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DR. SAMAH MOHAMED ELAIDY
1. Drug
Elimination (Clearance). 2. Secretion of Drugs. 3. Activation, Inactivation and Biotransformation of Drugs. 4. Secretion of Hormones.
It is controlled by the following factors:
Renal Blood Flow and Glomerular Filtration: ▪ ▪
C.
Increased by: vasodilators, digoxin, methyl xanthines. Decreased by: vasoconsrictors, ACEIs, ARBs, βblockers, verapamil.
Changes of PH of the Filtrate: ▪ ▪ ▪ ▪
Acidic drugs (e.g. salicylates) are better eliminated in alkaline urine. Basic drugs (e.g. Atropine) are better eliminated in acidic urine. Acidification of urine is produced by: Ascorbic acid , ammonium chloride. Alkalization of urine is produced by: sodium bicarbonate, sodium lactate, sodium citrate.
Tubular secretion of drugs or body excreta (e.g. uric acid) occurs in the proximal convoluted tubules, as: ▪ ▪
Some drugs inhibit the tubular secretion of other drugs→↑plasma levels of the latter, as: ▪ ▪
Acidic drugs (Anions): penicillins, thiazides, loop diuretics, salicylates. Basic drugs (Cations): atropine, quinidine, morphine, amiloride.
Probenicid inhibits tubular secretion of penicillins, cephalosporins →Beneficial effect. Quinidine inhibits tubular secretion of digitalis →digitalis toxicity.
Some drugs inhibit the tubular secretion of other drugs→ inhibit their
In the kidney vitamin D is converted to its active form [1,25(OH)2 Cholecalciferol], by 1alpha-hydroxylase enzyme. Some drugs are inactivated in the kidney, as imipinem (beta lactam antibiotic) is inactivated by renal dihydropeptidase (DHP). Oxidation of salicylates and acetaminophen in renal tissues shares for pathogenesis of renal toxicity of these drugs. Small molecular weight protein and polypeptides (e.g. insulin) are
As, secretion of erythropoeitin (EPO), to stimulate bone marrow or RBCs production. So, in CRF, anemia is a sign, which can be treated by EPO.
A.
Parathyroid Hormone (PTH): ▪ ▪ ▪
B.
Inhibits reabsorption of calcium and phosphate from all segments of nephron.
ADH (Vasopressin): ▪ ▪
D.
all
Calcitonin: ▪
C.
Stimulates reabsorption of calcium from DCT. Inhibits phosphate reabsorption from segments of nephron. Stimulate 1-alpha-hydroxylase enzyme → ↑ active form of vitamin D.
Increasing permeability to water in DCT and collecting tubules. Used in treatment of diabetes insipidus (pituitary type).
Aldosterone:
A. B.
C.
Renin: ▪
Secreted by juxtaglomerular apparatus.
▪ ▪ ▪ ▪ ▪
PGE2 (medullary) PGI2 (cortical) PGF2α PGD2 Thromboxane A2 (TXA2)
▪
ET1, ET2, ET3, acting on ETA&ETB receptors. Their levels increase in acute and chronic renal failure.
Prostaglandines:
Endothelins: ▪
1.
Absorption: ▪ ▪
2.
Volume of Distribution (Vd): ▪
3.
Impaired due to nausea and vomiting of uremia. Some unabsorbable drugs are absorbed (e.g.aminoglycosides). May be ↑or ↓, leading to change in total dose required (=serum conc. X Vd).
Protein Binding: ▪
Some patients are hypoproteinemic (e.g. nephrotic syndrome), thus increasing free drug level, and needing dose adjustment, esp. in highly protein-bound drugs.
▪
In CRF, excess H+ ocuppy the receptor sites for acidic drugs (e.g. sulpha, penicillin,
Changes in PK and PD of drugs in cases of impaired renal function 1.
Metabolism Biotransformation:
&
Small molecular weight protein and polypeptides (e.g. insulin) should be reduced in diabetics with renal impairment.
5. Renal clearance of drugs:
↓ due to accumulation of drugs or their metabolites.
They are drugs induced impairment of renal functions, which could be:
Pre-Renal Insult: ▪
3.
By drugs decreasing RBF, as: ▪ Drugs induced hypovolemia, e.g. loop diuretics. ▪ Drugs lowering cardiac output, e.g. Βblockers.
Renal Insult:
A. Acute Tubular Necrosis (ATN): • Direct nephrotoxicity resulting from prolonged use of: aminoglycosides, amphotericin B. B. Acute Tubulo-interstitial Nephropathy (ATIN): • Cell-mediated hypersensitivity
Nephrotoxic Drugs A. Chronic Tubulo-interstitial Nephropathy (CTIN): • Induced by: aspirin, paracetamol (analgesic nephropathy), lithium, cisplatin, cyclosporins.
B. Immune Complex Glomerulonephritis:
Mediated
• As: Penicillamine.
C. Nephrotic syndrome: • Induced by: heavy metals (e.g. gold, mercury), Penicillamine, lithum, NSAIDs, captopril, probenicid, rifampicin.
