CLINICAL USE OF MONOCLONAL

ANTIBODIES
Abciximab Anti-platelet-antagonist of IIb/IIIa
receptors
Infliximab Binds TNF, Rheumatoid arthritis and
Crohn disease
Trastuzumab Breast cancer- antagonist to ERB-B2
(Her2/neu)
Dacliximab Bloks interlukin-2 receptors, Kidney
transplants
Muromonab Blocks allograft rejections-Kidney
transplants
Rituximab Binds to surface protein-Non-Hodgkins
lymphoma
Palvizumab Blocks RSV protein
PRODRUG ACTIVE FORM USE
Dipivefrine Epinephrine Glaucoma
Levodopa Dopamine Parkinsonism
Sulindac Sulindac sulfide NSAID
Hydrazide Hydrazide derivative Depression
Enalapril Enalaprilat HT, CHF
Alpha-methyldopa Alpha-methylnorepinephrine HT
Sulfasalazine, 5-Aminosalicylic acid Ulcerative colitis,
Osalazine Rheumatoid arthritis
Prednisone Prednisolone Glucocorticoid
Cyclophosphamide Aldophosphamide Cancer
Becampicillin Ampicillin Broad spectrum pencillin
Chloramphenicol Chloramphenicol Antibiotic
palmitate
Proguanil Proguanil triazine Malaria
Valaciclovir Acyclovir Herpes
Famciclovir Penciclovir Herpes
Sulfasalazine 5 ASA Ulcerative colitis
(5-Amino Salicylic Acid)

DRUGS THAT PROLONG Q-T INTERVAL (HAVE POTENTIAL TO

PRECIPITATE TORSADES DE POINTES)
1. Antiarrhythmics : Quinidine, procainamide, disopyramide,
propafenone, amiodarone, SOTALOL
2. Antimicrobials : quinine, mefloquine, artemisinin,
halofantrine, sparfloxacin
3. Antihistaminics : Terfenadine, astemizole, ebastine
4. Antidepressant : Amitryptyline and other tricyclics
5. Antipsychotics : Thioridazine, risperidone
6. Prokinetic : Cisapride

ACTION OF DRUGS USED IN SHOCK

Receptors
Drug
Dopamine Beta1 Beta2 Alpha
Adrenaline $ Noradrenaline $$ – +++ +++ ++
– ++ – ++
(small doses) (large doses)
Dopamine ++ + – +

1
 Dobutamine – ++ + +
Isoprenaline – +++ +++ –
Glucagon: Positive inotropic and chronotropic action independent of beta-adrenergic receptors
$ Low doses elevate systolic and decrease diastolic pressure; higher doses elevate both
$$ Both systolic and diastolic pressured elevated
Dobutamine is a more potent ionotropic agent than isoprenaline
DRUG INTERACTIONS WITH NSAIDS
Pharmacodynamic
Diuretics Reduced diuresis
Beta blocker Reduces anti-hypertensive effect
ACE inhibitor Reduced anti-hypertensive effect
Anticoagulants Increased risk of bleeding
Sulfonylurea Increased risk of hypoglycemia
Alcohol Increased risk of GI bleeding
Cyclosporine Increased nephrotoxicity
Corticosteroids Increased risk of GI bleeding
Pharmacokinetic
Oral anticoagulants, Sulfonylurea, Metabolism inhibited; competition for
phenytoin, Valproate plasma binding
Digoxin, Lithium, Reduced renal excretion of interacting
Aminoglycosides, Methotrexate drug

Drug-induced pancreatitis

Class I medications (medications implicated in greater than 20 reported cases of acute pancreatitis with at least one
documented case following reexposure):

Didanosine, asparaginase, azathioprine, valproic acid, pentavalent antimonials, pentamidine, mercaptopurine,

mesalamine, estrogen preparations, opiates, tetracycline, cytarabine, steroids, trimethoprim/sulfamethoxazole,
sulfasalazine, furosemide, and sulindac.

Class II medications (medications implicated in more than 10 cases of acute pancreatitis):

Rifampin, lamivudine, octreotide, carbamazepine, acetaminophen, phenformin, interferon alfa-2b, enalapril,

hydrochlorothiazide, cisplatin, erythromycin, and cyclopenthiazide.

