
Health Dictionary
Reliable, easy-to-read patient information on common medical conditions β written in plain language, free of jargon, and grounded in current evidence. Browse the most frequent diagnoses, understand what they mean for everyday life, and learn which steps and questions help you have a focused conversation with your doctor.
Nephrotic syndrome medical therapy
Introduction
Overview
Overview
There are currently no guidelines for the management of edema associated with nephrotic syndrome. The slow reversal of edema is important at a rate of 0.5-1 kg daily to prevent electrolyte disturbances, hypotension, ischemic acute tubular necrosis, and hemoconcentration associated with aggressive diuretic therapy. Since proteinuria is one of the most significant factors for progression of a disease and is associated with outcome, treatment of proteinuria in nephrotic syndrome must always be considered a priority. Angiotensin-converting enzyme inhibitors (ACE-I), with or without angiotensin-II receptor blockers (ARB) have been extensively studied and are well-known to decrease proteinuria and the risk of progression of renal disease in patients with nephrotic syndrome. Pneumococcal vaccines are recommended for all patients with nephrotic syndrome.
Medical Therapy
Medical Therapy
Treatment of Edema
- There are currently no guidelines for the management of edema associated with nephrotic syndrome.
- The slow reversal of edema is important at a rate of 0.5-1 kg daily to prevent electrolyte disturbances, hypotension, ischemic acute tubular necrosis, and hemoconcentration associated with aggressive diuretic therapy.[1]
- Recommended sodium restriction: approximately 2 g/day.
Diuretics:
- IV loop diuretics, like furosemide or bumetanide, are mostly used as first line diuretics.[2]
- The use of oral medications is generally avoided due to poor absorption in cases of intestinal edema and due to presence of hypoalbuminemia.[1]
- Addition of thiazide-type diuretics, metolazone, or potassium-sparing diuretics are also reasonable options.[2]
- There are currently no guidelines to outline the appropriate dosages and drug selection.
Albumin:
- IV albumin, although generally not recommended for hypoalbuminemia due to its transient effects, has been shown to have synergistic effects with diuretics for an increased delivery of protein-bound diuretics to sites of action.[1]
- Nonetheless, albumin is still not widely recommended, and its risks may at times outweigh the benefits because it is associated with anaphylaxis, hypertension, and pulmonary edema.[1]
Treatment of Proteinuria
- Since proteinuria is one of the most significant factors for progression of disease and is associated with outcome, treatment of proteinuria in nephrotic syndrome must always be considered a priority.[3][4]
- Angiotensin-converting enzyme inhibitors (ACE-I), with or without angiotensin-II receptor blockers (ARB) have been extensively studied and are well-known to decrease proteinuria and the risk of progression of renal disease in patients with nephrotic syndrome.[5][6][7][8][9] In such cases, the indication of ACE-I is beyond blood pressure control. Patients must thus be started on ACE-I regardless of the presence of hypertension or not.
- Treatment with combined agents has been shown to effectively reduce proteinuria more than treatment with single agents.[5][6][7][10]
- Follow-up with measurements of serum electrolytes is recommended periodically.
- In adults, an addition of corticosteroids has not been proven to be beneficial, except if the underlying etiology necessitates the use of steroids or if no improvement on conservative therapy takes place. In converse, most children with nephrotic syndrome are diagnosed with minimal change disease (MCD) and require corticosteroids for the resolution of proteinuria.[11][12]
Treatment of Hyperlipidemia
- There are currently no reliable randomized clinical trials to recommend the use of lipid-lowering therapy in patients with nephrotic syndrome.[1]
- It is however well-established that treatment of nephrotic syndrome itself often resolves the associated hyperlipidemia.
- One meta-analysis and post hoc subgroup analysis showed that statin might be effective in reducing cardiovascular disease in patients with nephrotic syndrome. As such, nephrotic syndrome should not change the indication for lipid-lowering treatment.[13][14][15][16][17]
Dietary Recommendations
- There is currently no evidence to support or reject protein intake in patients with nephrotic syndrome. While a low protein diet may predispose to malnutrition, high protein diet has also been shown to exacerbate proteinuria.[1][18]
Other
Other recommendations, such as vaccinations and use of other prophylactic medications are listed below:[13]
- Pneumococcal vaccines are recommended for all patients with nephrotic syndrome.
- Prophylactic antibiotics are not recommended for patients with nephrotic syndrome.
- Prophylactic anticoagulation is not recommended. Anticoagulation may be initiated in thrombotic events, with special consideration to the decreased efficiency of heparin in patients with nephrotic syndrome due to the decreased serum antithrombin III levels needed for heparin anticoagulation.
Contraindicated Medications
Nephrosis or the nephrotic phase of nephritis is considered an absolute contraindication to the use of the following medications:
References
References
- β 1.0 1.1 1.2 1.3 1.4 1.5 Hull RP, Goldsmith DJ (2008). “Nephrotic syndrome in adults”. BMJ. 336 (7654): 1185β9. doi:10.1136/bmj.39576.709711.80. PMCΒ 2394708. PMIDΒ 18497417.
- β 2.0 2.1 Brater DC (1998). “Diuretic therapy”. N Engl J Med. 339 (6): 387β95. doi:10.1056/NEJM199808063390607. PMIDΒ 9691107.
