Depression of renal clearance of furosemide in man by azotemia

Rose, H; O’Malley, K; Pruitt, Albert W.

doi:10.1002/cpt1977212141

Cited by 52 publications

(14 citation statements)

References 8 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In the last period, all patients had an increase in urinary sodium excretion (minimum 25 to maximum of 101 mEq/8 h). These results indicate that in uremic patients furosemide is not a short-acting drug, possibly because the active secretion of this diuretic is inhibited both by accumulated endogenous acids [9] and reduced renal blood flow.…”

Section: Modalities O F Stabilization and Treatmentmentioning

confidence: 84%

Effects of Furosemide Therapy on Free-Water Excretion in Uremic Patients

Conte

Fuiano

Sabbatini

et al. 1988

Nephron

View full text Add to dashboard Cite

To assess the intrinsic effects of treatment with furosemide on free-water excretion in patients with chronic renal failure, two groups of patients with and without replacement of diuretic-induced salt losses have been studied. Furosemide therapy was administered for 1 week during constant sodium intake (100 mEq/day). In neither of the groups did furosemide cause hyponatremia, while it did decrease the urine to plasma osmolality ratio, an effect lasting even when the diuretic effect was exhausted. During water diuresis, furosemide decreased the fractional sodium reabsorption in diluting segments but not the absolute rate of the free-water generation (CH₂O). Presumably the expected decrease of CH₂O was masked by the increased distal delivery of tubular fluid mainly due to an additional effect of the diuretic on the proximal tubule. The hypotonicity of urine after furosemide treatment may be secondary to the dissipation of medullary hypertonicity, caused by furosemide, in the condition of decreased water permeability of the collecting duct due to uremic disease.

show abstract

Section: Modalities O F Stabilization and Treatmentmentioning

confidence: 84%

Effects of Furosemide Therapy on Free-Water Excretion in Uremic Patients

Conte

Fuiano

Sabbatini

et al. 1988

Nephron

View full text Add to dashboard Cite

show abstract

“…Furosemide is a highly protein-bound (>98%), weak organic acid which is actively secreted into the urine by organic acid transporters (OATs) in the proximal tubules (24,25). In patients with elevated plasma urea and creatinine concentrations, uremic acids may theoretically alter furosemide PK by competing for tubular secretion by OATs (26).…”

Section: Discussionmentioning

confidence: 99%

Determinants of Urinary Output Response to IV Furosemide in Acute Kidney Injury: A Pharmacokinetic/Pharmacodynamic Study

Silbert

Ho²,

Lipman³

et al. 2016

Critical Care Medicine

View full text Add to dashboard Cite

Objectives: This study assessed the determinants of urinary output response to furosemide in acute kidney injury; specifically, whether the response is related to altered pharmacokinetics or pharmacodynamics. Design: Prospective cohort.Setting: Tertiary intensive care unit. Patients:Thirty critically ill patients with acute kidney injury without preexisting renal impairment or recent diuretic exposure.Intervention: A single dose of IV furosemide. Measurements and Main Results:Baseline markers of intravascular volume status were obtained prior to administering furosemide. Six-hour creatinine clearance, hourly plasma/urinary furosemide concentrations, and hourly urinary output were used to assess furosemide pharmacokinetic/pharmacodynamic parameters. Of 30 patients enrolled, 11 had stage-1 (37%), nine had stage-2 (30%) and 10 had stage-3 (33%) Acute Kidney Injury Network acute kidney injury. Seventy-three percent were septic, 47% required norepinephrine, and 53% were mechanically ventilated. Urinary output doubled in 20 patients (67%) following IV furosemide. Measured creatinine clearance was strongly associated with the amount of urinary furosemide excreted and was the only reliable predictor of the urinary output after furosemide (area under the receiver-operating-characteristic curve, 0.75; 95% CI, 0.57-0.93). In addition to an altered pharmacokinetics (p<0.01), a reduced pharmacodynamic response to furosemide also became important when creatinine clearance was reduced to less than 40ml/min/1.73m 2 (p=0.01). Acute kidney injury staging and markers of intravascular volume, including central venous pressure, brain-natriuretic-peptide concentration and fractional urinary sodium excretion were not predictive of urinary output response to furosemide.3 Conclusions:The severity of acute kidney injury, as reflected by the measured creatinine clearance, alters both pharmacokinetics and pharmacodynamics of furosemide in acute kidney injury, and was the only reliable predictor of the urinary output response to furosemide in acute kidney injury.

show abstract

“…Renal function tests such as measurements of the creatinine clearance (CrCL), serum creatinine (CrJ, and blood urea nitrogen (BUN) all measure not only glomerular filtration rate specifically, but also overall renal function.610 Creatinine clearance is the most readily available measure of general renal function and therefore represents the logical choice for the independent variable in a predictive model of furosemide renal clearance. [11][12][13][14][15][16][17][18][19][20] Data Collection-Retrospective-The literature represents a substantial pool of information concerning the renal clearance of furosemide, including individual-specific renal clearance values. Renal clearance values and corresponding subject/patient-specific clinicall demographic information were gleaned from the literature.…”

Section: Methodsmentioning

confidence: 99%