Drug-induced lupus

The most common medicines known to cause drug-induced lupus are:

Isoniazid

Hydralazine

Procainamide

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Other less common drugs may also cause the condition. These may include:

Anti-seizure medications

Capoten

Chlorpromazine

Etanercept

Infliximab

Methyldopa

Minocycline

Penicillamine

Quinidine

Sulfasalazine

Drug induced pulmonary fibrosis

Amiodarone,

bleomycin,

busulfan,

nitrofurantoin,

methotrexate,

gold,

penicillamine,

and also illicit drugs - eg, crack cocaine, heroin.

Drug-Induced SIADH

Initially, pharmacologic agents that had antidiuretic action were prescribed to treat patients with diabetes
insipidus (DI). Later on, numerous reports documented serious adverse effects, such as water retention
and dilutional hyponatremia, associated with these drugs.

The proposed mechanism by which a drug interferes with the normal secretion and action of ADH
depends on the drug. Drugs that stimulate the release of ADH from the posterior pituitary gland
include nicotine, phenothiazines, and tricyclics. Some drugs increase or potentiate the renal
action of ADH. They include desmopressin, oxytocin, and prostaglandin synthesis inhibitors.

3
Drugs that cause SIADH by means of mixed or uncertain mechanism of action include
chlorpropamide, carbamazepine, cyclophosphamide, and vincristine

In 1994, researchers reported the first case suggesting a cause-effect relationship between omeprazole
and SIADH. However, the mechanism of omeprazole-induced SIADH needs to be established.

Ecstasy, or 3,4 methylene dioxymethamphetamine (MDMA), a powerful derivative of amphetamine that is

popular among adolescents, can cause SIADH. However, the mechanism of MDMA-induced SIADH is
not well understood.

SIADH induced by angiotensin-converting enzyme (ACE) inhibitors (eg, lisinopril) is a rare but possible
adverse effect of this category of drugs.The SIADH-type of dilutional hyponatremia induced by ACE
inhibitors may be mediated by the potentiation of the action of plasma renin, which results in increased
levels of brain angiotensin.This, in turn, results in the release of AVP from the hypothalamus and an
increase in thirst.

Drug-induced diabetes insipidus

Lithium, demeclocycline, foscarnet, Amphotericin B, Orlistat, Ifosfomide, Ofloxacin, Cidofovir,

Vaptanes.

Treatment is symptomatic in most patients and the offending drug should be stopped. If urine volumes
exceed 4 L/day, treatment with thiazides and amiloride has been advocated, and nonsteroidal anti-
inflammatory drugs, such as indomethacin, may be tried in severe cases.

Drugs withdrawn from the market secondary to hepatotoxicity / severe

limitations/precautions

In the last few years, the US Food and Drug Administration (FDA) has withdrawn 2 drugs from the market
for causing severe liver injury: bromfenac (NSAID) and troglitazone ( a thiazolidinedione was approved in
1997 as an antidiabetic agent. Over 3 years, more than 90 cases of hepatotoxicity were reported, which
resulted in withdrawal of this drug).

Kava kava, an herb used for anxiety, was reported as being hepatotoxic and was withdrawn from the
German market. The FDA has also issued a warning in this country. This demonstrates the importance of
postmarketing surveillance to identify reactions that are not reported or are underreported in drug trials.

Pemoline (Cylert), used for attention deficit disorder and narcolepsy is no longer available in the United
States. The Food and Drug Administration (FDA) concluded that the overall risk of liver toxicity from
pemoline outweighs the benefits.

Other drugs that have significant limitations of use because of their hepatotoxic effects are
felbamate (Felbatol), an antiepileptic used for complex partial seizures; zileuton (Zyflo), indicated
for asthma; tolcapone (Tasmar), used for Parkinson disease; trovafloxacin (Trovan), an antibiotic;
benoxaprofen, an NSAID; and tienilic acid, a diuretic.

Also remember the risk of hepatic injury with Acetaminophen and how to manage it.

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In April 2010, the US Food and Drug Administration (FDA) had added a boxed warning, the strongest
warning issued by the FDA, to the prescribing information for propylthiouracil. The boxed warning
emphasizes the risk for severe liver injury and acute liver failure, some of which have been fatal.

Severe hepatic injury, including cases of hepatic failure, has been reported in patients taking interferon
beta-1a (Avonex) used in treatment of multiple sclerosis.

In October 2005, the manufactures of duloxetine (an anti-depressant) reported postmarketing cases of
hepatitis and cholestatic jaundice.

