eMedicine Specialties > Nephrology > Glomerular Diseases

Nephrotic Syndrome: Treatment & Medication

Author: Eric P Cohen, MD, Professor of Medicine, Nephrology Fellowship Program Director, Department of Medicine, Division of Nephrology, Medical College of Wisconsin; Nephrology Section Chief, Zablocki Veterans Affairs Hospital
Contributor Information and Disclosures

Updated: Aug 25, 2009

Treatment

Medical Care

Acute management of childhood nephrotic syndrome

 With good parental and patient education and close outpatient follow-up care, hospitalization is not usually necessary. Hospitalization should be considered if a patient has generalized edema severe enough to cause respiratory distress, if a patient has tense scrotal or labial edema, if he or she has complications (eg, bacterial sepsis, peritonitis, pneumonia, thromboembolism, failure to thrive), or if patient or family compliance with treatment is in doubt.

Diuretics will be needed; furosemide (1 mg/kg/d) and spironolactone (2 mg/kg/d) will help when fluid retention is severe, provided no signs of renal failure or volume contraction are evident. Achieving a satisfactory diuresis is difficult when the patient's serum albumin level is less than 1.5 g/dL. Albumin at 1 g/kg may be given, followed by intravenous furosemide. Complications may occur, including pulmonary edema. Some evidence suggests that albumin may delay the response to steroids and may even induce more frequent relapses, probably by causing severe glomerular epithelial damage. Fluid removal and weight loss remain transient unless proteinuria remits.

With regard to infection, oral penicillin can be prescribed as prophylaxis for children with gross edema. Abdominal paracentesis should be performed if the patient develops signs of peritonitis, and any bacterial infection should be treated promptly. A nonimmune patient with varicella should receive zoster immunoglobulin therapy if exposed to chickenpox, and acyclovir should be given if the patient develops chickenpox.

Acute management of adult nephrotic syndrome

 The principles for acute management of adults with nephrotic syndrome are similar to those for children. Diuretics will be needed; furosemide, spironolactone, and even metolazone may be used. Volume depletion may occur with diuretic use, which should be monitored by assessment of symptoms, weight, pulse, and blood pressure.

Anticoagulation has been advocated by some for use in preventing thromboembolic complications, but its use in primary prevention is of unproven value.

Hypolipidemic agents may be used, but if the nephrotic syndrome cannot be controlled, there will be persistent hyperlipidemia.

In secondary nephrotic syndrome, such as that associated with diabetic nephropathy, angiotensin-converting enzyme (ACE) inhibitors and/or angiotensin II receptor blockers are widely used. These may reduce proteinuria by reducing the systemic blood pressure, by reducing intraglomerular pressure, and also by direct action on podocytes.

Specific treatment

 Specific treatment of nephrotic syndrome depends on the disease's cause. Thus, glucocorticosteroids, such as prednisone, are used for minimal-change nephropathy. Prednisone and cyclophosphamide are useful in some forms of lupus nephritis. Secondary amyloidosis with nephrotic syndrome may respond to anti-inflammatory treatment of the primary disease.

Surgical Care

Surgery is not applicable in itself for the treatment of nephrotic syndrome. It is possible that patients with nephrotic syndrome may have poor wound healing, which places emphasis on optimal medical treatments.

Consultations

Depending on the cause of nephrotic syndrome, a patient may need specialty consultation. For example, an individual with lupus nephritis may benefit from rheumatologic consultation.

Diet

  • For patients with nephrotic syndrome, their diet should provide adequate energy (caloric) intake and adequate protein (1-2 g/kg/d). Supplemental dietary protein is of no proven value.
  • A diet with no added salt will help to limit fluid overload.
  • Management of hyperlipidemia could be of some importance if the nephrotic state is prolonged.
  • Fluid restriction per se is not required.

Activity

There are no activity restrictions for patients with nephrotic syndrome. Ongoing activity, rather than bedrest, will reduce the risk of blood clots.

