scholarly journals Calculation of the renal perfusion and glomerular filtration rate from the renal impulse response obtained with MRI

2004 ◽  
Vol 51 (5) ◽  
pp. 1017-1025 ◽  
Author(s):  
L. Hermoye ◽  
L. Annet ◽  
Ph. Lemmerling ◽  
F. Peeters ◽  
F. Jamar ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Impulse Response ◽  
Filtration Rate ◽  
Renal Perfusion

The Effect of Glucagon on Glomerular Filtration Rate in Dogs During Reduction of Renal Blood Flow

1975 ◽  
Vol 53 (4) ◽  
pp. 660-668 ◽  
Author(s):  
Mortimer Levy
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Acute Tubular Necrosis ◽  
Filtration Rate ◽  
Renal Perfusion ◽  
Beneficial Effects ◽  
Tubular Necrosis ◽  
Arterial Blood ◽  
Urine Formation

Glucagon in small intravenous (i.v.) doses markedly increases glomerular filtration rate (GFR) in normal anesthetized dogs. In this study, the effects of glucagon 5 μg/min (i.v.) on renal hemodynamics was tested in four canine models of acute pre-renal failure (hemorrhage, barbiturate overdose; renal arterial clamping and renal arterial infusions of noradrenaline) and in a model of unilateral acute tubular necrosis at 4 h and 6–7 days following completion of the ischemic insult. Following hemorrhage and barbiturate excess, with arterial blood pressure maintained at 65–70 mm Hg, whole-kidney GFR and clearance rate of p-aminohippurate decreased by 50–70%. During this reduction of perfusion pressure, the subsequent infusion of glucagon increased GFR by 90–130%. In models where arterial pressure was normal during the period of ischemia (clamping and noradrenaline infusion), not only did glucagon significantly increase renal perfusion, but the ischemic kidney proved to be far more sensitive to the hemodynamic effects of glucagon (ΔGFR = 120–160%) than the contralateral control (ΔGFR = 30–40%). In three dogs completely anuric following renal arterial clamping, glucagon was able to improve blood flow and restart urine formation. Glucagon, but not dopamine, was able to simulate the beneficial effects of hypertonic mannitol on renal function in dogs with hemorrhagic hypotension. Glucagon was without effect in established acute tubular necrosis. This study, therefore, indicates that, during renal ischemia, glucagon may be quite effective in preserving urine output and perfusion of the kidneys.

Editor’s Choice-Diuretic resistance in acute heart failure

2018 ◽  
Vol 7 (4) ◽  
pp. 379-389 ◽  
Author(s):  
Frederik H Verbrugge
Keyword(s):  
Heart Failure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Acute Heart Failure ◽  
Filtration Rate ◽  
Loop Diuretic ◽  
Volume Overload ◽  
Renal Perfusion ◽  
Loop Diuretics ◽  
Diuretic Resistance

Diuretic resistance is a powerful predictor of adverse outcome in acute heart failure (AHF), irrespectively of underlying glomerular filtration rate. Metrics of diuretic efficacy such as natriuresis, urine output, weight loss, net fluid balance, or fractional sodium excretion, differ in their risk for measurement error, convenience, and biological plausibility, which should be taken into account when interpreting their results. Loop diuretic resistance in AHF has multiple causes including altered drug pharmacokinetics, impaired renal perfusion and effective circulatory volume, neurohumoral activation, post-diuretic sodium retention, the braking phenomenon and functional as well as structural adaptations in the nephron. Ideally, these mechanisms should guide specific treatment decisions with the goal of achieving complete decongestion. Therefore, volume overload needs to be identified correctly to avoid poor diuretic response due to electrolyte depletion or dehydration. Next, renal perfusion should be optimised if possible and loop diuretics should be prescribed above their threshold dose. Addition of thiazide-type diuretics should be considered when a progressive decrease in loop diuretic efficacy is observed with prolonged use (i.e., the braking phenomenon). Furthermore, thiazide-type diuretics are a useful addition in patients with low glomerular filtration rate. However, they limit free water excretion and are relatively contraindicated in cases of hypotonic hyponatremia, where acetazolamide is the better option. Finally, ultrafiltration should be considered in patients with refractory diuretic resistance as persistent volume overload after decongestive treatment is associated with worse outcomes. Whether more upfront use of any of these individually tailored decongestion strategies is superior to monotherapy with loop diuretics remains to be shown by adequately powered randomised clinical trials.