Pathological manifestations of drug-induced hepatotoxicity are as follows:

 Acute hepatocellular injury

 Acute viral hepatitis–like picture - INH, halothane, diclofenac, troglitazone

 Mononucleosis like picture - Phenytoin, sulfonamides, dapsone

 Chronic hepatocellular injury - Pemoline, methyldopa

 Massive necrosis - Acetaminophen, halothane, diclofenac

 Steatosis

 Macrovesicular steatosis - Alcohol, methotrexate, corticosteroids, minocycline, nifedipine, TPN

 Microvesicular steatosis - Alcohol, valproic acid, tetracycline, piroxicam

 Steatohepatitis - Amiodarone, nifedipine, synthetic estrogens, didanosine

 Pseudoalcoholic injury - Amiodarone

 Acute cholestasis - Amoxicillin-clavulanic acid, erythromycin, sulindac

 Chronic cholestasis - Chlorpromazine, sulfamethoxazole-trimethoprim, tetracycline, ibuprofen

 Granulomatous hepatitis - Carbamazepine, allopurinol, hydralazine

 Vascular injury - Steroids

 Neoplasia - Contraceptives, anabolic steroids

 Adenoma - Steroids

 Angiosarcoma - Vinyl chloride

 Hepatocellular carcinoma - Anabolic steroids, aflatoxin, arsenic, vinyl chloride

5
Drugs causing Gynacomastia

Drugs causing Ototoxicity

Aminoglycoside antibiotics (e.g., kanamycin, neomycin, amikacin, streptomycin, gentamicin)

Loop diuretics (e.g., furosemide, ethacrynic acid, bumetanide)

Antineoplastics. Cisplatin

Salicylates

Quinine

Phototoxic drugs

Common phototoxic drugs include the following:

Antibiotics

* the quinolones [for example, ciprofloxacin (Cipro, Cipro XR, Proquin XR), levofloxacin
(Levaquin)]

* tetracyclines [for example, tetracycline (Achromycin), doxycycline (Vibramycin, Oracea,

Adoxa,

Atridox and others)]

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 * sulfonamides [for example, sulfamethoxazole and trimethoprim; cotrimoxazole (Bactrim,
Septra),

sulfamethoxazole (Gantanol)]

Antihistamines

* diphenhydramine (Benadryl)

Malaria medications

* quinine (Quinerva, Quinite, QM-260)

* chloroquine (Aralen)

* hydroxychloroquine (Plaquenil)

Cancer chemotherapy drugs

* 5-fluorouracil (5-FU, Efudex, Carac, Fluoroplex)

* vinblastine (Velban, Velsar)

* dacarbazine (DTIC-Dome)

Cardiac drugs

* amiodarone (Cordarone)

* nifedipine (Procardia)

* quinidine (Quinaglute, Quinidex)

* diltiazem (Cardizem, Dilacor, Tiazac)

Diuretics

* furosemide (Lasix)

* thiazides [hydrochlorothiazide (Hydrodiuril)

Diabetic drugs

* sulfonylureas [chlorpropamide (Diabinese), glyburide (Micronase, DiaBeta, Glynase)]

Painkillers

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 * Non-steroidal antiinflammatory drugs [naproxen (Naprosyn, Naprelan, Anaprox, Aleve),
piroxicam

(Feldene)

Skin medications

* photodynamic therapy for skin cancer [ALA or 5-aminolevulinic acid (Levulan), Methyl-5-

aminolevulinic acid)

Acne medications

* isotretinoin (Accutane)

* acitretin (Soriatane)

Psychiatric drugs

* phenothiazines [chlorpromazine (Thorazine)]

* tricyclic antidepressants [desipramine (Norpramin), imipramine (Tofranil)

Imp points regarding Vitamins

 Iron deficiency causes hypochromic microcytic anemia, whereas folic acid or vitamin B 12
deficiency causes megaloblastic anemia.
 Ferrous sulfate and other ferrous salts are administered orally for several months in the treatment
of iron deficiency anemia.
 Folic acid supplementation is used during pregnancy to prevent anemia and birth defects.
 Folic acid treatment can partly mask the hematologic effect of vitamin B 12 deficiency but does not
prevent irreversible neurologic damage.
 Pernicious anemia is caused by inadequate secretion of intrinsic factor and reduced vitamin B 12
absorption. It is treated with intramuscular injections of cyanocobalamin or hydroxocobalamin.
 Epoetin-α, epoetin-β, and darbepoetin-α are recombinant forms of human erythropoietin
used to treat anemia caused by chronic renal failure, cancer-related anemia, and anemia caused
by other conditions.
 Filgrastim, pegfilgrastim, and sargramostim are recombinant forms of G-CSF or GM-CSF.
They are used to treat neutropenia associated with cancer chemotherapy, bone marrow
transplantation, and various disease states.
 ISOTRETINOIN
o Isotretinoin is a medication used for the treatment of severe acne. Isotretinoin is
classified as a retinoid, made from a synthetic form of vitamin A. It is taken orally,
in pill form, once or twice daily.
o MOA:Isotretinoin's exact mechanism of action is unknown. Recent research
suggests that the drug amplifies production of neutrophil-gelatinase associated
lipocalin (NGAL) in the skin, which has been shown to reduce sebum
production by inducing apoptosis in sebaceous gland cells while exhibiting
an antimicrobial effect on Propionibacterium acnes. The drug decreases the

