Treatment and prognosis of IgA nephropathy page-2 |
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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.
Please
proceed to next page of non Immunosuppressive treatment