Atrial appendectomy reduces ANF but not sodium excretion in acute vasopressin hypertension

1990 ◽  
Vol 258 (1) ◽  
pp. R77-R81
Author(s):  
R. S. Zimmerman ◽  
R. W. Barbee ◽  
A. Martinez ◽  
A. A. MacPhee ◽  
N. C. Trippodo
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Sprague Dawley ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Circulating Levels

The present study was designed to determine whether atrial appendectomy would decrease the sodium excretion associated with pressor doses of arginine vasopressin (AVP) infusion in rats by decreasing circulating levels of atrial natriuretic factor (ANF). Ten to 21 days after either sham (n = 9) or bilateral atrial appendectomy (n = 13) AVP (19 ng.kg-1.min-1) was infused for 90 min in anesthetized Sprague-Dawley rats. Atrial appendectomy decreased circulating ANF levels from 469 +/- 70 pg/ml in sham-operated animals to 259 +/- 50 pg/ml (P less than 0.05) in atrial-appendectomized animals after 90 min of AVP infusion. Despite a reduction in circulating levels of ANF, sodium excretion, potassium excretion, and urine flow increased and were not affected by bilateral atrial appendectomy. Glomerular filtration rate and mean arterial pressure significantly increased in both groups of rats. The present study supports non-ANF factors such as increases in renal perfusion pressure and/or glomerular filtration rate as potential mechanisms in AVP-induced natriuresis.

scholarly journals Dynamic Contrast Enhancement (DCE) MRI–Derived Renal Perfusion and Filtration: Basic Concepts

2021 ◽  
pp. 205-227
Author(s):  
Michael Pedersen ◽  
Pietro Irrera ◽  
Walter Dastrù ◽  
Frank G. Zöllner ◽  
Kevin M. Bennett ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Contrast Agents ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renal Perfusion ◽  
The European Union ◽  
Dce Mri ◽  
Indirect Measures ◽  
Renal Mri ◽  
The Cost

AbstractDynamic contrast-enhanced (DCE) MRI monitors the transit of contrast agents, typically gadolinium chelates, through the intrarenal regions, the renal cortex, the medulla, and the collecting system. In this way, DCE-MRI reveals the renal uptake and excretion of the contrast agent. An optimal DCE-MRI acquisition protocol involves finding a good compromise between whole-kidney coverage (i.e., 3D imaging), spatial and temporal resolution, and contrast resolution. By analyzing the enhancement of the renal tissues as a function of time, one can determine indirect measures of clinically important single-kidney parameters as the renal blood flow, glomerular filtration rate, and intrarenal blood volumes. Gadolinium-containing contrast agents may be nephrotoxic in patients suffering from severe renal dysfunction, but otherwise DCE-MRI is clearly useful for diagnosis of renal functions and for assessing treatment response and posttransplant rejection.Here we introduce the concept of renal DCE-MRI, describe the existing methods, and provide an overview of preclinical DCE-MRI applications to illustrate the utility of this technique to measure renal perfusion and glomerular filtration rate in animal models.This publication is based upon work from the COST Action PARENCHIMA, a community-driven network funded by the European Cooperation in Science and Technology (COST) program of the European Union, which aims to improve the reproducibility and standardization of renal MRI biomarkers. This introduction is complemented by two separate publications describing the experimental procedure and data analysis.

Renal autoregulation of blood flow and filtration rate in the rabbit

1979 ◽  
Vol 237 (6) ◽  
pp. F479-F482 ◽  
Author(s):  
C. E. Ott ◽  
R. C. Vari
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Pressure Range ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Rabbit Kidney ◽  
Renal Perfusion Pressure

Electromagnetic flow techniques and inulin clearance were used to determine the autoregulatory capabilities of the rabbit kidney in vivo. Renal blood flow was measured in 13 animals over a renal perfusion pressure range of 40–110 mmHg. Normal renal blood flow averaged 3.2 +/- 0.3 ml.min-1.g kidney-1 and was efficiently autoregulated above a renal artery pressure of 75 mmHg. For every 10 mmHg renal pressure change above 75 mmHg renal blood flow changed only 0.96%. Renal perfusion pressure was reduced from 102 +/- 3 to 74 +/- 2 mmHg in six animals. Over this pressure range glomerular filtration rate was not significantly decreased and averaged 4.2 +/- 0.5 ml/min at high pressure compared to 4.0 +/- 0.5 ml/min at low perfusion pressure. Results show that the rabbit kidney autoregulates renal blood flow and glomerular filtration rate efficiently above 75 mmHg. This range of autoregulation compares well with the autoregulatory range of the dog. The results also show that in the autoregulatory range the rabbit and the rat appear to autoregulate with equal efficiency but that the rabbit kidney begins to autoregulate at a low perfusion pressure than the average of approximately 100 mmHg usually found in the rat.