8
 size and sebum output of the sebaceous glands. Isotretinoin's combined impact
on several of acne's contributory factors distinguishes isotretinoin from alternative
remedies such as antibiotics and accounts for its greater efficacy in severe,
nodulocystic cases.
o The effect on sebum production is temporary. However, remission of the disease
can be "complete and prolonged.
o Increasingly higher dosages will result in higher toxicity, resembling vitamin A
toxicity.
o Adverse drug reactions associated with isotretinoin therapy include:
o Common: Extreme severe acne flare, dryness of skin, lips and mucous
membranes, infection of the cuticles, cheilitis, itch, rosacea, skin fragility, skin
peeling, rash, flushing, nose bleeds, dry eyes, diffuse alopecia areata, eye
irritation, conjunctivitis, reduced tolerance to contact lenses, hyperlipidaemia,
raised liver enzymes, permanent thin skin, headaches, temporary/permanent hair
thinning (this could start or continue after treatment), myalgia and/or arthralgia,
back pain.
o Infrequent: mild acne flare, raised blood glucose level, decreased libido/erectile
dysfunction, increased erythrocyte sedimentation rate, fatigue.
o Rare: impaired night vision; cataracts; optic neuritis; menstrual disturbances;
inflammatory bowel disease; pancreatitis; hepatitis; corneal opacities;
papilloedema; idiopathic intracranial hypertension; skeletal hyperostosis;
extraosseous calcification; psychosis; depression.

Drugs causing Short term memory loss

All the drugs below cause some degree of memory loss. The drugs listed in bold print indicates an
incidence of memory loss in 3% or more of users. Where possible we have noted the actual percentage
of users who experience memory loss with each drug. Special attention should be paid by users of
Xanax. Of all the drugs on the market, this drug has the highest incidence of memory loss in users.

• Abilify - Otsuka America (aripiprazole) Tablets

• Ambien see note below - Sanofi-Synthelabo (zolpidem tartrate)

• Abilify - Bristol-Myers Squibb (aripiprazole) Tablets

• Cogentin Injection - Merck (Benztropine Mesylate)

• Copaxone - Teva Neuroscience (glatiramer acetate injection)

• Copaxone tablets - Roche Laboratories (ribavirin, USP)

• Copegus tablets - 6% - Roche Laboratories (ribavirin, USP)

• Cozaar tablets - Merck (losartan potassium tablets)

9
• Eldepryl capsules (Somerset) (SELEGILINE HYDROCHLORIDE)

• Eskalith - GlaxoSmithKline (lithium carbonate)

• Eskalith - GlaxoSmithKline (lithium carbonate)

• Gleevec - Novartis (imatinib mesylate)

• Hyzaar tablets - Merck (losartan potassium-hydrochlorothiazide tablets)

• Imitrex Nasal Spray - GlaxoSmithKline (sumatriptan)

• Imitrex tablets - GlaxoSmithKline (sumatriptan succinate)

• Klonopin tablets - 4% - Roche Laboratories (clonazepam)

• Klonopin wafers - 4% - Roche Laboratories (clonazepam orally disintegrating)

• Lamictal tablets - GlaxoSmithKline (lamotrigine)

• Lamictal chewable dispersible tablets - GlaxoSmithKline (lamotrigine)

• Lupron Depot 3.75 mg - 6% - TAP (leuprolide acetate for depot suspension)

• Lupron Depot-3 Month 11.25 mg - TAP (leuprolide acetate for depot suspension)

• Lupron injection - TAP (leuprolide acetate)

• Maxalt tablets - Merck (rizatriptan benzoate)

• Maxalt-MLT orally disintegrating tablets - Merck (rizatriptan benzoate)

• Parcopa orally disintegrating tablets - Schwarz (carbidopa-levodopa)

• Pegasys - 5% - Roche Laboratories (peginterferon alfa-2a)