- β Ruggenenti P, Perna A, Mosconi L, Pisoni R, Remuzzi G (1998). “Urinary protein excretion rate is the best independent predictor of ESRF in non-diabetic proteinuric chronic nephropathies. “Gruppo Italiano di Studi Epidemiologici in Nefrologia” (GISEN)”. Kidney Int. 53 (5): 1209β16. doi:10.1046/j.1523-1755.1998.00874.x. PMIDΒ 9573535.
- β Locatelli F, Marcelli D, Comelli M, Alberti D, Graziani G, Buccianti G; et al. (1996). “Proteinuria and blood pressure as causal components of progression to end-stage renal failure. Northern Italian Cooperative Study Group”. Nephrol Dial Transplant. 11 (3): 461β7. PMIDΒ 8710157.
- β 5.0 5.1 Gansevoort RT, Sluiter WJ, Hemmelder MH, de Zeeuw D, de Jong PE (1995). “Antiproteinuric effect of blood-pressure-lowering agents: a meta-analysis of comparative trials”. Nephrol Dial Transplant. 10 (11): 1963β74. PMIDΒ 8643149.
- β 6.0 6.1 “Randomised placebo-controlled trial of effect of ramipril on decline in glomerular filtration rate and risk of terminal renal failure in proteinuric, non-diabetic nephropathy. The GISEN Group (Gruppo Italiano di Studi Epidemiologici in Nefrologia)”. Lancet. 349 (9069): 1857β63. 1997. PMIDΒ 9217756.
- β 7.0 7.1 Nakao N, Yoshimura A, Morita H, Takada M, Kayano T, Ideura T (2003). “Combination treatment of angiotensin-II receptor blocker and angiotensin-converting-enzyme inhibitor in non-diabetic renal disease (COOPERATE): a randomised controlled trial”. Lancet. 361 (9352): 117β24. doi:10.1016/S0140-6736(03)12229-5. PMIDΒ 12531578. Review in: ACP J Club. 2003 Sep-Oct;139(2):40
- β Ruggenenti P, Mosconi L, Vendramin G, Moriggi M, Remuzzi A, Sangalli F; et al. (2000). “ACE inhibition improves glomerular size selectivity in patients with idiopathic membranous nephropathy and persistent nephrotic syndrome”. Am J Kidney Dis. 35 (3): 381β91. PMIDΒ 10692263.
- β Korbet SM (2003). “Angiotensin antagonists and steroids in the treatment of focal segmental glomerulosclerosis”. Semin Nephrol. 23 (2): 219β28. doi:10.1053/snep.2003.50020. PMIDΒ 12704582.
- β Tsouli SG, Liberopoulos EN, Kiortsis DN, Mikhailidis DP, Elisaf MS (2006). “Combined treatment with angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers: a review of the current evidence”. J Cardiovasc Pharmacol Ther. 11 (1): 1β15. PMIDΒ 16703216.
- β Crook ED, Habeeb D, Gowdy O, Nimmagadda S, Salem M (2005). “Effects of steroids in focal segmental glomerulosclerosis in a predominantly African-American population”. Am J Med Sci. 330 (1): 19β24. PMIDΒ 16020995.
- β Schieppati A, Perna A, Zamora J, Giuliano GA, Braun N, Remuzzi G (2004). “Immunosuppressive treatment for idiopathic membranous nephropathy in adults with nephrotic syndrome”. Cochrane Database Syst Rev (4): CD004293. doi:10.1002/14651858.CD004293.pub2. PMIDΒ 15495098.
- β 13.0 13.1 Kodner C (2009). “Nephrotic syndrome in adults: diagnosis and management”. Am Fam Physician. 80 (10): 1129β34. PMIDΒ 19904897.
- β OrdoΓ±ez JD, Hiatt RA, Killebrew EJ, Fireman BH (1993). “The increased risk of coronary heart disease associated with nephrotic syndrome”. Kidney Int. 44 (3): 638β42. PMIDΒ 8231039.
- β Crew RJ, Radhakrishnan J, Appel G (2004). “Complications of the nephrotic syndrome and their treatment”. Clin Nephrol. 62 (4): 245β59. PMIDΒ 15524054.
- β Fried LF, Orchard TJ, Kasiske BL (2001). “Effect of lipid reduction on the progression of renal disease: a meta-analysis”. Kidney Int. 59 (1): 260β9. doi:10.1046/j.1523-1755.2001.00487.x. PMIDΒ 11135079.
- β Tonelli M, MoyΓ© L, Sacks FM, Cole T, Curhan GC, Cholesterol and Recurrent Events Trial Investigators (2003). “Effect of pravastatin on loss of renal function in people with moderate chronic renal insufficiency and cardiovascular disease”. J Am Soc Nephrol. 14 (6): 1605β13. PMIDΒ 12761262.
- β Guarnieri GF, Toigo G, Situlin R, Carraro M, Tamaro G, Lucchesli A; et al. (1989). “Nutritional state in patients on long-term low-protein diet or with nephrotic syndrome”. Kidney Int Suppl. 27: S195β200. PMIDΒ 2636656.
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2] ,Yazan Daaboul, Serge Korjian
