Excretion tubular reabsorption

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. 

Excretion via the kidney can be a straightforward question of glomerular filtration, followed by passage down the kidney tubules into the bladder. However, there can also be excretion and reabsorption across the tubular wall. This may happen if an ionized form within the tubule is converted into its nonpolar nonionized form because of a change in pH. The nonionized form can then diffuse across the tubular wall into plasma. Additionally, there are active transport systems for the excretion of lipophilic acids and bases across the wall of the proximal tubule. The antibiotic penicillin can be excreted in this way. 

Possible causes of increased ratio of Cgm/Ccr pancreatitis can be liberation of a more readily excretable form of amylase, a protein with a molecular weight of 55,000 or less which can be easily filtered via the glomerulus and undergoes no appreciable tubular reabsorption. 

Probenecid is a uricosuric agent that blocks the tubular reabsorption of uric acid, increasing its excretion. Because of its mechanism of action, probenecid is contraindicated in patients with a history of uric acid stones or nephropathy. Probenecid loses its effectiveness as renal function declines and should be avoided when the creatinine clearance is 50 mL/minute or less. Its uricosuric effect is counteracted by low aspirin doses, which many patients receive for prophylaxis of coronary heart disease. 

The renal excretion of drugs depends on glomerular filtration, tubular secretion, and tubular absorption. A twofold increase in glomerular filtration occurs in the first 14 days of life [36], The glomerular filtration rate continues to increase rapidly in the neonatal period and reaches a rate of about 86 mL/min per 1.73 m2 by 3 months of age. Children 3-13 years of age have an average clearance of 134 mL/min per 1.73 m2 [37]. Tubular secretion approaches adult values between 2 and 6 months [11], There is more variability observed in maturation of tubular reabsorption capacity. This is likely linked to fluctuations in urinary pH in the neonatal period [38],... 

The process of tubular reabsorption is essential for the conservation of plasma constituents important to the body, in particular electrolytes and nutrient molecules. This process is highly selective in that waste products and substances with no physiological value are not reabsorbed, but instead excreted in the urine. Furthermore, reabsorption of many substances, such as Na+, H+, and Ca++ ions, and water is physiologically controlled. Consequently, volume, osmolarity, composition, and pH of the extracellular fluid are precisely regulated. 

The a ns wer is a. (Hardman, pp 1525-1528.) Pa r a thyroid ho r m o ne is synthesized by and released from the parathyroid gland increased synthesis of PTI1 is a response to low serum Ca concentrations. Resorption and mobilization of Ca and phosphate from bone are increased in response to elevated PTI1 concentrations. Replacement of body stores of Ca is enhanced by the capacity of PTH to promote increased absorption of Ca by the small intestine in concert with vitamin D, which is the primary factor that enhances intestinal Ca absorption. Parathyroid hormone also causes an increased renal tubular reabsorption of Ca and excretion of phosphate. As a consequence of these effects, the extracellular Ca concentration becomes elevated. 

The answer is a. (Hardman, pp 16-20.) Sodium bicarbonate is excreted principally in the urine and alkalinizes it. Increasing urinary pH interferes with the passive renal tubular reabsorption of organic acids (such as aspirin and phenobarbital) by increasing the ionic form of the drug in the tubular filtrate. This would increase their excretion. Excretion of organic bases (such as amphetamine, cocaine, phencyclidine, and morphine) would be enhanced by acidifying the urine. 

Approximately 50% of the dose is excreted renally, and tubular reabsorption may be prominently involved. 

A plot of rate of transport against solute concentration in the tubule (Figure 8.3) shows fm, the tubular transport maximum to be analogous with Vmax for an enzyme, which is a maximum rate of solute transport across tubular cells. Assuming a fixed GFR, the point at which the plotted line begins to deviate from linearity, indicates that the substance exceeds a critical threshold concentration and begins to be excreted in the urine. When the plotted line reaches a plateau indicating that saturation point, that is tm has been reached, the rate of excretion is linear with increase in plasma concentration. The concept of fm as described here for tubular reabsorption applies equally well to carrier-mediated secretory processes. If the fm value for a particular is exceeded for any reason, there will be excretion of that solute in the urine. 

