Abstract

BackgroundIn SLE, new-onset proteinuria and albuminuria raise concern for renal involvement, even when isolated and subnephrotic. In women of childbearing age, pregnancy-related complications are other causes of renal protein loss. Distinguishing renal disease from pregnancy-related complications of SLE is difficult because SLE is associated with adverse maternal and fetal events, while pregnancy is also a cause of disease relapses. Common to all causes of pathologic proteinuria in SLE is that they are related to disease activity and/or the need for intervention, as proteinuria does not normalize on its own.ObjectivesWe report a case of a patient with inactive SLE who intermittently developed significant isolated proteinuria and albuminuria of glomerular origin that was directly related to spontaneous abortion in early (possibly twin-)pregnancy.MethodsA 39-year-old female with SLE on hydroxychloroquine presented at our clinic for a routine check-up. Physical examination and laboratory tests were performed. To that date, SLEDAI-2K during most visits had a score of 0, indicating inactive disease.ResultsThe patient reported feeling well, and the physical examination was unremarkable. Stable low-grade thrombocytopenia was the only relevant abnormality in recent years. On the current examination, the urine showed significant proteinuria and A3 albuminuria in the protein/albumin to creatinine ratio (uPCR 724 mg/g, uACR 488 mg/g). IgG/creatinine was markedly elevated (74.4 mg/g), and α1-microglobulin was normal, indicating nonselective glomerular proteinuria without tubular impairment. There were no other abnormalities suggestive of SLE activity. After she recalled having vaginal spotting a week earlier, a pregnancy test was performed and was positive. Subsequently, the βHCG level increased insufficiently, and ultrasound detection of a live embryo was not successful, but the presence of two amniotic cavities was suspected. An early incomplete miscarriage was diagnosed, and the gestational age was calculated to be 6 + 5 weeks. Shortly thereafter, a planned suckling curettage was performed. One week later, she had a final vaginal bleed. At this time, the urine showed a decrease in proteinuria of over 50% (uPCR 317 mg/g, uACR 210 mg/g, IgG 26.9 mg/g). Three weeks later, urine protein was completely normalized, which proved stable 12 weeks after initial diagnosis. Throughout the follow-up period, she did not show any SLE relapse.ConclusionAfter exclusion of differential diagnoses (chart), causality of the miscarriage with the urinary findings seems evident. To date, there have been no reports of the concomitant occurrence of early pregnancy miscarriage, possibly LN-indicative glomerular proteinuria, and its spontaneous regression in a clinically and serologically inactive SLE patient. Recently, observations were confirmed that a large proportion of patients with a uPCR <1g/g had LN histology, whereas a relevant proportion had inactive sediment or normal serology like our patient. As the kidney is the organ most affected in SLE pregnancy, it is important to be aware of intermittent proteinuria, as the consequences may be very different from persistent proteinuria as would be expected in nephritis.Figure 1.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

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