Histologic versus clinical remission in proliferative lupus nephritis

A Malvar, P Pirruccio, V Alberton… - Nephrology Dialysis …, 2017 - academic.oup.com
A Malvar, P Pirruccio, V Alberton, B Lococo, C Recalde, B Fazini, H Nagaraja, D Indrakanti…
Nephrology Dialysis Transplantation, 2017academic.oup.com
Background Treatment response in lupus nephritis (LN) is defined clinically, without
consideration of renal histology. Few studies have systematically examined histologic
responses to induction therapy. In LN patients who underwent protocol kidney biopsies after
induction immunosuppression, we describe the renal histology of the second biopsy and
correlate histologic activity and damage with short-and long-term kidney outcomes. Methods
Patients with suspected LN were biopsied for diagnosis (Biopsy 1), and those with …
Background
Treatment response in lupus nephritis (LN) is defined clinically, without consideration of renal histology. Few studies have systematically examined histologic responses to induction therapy. In LN patients who underwent protocol kidney biopsies after induction immunosuppression, we describe the renal histology of the second biopsy and correlate histologic activity and damage with short- and long-term kidney outcomes.
Methods
Patients with suspected LN were biopsied for diagnosis (Biopsy 1), and those with proliferative LN were rebiopsied after induction (Biopsy 2). Histologic activity and damage at each biopsy were calculated as the National Institutes of Health activity and chronicity indices. Complete and partial renal responses after induction and after long-term follow-up were determined clinically.
Results
One-third of patients who achieved a complete clinical response after induction had persistently high histologic activity, and 62% of patients who had complete histologic remission on rebiopsy were still clinically active. Chronic renal damage increased after induction even in complete clinical responders. Chronicity at Biopsy 2 associated with long-term kidney function and development of chronic kidney disease.
Conclusions
Early clinical and histologic outcomes are discordant in proliferative LN, and neither correlates with long-term renal outcome. The kidney accrues chronic damage rapidly and despite clinical response in LN. Preservation of kidney function may require therapeutic targeting of both chronic damage and inflammation during LN induction treatment.
Oxford University Press