eMedicine Specialties > Nephrology > Cystic Diseases of the Kidney

Polycystic Kidney Disease: Treatment & Medication

Author: Roser Torra, MD, PhD, Consulting Staff, Hereditary Renal Diseases, Department of Nephrology, Fundacio Puigvert, Spain
Contributor Information and Disclosures

Updated: Sep 17, 2009

Treatment

Medical Care

  • Ensure that a patient with ADPKD who is nonhypertensive and has normal renal function undergoes blood testing and ultrasonographic scanning once a year.
  • Schedule more frequent follow-up studies for patients with high blood pressure. Hypertension is common, occurring in as many as 50-70% of patients before the onset of renal failure.
  • Patients with renal failure require more frequent monitoring, based on the severity of their condition.
  • Medical therapy is necessary to accomplish the following:
    • Control blood pressure. In patients with renal disease, the goal is a blood pressure of less than 130/88 mm Hg. If more than 1 g/d of urinary protein is present, the target blood pressure is less than 125/75 mm Hg. Achieving good blood pressure control helps slow the progression of renal disease.
    • The best drugs for this condition are ACE inhibitors (ie, captopril, enalapril, lisinopril) or angiotensin II receptor antagonist blockers (ie, telmisartan, losartan, irbesartan, candesartan). Calcium channel blockers are not recommended.
    • Control abnormalities related to renal failure (ie, hyperkalemia, hyperphosphatemia, hypocalcemia, hyperparathyroidism, acidosis).
    • Treat urinary tract infections, which occur in 30-50% of patients and most frequently in women. Gram-negative bacteria are the most common pathogens.
    • Reduce abdominal pain produced by enlarged kidneys.
    • Avoid nonsteroidal anti-inflammatory drugs (NSAIDs).
    • With heart murmurs, institute routine American Heart Association antibiotic prophylaxis.
    • Treatment involves surgical cyst decompression, which is effective for pain relief in 60-80% of patients. See Surgical Care.
    • Distinguishing between infections of the bladder, renal parenchyma, and cysts is important because the treatment for each condition is different. Treating infected cysts requires antibiotics that penetrate into the cyst. Useful agents are ciprofloxacin, trimethoprim-sulfamethoxazole, clindamycin, and chloramphenicol.
    • Patients with ADPKD and ESRD may undergo hemodialysis, peritoneal dialysis, or renal transplantation.

Surgical Care

  • Infected renal or hepatic cysts
    • If infected cysts do not respond to conventional antibiotic therapy, surgical drainage may be necessary.
    • This procedure is usually performed with ultrasonographically guided puncture.
  • Large cysts causing abdominal pain
    • Cysts may become large enough to cause abdominal discomfort or pain. Typically, acute pain is from cyst hemorrhage or an obstruction by a clot, stone, or infection.7
    • When one or more cysts can be identified as causing the pain, the symptoms can often be abated by open- or fiber optic–guided surgery to excise the outer walls and to drain them.
    • In approximately one half of patients, however, candidate cysts cannot be identified as directly causing the pain. In these cases, indiscriminate excision of dozens of cyst walls that abut the capsule have produced complete symptomatic relief for months or years. Volumetric reduction of these kidneys usually exceeds 50% but still leaves kidneys larger than normal size. Not every cyst can be removed, and, with time, the residual cysts enlarge and symptoms may reappear.
    • Approximately one quarter of patients with the most severe pain do not gain relief from surgery or pharmacologic therapy with narcotics. These individuals usually have inaccessible cysts in the medullary portions of the kidneys. Nephrectomy is used as a last resort to control the pain in these patients.
  • Massive polycystic liver diseases (see image below and Image 2)
    • When the liver becomes so large that it prevents the patient from obtaining normal nutrition or causes severe abdominal discomfort, a surgical procedure is necessary.
    • Surgical intervention may range from unroofing several cysts to a partial hepatectomy.
    • Partial hepatectomy is difficult because of the characteristics of the polycystic liver. Only expert surgeons should proceed with this surgical procedure.
    • When the polycystic liver causes portal hypertension or is very large with nonresectable areas, liver transplantation may be necessary.
    • Special attention should be paid when bilateral nephrectomy has to be carried out in patients with severe liver involvement. Several cases of refractory ascites after bilateral nephrectomy have been reported in these patients.
Polycystic kidney disease and massive polycystic ...

Polycystic kidney disease and massive polycystic liver disease.

Polycystic kidney disease and massive polycystic ...

Polycystic kidney disease and massive polycystic liver disease.


Consultations

  • Nephrologist upon evidence of renal insufficiency, hypertension, microalbuminuria, or concentrating defect
  • Invasive radiologist for cyst sclerosis or drainage
  • General surgeon for nephrectomy, cyst decompression, unroofing, or surgical hepatic procedures
  • Neurosurgeon for ICAs
  • Cardiologist for valvular abnormalities

Diet

  • Although a low-salt diet is recommended when hypertension or renal failure is present, no other special diet reportedly is of benefit.

