A Unique Cause of Proteinuria in Pregnancy: Class II Lupus Nephritis with Concomitant Minimal Change Disease

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Abstract

We report the case of a 22-year-old African American female who presented to another facility for routine follow-up in the 34th week of pregnancy with lower extremity swelling and nephrotic-range proteinuria. Although she was normotensive, it was initially thought that she had preeclampsia. She was monitored carefully and delivery was induced at 37 weeks of gestation. She was transferred to our hospital, where she was diagnosed with systemic lupus erythematosus (SLE) based on clinical and laboratory criteria. Renal biopsy revealed a surprising finding of minimal change disease (MCD) concomitant with class II lupus nephritis (LN). She was managed with pulses and then tapering doses of steroid therapy with dramatic resolution of the nephrotic syndrome. This case demonstrates not only the rare de novo occurrence of SLE in pregnancy, but the unique finding of MCD coexisting with class II LN. We propose that altered T cell activity may be the link between these seemingly distinct entities.

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A glomerular permeability factor produced by human T cell hybridomas.

Akio Koyama, Masami Fujisaki, Masaki Kobayashi … (1991)

A glomerular permeability factor produced by human T cell hybridomas. T cell hybridomas derived from the T cells of a patient with mammal change nephrotic syndrome (MCNS) made a glomerular permeability factor (GPF). Sufficient quantities of GPF were available for further analysis and characterization. We obtained four stable clones of human T cell hybridomas which produced a glomerular permeability factor. When this factor was injected intravenously into rats, significant proteinurias were induced, and in normal human lymphocyte culture, GPF enhanced Concanavalin-A (Con-A) induced lymphocyte blastogenesis by greater than ten fold. GPF was cytotoxic to tumor cell lines of epithelial origin, but only cytostatic to tumor cells of hematopoietic origin. Electron microscopy studies, with polyethyleneimine (PEI) staining, indicated that GPF induced the changes in the arrangement of PEI particles and partial fusion of glomerular epithelial cells in the rats given this factor intravenously. The molecular weight of GPF were estimated to be between 60,000 and 160,000 daltons. The molecular weight of the factor and its TNF like activity, we speculated that the factor was a lymphokine, like lymphotoxins.

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Glomerular podocytopathy in patients with systemic lupus erythematosus.

Stephen M. Korbet, Katie Lewis, Timothy W Kraft … (2004)

A series of patients with systemic lupus erythematosus (SLE) and proteinuria were studied to determine whether nephrotic-range proteinuria was associated with diffuse epithelial cell foot process effacement in the absence of peripheral glomerular immune aggregate deposition. Biopsies from patients with known or suspected SLE and a histologic diagnosis of (1) normal by light microscopy, (2) mesangial proliferative glomerulonephritis, or (3) focal segmental glomerulosclerosis were studied. Biopsies were excluded when they demonstrated endocapillary proliferation or necrosis by light microscopy or electron-dense glomerular basement membrane deposits by electron microscopy. Patients were required to fulfill four of 11 American Rheumatologic Association criteria for the diagnosis of SLE, and proteinuria could not be associated with nonsteroidal anti-inflammatory drug use. Eighteen biopsies were studied, eight from patients with nephrotic-range proteinuria (>/=3 g/d) and 10 from patients with non-nephrotic proteinuria. The time from diagnosis of SLE to biopsy was shorter for nephrotic patients that for nonnephrotic patients. Seven of eight biopsies from nephrotic patients demonstrated at least 80% foot process effacement, whereas no biopsy from a nonnephrotic patient exhibited >20% effacement. There were no other significant pathologic differences between the nephrotic and nonnephrotic patients. The single common morphologic feature associated with nephrotic proteinuria was diffuse visceral epithelial cell foot process effacement. It is concluded that the development of nephrotic-range proteinuria in patients with SLE without peripheral immune aggregate deposition or endocapillary proliferation on renal biopsy is more likely a manifestation of SLE than the coexistence of idiopathic minimal-change glomerulopathy and SLE.

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Understanding and Managing Pregnancy in Patients with Lupus

Guilherme de Jesus, Claudia Mendoza-Pinto, Nilson de Jesus … (2015)

Systemic lupus erythematosus (SLE) is a chronic, multisystemic autoimmune disease that occurs predominantly in women of fertile age. The association of SLE and pregnancy, mainly with active disease and especially with nephritis, has poorer pregnancy outcomes, with increased frequency of preeclampsia, fetal loss, prematurity, growth restriction, and newborns small for gestational age. Therefore, SLE pregnancies are considered high risk condition, should be monitored frequently during pregnancy and delivery should occur in a controlled setting. Pregnancy induces dramatic immune and neuroendocrine changes in the maternal body in order to protect the fetus from immunologic attack and these modifications can be affected by SLE. The risk of flares depends on the level of maternal disease activity in the 6–12 months before conception and is higher in women with repeated flares before conception, in those who discontinue useful medications and in women with active glomerulonephritis at conception. It is a challenge to differentiate lupus nephritis from preeclampsia and, in this context, the angiogenic and antiangiogenic cytokines are promising. Prenatal care of pregnant patients with SLE requires close collaboration between rheumatologist and obstetrician. Planning pregnancy is essential to increase the probability of successful pregnancies.

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Author and article information

Journal

Journal ID (publisher-id): CND

Journal ID (pmc): CND

Journal ID (doi): 10.1159/issn.2296-9705

Title: Case Reports in Nephrology and Dialysis

Publisher: S. Karger AG

ISSN (Electronic): 2296-9705

Publication date Subscription-year: 2016

Publication date Collection: September – December 2016

Publication date (Electronic): 09 September 2016

Volume: 6

Issue: 3

Pages: 101-105

Affiliations

[_a] _aDepartment of Internal Medicine, University of Florida College of Medicine, Jacksonville, Florida, USA

[_b] _bDepartment of Nephrology, University of Florida College of Medicine, Jacksonville, Florida, USA

[_c] _cDepartment of Pathology, University of Florida College of Medicine, Jacksonville, Florida, USA

Author notes

*Ryan Kunjal, MD, Department of Internal Medicine, University of Florida College of Medicine, 655W 8th Street, Jacksonville, FL 32209 (USA), E-Mail ryan.kunjal@jax.ufl.edu

Article

Publisher ID: 448731 Pmcid ID: PMC5073675 Other ID: Case Rep Nephrol Dial 2016;6:101–105

DOI: 10.1159/000448731

PMC ID: PMC5073675

PubMed ID: 27781205

SO-VID: 6d1286db-ccba-4179-a02f-19706c9b9d10

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This article is licensed under the Creative Commons Attribution-NonCommercial 4.0 International License (CC BY-NC). Usage and distribution for commercial purposes requires written permission. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

History

Date received : 26 May 2016

Date accepted : 26 July 2016

Page count

Figures: 2, Pages: 5

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A Unique Cause of Proteinuria in Pregnancy: Class II Lupus Nephritis with Concomitant Minimal Change Disease

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Abstract

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Karger: Nephrology

Most cited references 16

A glomerular permeability factor produced by human T cell hybridomas.

Glomerular podocytopathy in patients with systemic lupus erythematosus.

Understanding and Managing Pregnancy in Patients with Lupus

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