Effect of Intraluminal Flow on Proximal Tubular Reabsorption

139

A B S T R A C T Tubular fluid flow, urine osmolality, and pH were selectively altered to determine the relative protective roles of these factors in a rat model of acute urate nephropathy. Various prehyperuricemic conditions were established in five groups of animals: (a) normopenic Wistar rats given no pretreatment (Group I); (b) Wistar rats given acetazolamide, 20 mg/kg, and isotonic NaHCO3 to produce urine alkalinization (Group II); (c) Wistar rats in which a moderate diuresis, similar to that observed in Group II but without urine alkalinization, was induced with furosemide, 2 mg/kg (Group III); (d) Wistar rats in which a high-flow solute diuresis was induced with furosemide, 15 mg/kg (Group IV); (e) Brattleboro rats, homozygous for pituitary diabetes insipidus, that had a spontaneous high-flow water diuresis (Group V). A comparable level of hyperuricemia (19.4+2.2 mg/100 ml) was achieved in all animals with intravenous urate infusion. Clearance and micropuncture studies were performed before and 1 h after induction of hyperuricemia. Group I rats had mean falls in renal plasma flow and glomerular filtration rate of 83 and 86%, respectively; nephron filtration rate decreased 66%, and tubular and microvascular pressures increased twofold. In Group II there were 45 and 47% declines in renal plasma flow and glomerular filtration rate, respectively, a 66% fall in nephron filtration rate, and a 30% increase in tubular and vascular pressures. Moderate amounts of urate were seen in the kidneys. Group III had changes in renal function identical to Group II suggesting that the moderate prehyperuricemic diuresis in the latter group and not urine alkalinization produced the partial protection observed. Groups IV Portions of this study appeared in abstract form in the

Section: Methodsmentioning

confidence: 99%

Intrarenal dynamics in the pathogenesis and prevention of acute urate nephropathy.

Conger¹,

Falk²

1977

139

“…14 littermate 10-d postpartum Munich Wistar rats weighing 200-265 g were prepared for clearance and micropuncture studies as described (13 (10 ,ul) were taken at the beginning and end of the series of efferent arteriolar blood collections. The animals were then infused via the femoral vein with endotoxin for two h as in the preceding set of experiments and the measurements described above were repeated.…”

Section: Snffmentioning

confidence: 99%

Glomerular dynamics and morphologic changes in the generalized Shwartzman reaction in postpartum rats.

Conger¹,

Falk²,

Guggenheim³

1981

A B S T R A C T The roles of glomerular functional and morphologic changes were examined in the acute renal failure associated with generalized Shwartzman reaction in postpartum Munich Wistar rats. The susceptibility of postpartum rats to acute deterioration in renal function after a 2-h endotoxin infusion was found to be greater than in virgin litter mates: glomerular filtration rate fell by 93% in the former vs. 24% in the latter group (P < 0.001). In postpartum rats there were marked changes in platelet count and fibrinogen level (P <0.025) compatible with consumption coagulopathy. Renal blood flow and glomerular filtration rate fell from 5.5+0.9 and 0.74+0.12 to 2.0+0.7 and 0.12±0.01 ml/min, respectively (both P < 0.001). Blood pressure did not change. Results ofglomerular dynamics studies showed decreases in single nephron filtration rate from 28±7 to 6±4 nl/min and in glomerular plasma flow rate from 77± 26 to 23± 12 nl/min (both P < 0.001). Afferent net ultrafiltration pressure fell from 20±3 to 5±4 mm Hg due to a fall in glomerular capillary hydraulic pressure from 47±1 to 29±5 mm Hg (P < 0.001). There were four-and twofold increases in afferent and efferent arteriolar resistances, respectively. Less

“…Recent studies have shown that GFR calculated from distal tubular fluid collections are consistently lower than those calculated from proximal tubular fluid collections in that nephron, when distal tubular sodium concentration are presumably very low due to the proximal oil block (57,58). Others have failed to substantiate these findings (59).…”

Section: Microinjection Studiesmentioning

confidence: 99%

Pathophysiology of Experimental Glomerulonephritis in Rats

Allison¹,

Wilson²,

Gottschalk³

1974

158

A B S T R A C T Micropuncture, clearance, immunofluorescence and light microscopy techniques were used to study kidney structure and single nephron function in rats with autologous immune complex nephritis (AICN), a membranous glomerulonephritis developing over 5 to 20 mo, in the more acute and proliferative glomerular basement membrane (GBM) nephritis and in controls. Both models are known to have clinical counterparts in human disease. Kidney functional abnormalities correlated with the degree of architectural derangement. In both AICN and anti-GBM nephritis filtration fraction fell in direct proportion to the fall in glomerular filtration rate (GFR), renal plasma flow being unchanged. Fractional electrolyte excretion increased as the GFR fell. Despite marked heterogeneity of single nephron filtration rate (SNGFR) (AICN, 5-93 nl/min; anti-GBM, 0-50 nl/min) and of proximal tubular hydrostatic pressure (4-48 mm Hg), each nephron showed almost complete glomerulotubular balance, absolute reabsorption to the late proximal convolution varying directly with filtration rate. In addition SNGFR could be related both to proximal intratubular hydrostatic pressure and to calculated glomerular capillary pressure (Pg), being lowest in those nephrons with the highest intratubular pressure. Nephrons with very high filtration rates did not apparently reach filtration equilibrium. Mean SNGFR was significantly lower in the anti-GBM group, while calculated Pg was the same in both. This probably reflects the acute and diffuse involvement of the anti-GBM lesion with different filtration characteristics from Dr.