1. Drug
Elimination (Clearance). 2. Secretion of Drugs. 3. Activation, Inactivation and Biotransformation of Drugs. 4. Secretion of Hormones.
It is controlled by the following factors:
Renal Blood Flow and Glomerular Filtration: ▪ ▪
C.
Increased by: vasodilators, digoxin, methyl xanthines. Decreased by: vasoconsrictors, ACEIs, ARBs, βblockers, verapamil.
Changes of PH of the Filtrate: ▪ ▪ ▪ ▪
Acidic drugs (e.g. salicylates) are better eliminated in alkaline urine. Basic drugs (e.g. Atropine) are better eliminated in acidic urine. Acidification of urine is produced by: Ascorbic acid , ammonium chloride. Alkalization of urine is produced by: sodium bicarbonate, sodium lactate, sodium citrate.
Tubular secretion of drugs or body excreta (e.g. uric acid) occurs in the proximal convoluted tubules, as: ▪ ▪
Some drugs inhibit the tubular secretion of other drugs→↑plasma levels of the latter, as: ▪ ▪
Acidic drugs (Anions): penicillins, thiazides, loop diuretics, salicylates. Basic drugs (Cations): atropine, quinidine, morphine, amiloride.
Probenicid inhibits tubular secretion of penicillins, cephalosporins →Beneficial effect. Quinidine inhibits tubular secretion of digitalis →digitalis toxicity.
Some drugs inhibit the tubular secretion of other drugs→ inhibit their
In the kidney vitamin D is converted to its active form [1,25(OH)2 Cholecalciferol], by 1alpha-hydroxylase enzyme. Some drugs are inactivated in the kidney, as imipinem (beta lactam antibiotic) is inactivated by renal dihydropeptidase (DHP). Oxidation of salicylates and acetaminophen in renal tissues shares for pathogenesis of renal toxicity of these drugs. Small molecular weight protein and polypeptides (e.g. insulin) are
As, secretion of erythropoeitin (EPO), to stimulate bone marrow or RBCs production. So, in CRF, anemia is a sign, which can be treated by EPO.
A.
Parathyroid Hormone (PTH): ▪ ▪ ▪
B.
Inhibits reabsorption of calcium and phosphate from all segments of nephron.
ADH (Vasopressin): ▪ ▪
D.
all
Calcitonin: ▪
C.
Stimulates reabsorption of calcium from DCT. Inhibits phosphate reabsorption from segments of nephron. Stimulate 1-alpha-hydroxylase enzyme → ↑ active form of vitamin D.
Increasing permeability to water in DCT and collecting tubules. Used in treatment of diabetes insipidus (pituitary type).
Aldosterone:
A. B.
C.
Renin: ▪
Secreted by juxtaglomerular apparatus.
▪ ▪ ▪ ▪ ▪
PGE2 (medullary) PGI2 (cortical) PGF2α PGD2 Thromboxane A2 (TXA2)
▪
ET1, ET2, ET3, acting on ETA&ETB receptors. Their levels increase in acute and chronic renal failure.
Prostaglandines:
Endothelins: ▪
1.
Absorption: ▪ ▪
2.
Volume of Distribution (Vd): ▪
3.
Impaired due to nausea and vomiting of uremia. Some unabsorbable drugs are absorbed (e.g.aminoglycosides). May be ↑or ↓, leading to change in total dose required (=serum conc. X Vd).
Protein Binding: ▪
Some patients are hypoproteinemic (e.g. nephrotic syndrome), thus increasing free drug level, and needing dose adjustment, esp. in highly protein-bound drugs.
▪
In CRF, excess H+ ocuppy the receptor sites for acidic drugs (e.g. sulpha, penicillin,
Changes in PK and PD of drugs in cases of impaired renal function 1.
Metabolism Biotransformation:
&
Small molecular weight protein and polypeptides (e.g. insulin) should be reduced in diabetics with renal impairment.
5. Renal clearance of drugs:
↓ due to accumulation of drugs or their metabolites.
They are drugs induced impairment of renal functions, which could be:
Pre-Renal Insult: ▪
3.
By drugs decreasing RBF, as: ▪ Drugs induced hypovolemia, e.g. loop diuretics. ▪ Drugs lowering cardiac output, e.g. Βblockers.
Renal Insult:
A. Acute Tubular Necrosis (ATN): • Direct nephrotoxicity resulting from prolonged use of: aminoglycosides, amphotericin B. B. Acute Tubulo-interstitial Nephropathy (ATIN): • Cell-mediated hypersensitivity
Nephrotoxic Drugs A. Chronic Tubulo-interstitial Nephropathy (CTIN): • Induced by: aspirin, paracetamol (analgesic nephropathy), lithium, cisplatin, cyclosporins.
B. Immune Complex Glomerulonephritis:
Mediated
• As: Penicillamine.
C. Nephrotic syndrome: • Induced by: heavy metals (e.g. gold, mercury), Penicillamine, lithum, NSAIDs, captopril, probenicid, rifampicin.
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