Dense Deposit Disease When Blood Pressure Control and ACE Inhibitor Therapy Has Not Met Targets
In dense deposit disease, the initial approach centres on renin-angiotensin system blockade to reduce proteinuria and control blood pressure. When this strategy is insufficient — proteinuria persists and blood pressure goals remain unmet — escalation to a second-line protocol is warranted.
First-Line Failure Condition
Aggressive blood pressure control with ACE inhibitors and/or angiotensin II receptor blockers, with lipid-lowering therapy added where indicated, did not achieve the required reduction in proteinuria or sustained blood pressure targets. This failure triggers escalation to the next step.
Second-Line Approach (Partial Overview)
The next step involves complement-targeted therapy, initiated when end organ damage is evident from proteinuria or haematuria — the full selection criteria, specific agents, and duration are available in the complete protocol.
Clinical Goals
The aim is to prevent further decline in renal function — assessed by the degree of proteinuria and haematuria — while also normalising alternative complement pathway activity levels and reducing relevant complement biomarkers.
References
DOI: 10.1681/ASN.2007030356
Treatment with rituximab, plasma exchange or infusion, eculizumab, or sulodexide should be initiated in the presence of end organ damage (proteinuria/hematuria) and be continuous for 6 to 12 wk.
Other treatments that should be considered include eculizumab (an anti-C5 antibody) and sulodexide (a heparanase inhibitor).
The primary criterion for success at the end of this period should be prevention of disease progression (either maintenance of or prevention of decrease in renal function) as measured by the degree of proteinuria/hematuria.
Secondary criteria for success should be normalization of activity levels of the alternative complement pathway and reduction in C3NeF levels.
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