IgA Np is the most commonly observed etiology of primary (idiopathic) GN in developed world. Slowly progressing to ESRD can be seen in up to 50 % of p
IgA Np is the most commonly observed etiology of primary (idiopathic) GN in developed world. Slowly progressing to ESRD can be seen in up to 50 % of ptns, usually > ys of observation. The rest of ptns develop persistent clinical remission or have sustained low-grade hematuria and/or proteinuria. The clinical predictors denoting progression of IgA Np may include:
o Higher SCr,
o HT, and
o Sustained proteinuria > 1000 mg/d.
Ptns having recurrent attacks of gross hematuria with no proteinuria considered at a lowered risk for progressive renal disease.
AKI can be seen in ptns with episodic gross hematuria that can be related to ATN, & SCr typically comes back to its baseline within few weeks. However, AKI may alarm to crescentic lesion requiring urgent therapy. In IgA Np ptn with acute decline in renal function and not improving within a week's follow up, repeating kidney biopsy is suggested to exclude crescentic formation.
2 major approaches have been suggested:
o Non-im/m therapy to slow down disease progression:
1. Fish oil.
2. BP control,
3. ACEi/ARBs; for proteinuric ptns.
o im/m therapy with GC, with/without other im/m medications, to manage the underlying inflammatory lesions.
o Angiotensin inhibition with ACEi or ARB. Target of urinary proteinuria < 500 mg/d or 1 g/d & BP < 130/80 mmHg.
o Fish oil (3.3 g/d. or more), that can be tried with proteinuria > 1 g/d despite mo of therapy with ACEi/ARB. Fish oil may have CVS benefits.
Anti-inflammatory with GC with progressively active disease including hematuria + one or more of:
o Rising SCr
o Persistent proteinuria > 1 g/d after maximal anti-proteinuric non-im/m ttt
o Morphologic evidence of active disease in renal biopsy (e.g., proliferative or necrotizing glomerular alterations)
o No need to introduce GC with chronic rise in SCr or histologic findings of prominent GS and IF/TA
Either of the following 2 protocols is accepted for ptns selected for GC therapy:
o IV. Mp, 1 g, for 3 successive days at the beginning of mo 1, 3, & 5, + Pred on alternate days for 6 more mo. mg/kg oral
o Pred, 2 mo followed by monthly dose decline of mg/kg/d. in the next 4 mo. mg/kg/d, for