MIRROR SYNDROME AND SEVERE PREECLAMPSIA: A CASE REPORT

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https://storage.unitedwebnetwork.com/files/1099/5220422502deff7608bc8f78afc9cb82.pdf

Abstract Title

First Name *

Martin

Last Name *

Frisch

Co-author 1

Lucía Facal luciafacalferreira@gmail.com Hospital de Clínicas Dr. Manuel Quintela Montevideo Montevideo

Co-author 2

Paula Parnizari paulaparnizari@gmail.com Hospital de Clínicas Dr. Manuel Quintela Montevideo Montevideo

Co-author 3

Gabriela Ottati gottati@gmail.com Hospital de Clínicas Dr. Manuel Quintela Montevideo Montevideo

Co-author 4

José Boggia ppboggia@gmail.com Hospital de Clínicas Dr. Manuel Quintela Montevideo Montevideo

Co-author 5

Oscar Noboa onoboa@gmail.com Hospital de Clínicas Dr. Manuel Quintela Montevideo Montevideo

Co-author 6

Co-author 7

Co-author 8

Co-author 9

Co-author 10

Co-author 11

Co-author 12

Co-author 13

Co-author 14

Co-author 15

Introduction

Ballantyne syndrome or Mirror syndrome is a rare condition, associated with high fetal and maternal morbi-mortality. It is characterized by the triad of maternal, placental and fetal edema.

Methods

Report the case of a patient with Mirror syndrome complicated with severe and early onset preeclampsia and acute kidney injury.

Results

A 29-year old white female, with unremarkable medical background, was hospitalized while undergoing 17 weeks of her first pregnancy, complicated with gestational diabetes. She had no previous diagnosis of hypertension or proteinuria. She presented with generalized edema and weight gain of 6 kg in one month. She denied headache or visual disturbances.

Physical examination: BP 170/120 mmHg, generalized edema, without other signs of congestive heart failure.

Laboratory tests: urinary protein to creatinine ratio 0,35 g/g, bland urinary sediment, negative urine culture, serum creatinine 0,66 mg/dl, azotemia 37 mg/dl, Na 139 mEq/l, hemoglobin 11,9 g/dl, platelet count 153000 cel/mm3, albumin 3,4 g/dl and normal liver enzymes. Negative inmunologic work-out. Maternal transthoracic echocardiography and renal ultrasound were unremarkable.

The patient had a rapid deterioration within 72 hours from admission, with sustained oligoanuria, creatininemia 0,77mg/dl, acute hyponatremia (118 mEq/l), a decrease in platelet count, hematocrit and albumin. She also developed a slight increase in transaminases and uricemia (5,9 mg/dl). Fetal structural ultrasound reported anhydramnios, fetus with ascites, displaced mediastinum and a compressed heart by both enlarged lungs, echogenic and with cysts, suggesting bilateral renal agenesis or hypoplasia. Serum sFlt-1/PIGF ratio was 239 (reference value < 33).

With diagnosis of acute kidney injury secondary to severe preeclampsia in the context of Mirror syndrome due to fetal hydrops, termination of the pregnancy was decided. The patient had a favorable evolution, with resolution of the kidney injury, improvement of edema and dilutional hyponatremia, and was discharged from hospital after 10 days. On follow-up she continues normotensive with normal renal function and negativization of proteinuria.

Conclusions

Given the development of severe hypertension in the context of edema and oliguria, in absence of inflammatory urinary sediment, the first diagnostic approach was early onset severe preeclampsia.

The originality of the clinical case is that the cause of preeclampsia was Mirror Syndrome. The evolution confirmed this infrequent entity, with resolution after termination of the pregnancy. This is an extremely rare condition, probably underdiagnosed, highlighting the importance of acknowledging it in nephrology practice. It should be suspected in a patient with early onset preeclampsia with signs of maternal hemodilution, ruling out other causes such as mole, multiple gestation and chronic kidney disease. The pathogenesis is unclear, but at least in some cases the placenta edema increases the production of the soluble form of tyrosine kinase 1 (sFlt1), an important mediator of endothelial and vascular abnormalities in preeclampsia. Therefore, sFlt-1/PIGF ratio could be a diagnostic tool. The clinical case emphasizes creatinine is a poor marker of glomerular filtration, particularly in pregnancy. In this case diuresis was a more sensitive indicator of acute renal failure.

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