• Prinivil tablets - Merck (Lisinopril)

• Prinzide tablets - Merck (Lisinopril-Hydrochlorothiazide)

• Rifamate capsules - Aventis (rifampin and isoniazid)

• Rifater tablets - Aventis (rifampin, isoniazid and pyrazinamide)

• Roferon -A - Roche Laboratories (Interferon alfa-2a, recombinant)

• Seromycin capsules - Lilly (Cycloserine)

• Stalevo 50, 100 and 150 tablets - Novartis (carbidopa, levodopa and entacapone)

10
• Timolide tablets - Merck (Timolol Maleate-Hydrochlorothiazide)

• Topamax tablets - 3.2% - Ortho-McNeil (topiramate)

• Topamax sprinkle capsules - 3.2% - Ortho-McNeil (topiramate capsules)

• Transderm Scop - Novartis (scopolamine 1.5 mg Transdermal Therapeutic System)

• Vesanoid capsules - 3% - Roche Laboratories (tretinoin)

• Wellbutrin - GlaxoSmithKline (bupropion hydrochloride)

• Wellbutrin SR sustained-release tablets - GlaxoSmithKline (bupropion hydrochloride)

• Wellbutrin XL extended-release tablets - GlaxoSmithKline (bupropion hydrochloride)

• Xanax - 33.1%- Pharmacia & Upjohn (alprazolam)

• Xanax XR - 15.4% extended-release tablets - Pharmacia & Upjohn (alprazolam)

• Zonegran capsules - 6% - Eisai (zonisamide)

• Zyban Sustained-Release tablets - GlaxoSmithKline (bupropion hydrochloride)

Note: Although not expressed as a percentage, Ambien has been documented to cause a "significant
decrease in next-morning recall" of information presented to subjects.

Management of Headaches:

* Migraine, the most common headache disorder, is believed to result from neurovascular dysfunction at several
levels in the CNS. Cerebral vasoconstriction and ischemia are followed by vasodilation, inflammation, and a
unilateral, pulsatile headache.
* Drugs for migraine prophylaxis should aim to reduce the frequency of migraine attacks by 50%. These include
anticonvulsants (valproate), antidepressants (amitriptyline and fluoxetine), NSAIDs (naproxen), β-adrenoceptor
antagonists (propranolol, timolol), calcium channel blockers (verapamil, nimodipine), and serotonin 5-HT2 receptor
antagonists (methysergide).

* Prophylactic drugs often must be taken for 3 to 4 weeks before benefits are observed.

* Drugs for aborting migraine headaches include ergot alkaloids (ergotamine and dihydroergotamine) and so-
called triptan drugs (sumatriptan and others). These drugs act primarily by stimulating serotonin 5-HT1D/1B
receptors. This stimulation causes cerebral vasoconstriction, inhibits the release of peptides and other mediators of
inflammation and vasodilation from trigeminal neurons, and inhibits activation of the trigeminal nucleus in the brain
stem.

* Ergot alkaloids and triptan drugs can cause marked vasoconstriction, so their dosage and frequency of use must
be restricted to avoid rebound headache and adverse effects. Common adverse effects of ergots include nausea,
vomiting, and muscle cramps; those of triptans include chest tightness and drowsiness. Use of ergots or triptans is
contraindicated in patients with coronary artery disease.

* Other agents for aborting migraine headaches include NSAIDs (e.g., naproxen), opioid analgesics (e.g.,
tramadol), and a sympathomimetic drug called isometheptene.

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 * Cluster headaches can be prevented with lithium, methysergide, or verapamil. They can be terminated with ergot
alkaloids, sumatriptan, inhaled oxygen, intranasal lidocaine, or glucocorticoids.

* Tension headaches often respond to NSAIDs and muscle relaxants. Nonpharmacologic therapies (e.g.,
biofeedback and physiotherapy) are also useful.

TREATMENT OF CHRONIC OPEN-ANGLE GLAUCOMA

In the normal eye, aqueous humor is secreted by the ciliary processes and flows through the pupillary aperture of the
iris and into the anterior chamber. It then drains through the trabecular meshwork in Schlemm's canal. In patients with
open-angle glaucoma, persistently elevated intraocular pressure is associated with narrowing of the anterior chamber
angle, a decrease in the rate of aqueous outflow, and the gradual loss of peripheral vision.

Various types of drugs can be used to reduce intraocular pressure before irreversible optic nerve damage occurs.
The sites of action of these drugs are shown below.

