Kidney excretion ratio

The hypocupremia in nephrosis where the albumin globulin ratio is reversed and total protein levels are low remains to be explained. In these cases, however, there is a considerable loss by kidney excretion, as has been described by Markowitz et al. (1955). The ceruloplasmin excretion has been determined in 4 of his 7 nephrosis patients. The loss proved to be as high as 46-75 mg. ceruloplasmin a day. The serum copper values of these 7 patients were between 36 and 129 fig. %, with corresponding decreases in ceruloplasmin values. 

The study of the mechanism of urinary excretion of amylase and the amylase clearance has been the subject of many studies in recent years. Levitt et. al (79) studied the renal clearance of amylase in renal insufficiency, acute pancreatitis and macro-amylasemia. In acute pancreatitis, the kidney cleared amylase at a markedly increased rate. The ratio of the amylase clearance rate to the creatinine clearance rate (Cgm/Ccr) averaged 3 times normal early in the course of acute pancreatitis, and this elevation could persist after the serum amylase returned to normal. Comparison of an lase clearance to creatinine clearance was to minimize irrelevant changes due to variation in renal function. The increased clearance of amylase makes the urinary amylase a more sensitive indicator of pancreatitis. 

There are several pharmacokinetic differences between loop diuretics. Fifty to sixty percent of a dose of furosemide is excreted unchanged by the kidney with the remainder undergoing glucuronide conjugation in the kidney.17 In contrast, liver metabolism accounts for 50% and 80% of the elimination of bumetanide and torsemide, respectively.17 Thus, patients with ARF may have a prolonged half-life of furosemide. The bioavailability of both torsemide and bumetanide is higher than for furosemide. The intravenous (IV) oral ratio for bumetanide and torsemide is 1 1, bioavailability of oral furosemide is approximately 50%, with a reported range of 10% to 100%.18... 

Taken together, these data are consistent with those of a BPA (low Vp, C5/C0 ratio greater than that of iobitridol) that is freely excreted by the kidney with a very short elimination half-life. Furthermore, no biliary excretion was observed up to 6 hours after intravenous injection of P743 at the dose of 300 mgl kg in awake rats. 

Pharmacokinetics Sodium bicarbonate in water dissociates to provide sodium and bicarbonate ions. Sodium is the principal cation of extracellular fluid. Bicarbonate is a normal constituent of body fluids and normal plasma level ranges from 24 to 31 mEq/L. Plasma concentration is regulated by the kidney. Bicarbonate anion is considered labile because, at a proper concentration of hydrogen ion, it may be converted to carbonic acid, then to its volatile form, carbon dioxide, excreted by lungs. Normally, a ratio of 1 20 (carbonic acid bicarbonate) is present in extracellular fluid. In a healthy adult with normal kidney function, almost all the glomerular filtered bicarbonate ion is reabsorbed less than 1% is excreted in urine. 

Isoniazid is acetylated to acetyl isoniazid by A-acetyl-transferase, an enzyme in fiver, bowel, and kidney. Individuals who are genetically rapid acetylators will have a higher ratio of acetyl isoniazid to isoniazid than will slow acetylators. Rapid acetylators were once thought to be more prone to hepatotoxicity, but this is not proved. The slow or rapid acetylation of isoniazid is rarely important clinically, although slow inactivators tend to develop peripheral neuropathy more readily. Metabolites of isoniazid and small amounts of unaltered drug are excreted in the urine within 24 hours of administration. 

As indicated earher, sulfonamides are effective in both gram-positive and gramnegative bacteria. Mostly prescribed for humans in the United States, in this class is sulfamethoxazole, mostly in combination with trimethoprim (SMZ-TMP) in a 5 1 ratio. Trimethoprim inhibits dihydropholic acid reductase and this, just like sulfonamides, also interferes with the synthesis of folic acid (Fig. 1.8). As a matter of fact, use of the combined SMZ-TMP has been steadily increasing recently as is displayed by the number of prescriptions (Fig. 1.7). Oral doses of sulfonamides are absorbed well and eliminated by the liver and kidney with 20-60% excreted as the parent compound (Queener and Gutierrez, 2003). 

In general, the macrolides are administered orally but sometimes also paren-terally. All the members of this group are well absorbed and are distributed extensively in tissues, especially in the lungs, liver, and kidneys, with high tissue to plasma ratios. They are retained in the tissues for long periods after the levels in the blood have ceased to be detectable. Elimination of all macrolides occurs primarily through hepatic metabolism, which accounts for approximately 60% of an administered intravenous dose the remainder is excreted in active form in the urine and bile. With oral and intramuscular administration, urinary excretion decreases, but biliary excretion and hepatic metabolism increase proportionally. Milk has often macrolide concentrations severalfold greater than in plasma (7). 

For example, once in sy.stemic circulation, the plasma pH of 7.4 will be one of the determinants of whether the drug will lend to remain in the aqueous environment of the blood nr partition across lipid membranes into hepatic tissue to he metabolized, into the kidney for excretion, into ii.ssue depots, or to the receptor tissue. A useful exercise is to culculalc cither the conj. ba.se / acid ratio using the Henderson-Has-sclbalch equation (Eq. 2-11) or percent ionization for ephed-rinc (pK , 9.6 Bq. 2-14) and indomclhacin (pK 4.. i 2-... 

When plasma HCOJ concentration increases above 28 mmol/L, the capacity of the proximal and distal tubules to reclaim is exceeded, and HCOf is excreted in the urine. The process of bicarbonate reclamation is enhanced in acidosis (and decreased in alkalosis), most likely as a result of increased Na -H exchange. In this way, the kidneys in acidosis or alkalosis support the other compensatory mechanisms to restore the normal cHC03/cdC02 ratio. Type II RTA is a decreased ability to reabsorb HCO3 in the proximal tubules, leading to a decrease in blood pH. 

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