Medication

Drugs used in the remittive treatment of nephrotic syndrome include corticosteroids (prednisone), cyclophosphamide, and cyclosporine, while drugs used to reduce edema include diuretics and those administered to reduce the proteinuria include ACE inhibitors and angiotensin II receptor blockers.

Corticosteroids

Have anti-inflammatory properties and modify the body's immune response to diverse stimuli.


Prednisone (Sterapred)

Immunosuppressant for treatment of autoimmune disorders. May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. May be administered as a single dose in the morning or as divided doses. Studies show that a single dose is equally effective and greatly improves compliance.

Adult

60 mg/m2/d PO, titrate to a maximum 80 mg/m2/d until remission; then, 40 mg/m2/d, titrate to 60 mg/m2 qod for 4 wk

Pediatric

1 to 2 mg/kg/d; taper over 2 wk as symptoms resolve

Coadministration with estrogens may decrease clearance; concurrent use with digoxin may cause digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids (consider increasing maintenance dose); monitor for hypokalemia with coadministration of diuretics

Documented hypersensitivity, viral infection, peptic ulcer disease, hepatic dysfunction, connective tissue infections, fungal or tubercular infections, GI disease

Pregnancy

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

Precautions

Edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections may occur with glucocorticoid use; blood pressure may increase and should be treated; sudden stopping may cause adrenal crisis, ie, hypoadrenalism

Immunomodulators

These agents regulate key steps of the immune system.


Cyclophosphamide (Cytoxan)

Antineoplastic drug chemically related to nitrogen mustard. Potent immunomodulator that has been used successfully in conditions that require immunosuppression. Highly effective for frequently relapsing steroid-sensitive nephrotic syndrome; half of the children enter a prolonged remission.
Doses (below) are based on published studies. This drug is used for the time required to induce remission and should be continued thereafter, but probably not for more than a year.

Adult

1-2 mg/kg/d PO; continue for 3-6 mo beyond remission

Pediatric

2 mg/kg/d PO

Allopurinol may increase risk of bleeding or infection and may enhance myelosuppressive effects; may potentiate doxorubicin-induced cardiotoxicity; may reduce digoxin serum levels and antimicrobial effects of quinolones
Chloramphenicol may increase half-life while decreasing metabolite concentrations; may increase effect of anticoagulants; coadministration with high doses of phenobarbital may increase rate of metabolism and leukopenic activity of cyclophosphamide; thiazide diuretics may prolong cyclophosphamide-induced leukopenia and neuromuscular blockade by inhibiting cholinesterase activity

Documented hypersensitivity, severely depressed bone marrow function

Pregnancy

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

Precautions

Regularly examine hematologic profile (particularly neutrophils and platelets) to monitor for hematopoietic suppression; regularly examine urine for RBCs, which may precede hemorrhagic cystitis


Cyclosporine (Sandimmune, Neoral, Gengraf)

Cyclic polypeptide that suppresses cell-mediated immune reactions.
For children and adults, base dosing on ideal body weight.

Adult

Up to 3 mg/kg PO in divided doses

Pediatric

Administer as in adults

Carbamazepine, phenytoin, isoniazid, rifampin, and phenobarbital may decrease concentrations; azithromycin, itraconazole, nicardipine, ketoconazole, fluconazole, erythromycin, verapamil, grapefruit juice, diltiazem, aminoglycosides, acyclovir, amphotericin B, and clarithromycin may increase toxicity; risk of acute renal failure, rhabdomyolysis, myositis, and myalgias increases when taken concurrently with lovastatin

Documented hypersensitivity; uncontrolled hypertension or malignancies; do not administer concomitantly with PUVA or UVB radiation in psoriasis because may increase risk of cancer

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

Evaluate renal and liver functions often by measuring BUN, serum creatinine, serum potassium, serum bilirubin, and liver enzyme levels; may increase risk of infection and lymphoma; reserve IV use only for those who cannot take PO

Immunosuppressants

Inhibit key steps that mediate immune reactions.


Mycophenolate (CellCept, Myfortic)

Inhibits inosine monophosphate dehydrogenase and suppresses de novo purine synthesis by lymphocytes, thereby inhibiting their proliferation. Inhibits antibody production.

