• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/3

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

3 Cards in this Set

  • Front
  • Back

What

Q

What

Q

This site is intended for healthcare professionalsMedscape LogoDrugs & Diseases > NephrologyProteinuria MedicationUpdated: Apr 28, 2018 Author: Beje Thomas, MD; Chief Editor: Vecihi Batuman, MD, FASN more...Share FeedbackSECTIONSMedication SummaryAngiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) reduce intraglomerular pressure by inhibiting angiotensin II ̶ mediated efferent arteriolar vasoconstriction. [34] These drugs also have a proteinuria-reducing effect that is independent of their antihypertensive effect.In addition, ACE inhibitors have renoprotective properties, which may be partially due to the other hemodynamic and nonhemodynamic effects of these drugs. ACE inhibitors reduce the breakdown of bradykinin (an efferent arteriolar vasodilator); restore the size and charge selectivity to the glomerular cell wall; and reduce the production of cytokines, such as transforming growth factor–beta (TGF-beta), that promote glomerulosclerosis and fibrosis.ACE InhibitorsClass SummaryACE inhibitors reduce intraglomerular pressure and may restore size and charge integrity to the GCW. They also reduce level of profibrotic cytokines. ACE inhibitors reduce proteinuria and also reduce rate of deterioration of renal function in patients with diabetic and nondiabetic renal disease associated with proteinuria.Lisinopril (Zestril, Prinivil)View full drug informationLisinopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. The target blood pressure is less than 125/75 mm Hg in patients with proteinuria of greater than 1 g/day.Patients who develop a cough, angioedema, bronchospasm, or other hypersensitivity reactions after starting ACE inhibitors should receive an angiotensin receptor blocker.Ramipril (Altace)View full drug informationRamipril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.CaptoprilView full drug informationCaptopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.Enalapril (Vasotec)View full drug informationEnalapril is a competitive inhibitor of ACE. It reduces angiotensin II levels, decreasing aldosterone secretion.Angiotensin II Receptor Antagonists (ARBs)Class SummaryAngiotensin II receptor blockers reduce blood pressure and proteinuria, protecting renal function and delaying the onset of end-stage renal disease.Candesartan (Atacand)View full drug informationCandesartan blocks the vasoconstrictive and aldosterone-secreting effects of angiotensin II. It may induce more complete inhibition of the renin-angiotensin system than ACE inhibitors do. In addition, candesartan does not affect the response to bradykinin and is less likely to be associated with cough and angioedema. This drug can be used in patients who are unable to tolerate ACE inhibitors.Eprosartan (Teveten)View full drug informationEprosartan is a nonpeptide angiotensin II receptor antagonist that blocks the vasoconstrictive and aldosterone-secreting effects of angiotensin II. It may induce more complete inhibition of the renin-angiotensin system than ACE inhibitors do. In addition, eprosartan does not affect the response to bradykinin and is less likely to be associated with cough and angioedema. This drug can be used in patients who are unable to tolerate ACE inhibitors.Irbesartan (Avapro)View full drug informationIrbesartan blocks the vasoconstrictive and aldosterone-secreting effects of angiotensin II at the tissue receptor site. It may induce more complete inhibition of the renin-angiotensin system than ACE inhibitors do. In addition, it does not affect the response to bradykinin and is less likely to be associated with cough and angioedema.Losartan (Cozaar)View full drug informationLosartan blocks the vasoconstrictive and aldosterone-secreting effects of angiotensin II. It may induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors do. In addition, Losartan does not affect the response to bradykinin and is less likely to be associated with cough and angioedema. It can be used in patients who are unable to tolerate ACE inhibitors.Olmesartan (Benicar)View full drug informationOlmesartan blocks the vasoconstrictive effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptors in vascular smooth muscle. Its action is independent of the pathways for angiotensin II synthesis.Valsartan (Diovan)View full drug informationValsartan is a prodrug that produces direct antagonism of angiotensin II receptors. It displaces angiotensin II from AT1 receptors and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses.Valsartan may induce more complete inhibition of the renin-angiotensin system than ACE inhibitors do. In addition, it does not affect the response to bradykinin and is less likely to be associated with cough and angioedema. Valsartan can be used in patients who are unable to tolerate ACE inhibitors.Diuretics, LoopClass SummaryPatients with fluid overload should be treated with diuretics. Use a combination of diuretics acting at different sites of the nephron (eg, loop diuretic ± thiazide ± spironolactone). They increase urine excretion by inhibiting sodium and chloride transporters.Furosemide (Lasix)View full drug informationFurosemide is the diuretic of choice. It increases excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule.Bumetanide (Bumex)View full drug informationBumetanide increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium, potassium, and chloride reabsorption in the ascending loop of Henle. These effects increase the urinary excretion of sodium, chloride, and water, resulting in profound diuresis. Renal vasodilation occurs after administration, renal vascular resistance decreases, and renal blood flow is enhanced. In terms of effect, 1 mg of bumetanide is equivalent to approximately 40 mg of furosemide.Ethacrynic acid (Edecrin)View full drug informationEthacrynic acid increases the excretion of water by interfering with the chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule. This agent is used only in refractory cases. Continuous IV infusion is preferable in many cases. It is indicated for temporary treatment of