The topic of IgA nephropathy has been discussed in multiple posts here in the past. IgA is the commonest primary GN with a wide variety of presentations and prognoses ranging from isolated hematuria to a rapidly progressive GN. Over the last few years, my practice has been that if I see a patient with isolated hematuria, no adverse family history and minimal proteinuria, I will not biopsy them and reassure them that their chance of progression is very low. This is an approach that has also been supported by previous posters.
An article and accompanying editorial in this month's JASN would appear to support this approach. This was a retrospective review of the outcomes in 141 patients diagnosed with IgA nephropathy with minimal proteinuria (less than 0.5g) between 1975 and 2008 in 8 Spanish hospitals. During this period there was an aggressive policy in place with a very low threshold for renal biopsy. At the time of biopsy, only 16% were hypertensive while 17.7% had no detectable proteinuria. All patients had a normal eGFR at baseline.
Over a mean follow-up of 9 years, no patients were treated with immunosuppressive agents and 41% were treated with RAAS blockade. 5 patients (3.5%) had an increase of 50% from baseline creatinine while 1 patient had a doubling of creatinine (following pregnancy). 14.9% of patients developed proteinuria (more than 0.5g) while it increased above 1g in 6 patients. The only factor predicting increased proteinuria or an increased creatinine after multivariable analysis was the presence of FSGS (S1 by the Oxford Classification).
These results are very reassuring and for me reinforce the idea that we should not be routinely biopsying patients who present like with isolated hematuria. It is notable that most of the hospitals in this study have stopped this aggressive biopsy policy and it is unlikely that a similar study will be done in the future. However, there is no doubt that they should be followed long term because there is a (small) risk of progression. It should be stated that these results are not necessarily generalizable to other populations - studies in Asian populations have found a much higher rate of progression and the indication for biopsy might be different in this group. It would be interesting to know what the genetic factors underlying this difference in outcomes might be.
An article and accompanying editorial in this month's JASN would appear to support this approach. This was a retrospective review of the outcomes in 141 patients diagnosed with IgA nephropathy with minimal proteinuria (less than 0.5g) between 1975 and 2008 in 8 Spanish hospitals. During this period there was an aggressive policy in place with a very low threshold for renal biopsy. At the time of biopsy, only 16% were hypertensive while 17.7% had no detectable proteinuria. All patients had a normal eGFR at baseline.
Over a mean follow-up of 9 years, no patients were treated with immunosuppressive agents and 41% were treated with RAAS blockade. 5 patients (3.5%) had an increase of 50% from baseline creatinine while 1 patient had a doubling of creatinine (following pregnancy). 14.9% of patients developed proteinuria (more than 0.5g) while it increased above 1g in 6 patients. The only factor predicting increased proteinuria or an increased creatinine after multivariable analysis was the presence of FSGS (S1 by the Oxford Classification).
These results are very reassuring and for me reinforce the idea that we should not be routinely biopsying patients who present like with isolated hematuria. It is notable that most of the hospitals in this study have stopped this aggressive biopsy policy and it is unlikely that a similar study will be done in the future. However, there is no doubt that they should be followed long term because there is a (small) risk of progression. It should be stated that these results are not necessarily generalizable to other populations - studies in Asian populations have found a much higher rate of progression and the indication for biopsy might be different in this group. It would be interesting to know what the genetic factors underlying this difference in outcomes might be.
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