Adult

Mycophenolate mofetil (CellCept): 500 to 1500 mg PO bid
Mycophenolate sodium (Myfortic): 360 to 720 mg PO bid

Pediatric

CellCept oral suspension: 600 mg/m² PO bid; 1 g PO bid maximum

May elevate levels of acyclovir and ganciclovir; antacids and cholestyramine decrease absorption, reducing levels (do not administer together); probenecid may increase levels of mycophenolate; salicylates may increase toxicity of mycophenolate

Pregnancy

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

Precautions

May cause nausea, vomiting, and diarrhea; may experience less gastrointestinal side effects with Myfortic preparation

Diuretics

Used for symptomatic treatment of edema.


Furosemide (Lasix)

Increases urine output by inhibiting sodium transport in ascending loop of Henle and distal renal tubule. Dose must be individualized to patient. Depending on response, administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until desired diuresis occurs.

Adult

20-80 mg/d PO/IV; titrate up to 200 mg/d for severe edema

Pediatric

1-2 mg/kg/dose PO; not to exceed 6 mg/kg/dose; do not administer >q6h
When treating infants, titrate in increments of 1 mg/kg/dose until satisfactory effect achieved
1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration with aminoglycosides; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently

Documented hypersensitivity; hepatic coma, anuria, state of severe electrolyte depletion

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

Perform frequent serum electrolyte, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter


Spironolactone (Aldactone)

For management of edema resulting from excessive aldosterone excretion. Competes with aldosterone for receptor sites in distal renal tubules, thus enhancing sodium excretion.

Adult

25-200 mg/d PO qd or divided bid

Pediatric

1.5-3.5 mg/kg/d PO divided q6-24h

May decrease effect of anticoagulants; simultaneous use of potassium, potassium-sparing diuretics, or ACE inhibitors may cause hyperkalemia.

Documented hypersensitivity; anuria, renal failure or hyperkalemia

Pregnancy

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

Precautions

Caution in renal and hepatic impairment

Angiotensin-converting Enzyme (ACE) Inhibitors

These agents improve hypertension by inhibiting renin or angiotensin II production.


Lisinopril (Prinivil, Zestril)

Inhibitor of the enzyme that converts angiotensin I to angiotensin II.

Adult

2.5 mg PO qd, increasing to 20 mg/d, as required

Pediatric

Not established

NSAIDs may reduce hypotensive effects of lisinopril; ACE inhibitors may increase digoxin, lithium, and allopurinol levels; rifampin decreases lisinopril levels; probenecid may increase lisinopril levels; the hypotensive effects of ACE inhibitors may be enhanced when given concurrently with diuretics; may cause hyperkalemia when used together with potassium-sparing diuretics such as spironolactone, or when used together with potassium supplements

Documented hypersensitivity to drug and related products

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 of pregnancy, causes fetal malformations if used during a late-term pregnancy; may cause elevations in the serum creatinine related to hemodynamic change, or even renal failure when used in a subject with renal artery stenosis; caution in severe congestive heart failure; may cause cough in up to 5% of subjects on this drug or other drugs in its class

Angiotensin II Receptor Antagonist

These agents inhibit angiotensin II activity by interfering with the binding of formed angiotensin II to its endogenous receptor.


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

Not established

May increase digoxin, lithium, and allopurinol levels; probenecid may increase losartan levels; coadministration with diuretics increases hypotensive effects of losartan; 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 of pregnancy, caution in patients with unilateral or bilateral renal artery stenosis

More on Nephrotic Syndrome

Overview: Nephrotic Syndrome
Differential Diagnoses & Workup: Nephrotic Syndrome
Treatment & Medication: Nephrotic Syndrome
Follow-up: Nephrotic Syndrome
Multimedia: Nephrotic Syndrome
References
Further Reading
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References

  1. Neelakantappa K, Gallo GR, Baldwin DS. Proteinuria in IgA nephropathy. Kidney Int. Mar 1988;33(3):716-21. [Medline].

  2. Wong W. Idiopathic nephrotic syndrome in New Zealand children, demographic, clinical features, initial management and outcome after twelve-month follow-up: results of a three-year national surveillance study. J Paediatr Child Health. May 2007;43(5):337-41. [Medline].

