IgA nephropathy medical therapy: Difference between revisions
Rim Halaby (talk | contribs) |
Olufunmilola (talk | contribs) No edit summary |
||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{IgA nephropathy }} | {{IgA nephropathy }} | ||
{{CMG}} | {{CMG}}{{APM}} {{AE}}{{OO}] | ||
==Overview== | ==Overview== | ||
==[[IgA nephropathy|Medical Therapy]]== | ==[[IgA nephropathy|Medical Therapy]]== | ||
Revision as of 19:04, 23 January 2017
|
IgA nephropathy Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
IgA nephropathy medical therapy On the Web |
|
American Roentgen Ray Society Images of IgA nephropathy medical therapy |
|
Risk calculators and risk factors for IgA nephropathy medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Ali Poyan Mehr, M.D. [2] Associate Editor(s)-in-Chief: {{OO}]
Overview
Medical Therapy
According to “The National Kidney Foundation: Kidney Disease - Improving Global Outcomes” (NKF-KDIGO)[1] in 2012, the management and treatment recommendations of primary IgA nephropathy are as follows:
Goals of Management
- Prevent the occurrence of repeated episodes of AKI and persistent macroscopic hematuria[2]
- Reduce proteinuria to less than 1 g/24 hrs in adults and to less than 0.5 g/24 hrs in children regardless of baseline proteinuria at diagnosis[2][3]
- Control blood pressure to < 130/80 mmHg if proteinuria is > 0.3 g/24 hrs and more aggressively to <125/75 mmHg if proteinuria is 1g/24 hrs[2]
- Reduce avoidable risk factors, such as obesity. Weight loss to a BMI<25 kg/m2 is recommended to patients with IgA nephropathy to reduce obesity and cardiovascular co-morbidities and degree of proteinuria[2]
Treatment
Supportive Measures
Supportive measures are to performed in IgA nephropathy similar to the measures required for management of ATN[2]
- Indication: Remarkable presence of only ATN and intratubular RBC casts
Pharmacologic Therapy
- Angiotensin-converting enzyme inhibitor (ACE-I) or angiotensin II-receptor blocker (ARB)[2]
- To titrate dosages as required and as tolerated[2]
- Duration: Chronic
- Indications:
- Proteinuria > 1g/24 hrs in adults or 0.5 g/24 hrs in children
- Blood pressure > 130/80 mmHg if proteinuria < 1g/24 hrs
- Blood pressure > 125/75 mm Hg if proteinuria > 1g/24 hrs
ACE-I or ARB are helpful to reduce proteinuria. Nonetheless, randomized clinical trials (RCT) have not yet been conducted to assess their role in reducing the progression to ESRD. Although combination therapy has been proven more effective in monotherapy in some studies[4][5], KDIGO guidelines have not made recommendations about combination therapy yet pending RCTs.
- Corticosteroids[2]
- Duration: 6 months
- Indication: GFR > 50 ml/min/1.73m2 and persistent proteinuria > 1g/24 hrs despite ACE-I or ARB and BP control
The use of steroids in patient with a GFR<50 ml/min/1.73m2 has not been studied yet. Specific dosage is not yet recommended according to KDIGO guidelines. There are more observed side-effects with high-dose pulse corticosteroids.
- Immunosuppressive agents (cyclophosphamide, azathioprine)[2]
- Duration: Cyclophosphamide: 3 months and azathrioprine: minimum 2 years.
- Indication: Patients on steroid therapy with rapidly progressive IgA nephropathy and >50% crescent formation on biopsy
Immunosuppressive agents should not be used in patients with low GFR < 30 ml/min/1.73m2 except if indicated as above. The dose of steroid must be reduced when using concomitant immunosuppressive therapy. One RCT showed better kidney function by reducing corticosteroiddose from 40mg/d to 10mg/d with use of cyclophosphamide at 1.5mg/kg/d for 3 months followed by azathioprine at 1.5mg/kg/d for at least 2 years.
- Fish oil[2]
- Indication: Persistent proteinuria > 1g/24 hrs despite 3-6 months of optimal ACE-I or ARB and blood pressure control.
Fish oil at a dose of 12g/d was shown to improve renal outcome in patients with IgA nephropathy in trials by reducing rate of ESRD in 4 years from 40% to only 4%.[6] In another 6-month study, 3g/d dose also showed better prognosis with less proteinuria.[7]
References
- ↑ Haubitz M, Wittke S, Weissinger EM, Walden M, Rupprecht HD, Floege J; et al. (2005). "Urine protein patterns can serve as diagnostic tools in patients with IgA nephropathy". Kidney Int. 67 (6): 2313–20. doi:10.1111/j.1523-1755.2005.00335.x. PMID 15882273.
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 2.7 2.8 2.9 Radhakrishnan J, Cattran DC (2012). "The KDIGO practice guideline on glomerulonephritis: reading between the (guide)lines--application to the individual patient". Kidney Int. 82 (8): 840–56. doi:10.1038/ki.2012.280. PMID 22895519.
- ↑ Reich HN, Troyanov S, Scholey JW, Cattran DC, Toronto Glomerulonephritis Registry (2007). "Remission of proteinuria improves prognosis in IgA nephropathy". J Am Soc Nephrol. 18 (12): 3177–83. doi:10.1681/ASN.2007050526. PMID 17978307.
- ↑ Russo D, Pisani A, Balletta MM, De Nicola L, Savino FA, Andreucci M; et al. (1999). "Additive antiproteinuric effect of converting enzyme inhibitor and losartan in normotensive patients with IgA nephropathy". Am J Kidney Dis. 33 (5): 851–6. PMID 10213639.
- ↑ Yang Y, Ohta K, Shimizu M, Nakai A, Kasahara Y, Yachie A; et al. (2005). "Treatment with low-dose angiotensin-converting enzyme inhibitor (ACEI) plus angiotensin II receptor blocker (ARB) in pediatric patients with IgA nephropathy". Clin Nephrol. 64 (1): 35–40. PMID 16047643.
- ↑ Donadio JV, Bergstralh EJ, Offord KP, Spencer DC, Holley KE (1994). "A controlled trial of fish oil in IgA nephropathy. Mayo Nephrology Collaborative Group". N Engl J Med. 331 (18): 1194–9. doi:10.1056/NEJM199411033311804. PMID 7935657.
- ↑ Donadio JV, Grande JP, Bergstralh EJ, Dart RA, Larson TS, Spencer DC (1999). "The long-term outcome of patients with IgA nephropathy treated with fish oil in a controlled trial. Mayo Nephrology Collaborative Group". J Am Soc Nephrol. 10 (8): 1772–7. PMID 10446945.