In calves and cows, SDM was excreted by glomerular filtration minus tubular reabsorption its renal clearance was urine flow correlated, and amounts to half of the creatinine clearance. The SCH2OH hydroxy metabolite was excreted by glomerular filtration and partly by tubular secretion, whereas both Na-SDM and SOH were excreted predominantly by tubular secretion (15 . The main metabolite in urine SCH2OH was 23 to 55 % of the administered dose (Table III). The urine concentration—time curves for SDM and its metabolites are illustrated in Figure 7 for a high SDM dosage. 

Pharmacology A uricosuric and renal tubular blocking agent, probenecid inhibits the tubular reabsorption of urate, thus increasing the urinary excretion of uric acid and decreasing serum uric acid levels. 

Pregabalin is eliminated from the systemic circulation primarily by renal excretion as unchanged drug, with a mean elimination half-life of 6.3 hours in subjects with normal renal function. Mean renal clearance was estimated to be 67 to 80.9 mL/min in young healthy subjects. Because pregabalin is not bound to plasma proteins, this clearance rate indicates that renal tubular reabsorption is involved. Pregabalin elimination is nearly proportional to Ccr. 

Excretion - Nonrenal clearance accounts for approximately 65% of the total clearance of linezolid. The renal clearance of linezolid is low and suggests net tubular reabsorption. 

Excretion - Renal excretion is mainly by glomerular filtration tubular reabsorption occurs in varying degrees. 

The sulfonamides are degraded in the liver by acetylation and oxidation metabolites have reduced bacteriological activity. The parent compound and the metabolites are excreted in the urine, primarily by glomerular filtration followed by tubular reabsorption. Some sulfonamides exhibit diurnal variations in excretion, being three times greater at night than during the day. 

Small molecules are eliminated from the body largely by means of drug metabolism enzymes in the liver and other tissues and by urinary excretion. Large molecules are also eliminated by renal and hepatic mechanisms. Proteins that are less than 40 to 50 kDa are cleared by renal filtration with little or no tubular reabsorption. Larger proteins are less likely to be filtered but may be subject to phagocytosis in hepa-tocytes and Kupfer cells in the liver. Protein biotransformation—denaturation, proteolysis, and oxidative metabolism—is also important. 

While theoretically it is possible that botanicals with diuretic effects can increase drug excretion, most botanical diuretics are not as potent as furo-semide and are unlikely to result in significant interactions. Most botanicals also do not affect urinary pH significantly, and hence are unlikely to affect renal tubular reabsorption of drugs. Nevertheless, lithium toxicity was thought to be related to the use of a botanical diuretic mixture in a patient. If the toxicity indeed is related to the use of the botanical diuretic, the mechanism of action or the responsible constituent(s) is not known (48). 

Mannitol is poorly absorbed by the GI tract, and when administered orally it causes osmotic diarrhea. For systemic effect, mannitol must be given parenterally. Mannitol is not metabolized and is excreted by glomerular filtration within 30-60 minutes, without any important tubular reabsorption or secretion. 

The drug is approximately 70% absorbed after oral administration (see Chapter 54). It is metabolized to a less active hydroxylated metabolite, and both the parent compound and the metabolite are polyglutamated within cells, where they stay for prolonged periods. Methotrexate s serum half-life is usually only 6-9 hours, although it may be as long as 24 hours in some individuals. Methotrexate s concentration is increased in the presence of hydroxychloroquine, which can reduce the clearance or increase the tubular reabsorption of methotrexate. This drug is excreted principally in the urine, but up to 30% may be excreted in bile. 

In six healthy subjects, ampicillin caused an increase in urinary uric acid excretion this effect was attributed to competition for active renal tubular reabsorption of urate (SEDA-13, 212). 

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