  3. Niaudet P. Genetic forms of nephrotic syndrome. Pediatr Nephrol. Dec 2004;19(12):1313-8. [Medline].

  4. International Study of Kidney Disease in Children. Primary nephrotic syndrome in children: clinical significance of histopathologic variants of minimal change and of diffuse mesangial hypercellularity. A Report of the International Study of Kidney Disease in Children. Kidney Int. Dec 1981;20(6):765-71. [Medline].

  5. International Study of Kidney Disease in Children. The primary nephrotic syndrome in children. Identification of patients with minimal change nephrotic syndrome from initial response to prednisone. J Pediatr. Apr 1981;98(4):561-4. [Medline].

  6. Haraldsson B, Nyström J, Deen WM. Properties of the glomerular barrier and mechanisms of proteinuria. Physiol Rev. Apr 2008;88(2):451-87. [Medline].

  7. Russo LM, Bakris GL, Comper WD. Renal handling of albumin: a critical review of basic concepts and perspective. Am J Kidney Dis. May 2002;39(5):899-919. [Medline].

  8. Norden AG, Lapsley M, Lee PJ, Pusey CD, Scheinman SJ, Tam FW. Glomerular protein sieving and implications for renal failure in Fanconi syndrome. Kidney Int. Nov 2001;60(5):1885-92. [Medline].

  9. Hamm LL, Batuman V. Edema in the nephrotic syndrome: new aspect of an old enigma. J Am Soc Nephrol. Dec 2003;14(12):3288-9. [Medline].

  10. Rostoker G, Behar A, Lagrue G. Vascular hyperpermeability in nephrotic edema. Nephron. Jul 2000;85(3):194-200. [Medline].

  11. Mahmoodi BK, ten Kate MK, Waanders F, Veeger NJ, Brouwer JL, Vogt L. High absolute risks and predictors of venous and arterial thromboembolic events in patients with nephrotic syndrome: results from a large retrospective cohort study. Circulation. Jan 15 2008;117(2):224-30. [Medline].

  12. Mittal SK, Dash SC, Tiwari SC, Agarwal SK, Saxena S, Fishbane S. Bone histology in patients with nephrotic syndrome and normal renal function. Kidney Int. May 1999;55(5):1912-9. [Medline].

  13. Kumar J, Gulati S, Sharma AP, Sharma RK, Gupta RK. Histopathological spectrum of childhood nephrotic syndrome in Indian children. Pediatr Nephrol. Jul 2003;18(7):657-60. [Medline].

  14. Ozkaya N, Cakar N, Ekim M, Kara N, Akkök N, Yalçinkaya F. Primary nephrotic syndrome during childhood in Turkey. Pediatr Int. Aug 2004;46(4):436-8. [Medline].

  15. Kazi JI, Mubarak M. Pattern of glomerulonephritides in adult nephrotic patients--report from SIUT. J Pak Med Assoc. Nov 2007;57(11):574. [Medline].

  16. Barsoum R. The changing face of schistosomal glomerulopathy. Kidney Int. 2004;66:2472-2484.

  17. Doe JY, Funk M, Mengel M, et al. Nephrotic syndrome in African children: lack of evidence for 'tropical nephrotic syndrome'?. Nephrol Dial Transplant. 2006;21:672-676.

  18. Pakasa NM, Sumaili EK. The nephrotic syndrome in the Democratic Republic of Congo. N Engl J Med. Mar 9 2006;354(10):1085-6. [Medline].

  19. Sumaili EK, Krzesinski JM, Zinga CV, Cohen EP, Delanaye P, Munyanga SM, et al. Prevalence of chronic kidney disease in Kinshasa: results of a pilot study from the Democratic Republic of Congo. Nephrol Dial Transplant. Jan 2009;24(1):117-22. [Medline].