Activity

  • Patients should avoid contact sports in which direct trauma to the back or abdomen is likely. This is especially important with larger, palpable kidneys in order to minimize the risk of rupture.

Medication

No specific medication is available for ADPKD; however, clinical trials with vasopressin 2 receptor antagonists (Tolvaptan), somatostatin, and rapamycin are ongoing. The drugs of choice for hypertension are ACE inhibitors and angiotensin II receptor antagonist blockers. Do not treat abdominal pain with NSAIDs because of its 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.

ACE inhibitors

These peptides suppress the renin-angiotensin-aldosterone system.


Enalapril (Vasotec)

Competitive inhibitor of ACE. Reduces angiotensin II levels, decreasing aldosterone secretion.

Adult

2.5-5 mg/d PO, increase prn
Dosing range: 10-40 mg/d PO in 1-2 divided doses
Alternatively: 1.25 mg/dose IV over 5 min q6h

Pediatric

Not established

NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects may be enhanced when administered concurrently with diuretics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Renal impairment, valvular stenosis, or severe congestive heart failure


Lisinopril (Prinivil, Zestril)

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

Adult

10 mg/d PO; increase 5-10 mg/d at 1- to 2-wk intervals; not to exceed 40 mg

Pediatric

Not established

NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects may be enhanced when administered concurrently with diuretics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Renal impairment, valvular stenosis, or severe congestive heart failure


Captopril (Capoten)

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

Adult

12.5-25 mg PO bid/tid; may increase by 12.5-25 mg/dose at 1- to 2-wk intervals; not to exceed 50 mg tid

Pediatric

6.25-12.5 mg/dose PO q12-24h; not to exceed 6 mg/kg/d

NSAIDs may reduce hypotensive effects; may increase digoxin, lithium, and allopurinol levels; rifampin decreases levels; probenecid may increase levels; hypotensive effects may be enhanced when administered concurrently with diuretics

Documented hypersensitivity; renal impairment

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Renal impairment, valvular stenosis, or severe congestive heart failure

Electrolyte supplements

Administer to maintain electrolyte levels in renal failure.


Calcium carbonate (Oystercal)

Reduces phosphorus load.

Adult

1-2 g divided PO bid/qid

Pediatric

45-65 mg/kg/d PO divided qid

May decrease effects of tetracyclines, atenolol, salicylates, iron salts, and fluoroquinolones; IV administration antagonizes effects of verapamil; large intakes of dietary fiber may decrease calcium absorption and levels

Renal calculi; hypercalcemia; hypophosphatemia; renal or cardiac disease; patients with digitalis toxicity

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Digitalized patients and respiratory failure or acidosis

Antibiotics

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


Ciprofloxacin (Cipro)

Inhibits bacterial DNA synthesis and, consequently, growth. Fluoroquinolone with activity against pseudomonads, streptococci, MRSA, Staphylococcus 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

Adult

250-500 mg PO bid for 7-14 d

Pediatric

<18 years: Not recommended
>18 years: Administer as in adults

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy


Levofloxacin (Levaquin)

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

Adult

750 mg PO q24h for 7-14 d

Pediatric

Not established

Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism; reduces therapeutic effects of phenytoin; probenecid may increase serum concentrations; may increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy


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

Inhibits bacterial growth by inhibiting synthesis of dihydrofolic acid.

Adult

20 mg TMP/kg/d IV divided qid

Pediatric

Administer as in adults

May increase PT when used with warfarin (perform coagulation tests and adjust dose accordingly); coadministration with dapsone may increase blood levels of both drugs; coadministration with diuretics increases incidence of thrombocytopenic purpura in elderly people; phenytoin levels may increase with coadministration; may potentiate effects of methotrexate in bone marrow depression; hypoglycemic response to sulfonylureas may increase with coadministration; may increase levels of zidovudine

Documented hypersensitivity; megaloblastic anemia due to folate deficiency

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Discontinue at first appearance of skin rash or sign of adverse reaction; obtain CBC counts frequently; discontinue therapy if significant hematologic changes occur; goiter, diuresis, and hypoglycemia may occur with sulfonamides; prolonged IV infusions or high doses may cause bone marrow depression (if signs occur, administer 5-15 mg/d leucovorin); caution in folate deficiency (eg, chronic alcoholism, elderly people, anticonvulsant therapy, malabsorption syndrome); hemolysis may occur in G-6-PD deficiency; AIDS patients may not tolerate or respond to TMP-SMZ; caution in renal or hepatic impairment (perform urinalyses and renal function tests during therapy); administer fluids to prevent crystalluria and stone formation