Some types of drugs act by enhancing the drainage of aqueous humor. Muscarinic receptor agonists (e.g.,
pilocarpine) stimulate the contraction of meridional ciliary muscle fibers that insert near the trabecular meshwork.
Contraction of these fibers opens the trabecular spaces so that aqueous humor drains more easily.

Prostaglandins (e.g., latanoprost) increase aqueous drainage through an alternative pathway known as the
uveoscleral route. In this pathway, aqueous humor flows through the ciliary muscles into the suprachoroidal space.

Other types of drugs act by reducing the amount of aqueous humor produced by the ciliary processes. The β-
adrenoceptor blockers (e.g., timolol) and the α2-adrenoceptor agonists (e.g., apraclonidine) reduce the formation
of cyclic AMP, a substance that stimulates aqueous humor production. Carbonic anhydrase inhibitors (e.g.,
dorzolamide) block the formation of bicarbonate by carbonic anhydrase, an enzyme that is required for aqueous
humor secretion. Epinephrine probably acts by reducing blood flow in the ciliary processes.

AGENTS ACTING ON NEUROMUSCULAR JUNCTION AND

AUTONOMIC GANGLIA
Drug Effect on Effect on cardiac Tendency to cause
autonomic muscarinic receptor histamine release

12
 ganglion
(A) Isoquinoline derivatives
Atracurium None None Yes
Doxacurium None None Yes
Metocurine Weak block None Yes
Mivacurium More None Yes
Tubocurarine Weak block None Yes
(B) Steroid derivatives
Pancuronium None Moderate block Lesser tendency
Pipecuronium None None Lesser tendency
Rocuronium None Slight Lesser tendency
Vecuronium None None Lesser tendency
(C) Other agents
Gallamine None Strong block None
Succinyl choline Stimulation Stimulation Yes

Drugs which are highly

Drugs which are poorly protein bound
protein bound
Aspirin, Indomethacin Paracetamol
Warfarin Atenolol, Metaprolol
Tolbutamide,
Gentamicin, Amikacin, Tobramycin
Chlorpropamide
Digitoxin (but not digoxin) Acyclovir
Phenytoin, valproic acid Ethambutol
Imipramine,
Metronidazole
Chlordiazepoxide
Nifedipine, Verapamil Ranitidine
Drugs which are not bound to
Propranolol
proteins
Prazosin Ethosuximide
Furosemide Lithium
Erythromycin, Rifampicin INH
Ribavirin

Nephrotoxic drugs

Antibiotics

* Aminoglycosides (10-15% Incidence of Acute Tubular Necrosis)

* Sulfonamides

* Amphotericin B (Incidence 80-90%)

* Levofloxacin

* Ciprofloxacin

* Rifampin

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 * Tetracycline

* Acyclovir (only nephrotoxic in intravenous form)

* Pentamidine

Chemotherapy and Immunosuppressants

* Cisplatin

* Methotrexate

* Mitomycin

* Cyclosporine

Heavy Metals

* Mercury Poisoning

* Lead Poisoning

* Arsenic Poisoning

* Bismuth

* Lithium related kidney disorders

* Polydipsia and Nephrogenic Diabetes Insipidus

* Acute Renal Failure

* Chronic kidney disease with fibrosis

AntiHyperlipidemics

* Statins

* Gemfibrozil

* Associated with Acute Renal Failure due to Rhabdomyolysis

* Fenofibrate (Tricor)

* Increases Serum Creatinine without significant decrease in GFR

* Serum Creatinine rise is reversible on stopping Fenofibrate

Chemotherapy

* Cisplatin

* Ifosphamide

* Causes Fanconi's Syndrome

14
Miscellaneous Drugs

* Chronic Stimulant Laxative use

* Resulting chronic volume depletion and Hypokalemia causes nephropathy

* Radiographic contrast

* ACE Inhibitors

* Expect an increase of Serum Creatinine in Chronic kidney disease

* NSAIDs

* Aspirin

* Low dose Aspirin reduces Renal function in elderly

* Mesalamine (Asacol, Pentasa)

o Mesalamine is an NSAID analog and has systemic absorption from the bowel

* Penicillins and Cephalosporins

* Hypersensitivity (fever, rash, arthralgia)

* Sulfonamides

* Vasculitis reaction

* NSAIDs

* Nephrotic Syndrome type reaction

* Rifampin

* Diuretics (Thiazides and furosemide)

* Allopurinol

* Cimetidine

* Ciprofloxacin

* Dilantin

Drugs of abuse

* Cocaine

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