  20. Arneil GC, Lam CN. Long-term assessment of steroid therapy in childhood nephrosis. Lancet. Oct 15 1966;2(7468):819-21. [Medline].

  21. Donadio JV Jr, Torres VE, Velosa JA, Wagoner RD, Holley KE, Okamura M. Idiopathic membranous nephropathy: the natural history of untreated patients. Kidney Int. Mar 1988;33(3):708-15. [Medline].

  22. du Buf-Vereijken PW, Branten AJ, Wetzels JF. Idiopathic membranous nephropathy: outline and rationale of a treatment strategy. Am J Kidney Dis. Dec 2005;46(6):1012-29. [Medline].

  23. Jude EB, Anderson SG, Cruickshank JK, et al. Natural history and prognostic factors of diabetic nephropathy in type 2 diabetes. Quart J Med. 2002;95:371-7. [Medline].

  24. Kopp JB, Winkler C. HIV-associated nephropathy in African Americans. Kidney Int Suppl. Feb 2003;S43-9. [Medline].

  25. Bonilla-Felix M, Parra C, Dajani T, Ferris M, Swinford RD, Portman RJ. Changing patterns in the histopathology of idiopathic nephrotic syndrome in children. Kidney Int. May 1999;55(5):1885-90. [Medline].

  26. Lefaucheur C, Stengel B, Nochy D, et al. Membranous nephropathy and cancer: Epidemiologic evidence and determinants of high-risk cancer association. Kidney Int. Oct 2006;70(8):1510-7. [Medline].

  27. George BA, Zhou XJ, Toto R. Nephrotic syndrome after bevacizumab: case report and literature review. Am J Kidney Dis. Feb 2007;49(2):e23-9. [Medline].

  28. Cohen EP, Lemann J. The role of the laboratory in evaluation of kidney function. Clin Chem. 1991;37:785-796.

  29. Gupta K, Iskandar SS, Daeihagh P, et al. Distribution of pathologic findings in individuals with nephrotic proteinuria according to serum albumin. Nephrol Dial Transplant. May 2008;23(5):1595-9. [Medline].

  30. Varghese SA, Powell TB, Budisavljevic MN, et al. Urine biomarkers predict the cause of glomerular disease. J Am Soc Nephrol. 2007;18:913-22. [Medline].

  31. Rapola J. Congenital nephrotic syndrome. Pediatr Nephrol. Jul 1987;1(3):441-6. [Medline].

  32. Appel GB, Blum CB, Chien S, Kunis CL, Appel AS. The hyperlipidemia of the nephrotic syndrome. Relation to plasma albumin concentration, oncotic pressure, and viscosity. N Engl J Med. Jun 13 1985;312(24):1544-8. [Medline].

  33. Curry RC Jr, Roberts WC. Status of the coronary arteries in the nephrotic syndrome. Analysis of 20 necropsy patients aged 15 to 35 years to determine if coronary atherosclerosis is accelerated. Am J Med. Aug 1977;63(2):183-92. [Medline].

  34. Tessitore N, Bonucci E, D'Angelo A, Lund B, Corgnati A, Lund B, et al. Bone histology and calcium metabolism in patients with nephrotic syndrome and normal or reduced renal function. Nephron. 1984;37(3):153-9. [Medline].

  35. Gulati S, Godbole M, Singh U, Gulati K, Srivastava A. Are children with idiopathic nephrotic syndrome at risk for metabolic bone disease?. Am J Kidney Dis. Jun 2003;41(6):1163-9. [Medline].

  36. Leonard MB, Feldman HI, Shults J, Zemel BS, Foster BJ, Stallings VA. Long-term, high-dose glucocorticoids and bone mineral content in childhood glucocorticoid-sensitive nephrotic syndrome. N Engl J Med. Aug 26 2004;351(9):868-75. [Medline].

  37. Palmer SC, Nand K, Strippoli GF. Interventions for minimal change disease in adults with nephrotic syndrome. Cochrane Database Syst Rev. Jan 23 2008;CD001537. [Medline].

