An unrecognized cause of oedema in a patient with lupus nephritis: protein losing enteropathy

Chia-Chao Wu1, Shih-Hua Lin1, Pauling Chu1, Jenn-Haung Lai2, Deh-Ming Chang2 and Yuh-Feng Lin1

1 Division of Nephrology and 2 Division of Immunology/Rheumatology and Allergy, Department of Medicine, Tri-Service General Hospital, Taipei, Taiwan, R.O.C.

Correspondence and offprint requests to: Yuh-Feng Lin, Division of Nephrology, Department of Medicine, Tri-Service General Hospital, Number 325, Section 2, Chung-Kung Road, Neihu 114, Taipei, Taiwan. Email: linyf{at}ndmctsgh.edu.tw

Keywords: hypoalbuminaemia; oedema; protein losing enteropathy; systemic lupus erythematosus

A 39-year-old woman was admitted because of marked peripheral oedema. Her haematocrit was 31.0% and her white-cell count was 3500. The urea nitrogen was 9 mg/dl, the creatinine 0.7 mg/dl, the total cholesterol 244 mg/dl, the triglyceride 408 mg/dl and total protein 3.4 g/dl with an albumin of 1.5 g/dl. Other biochemistries were normal. Urinalysis revealed microscopic haematuria with red blood cell casts and a negative dipstick for protein, and twice the 24-h urine collection contained 0.100 and 0.350 g of protein. Anti-nuclear antibody (1:1280), and anti-dsDNA (41 IU/ml, normal <30 IU/ml) were positive. Systemic lupus erythematosus (SLE) was impressed. Renal protein loss due to lupus nephritis was first considered. Kidney biopsy was performed and lupus nephritis WHO class IIa was found. However, the proteinuria was too little to account for the hypoalbuminaemia. Protein losing enteropathy (PLE) was finally proved by Tc-99m albumin scintigraphy, which revealed clear visualization of tracer in the small bowel at 30 min (Figure 1A) and in the large bowel at 24 h (Figure1B), but is normally not seen in normal people (Figure 1C). The patient's symptoms improved excellently with 50 mg prednisolone daily treatment. The dosage of prednisolone was gradually tapered and the patient remained clinically well for 3 years on a maintenance treatment of 5 mg of prednisolone.



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Fig. 1. Images of abdomen after i.v. injection of Tc-99m labelled human serum albumin. (A) Abdominal image 30 min after i.v. injection in the patient showing tracer in small bowel. (B) Abdominal image 24 h after injection in the patient showing tracer in large bowel. (C) Abdominal image 24 h after injection in normal control.

 
PLE has been reported in a heterogenous group of disease. Lesser known is PLE associated with SLE. Lupus-associated PLE typically occurs in young women and was characterized by the onset of profound oedema and hypoalbuminaemia [1]. In many patients, it may be the first obvious manifestation of SLE. Despite the existence of lupus nephritis, PLE still should be kept in mind as a cause of oedema and hypoalbuminaemia as shown in our case. On the other hand, Tc-99m albumin scintigraphy offers a non-invasive, rapid, safe and convenient way to demonstrate gastrointestinal loss of albumin and has the potential to localize the region responsible for leakage [2]. It should be evaluated in patients presenting with unexplained hypoalbuminaemia and oedema to avoid missing the correct diagnosis.

Conflict of interest statement. None declared.

References

  1. Perednia DA, Curosh NA. Lupus-associated protein-losing enteropathy. Arch Intern Med 1990; 150: 1806–1810[Abstract]
  2. Divgi CR, Lisann NM, Yeh SD, Benua RS. Technitium-99m albumin scintigraphy in the diagnosis of protein-losing enteropathy. J Nucl Med 1986; 27: 1710–1712[Abstract]