Gilbert’s Syndrome and Proteinuria: A Case Report

Case Report

Chronic Dis Int. 2015;2(2): 1016.

Gilbert’s Syndrome and Proteinuria: A Case Report

Vaia D. Raikou1* and Despina Kyriaki2

1Department of Medicine, National & Kapodistrian University of Athens, Greece

2Department of Nuclear Medicine, General Hospital Athens, Greece

*Corresponding author: Vaia Raikou, Department of Medicine, National & Kapodistrian University of Athens, 17 Agiou Thoma -Athens, Greece

Received: May 13, 2015; Accepted: June 22, 2015; Published: June 23, 2015

Abstract

Gilbert’s syndrome is characterized by increased unconjugated bilirubin in the plasma. Bilirubin may be associated with chronic antihypertensive actions, due to its role on renal hemodynamic and renal tubule function. We describe a case of patient with Gilbert’s disease and proteinuria.

Keywords: Gilbert’s syndrome; Proteinuria; Bilirubin

Introduction

Gilbert’s syndrome, with a prevalence of 1% to 3% in general population, is a common, harmless genetic condition characterized by increased unconjugated bilirubin in the plasma, due to mutations in hepatic UDP-glucuronosyltransferase (UGT1A1), which decrease the conjugation of bilirubin in the liver. Bilirubin is derived from the breakdown of red blood cells produced heme by Heme Oxygenase (HO) enzymes in the spleen. In the blood, bilirubin travels to the liver and is conjugated by hepatic UGT1A1 enzymes. The conjugated bilirubin then exits the liver through the biliary ducts into the bile where it is eliminated through the digestive system.

The enzyme abnormality in Gilbert’s syndrome results in mild elevations of bilirubin in the blood, particularly after starvation or dehydration. The elevated bilirubin pigment can sometimes cause mild yellowing (jaundice) of the eyes. People with Gilbert syndrome are otherwise entirely normal with no other signs or symptoms. Their liver enzyme levels in blood serum are also entirely normal. Gilbert syndrome is most commonly diagnosed after puberty, when alterations in sex hormone levels cause the blood bilirubin levels to rise, or it is diagnosed in the course of routine blood screening. There is no need for treatment, and the prognosis is excellent.

Previous studies have shown that mutations in UGT1A1, such as in Gilbert’s syndrome, which resulted in moderated increases in plasma bilirubin (twofold) were protective against atherosclerosis, coronary heart disease, metabolic syndrome, diabetic nephropathy and end stage of renal disease [1,2,3]. Also, it has been reported that bilirubin is associated with chronic antihypertensive actions, due to its role on renal hemodynamic attenuating constriction from vasoconstrictors such as AII and also acting as an antioxidant in the body [4].

In present report, we describe a case of patient with Gilbert’s disease and proteinuria.

Case Description

A female Gilbert’s disease patient, 30 years old, is coming for examination of proteinuria after recommendation by a practitioner. Proteinuria was found in a annual checkup in urine spot since 2 years. The patient was an official, in a physical activity, with a Body Mass Index (BMI) equal to 28 and she was receiving food supplements.

Her past medical history was free of illnesses. The physical examination did not reveal any significant findings and she was receiving no drugs. She had a normal blood pressure. Her family history was positive for hypertension and dyslipidemia.

The laboratory measurements showed normal findings, except of a mild elevation of Gamma-glutamyltranspeptidase (γGT) and triglycerides. She had a fatty liver history. An urine spot examination showed a single proteinuria without hematuria nor cylindruria and with a normal specific gravity. The echocardiography examination of kidneys was normal and a triplex renal vascular examination was also normal.

Clearance creatinine was equal to 93 ml/min and capillary protein electrophoresis was normal (Figure 1). The average value of proteinuria of three sequences measurements in daily urine per 6 months was equal to 492.3 mg/24 hours. Urine protein electrophoresis and analysis with immunoreactions showed albumin fraction, a1-antitrypsin, transferrin and multiclonical bound with A, G, M immunoglobins κ chains excretion (Figure 2).

Citation: Raikou VD and Kyriaki D. Gilbert’s Syndrome and Proteinuria: A Case Report. Chronic Dis Int. 2015;2(2): 1016.