Clindamycin (Cleocin)

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

Adult

150-450 mg/dose PO q6-8h; not to exceed 1.8 g/d
600-1200 mg/d IV/IM divided q6-8h depending on degree of infection

Pediatric

8-20 mg/kg/d PO as hydrochloride and 8-25 mg/kg/d as palmitate divided tid/qid
20-40 mg/kg/d IV/IM divided tid/qid

Increases duration of neuromuscular blockade induced by tubocurarine and pancuronium; erythromycin may antagonize effects; antidiarrheals may delay absorption

Documented hypersensitivity; regional enteritis; ulcerative colitis; hepatic impairment; antibiotic-associated colitis

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in severe hepatic dysfunction; no adjustment necessary in renal insufficiency; associated with severe and possibly fatal colitis


Chloramphenicol (Chloromycetin)

Binds to 50S bacterial-ribosomal subunits and inhibits bacterial growth by inhibiting protein synthesis. Effective against gram-negative and gram-positive bacteria.

Adult

50-100 mg/kg/d PO/IV divided q6h for 10 d; not to exceed 4 g/d

Pediatric

50-75 mg/kg/d PO/IV divided q6h

With concurrent administration with barbiturates, serum levels may decrease while barbiturate levels may increase, causing toxicity; manifestations of hypoglycemia may occur with sulfonylureas; rifampin may reduce serum levels, presumably through hepatic enzyme induction; may increase effects of anticoagulants; may increase serum hydantoin levels, possibly resulting in toxicity (chloramphenicol levels may increase or decrease)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use only for indicated infections or as prophylaxis for bacterial infections; serious and fatal blood dyscrasias (eg, aplastic anemia, hypoplastic anemia, thrombocytopenia, granulocytopenia) can occur; evaluate baseline and perform periodic blood studies approximately q2d while on therapy; discontinue upon appearance of reticulocytopenia, leukopenia, thrombocytopenia, anemia, or findings attributable to chloramphenicol; adjust dose in liver or kidney dysfunction; caution in pregnancy at term or during labor because of potential toxic effects on fetus (gray syndrome)

Phosphate binders

Administer to maintain phosphate levels in renal failure.


Lanthanum carbonate (Fosrenol)

Noncalcium, nonaluminum phosphate binder indicated for reduction of high phosphorus levels in patients with ESRD. Directly binds dietary phosphorus in upper GI tract, thereby inhibiting phosphorus absorption.

Adult

Initial: 250-500 mg PO tid pc (chewable tabs); adjust dose q2-3wk to target serum phosphorus level
Maintenance: 500-1000 mg PO tid pc

Pediatric

Not established

Drugs known to interact with antacids (eg, alendronate, amprenavir, ciprofloxacin, itraconazole, tetracycline, thyroid hormones) should not be administered within 2 h

Documented hypersensitivity; bowel obstruction; hypophosphatemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Deposited into developing bone, including growth plate (long-term effects unknown); common adverse effects typically diminish over time but include headache, abdominal pain, nausea, diarrhea, constipation, and vomiting; in clinical trials, dialysis graft occlusion occurred more frequently than with placebo; caution with GI motility diseases (eg, Crohn disease, ulcerative colitis) or recent GI surgery


Sevelamer hydrochloride (Renagel)

Polymeric phosphate binder for oral administration. Does not contain aluminum and, thus, aluminum intoxication is not a concern.

Adult

2-4 cap PO pc; adjust based on serum phosphorus concentrations to lower serum phosphorus to <6 mg/dL

Pediatric

Not established

May reduce absorption of drugs co-administered with sevelamer

Documented hypersensitivity; bowel obstruction; hypophosphatemia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in patients with dysphagia, severe GI motility disorders, or swallowing disorders; can cause hypophosphatemia in patients with low or normal serum phosphate levels; when changes in absorption of oral medications may have clinical consequences (eg, antiseizure or antiarrhythmic drugs), medications should be taken 1 h before or 3 h after a dose of sevelamer

Angiotensin II receptor antagonists

These agents interfere with the binding of formed angiotensin II to its endogenous receptor.


Valsartan (Diovan)

Prodrug that produces direct antagonism of angiotensin II receptors. Displaces angiotensin II from AT1 receptor and may lower blood pressure by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. For use in patients unable to tolerate ACE inhibitors.

