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Polycystic Kidney Disease Medication

  • Author: Roser Torra, MD, PhD; Chief Editor: Vecihi Batuman, MD, FACP, FASN  more...
 
Updated: Feb 22, 2016
 

Medication Summary

No specific medication is available for autosomal dominant polycystic kidney disease (ADPKD); however, clinical trials with vasopressin 2 receptor antagonists (tolvaptan), somatostatin analogs, and other drugs are ongoing. A 2012 phase III, double-blind, 3-year trial suggested that tolvaptan may modify the natural course of ADPKD. A significant reduction in the increase of renal volume and decline of glomerular filtration rate (GFR) was demonstrated in patients randomized to tolvaptan. There was a high rate of discontinuation due to side effects of the drug, mainly related to polyuria and elevation of liver enzymes.[41]

Further studies may be necessary and tolvaptan should not be prescribed to patients until such time as it is approved by the US Food and Drug Administration for this indication. Currently, the drugs of choice for hypertension related to ADPKD are angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs). Do not treat abdominal pain with nonsteroidal anti-inflammatory drugs (NSAIDs) because of their potential nephrotoxic effect.

Cyst infections require gyrase inhibitors (eg, ciprofloxacin, chloramphenicol, clindamycin). Trimethoprim-sulfamethoxazole is also an effective antibiotic for reaching the inner cavity of the cyst.

Renal failure requires drugs to maintain electrolyte levels (eg, calcium carbonate, calcium acetate, sevelamer, lanthanum carbonate, calcitriol [possibly], diuretics, blood pressure medications). Approximately 62% of patients with renal insufficiency require at least 2 antihypertensive agents for optimal blood pressure control.

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Angiotensin-Converting Enzyme Inhibitors

Class Summary

ACE inhibitors suppress the renin-angiotensin-aldosterone system.

Enalapril (Vasotec)

 

Enalapril is a competitive inhibitor of ACE. It reduces angiotensin II levels, decreasing aldosterone secretion.

Lisinopril (Prinivil, Zestril)

 

This agent prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

Captopril

 

Captopril prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

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Angiotensin II Receptor Antagonists

Class Summary

ARBs interfere with the binding of formed angiotensin II to its endogenous receptor. These agents reduce blood pressure and proteinuria, protecting renal function and delaying onset of end-stage renal disease (ESRD).

Valsartan (Diovan)

 

Valsartan is a prodrug that produces direct antagonism of angiotensin II receptors. It displaces angiotensin II from the AT1 receptor 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, it does not affect response to bradykinin, and it is less likely to be associated with cough and angioedema. It is for use in patients unable to tolerate ACE inhibitors.

Losartan (Cozaar)

 

Losartan is an ARB that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. It may induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, it does not affect the response to bradykinin, and it is less likely to be associated with cough and angioedema. It is used for patients unable to tolerate ACE inhibitors.

Candesartan (Atacand)

 

Candesartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. It may induce more complete inhibition of renin-angiotensin system than ACE inhibitors, it does not affect response to bradykinin, and it is less likely to be associated with cough and angioedema. It is used in patients unable to tolerate ACE inhibitors.

Olmesartan (Benicar)

 

Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking binding of angiotensin II to the AT-1 receptor in vascular smooth muscle. Its action is independent of pathways for angiotensin II synthesis.

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Antibiotics

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Ciprofloxacin (Cipro)

 

Ciprofloxacin inhibits bacterial DNA synthesis and, consequently, growth. It is a fluoroquinolone with activity against pseudomonads, streptococci, methicillin-resistant Staphylococus aureus (MRSA), S epidermidis, and most gram-negative organisms, but no activity against anaerobes. Levofloxacin (Levaquin) overcomes many of these limitations. Continue treatment for at least 2 d (7-14 d typical) after signs and symptoms have disappeared.

Levofloxacin (Levaquin)

 

Levofloxacin inhibits growth of susceptible organisms by inhibiting DNA gyrase and promoting breakage of DNA strands.

Trimethoprim-sulfamethoxazole (Bactrim, Bactrim DS, Septra, Septra DS)

 

This agent inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.

Clindamycin (Cleocin)

 

Clindamycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Chloramphenicol

 

Chloramphenicol binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. It is effective against gram-negative and gram-positive bacteria.

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Phosphate Binders

Class Summary

Administer phosphate binders to maintain phosphate levels in renal failure.

Calcium Acetate ( PhosLo, Eliphos)

 

Calcium acetate reduces the phosphorus load.

Lanthanum carbonate (Fosrenol)

 

Lanthanum is a noncalcium, nonaluminum phosphate binder indicated for reduction of high phosphorus levels in patients with ESRD. It directly binds dietary phosphorus in the upper GI tract, thereby inhibiting phosphorus absorption.

Sevelamer hydrochloride (Renagel, Renvela)

 

This polymeric phosphate binder for oral administration does not contain aluminum. Thus, aluminum intoxication is not a concern.

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Contributor Information and Disclosures
Author

Roser Torra, MD, PhD Consulting Staff, Hereditary Renal Diseases, Department of Nephrology, Fundacio Puigvert, Spain

Roser Torra, MD, PhD is a member of the following medical societies: American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

George R Aronoff, MD Director, Professor, Departments of Internal Medicine and Pharmacology, Section of Nephrology, Kidney Disease Program, University of Louisville School of Medicine

George R Aronoff, MD is a member of the following medical societies: American Federation for Medical Research, American Society of Nephrology, Kentucky Medical Association, National Kidney Foundation

Disclosure: Nothing to disclose.

Chief Editor

Vecihi Batuman, MD, FACP, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System

Vecihi Batuman, MD, FACP, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology

Disclosure: Nothing to disclose.

Additional Contributors

Laura Lyngby Mulloy, DO, FACP Professor of Medicine, Chief, Section of Nephrology, Hypertension, and Transplantation Medicine, Glover/Mealing Eminent Scholar Chair in Immunology, Medical College of Georgia, Georgia Regents University

Disclosure: Nothing to disclose.

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Polycystic kidney disease and massive polycystic liver disease.
 
 
 
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