Renal Distribution Volumes of Indocyanine Green, [51Cr]EDTA, and 24Na in Man during Acute Renal Failure after Shock. IMPLICATIONS FOR THE PATHOGENESIS OF ANURIA

Reubi, F; Vorburger, C; Tuckman, John

doi:10.1172/jci107179

Cited by 37 publications

(10 citation statements)

References 38 publications

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“…With nonoliguria, the corresponding measures of GFR are less depressed to a range similar to that found immediately following clamp release in the present study (30,31). By contrast, renal blood flow, as measured by inert gas (36)(37)(38) or dye dilution techniques (39,40) in sustained ARF, has been depressed to only 50-67% of normal, a finding again quite similar to that following TRI. Furthermore, features of proximal and distal tubule dysfunction similar to those demonstrated in the post-TRI population, have also been observed in patients with sustained forms of ARF.…”

Section: Discussionsupporting

confidence: 83%

Nature of the renal injury following total renal ischemia in man.

Myers¹,

Miller²,

Mehigan³

et al. 1984

J. Clin. Invest.

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As bstract. The effects of total renal ischemia (TRI) of 15-87 min duration due to suprarenal clamping of the aorta were studied in 15 mannitol-treated patients undergoing abdominal aortic surgery. 15 patients undergoing similar surgery but requiring only infrarenal clamping served as controls. 1-2 h following TRI, GFR was reduced to only 39% of that in controls, 23±5 vs. 59±7 ml/min (P < 0.001). This could not be ascribed to impaired renal plasma flow (RPF), which was mildly reduced to 331±71 and was not different from the value in controls, 407±66 ml/min. However, impaired PAH extraction (43±7%) and isosthenuria, not present in controls, suggest a primary role for tubular injury in lowering GFR at this time.24 h following TRI, the GFR remained depressed below controls, 45±8 vs. 84±8 ml/min (P < 0.005), while the transglomerular sieving of neutral dextrans was significantly enhanced (radius interval, 24-40 A). A theoretical analysis of transcapillary solute exchange revealed that these findings could be largely explained by a selective reduction of either RPF (-61%) or of transmembrane hydraulic pressure difference (-18%) below control values. Alternately, a combination of these two factors with changes of smaller magnitude could explain the findings. In contrast, a selective increase in oncotic pressure or decrease ofthe glomerular ultrafiltration coefficient could be excluded as a cause of hypofiltration 24 h after TRI. These observations lead us to suggest that the transient azotemia observed following TRI is due to a self-limited

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Section: Discussionsupporting

confidence: 83%

Nature of the renal injury following total renal ischemia in man.

Myers¹,

Miller²,

Mehigan³

et al. 1984

J. Clin. Invest.

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“…Studies carried out on rats show a progressive decrease in renal blood flow rate and whole kidney and single nephron glomerular filtration rates6). Renal hemodynamic alterations similar to those observed after uranil nitrate administration have been reported in human acute renal impairment of varied etiologies9, 10,14).…”

Section: Animalssupporting

confidence: 53%

Pharmacokinetics of cefamandole in rabbits with experimentally induced renal impairment.

1980

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“…The observation of collapsed tubules and low efferent arteriolar pressures in methemoglobin-induced acute renal failure (Ruiz-Guinazu et al, 1975) is compatible with this hypothesis. In addition, Reubi et al (1973) have indicated also that the lack of correlation of GFR with relatively well preserved RBF in humans with acute renal failure may be due to a combination of afferent vasoconstriction and efferent vasodilation.…”

Section: Discussionmentioning

confidence: 99%

Intrarenal vascular resistance in glycerol-induced acute renal failure in the rat.

Hsu¹,

Kurtz²,

Sands³

1979

Circulation Research

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SUMMARYWe measured mean afferent arteriolar diameter and renal blood flow with microsphere techniques in awake rats 24 hours after induction of acute renal failure by glycerol injection. Renal blood flow, mean arterial pressure, and total renal vascular resistance in rats with acute renal failure were not different from control levels, despite significantly elevated serum urea nitrogen. Mean afferent arteriolar diameter was decreased in rats with acute renal failure compared to controls (21.1 ± 0.10 vs. 22.0 ± 0.16 jun, mean ± SE, n -5, respectively, P < 0.01). The percentage of renal intravascular microspheres (mean diameter of spheres « 22.3 ± 2.1 jim) entering the glomeruli also was decreased in rats with acute renal failure compared to control (75.9 ± 1.4 vs. 85.7 ± 0.8%, n -7, respectively, P < 0.001). Blood viscosity values of rats injected with glycerol and measured at shear rates of 61.8/sec (4.36 ± 0.06 centipoise (cP, n -6) and 123.6/sec [3.78 ± 0.05 cP, n -6] were significantly higher than those of controls (3.84 ± 0.08 cP, n = 6, P < 0.005, and 3.36 ± 0.09 cP, n = 6, P < 0.005). Therefore, preglomerular resistance is increased during glycerol-induced acute renal failure due to a combination of afferent arteriolar vasoconstriction and increased blood viscosity. The increase in preglomerular resistance will cause a reduced glomerular capillary hydrostatic pressure in glycerol-induced acute renal failure. Ore Ret 45: 583-587, 1979 A SUBSTANTIAL number of studies have demonstrated that a decreased glomerular filtration rate (GFR) is not necessarily associated with impaired renal perfusion in acute renal failure (Churchill et al., 1977;Eisenbach et al, 1974; Hsu et ai, 1977;Kurtz et al., 1976; Stein et al., 1975). These studies contrast sharply with earlier reports documenting a relationship between decreased GFR and decreased renal blood flow (RBF) in acute renal failure (Ayer et al., 1971;Chedru et al., 1972;Flamenbaum et al., 1972;Flamenbaum et al., 1974). Initially, preglomerular vasoconstriction was suggested to be the hemodynamic mechanism responsible for the impaired GFR (Chedru et al., 1972; Ruiz-Guinazu et al., 1975). The recent demonstration of normal renal blood flow in acute renal failure, however, does not preclude this concept, provided that postglomerular resistance decreases simultaneously with an increase in afferent arteriolar resistance. Thus, preglomerular vasoconstriction is still a viable hemodynamic explanation for the decreased GFR of acute renal failure. To test this hypothesis, we measured afferent arteriolar diameter in glycerol-induced acute renal failure, using a recently developed microsphere method (Chenitz et al., 1976;Ishikawa and Hollenberg, 1977;Ofstad et al., 1975). MethodsMale Sprague-Dawley rats, weighing 200-240 g, were given Purina rat chow and tap water ad libitum. Acute renal failure was induced by hindlimb intramuscular injection of 50% glycerol, 1 ml/100 g, after 15 hours of dehydration. Water was freely available thereafter. Controls were injected with equ...

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Renal Distribution Volumes of Indocyanine Green, [51Cr]EDTA, and 24Na in Man during Acute Renal Failure after Shock. IMPLICATIONS FOR THE PATHOGENESIS OF ANURIA

Cited by 37 publications

References 38 publications

Nature of the renal injury following total renal ischemia in man.

Nature of the renal injury following total renal ischemia in man.

Pharmacokinetics of cefamandole in rabbits with experimentally induced renal impairment.

Intrarenal vascular resistance in glycerol-induced acute renal failure in the rat.

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