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Patients who have only recurrent episodes of gross hematuria seem to be at less risk than those with persistent microscopic hematuria and proteinuria [1,23] . Why this might occur is not clear.
Acute renal failure with gross hematuria  Acute renal failure can occur during episodes of gross hematuria [24-26] . Renal biopsy in these patients reveals mesangial proliferation and segmental crescents in a small proportion of glomeruli (usually less than 25 percent) [24,26] . These findings are insufficient to account for the acute renal failure, which has been ascribed to tubular obstruction by red cell casts . However, the most common histologic lesion is acute tubular necrosis, which may be induced by the iron released from lysed red cells in the tubules  .


This form of acute renal failure is generally a benign complication; the serum creatinine concentration most commonly returns to baseline levels within several weeks to months, even if dialysis is temporarily required [24] . However, incomplete recovery of renal function has been described in up to 25 percent of affected patients [27] .


Histologic predictors of progression  Although clinical features appear to be stronger prognostic indicators [18] , certain findings on renal biopsy have been associated with an increased risk of progressive disease. These include glomerulosclerosis, tubular atrophy, interstitial fibrosis, immune deposits in the capillary loops as well as the mesangium, vascular disease, and crescent formation  .
Several schema for classifying renal biopsy findings have been described that appear to correlate with prognosis; in multivariate analyses, the extent of glomerulosclerosis and tubulointerstitial disease are most commonly associated with a poor prognosis . These indicators are typical of most glomerular diseases. (See "Secondary factors and progression of chronic kidney disease", section on Tubulointerstitial disease).

APPROACH TO THERAPY 

 The optimal approach to the treatment of IgA nephropathy is uncertain [42,43] . The slow rate of loss of GFR (1 to 3 mL/min per year) seen in many patients hinders the ability to perform adequate studies.


There are two separate approaches to the therapy of IgA nephropathy:
General interventions to slow progression that are not specific to IgA nephropathy, include blood pressure control, angiotensin converting enzyme (ACE) inhibitors and/or angiotensin II receptor blockers (ARBs) in patients with proteinuria.

Issues related to statin therapy in patients with chronic kidney disease and serum LDL-cholesterol concentrations above goal values are discussed below and separately. (See "Nonimmunosuppressive therapies" below and see "Statins and chronic kidney disease").


Therapy with corticosteroids with or without other immunosuppressive agents to treat the underlying inflammatory disease. (See "Immunosuppressive therapy" below).


Patient selection  Patient selection for therapy is based in part upon the perceived risk of progressive kidney disease. (See "Clinical predictors of progression" above):


Patients with isolated hematuria, no or minimal proteinuria, and a normal GFR are typically not treated (and often not biopsied and identified), unless they have evidence of progressive disease such as increasing proteinuria, blood pressure, and/or serum creatinine.


Patients with persistent proteinuria (above 500 to 1000 mg/day), normal or only slightly reduced GFR that is not declining rapidly, and only mild to moderate histologic findings on renal biopsy are managed with general interventions to slow progression and perhaps with fish oil. (See "Nonimmunosuppressive therapies" below).


Hematuria Persistent hematuria is generally a marker of persistent immunologic activity, but not necessarily of progressive disease. This finding may be a sign of a "smoldering" segmental necrotizing lesion, suggestive of "capillaritis." Hematuria alone does not require any form of therapy.
Proteinuria Proteinuria, rather than hematuria alone, is a marker of more severe disease [21] . Increasing proteinuria may be due to one of two factors: ongoing active disease; and secondary glomerular injury due to nonimmunologic progression.


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