Membranous glomerulonephritis secondary to Borrelia burgdorferi infection presenting as nephrotic syndrome.

Sir,

A few months following a tick bite an adult patient presented with progressive oedema, hypoalbuminaemia and nephrotic range proteinuria. Serology was positive for Borrelia burgdorferi and renal biopsy confirmed secondary membranous glomerulonephritis (MGN).

A 64-year-old male sustained a tick bite on his left leg whilst holidaying on an island near Stockholm. There was no localized reaction or febrile illness associated with the bite. Over the next few months he experienced progressive oedema. Blood tests showed elevated serum creatinine at 147 μmol (106 μmol 2 months prior to holiday), serum albumin 11 g/L and serum cholesterol/HDL ratio 28.8. Urine dipstick showed 4+ of protein and 1+ of blood. Twenty-four-hour urinary collection for protein excretion was 15.46 g/24 h (<0.15 g/24 h). Hepatitis serology and autoimmune screen were negative and complement levels were normal.

Initial enzyme immunoassay to Borrelia C6 peptide was reactive. This was followed by western immunoblot which was Borrelia burgdorferi IgG antibody positive and IgM antibody negative, consistent with recent infection. The patient was treated with doxycycline 100 mg twice daily for 1 month.

Ultrasound of the renal tract revealed normal sized kidneys and a renal biopsy was performed. Histological examination showed diffuse thickening of the glomerular basement membrane (GBM). Immunohistology demonstrated IgG and C3 in a diffuse granular intensive reaction along the GBM in a membranous pattern. Electron microscopy revealed large electron dense deposits on the mesangial surface.

The patient is on an angiotensin-converting enzyme inhibitor to reduce the intraglomerular pressure, thereby reducing the rate of his disease progression, and on warfarin therapy to reduce the risk of thrombotic complications. His oedema has subsided and the proteinuria has decreased to 650 mg/mmol/L on a recent urine PCR (protein/creatinine ratio) determined in our clinic.

Lyme disease is caused by the tick-borne spirochete Borrelia burgdorferi [1].

Clinical manifestations of Lyme disease include a slowly expanding skin lesion, erythema migrans, which occurs at the site of tick bite. The skin lesion is frequently accompanied by malaise, headache, arthralgia, fever or regional lymphadenopathy, followed within days or weeks by disseminated infection that affects the nervous system, heart or joints [2]. Infection with Borrelia burgdorferi is well described as a cause of glomerulonephritis in animals, particularly canines [3]. This is rarer in humans, and association of Lyme disease with membranoproliferative glomerulonephritis (MPGN) in humans has been described in the literature only twice [4,5].

Most membranous glomerulonephritis is idiopathic but MGN may be secondary to immunological conditions, infections (hepatitis B and C, malaria), neoplasms or drugs.

To our knowledge, this is the first case of membranous glomerulopathy and Borrelia burgdorferi infection as a possible aetiology. The outcome of MGN is variable as the degree of renal recovery is dependent on the causative infectious agent and treatment modalities available.

Conflict of interest statement. None declared.