RENAL METABOLISM Of DRUGS
A large number of drugs are eliminated from the body by renal excretion. Excretion of drugs by the kidney may involve filtration, secretion, and reab-sorption depending upon the agent in question. Filtration of a drug through the glomerulus depends on the chemical characteristics of the drug itself and the degree of binding of the drug to plasma proteins. Drugs that are highly bound to plasma proteins are poorly filtered, while those that are bound less avidly or not at all can gain access to the tubular fluid. Drugs that are organic anions or cations can be secreted from the peritubular capillary blood into the lumen of the tubule by specific transport mechanisms in renal tubular cells. Some drugs that gain access to the tubular fluid by filtration and/or secretion may be reabsorbed back into the systemic circulation by mediated or passive transport mechanisms. For some drugs, bidirectional transport across renal tubules is known to occur, so that the net rate of excretion is dependent on the relative activities of the secretory and absorptive processes. For organic anions and cations whose pK is in the range of the pH normally attainable in the tubular fluid, any change in the pH of the urine may have aprofound and clinically important effect on the rate of excretion of the drug. These principles are known as the effects of “nonionic diffusion” and indicate the differences in the permeabilities of drugs across renal membranes when the drug is in its ionized or un-ionized form (Table 35-1}. Alkalinization of the urine significantly increases the excretion of organic anions such as aspirin and phenobarbital. Acidification of the urine increases the renal excretion of organic bases such as amphetamines.
In addition to modulating the rates of excretion of drugs, the kidney accumulates certain drugs. The kidney is also capable of metabolizing specific types of pharmaceutical agents. Owing to an effect on specific transport pathways, drug-drug interactions may occur. For example, probenecid, an inhibitor of organic anion secretion, inhibits the tubular secretion of penicillin. Such an interaction may have clinical utility when it is necessary to achieve high blood concentrations of this antibiotic.
- CHROMIC PANCREATITIS
- PHYSIOLOGICAL EFFECTS OF PULMONARY HYPERTENSION ON CARDIAC FUNCTION
- MEDICAL MANAGEMENT OF ANGINA
- PERICARDIAL EFFUSIOH
- CHROMC BROriCMITIS
- ARTERIAL TRAUMA
- PATHOLOGY
- Gardner's Syndrome
- POLYPS OF THE GASTROINTESTINAL TRACT
- DISEASES OF THE ESOPHAGUS
- Diabetes Mellitus (DM)
- CAUSES OF PULMONARY HYPERTENSION
- Alterations in Glomerular Hemodynamics, Parathyroid Hormone Metabolism, and Systemic Arterial Blood Pressure
- Disorders of Pregnancy
- Magnetic Resonance Imaging (MRI)
- CLINICAL MANIFESTATIONS OF ENDSTAGE RENAL DISEASE
- FACTORS AFFECTING THE RATE OF LOSS OF NEPHRONS
- MULTIVALVULAR DISEASE
- NAUSEA AND VOMITING
- MYOCARDIAL DISEASE - MYOCARDITIS
- Amiodarone
- Phosphate Balance
- GENERAL MANAGEMENT OF MYOCARDIAL INFARCTION
- Pulmonary Vasculitis
- Clinical Manifestations
- CARDIAC DEVELOPMENT
- Renal Venous Occlusion
- Improving Case Management
- Blood Chemistries
- SMOKING CESSATION
- CARDIOVASCULAR RESPONSE TO EXERCISE
- Lower GI Bleeding
- Conjugated Hyperbilirubinemia
- ANTIBIOTICS
- Factors Involved in the Choice of Type of Dialysis