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Glomerular Filtration Rate GFR

As a general rule, increases of renal blood flow and/ or glomerular filtration rate (GFR) correlate rather well with increased urinary excretion of solutes and water. The underlying causes for this correlation are not fully understood, but they reflect incomplete adjustments of tubular reabsorption to an increase of tubular electrolyte load. [Pg.429]

Glomerular filtration rate (GFR) is the volume of plasma-like fluid that is filtered per unit time across the glomerular capillary membranes to enter the tubular space. Filtrate formation is driven by the net filtration pressure that is equal to the capillary hydrostatic pressure diminished by the sum of capillary oncotic... [Pg.537]

Another key feature of the thiazide-type diuretics is their limited efficacy in patients whose estimated renal function is reduced, such as the elderly. For example, patients with estimates of reduced renal function, such as those with a glomerular filtration rate (GFR) below 30 mL/minute, should be considered for more potent loop type diuretics such as furosemide. Clinicians often fail to either reconsider the role of thiazide diuretics prescribed to individuals whose renal function has been declining or fail to recognize the likely prevalence of renal compromise in the elderly to begin with. [Pg.21]

Within normal limits estimated glomerular filtration rate (GFR) 101 mL/minute... [Pg.155]

Acute renal failure (ARF) is a potentially life-threatening clinical syndrome that occurs primarily in hospitalized patients and frequently complicates the course of the critically ill. It is characterized by a rapid decrease in glomerular filtration rate (GFR) and the resultant accumulation of nitrogenous waste products (e.g., creatinine and urea nitrogen), with or without a decrease in urine output. A recent consensus statement... [Pg.361]

Glomerular filtration rate (GFR) The volume of plasma that is filtered by the glomerulus per unit time, usually expressed as mL/minute or mL/minute/1.73 m2, which adjusts the value for body surface area. GFR is the primary index used to describe overall renal function. [Pg.1567]

The glomerular filtration rate (GFR) in normal males is estimated to be 125mL/min, and the results of the example calculation suggest that the drug is cleared by GFR. If the RCR had been less than 125 mL/min, tubular reabsorption of the drug would have been suspected. If it had been greater than 125 mL/min, tubular secretion would have been involved in the drug elimination. [Pg.85]

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). [Pg.99]

Acute renal failure (ARF) is broadly defined as a decrease in glomerular filtration rate (GFR) occurring over hours to weeks that is associated with an accumulation of waste products, including urea and creatinine. Clinicians use a combination of the serum creatinine (Scr) value with change in either Scr or urine output (UOP) as the primary criteria for diagnosing ARF. [Pg.862]

Dosingof selected agents by class fibrate (gemfibrozil 600 mg twice a day) niacin (1.5-3 g/day of immediate-release product) statin (simvastatin 10-40 mg/day if glomerular filtration rate [GFR] <30 mL/min, 20-80 mg/day if GFR >30 mL/min) bile acid sequestrant (cholestyramine 4-16 g/day). [Pg.877]

Blood samples were centrifuged at 1000 x g for 20 min at 0-4°. Ionized calcium levels were immediately determined in serum and urine samples using a calcium ion-selective electrode (Ionetics, Inc., Costa Mesa, CA) urine volumes were recorded. The remaining serum and urine were aliquoted for various analyses and stored at -40°. Serum insulin was analysed by radioimmunoassay (Amersham Corp., Arlington Heights, IL). Serum levels of total calcium, phosphorus and creatinine as well as urine creatinine were determined by colorimetric procedures using an automated analyzer (Centrifichem, Baker Instruments Corp., Pleasantville, NY). Glomerular filtration rates (GFR) were calculated from serum and urine creatinine data GFR = urine creatinine/serum creatinine. [Pg.127]

The glomerular filtration rate (GFR) defines how much plasma water passes from the blood into the top of the nephron per minute. In health, the true GFR for a 70 kg adult is typically 100-120 ml/minute. Expressed another way, we can say that, in health, every minute each of the approximately 2 million glomeruli present in both adult kidneys filters between 0.05 and 0.06 pi of plasma water. The GFR is a good overall measure of renal function and the clinical laboratory has many ways of estimating its value. [Pg.264]

The marker remains in the plasma without binding to proteins, and the filtrate is neither reabsorbed nor secreted by the renal tubule. Clearance rate of the marker from plasma equals the glomerular filtration rate (GFR). The polysaccharide, inulin, typifies this class of markers. [Pg.53]

Jenkins et al. developed a capillary electrophoresis system for the measurement of iohexol as a marker of the glomerular filtration rate (GFR) with a run time of 5.25 min and a coefficient of variation (CV) of 4.3% at 80 mg L" [121]. The GFR, calculated from the plasma clearance, had a reproducibility of 5.47 %. A similar approach (liquid chromatography-mass spectrometry with positive electrospray ionization after enrichment by solid phase extraction) was applied by Putschew et al. for the determination of iodinated contrast agents in treatment plant effluents and surface waters [118]. [Pg.126]

Renal function Impairment- Ceftazidime is excreted by the kidneys, almost exclusively by glomerular filtration. In patients with impaired renal function (glomerular filtration rate (GFR) less than 50 mL/min), reduce dosage to compensate for slower excretion. In patients with suspected renal insufficiency, give an initial loading dose of 1 g. Estimate GFR to determine the appropriate maintenance dose. [Pg.1505]

Dosage adjustments - In renal transplant patients with severe chronic renal impairment (glomerular filtration rate [GFR] less than 25 mL/min per 1.73 m ) outside the immediate posttransplant period, avoid dosages of mycophenolate greater than 1 g administered twice a day. [Pg.1947]

Serum creatinine - During the first 1 to 3 days of therapy, some patients have experienced an acute and transient decline in the glomerular filtration rate (GFR) and diminished urine output with a resulting increase in the level of serum creatinine. [Pg.1977]

During pregnancy, serum lithium levels need to be carefully monitored. The 50% to 100% increase in glomerular filtration rate (GFR) that normally occurs in the third trimester will proportionally lower lithium levels due to its increased clearance. Thus, dosage may need to be increased to maintain a therapeutic range ( 341). Because the GFR and lithium clearance quickly return to normal after delivery, it may be wise to stop the drug shortly before delivery and restart a few days after delivery at a lower dose. In summary ... [Pg.215]

Increased delivery of salt to the TAL leads to activation of the macula densa and a reduction in glomerular filtration rate (GFR) by tubuloglomerular (TG) feedback. The mechanism of this feedback is secretion of adenosine by macula densa cells, which locally causes afferent arteriolar vasoconstriction. This vasoconstriction reduces GFR. Tubuloglomerular feedback-mediated reduction in GFR exacerbates the reduction that was initially caused by decreased cardiac output. Recent work with adenosine receptor antagonists (eg, rolofylline) has shown that it will soon be possible to circumvent this complication of diuretic therapy in heart failure patients. Using rolofylline with a diuretic will make it possible to produce an effective diuresis in patients with heart failure without causing renal decompensation. [Pg.339]


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