  38. Savin VJ, McCarthy ET, Sharma R, Charba D, Sharma M. Galactose binds to focal segmental glomerulosclerosis permeability factor and inhibits its activity. Transl Res. Jun 2008;151(6):288-92. [Medline].

  39. Alkjaersig N, Fletcher AP, Narayanan M, Robson AM. Course and resolution of the coagulopathy in nephrotic children. Kidney Int. Mar 1987;31(3):772-80. [Medline].

  40. Bergesio F, Ciciani AM, Santostefano M, et al. Renal involvement in systemic amyloidosis-an Italian retrospective study on epidemiological and clinical data at diagnosis. Nephrol Dial Transplant. 2007;22:1608-1618. [Medline].

  41. Brukamp K, Doyle AM, Bloom RD, Bunin N, Tomaszewski JE, Cizman B. Nephrotic syndrome after hematopoietic cell transplantation: do glomerular lesions represent renal graft-versus-host disease?. Clin J Am Soc Nephrol. Jul 2006;1(4):685-94. [Medline].

  42. Cattran DC, Alexopoulos E, Heering P, Hoyer PF, Johnston A, Meyrier A, et al. Cyclosporin in idiopathic glomerular disease associated with the nephrotic syndrome : workshop recommendations. Kidney Int. Dec 2007;72(12):1429-47. [Medline].

  43. Chesney RW, Novello AC. Forms of nephrotic syndrome more likely to progress to renal impairment. Pediatr Clin North Am. Jun 1987;34(3):609-27. [Medline].

  44. Deen WM. What determines glomerular capillary permeability?. J Clin Invest. Nov 2004;114(10):1412-4. [Medline].

  45. Eddy AA, Symons JM. Nephrotic syndrome in childhood. Lancet. Aug 23 2003;362(9384):629-39. [Medline].

  46. Filler G, Young E, Geier P. Is there really an increase in non-minimal change nephrotic syndrome in children?. Am J Kidney Dis. Dec 2003;42(6):1107-13.

  47. Fliser D, Zurbruggen, Mutschler E, et al. Coadministration of albumin and furosemide in patients with the nephrotic syndrome. Kidney Int. 1999;55:629-634. [Medline].

  48. Gorensek MJ, Lebel MH, Nelson JD. Peritonitis in children with nephrotic syndrome. Pediatrics. Jun 1988;81(6):849-56. [Medline].

  49. Grundy SM, Vega GL. Rationale and management of hyperlipidemia of the nephrotic syndrome. Am J Med. Nov 1989;87(5N):3N-11N. [Medline].

  50. Haws RM, Baum M. Efficacy of albumin and diuretic therapy in children with nephrotic syndrome. Pediatrics. Jun 1993;91(6):1142-6. [Medline].

  51. Hodson EM, Craig JC, Willis NS. Evidence-based management of steroid-sensitive nephrotic syndrome. Pediatr Nephrol. Nov 2005;20(11):1523-30. [Medline].

  52. Hoyer PF, Gonda S, Barthels M, et al. Thromboembolic complications in children with nephrotic syndrome. Risk and incidence. Acta Paediatr Scand. Sep 1986;75(5):804-10. [Medline].

  53. Ingulli E, Tejani A. Racial differences in the incidence and renal outcome of idiopathic focal segmental glomerulosclerosis in children. Pediatr Nephrol. Jul 1991;5(4):393-7. [Medline].

  54. Keane WF, St Peter JV, Kasiske BL. Is the aggressive management of hyperlipidemia in nephrotic syndrome mandatory?. Kidney Int (suppl). 1992;38:s134-s141. [Medline].

  55. Koskimies O, Vilska J, Rapola J, Hallman N. Long-term outcome of primary nephrotic syndrome. Arch Dis Child. Jul 1982;57(7):544-8. [Medline].

  56. Lewis MA, Baildom EM, Davis N, et al. Nephrotic syndrome: from toddlers to twenties. Lancet. Feb 4 1989;1(8632):255-9. [Medline].