edema associated with heart failure when greater diuretic potential is needed.Diuretics, ThiazideClass SummaryPatients with fluid overload should be treated with diuretics. Use a combination of diuretics acting at different sites of the nephron (eg, loop diuretic ± thiazide ± spironolactone). Diuretics are used to treat edema and hypertension. They increase urine excretion by inhibiting sodium and chloride transporters.Metolazone (Zaroxolyn)View full drug informationMetolazone treats edema in congestive heart failure. It increases excretion of sodium, water, potassium, and hydrogen ions by inhibiting reabsorption of sodium in distal tubules. It may be more effective in cases of impaired renal function.Hydrochlorothiazide (Microzide)View full drug informationHydrochlorothiazide inhibits reabsorption of sodium in distal tubules, causing increased excretion of sodium and water as well as potassium and hydrogen ions.Aldosterone Antagonists, SelectiveClass SummaryPatients with fluid overload should be treated with diuretics. Use a combination of diuretics acting at different sites of the nephron (eg, loop diuretic ± thiazide ± spironolactone). Aldosterone antagonists are used to lower the blood pressure and normalize serum potassium.Spironolactone (Aldactone)View full drug informationSpironolactone is the agent most commonly used to treat hyperaldosteronism because it directly antagonizes aldosterone effects at the distal tubule.Calcium Channel AntagonistsClass SummaryThese agents may help to reduce proteinuria.Diltiazem (Cardizem, Dilacor, Tiazac, Dilacor, Cartia XT)View full drug informationDuring depolarization, diltiazem inhibits the influx of extracellular calcium across myocardial and vascular smooth muscle cell membranes. (Serum calcium levels remain unchanged.) The resultant decrease in intracellular calcium inhibits the contractile processes of myocardial smooth muscle cells, resulting in dilation of the coronary and systemic arteries and improved oxygen delivery to the myocardial tissue.Diltiazem decreases conduction velocity in the atrioventricular node. In addition, it increases the refractory period by blocking calcium influx. This, in turn, stops the reentrant phenomenon.The drug decreases myocardial oxygen demand by reducing peripheral vascular resistance, reducing the heart rate by slowing conduction through the sinoatrial and atrioventricular nodes and reducing left ventricular inotropy.Diltiazem slows atrioventricular nodal conduction time and prolongs the atrioventricular nodal refractory period, which may convert supraventricular tachycardia or slow the rate in atrial fibrillation. It also has vasodilator activity but may be less potent than other agents. Total peripheral resistance, systemic blood pressure, and afterload are decreased.Amlodipine (Norvasc)View full drug informationAmlodipine blocks slow calcium channels, causing relaxation of vascular smooth muscles.Nifedipine (Procardia)View full drug informationNifedipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Sublingual administration is generally safe, theoretical concerns notwithstanding.FelodipineView full drug informationFelodipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery. Calcium channel blockers potentiate ACE inhibitor effects. Renal protection is not proven, but these agents reduce morbidity and mortality rates in congestive heart failure. Calcium channel blockers are indicated in patients with diastolic dysfunction. They are effective as monotherapy in black patients and elderly patients.Isradipine (DynaCirc)View full drug informationIsradipine is a dihydropyridine calcium-channel blocker. It inhibits calcium from entering select voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization. This causes relaxation of coronary vascular smooth muscle, which results in coronary vasodilation. Vasodilation reduces systemic resistance and blood pressure, with a small increase in resting heart rate. Isradipine also has negative inotropic effects.Verapamil (Calan, Isoptin, Verelan)View full drug informationDuring depolarization, verapamil inhibits calcium ions from entering slow channels and voltage-sensitive areas of vascular smooth muscle and myocardium. It can diminish premature ventricular contractions (PVCs) associated with perfusion therapy and decrease risk of ventricular fibrillation and ventricular tachycardia.eMedicine LogoQuestionsSECTIONSProteinuriaOverviewPresentationDDxWorkupTreatmentMedicationMedication SummaryACE InhibitorsAngiotensin II Receptor Antagonists (ARBs)Diuretics, LoopDiuretics, ThiazideAldosterone Antagonists, SelectiveCalcium Channel AntagonistsQuestions & AnswersReferencesWhat to Read Next on MedscapeRelated Conditions and DiseasesDialysis Complications of Chronic Renal FailurePerioperative Management of the Patient With Chronic Renal FailureChronic Kidney DiseaseChronic Kidney Disease in ChildrenFast Five Quiz: Is Your Knowledge of Chronic Kidney Disease Sufficient?Anemia of Chronic Disease and Renal FailureNEWS & PERSPECTIVE Implications of the Type 2 Diabetes-Cardiovascular Disease-Chronic Kidney Disease Link: New UnderstandingsThe Case for Cautious Consumption: NSAIDs in Chronic Kidney DiseaseNSAID Kidney Risk Underestimated in Young, Active AdultsTOOLSDrug Interaction CheckerPill IdentifierCalculatorsFormularySLIDESHOW Fingernail and Toenail Abnormalities: Nail the DiagnosisMost Popular ArticlesAccording to Nephrologists NSAID Kidney Risk Underestimated in Young, Active Adults Novel Oral Anticoagulants in Patients With Chronic Kidney Disease and Atrial Fibrillation The Case for Cautious Consumption: NSAIDs in Chronic Kidney Disease Do Neprilysin Inhibitors Have a Role in Patients With CKD? Is Vitamin D3 Bad for the Kidney?View More Medscape LogoFIND US ON ABOUTAbout MedscapePrivacy PolicyCookiesTerms of UseAdvertising PolicyHelp CenterMEMBERSHIPEmail NewslettersManage My AccountAPPSMedscapeMedPulse NewsCME & EducationWEBMD NETWORKWebMDMedicineNeteMedicineHealthRxListWebMD CorporateEDITIONSEnglishDeutschEspañolFrançaisPortuguêsAll material on this website is protected by copyright, Copyright © 1994-2019 by WebMD LLC. This website also contains material copyrighted by 3rd parties.


Q