Insulin-like growth factor I increases glomerular filtration rate and renal plasma flow in man

1989 ◽  
Vol 121 (1) ◽  
pp. 101-106 ◽  
Author(s):  
Hans-Peter Guler ◽  
Kai-U. Eckardt ◽  
Jürgen Zapf ◽  
Christian Bauer ◽  
E. Rudolf Froesch
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Fasting Blood Glucose ◽  
Serum Levels ◽  
Renal Perfusion ◽  
Igf I ◽  
Clinical Potential

Abstract. Recombinant IGF-I was infused sc at a dose of 20 μg · kg−1 · h−1 to 2 healthy subjects during a total of 79 h. Serum levels of IGF-I rose from 93 and 177 to 502 and 616 μg/l, respectively. Fasting blood glucose remained normal. During the infusion, glomerular filtration rate increased by 31% in subject No. 1 and by 32% in subject No.2. Concomitantly, renal plasma flow increased by 26% and 22%, respectively. Proximal and distal tubular reabsorption of fluid and sodium as determined by lithium clearance was elevated to a similar extent. When determined again one week after the end of the IGF-I infusion, all parameters of renal function had returned to baseline. Sodium excretion, body weight and blood pressure did not change. We conclude that IGF-I infused at pharmacological doses has marked effects on kidney function. Future studies will be necessary to define the clinical potential of recombinant IGF-I in the treatment of diseases characterized by impaired renal perfusion and filtration.

Glomerular filtration dynamics during renal vasodilation with acetylcholine in the dog

1983 ◽  
Vol 244 (6) ◽  
pp. F606-F611 ◽  
Author(s):  
C. E. Thomas ◽  
C. E. Ott ◽  
P. D. Bell ◽  
F. G. Knox ◽  
L. G. Navar
Keyword(s):  
Glomerular Filtration Rate ◽  
Proximal Tubule ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Effective Filtration Pressure ◽  
Single Nephron ◽  
Flow Dependency

The reason for the failure of glomerular filtration rate (GFR) to exhibit plasma flow dependency during pharmacologic vasodilation remains unclear although it has been suggested on the basis of experiments in rats that vasodilators may lead to a reduction in the glomerular filtration coefficient (Kf). To evaluate the applicability of this hypothesis to the dog, the effects of vasodilation with acetylcholine on glomerular dynamics and Kf were evaluated in two groups of dogs. One group (n = 19) was studied at spontaneous arterial pressures to allow maximum vasodilation to occur. In the other group (n = 5), renal arterial pressure was reduced and maintained at approximately 89 mmHg. Glomerular filtration rate and single nephron glomerular filtration rate were not altered significantly during acetylcholine infusion in either of the two groups. Both whole kidney and superficial filtration fractions decreased significantly. At spontaneous arterial pressures, transglomerular hydrostatic pressure was not altered significantly because of equivalent increases in proximal tubule pressure and in glomerular pressure. In the dogs studied at reduced renal perfusion pressure, glomerular capillary pressure did not change, but proximal tubule pressure increased slightly. Average effective filtration pressures and Kf were not significantly altered during the infusion of acetylcholine either at spontaneous or reduced renal perfusion pressures. These observations indicate that Kf in the dog is not significantly decreased by acetylcholine and that GFR is not affected during infusion of this agent because the effective filtration pressure is not significantly altered.

Autoregulation of renal blood flow and glomerular filtration rate in the pregnant rabbit

1987 ◽  
Vol 252 (1) ◽  
pp. R69-R72 ◽  
Author(s):  
L. L. Woods ◽  
H. L. Mizelle ◽  
J. E. Hall
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Pregnant Rabbit ◽  
In Pregnancy

Our purpose was to determine whether renal autoregulatory capability is retained in pregnancy despite the marked renal vasodilation that occurs at this time. Renal blood flow and glomerular filtration rate (GFR) were measured in anesthetized pregnant (22–27 days gestation) and nonpregnant rabbits during step reductions in renal perfusion pressure from control (100 +/- 3 mmHg) to 50 mmHg. Control renal blood flow and GFR were significantly higher in pregnant animals, averaging 65 +/- 5 and 13.1 +/- 1.1 ml/min, respectively, compared with 50 +/- 5 and 9.4 +/- 1.2 ml/min in nonpregnant rabbits. Filtration fraction was also significantly elevated in pregnant animals (0.33 +/- 0.02 vs. 0.27 +/- 0.01 in nonpregnant rabbits). During step reductions in renal perfusion pressure, renal blood flow was well autoregulated down to approximately 70 mmHg in both nonpregnant and pregnant animals, falling by only 9 +/- 4 and 12 +/- 5%, respectively. Likewise, GFR was also well autoregulated, falling by 10 +/- 2 and 8 +/- 3% in nonpregnant and pregnant animals, respectively, when perfusion pressure was reduced from 90 to 70 mmHg. These results suggest that renal autoregulation is preserved in pregnancy despite the fact that the renal circulation is already markedly vasodilated.

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