  57. Mendoza SA, Tune BM. Management of the difficult nephrotic patient. Pediatr Clin North Am. Dec 1995;42(6):1459-68. [Medline].

  58. Mongeau JG, Corneille L, Robitaille P, et al. Primary nephrosis in childhood associated with focal glomerular sclerosis: is long-term prognosis that severe?. Kidney Int. Dec 1981;20(6):743-6. [Medline].

  59. Niaudet P, Broyer M, Habib R. Treatment of idiopathic nephrotic syndrome with cyclosporin A in children. Clin Nephrol. 1991;35 Suppl 1:S31-6. [Medline].

  60. Ozanne P, Francis RB, Meiselman HJ. Red blood cell aggregation in nephrotic syndrome. Kidney Int. Mar 1983;23(3):519-25. [Medline].

  61. Salcedo JR, Thabet MA, Latta K, Chan JC. Nephrosis in childhood. Nephron. 1995;71(4):373-85. [Medline].

  62. Southwest Pediatric Nephrology Study Group. Childhood nephrotic syndrome associated with diffuse mesangial hypercellularity. A report of the Southwest Pediatric Nephrology Study Group. Kidney Int. Jul 1983;24(1):87-94. [Medline].

  63. Swaminathan S, Leung N, Lager DJ, Melton LJ 3rd, Bergstralh EJ, Rohlinger A. Changing incidence of glomerular disease in Olmsted County, Minnesota: a 30-year renal biopsy study. Clin J Am Soc Nephrol. May 2006;1(3):483-7. [Medline].

  64. Tejani A, Nicastri AD, Sen D, et al. Long-term evaluation of children with nephrotic syndrome and focal segmental glomerular sclerosis. Nephron. 1983;35(4):225-31. [Medline].

  65. Waldman M, Crew RJ, Valeri A, Busch J, Stokes B, Markowitz G, et al. Adult minimal-change disease: clinical characteristics, treatment, and outcomes. Clin J Am Soc Nephrol. May 2007;2(3):445-53. [Medline].

  66. Warshaw BL, Hymes LC. Daily single-dose and daily reduced-dose prednisone therapy for children with the nephrotic syndrome. Pediatrics. May 1989;83(5):694-9. [Medline].

  67. Wyatt RJ, Marx MB, Kazee M, Holland NH. Current estimates of the incidence of steroid responsive idiopathic nephrosis in Kentucky children 1-9 years of age. Int J Pediatr Nephrol. Jun 1982;3(2):63-5. [Medline].

  68. Wynn SR, Stickler GB, Burke EC. Long-term prognosis for children with nephrotic syndrome. Clin Pediatr (Phila). Feb 1988;27(2):63-8. [Medline].

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Keywords

nephrotic syndrome, nephrotic, syndrome nephrotic, nephrosis, nephropathy, proteinuria, diabetic nephropathy, glomerulosclerosis, IgA nephropathy, focal segmental glomerulosclerosis, focal glomerulosclerosis, membranous nephropathy, minimal change disease, minimal-change disease, hypoalbuminemia, hypercholesterolemia, minimal change nephropathy, pediatric nephrotic syndrome, collagen vascular disease, IgA nephropathy, amyloidosis, congenital nephrotic syndrome Finnish type, focal segmental glomerulosclerosis

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Contributor Information and Disclosures

Author

Eric P Cohen, MD, Professor of Medicine, Nephrology Fellowship Program Director, Department of Medicine, Division of Nephrology, Medical College of Wisconsin; Nephrology Section Chief, Zablocki Veterans Affairs Hospital
Eric P Cohen, MD is a member of the following medical societies: American Society of Nephrology, Central Society for Clinical Research, International Society of Nephrology, and Radiation Research Society
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

Eleanor Lederer, MD, Consulting Staff, Louisville VA Hospital; Professor of Medicine; Interim Chief of Nephrology; Director of Nephrology Training Program; Director, Metabolic Stone Clinic; Director of Outpatient Clinics, Kidney Disease Program, University of Louisville School of Medicine
Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa
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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