Adult

80 mg/d PO; may increase to 160 mg/d if needed

Pediatric

<6 years: Not established
>6 years: 1.3 mg/kg PO qd initially, not to exceed 40 mg/d; may adjust dose according to blood pressure response up to 2.7 mg/kg/d (not to exceed 160 mg/d)

May increase digoxin, lithium, and allopurinol levels; probenecid may increase valsartan levels; coadministration with diuretics increases hypotensive effects; NSAIDs may reduce hypotensive effects of valsartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Documented hypersensitivity; severe hepatic insufficiency; biliary cirrhosis or obstruction; primary hyperaldosteronism; bilateral renal artery stenosis

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimesters; caution in hyperkalemia, suspected bilateral renal artery stenosis, or suspected solitary kidney with unilateral renal artery stenosis


Losartan (Cozaar)

Angiotensin II receptor antagonist that blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. May induce a more complete inhibition of the renin-angiotensin system than ACE inhibitors, does not affect the response to bradykinin, and is less likely to be associated with cough and angioedema. For patients unable to tolerate ACE inhibitors.

Adult

25-100 mg PO qd or divided bid

Pediatric

<6 years: Not established
6-16 years: 0.7 mg/kg PO qd; not to exceed 50 mg/d if <50 kg or 100 mg/d if >50 kg
CrCl <30 mL/min: Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase losartan levels; coadministration with diuretics increases hypotensive effects; NSAIDs may reduce hypotensive effects of losartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimesters; caution in patients with unilateral or bilateral renal artery stenosis


Candesartan (Atacand)

Blocks vasoconstriction and aldosterone-secreting effects of angiotensin II. May induce more complete inhibition of renin-angiotensin system than ACE inhibitors, does not affect response to bradykinin, and is less likely to be associated with cough and angioedema. Use in patients unable to tolerate ACE inhibitors.
Angiotensin II receptor antagonist blockers reduce blood pressure and proteinuria, protecting renal function and delaying onset of ESRD.

Adult

8-16 mg/d PO initially; not to exceed 32 mg/d

Pediatric

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase candesartan levels; coadministration with diuretics increases hypotensive effects; NSAIDs may reduce hypotensive effects of candesartan; may increase risk of hyperkalemia if taken concurrently with potassium supplements or other potassium-sparing diuretics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimesters; caution in renal impairment (serum creatinine >3.5), valvular stenosis, or severe congestive heart failure; watch for serum potassium


Olmesartan (Benicar)

Blocks vasoconstrictor effects of angiotensin II by selectively blocking binding of angiotensin II to AT-1 receptor in vascular smooth muscle. Action is independent of pathways for angiotensin II synthesis.

Adult

20 mg PO qd initially; may increase to 40 mg/d after 2 wk if further BP reduction required; lower dose in volume- or salt-depleted patients

Pediatric

Not established

Diuretics may enhance hypotensive effect

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Pregnancy category D in second and third trimesters; may cause injury or even death to the developing fetus due to effect on renin-angiotensin system if given in second or third trimesters of pregnancy; serum levels and AUC increase with renal and hepatic insufficiency, respectively; may cause oliguria, azotemia, and acute renal failure; facial edema, angioedema, or decreased hemoglobin or hematocrit occur rarely

More on Polycystic Kidney Disease

Overview: Polycystic Kidney Disease
Differential Diagnoses & Workup: Polycystic Kidney Disease
Treatment & Medication: Polycystic Kidney Disease
Follow-up: Polycystic Kidney Disease
Multimedia: Polycystic Kidney Disease
References
Further Reading

References

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Keywords

polycystic kidney disease, PKD, polycystic kidney, kidney cyst, kidney cysts, kidney disease, renal cyst, renal cysts, autosomal dominant polycystic kidney disease, ADPKD, adult polycystic kidney disease, polycystic kidney disease type 1, PKD1, polycystic kidney disease type 2, PKD2, kidney failure, renal failure, dialysis-dependent kidney disease, end-stage renal disease, ESRD, end-stage kidney disease, ESKD, renal transplantation, renal transplant, kidney transplantation, kidney transplant, hemodialysis, peritoneal dialysis, ADPKD type 1, ADPKD1, ADPKD type 2, ADPKD2

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 and International Society of Nephrology
Disclosure: Nothing to disclose.

Medical Editor

Laura L 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
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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, and National Kidney Foundation
Disclosure: Nothing to disclose.

CME Editor

Rebecca J Schmidt, DO, FACP, FASN, Professor of Medicine, Section Chief, Department of Medicine, Section of Nephrology, West Virginia University School of Medicine
Rebecca J Schmidt, DO, FACP, FASN is a member of the following medical societies: American College of Osteopathic Internists, American College of Physicians, American Medical Association, American Society of Nephrology, International Society of Nephrology, National Kidney Foundation, Renal Physicians Association, and West Virginia State Medical Association
Disclosure: Abbott Grant/research funds Speaking and teaching; Genzyme Honoraria Consulting; Amgen Honoraria Speaking and teaching; Ortho Biotech Honoraria Speaking and teaching

Chief Editor

Vecihi Batuman, MD, FACP, FASN, Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Medicine Service, 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, and International Society of Nephrology
Disclosure: Nothing to disclose.

 
 
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