the model of ultrafiltration of Deen et al (6). In this modification, it is assumed that, for the range of plasma protein concentrations observed in humans, the plasma oncotic pressure ( ) is approximately proportional to the total protein concentration (C), an assumption that is consistent with an earlier study from our laboratory (4).…”

Section: Methodsmentioning

confidence: 99%

“…If this is the case, then Kf can be estimated without knowing the value of ␣. With a linear function of C and ⌬P a constant, a derivation like that in Deen et al (6) leads to:…”

Section: Methodsmentioning

confidence: 99%

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Course of preeclamptic glomerular injury after delivery

Hladunewich

Myers²,

Derby³

et al. 2008

American Journal of Physiology-Renal Physiology

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Hladunewich MA, Myers BD, Derby GC, Blouch KL, Druzin ML, Deen WM, Naimark DM, Lafayette RA. Course of preeclamptic glomerular injury after delivery. Am J Physiol Renal Physiol 294: F614-F620, 2008. First published January 16, 2008 doi:10.1152/ajprenal.00470.2007.-We evaluated the early postpartum recovery of glomerular function over 4 wk in 57 women with preeclampsia. We used physiological techniques to measure glomerular filtration rate (GFR), renal plasma flow, and oncotic pressure ( A) and computed a value for the two-kidney ultrafiltration coefficient (Kf). Compared with healthy, postpartum controls, GFR was depressed by 40% on postpartum day 1, but by only 19% and 8% in the second and fourth postpartum weeks, respectively. Hypofiltration was attributable solely to depression, at corresponding postpartum times, of Kf by 55%, 30%, and 18%, respectively. Improvement in glomerular filtration capacity was accompanied by recovery of hypertension to near-normal levels and significant improvement in albuminuria. We conclude that the functional manifestations of the glomerular endothelial injury of preeclampsia largely resolve within the first postpartum month. glomerular filtration rate; ultrafiltration coefficient; postpartum recovery AFFECTING 5-7% of pregnancies, preeclampsia remains a leading cause of maternal and fetal morbidity and mortality. Because the primary target of injury in preeclampsia is the glomerular endothelial cell, affected patients invariably present with depression of the glomerular filtration rate (GFR), proteinuria, and hypertension. We previously (13) evaluated glomerular morphology immediately after delivery. We demonstrated severe endothelial cell swelling with diminished size and density of the endothelial fenestrae, along with mesangial cell interposition and subendothelial fibrinoid deposits. These findings were computed to lower glomerular filtration capacity sufficiently to account for the observed depression of GFR by 40% (13).Despite the profound alterations in glomerular morphology, clinical recovery is usually rapid after delivery of the placenta. However, few detailed physiological evaluations of preeclampsia have been undertaken in the postpartum period. The characteristic glomerular pathological lesion has been reported to improve within days after delivery (21). Although complete recovery can occasionally require in excess of 6 mo, the majority of cases demonstrate complete resolution of the renal pathology within 3 mo (25). With the exception of those women with persistent postpartum hypertension, GFR and proteinuria also normalize over several months (18,(32)(33)(34).In the present study, we have employed precise physiological techniques to evaluate the postpartum course of the GFR and its determinants in women with preeclampsia. We combined our physiological findings with mathematical modeling to estimate glomerular ultrafiltration capacity. We observed a profound initial injury, which improved significantly after 4 wk. METHODSPatient population. This paper represents a...

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Section: Discussionsupporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…If this is the case, then Kf can be estimated without knowing the value of ␣. With a linear function of C and ⌬P a constant, a derivation like that in Deen et al (6) leads to:…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Course of preeclamptic glomerular injury after delivery

Hladunewich

Myers²,

Derby³

et al. 2008

American Journal of Physiology-Renal Physiology

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“…Previous studies from this laboratory (11)(12)(13)(14)17) and the laboratory of Brenner and co-workers (21)(22)(23) Utilizing mathematical models of glomerular filtration as previously described (11,17) and applying data to the computer, a profile for EFP and the integrated value for EFP can be generated. A value for the glomerular permeability coefficient (LpA) is also generated by this method (sngfr = LpA -EFP).…”

Section: Introductionmentioning

confidence: 99%

Acute effects of antiglomerular basement membrane antibody on the process of glomerular filtration in the rat.

Blantz¹,

Wilson²

1976

J. Clin. Invest.

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A B S T R A C T Nephron filtration rate (sngfr) and the factors controlling filtration were examined before and within 60 min of the intravenous infusion of 225-450 Ag of antiglomerular basement membrane antibody (AGBM Ab) (> 50% antigenic saturation) in plasma-expanded (2.5% body wt) Munich-Wistar rats. Pressures in glonmerular capillaries (PG) and Bowman's space (Pt) were measured with a servo-nulling device, systemic (l7rA) and efferent arteriolar oncotic pressures (irE) were measured by microprotein methods, and nephron plasma flow (rpf) and sngfr were measured by micropuncture techniques in both control and post-AGBM Ab conditions in each rat. The sngfr fell from 52.7±2.9 to 24.1±+1.9 nl/min per g kidney wt (n = 7, P <0.001).Both afferent and efferent arteriolar resistances increased and rpf fell from 221±25 to 90±9 nl/min per g kidney wt (P < 0.001) but the hydrostatic pressure gradient across the glomerular membrane (AP = PG -Pt) increased from 37±1 to 50±2 mm Hg (P < 0.001). The increase in AP and a numerical decrease in TA both acted to maintain sngfr after AGBM Ab and effectively nullified the influence of decreased rpf upon sngfr. The nmean effective filtration pressure (EFP = AP -i) increased from 14±2 to 30±3 mm Hg (P < 0.001) while sngfr decreased. The major and critical reason for this reduction in sngfr was a decrease in the glomerular permeability coefficient from 0.077+0.017 to 0.014+0.001 nl/s per g kidney wt per mm Hg (P <0

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Renal Manifestations of Sickle Cell Disease

Buckalew¹

1974

Arch Intern Med

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A model of glomerular ultrafiltration in the rat

Cited by 332 publications

References 0 publications

Course of preeclamptic glomerular injury after delivery

Course of preeclamptic glomerular injury after delivery

Acute effects of antiglomerular basement membrane antibody on the process of glomerular filtration in the rat.

Renal Manifestations of Sickle Cell Disease

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