Introduction

A patient with membranoproliferative glomerulonephritis secondary to Lyme disease is presented. This is the first report of glomerulonephritis secondary to Lyme disease in a human. We propose that the pathogenesis in this case is similar to that proposed for glomerulonephritis in chronic hepatitis B infection.

Case Report

A 65-year old man presented with a three week history of severe right-sided frontal headache, which radiated to the neck and was triggered by touch. He also complained of nausea, dizziness, loss of taste and double-vision. On examin-ation, the right temple was exquisitely tender to touch, and there was a right sixth cranial nerve palsy. Horizontal diplopia was present in the centre of the visual field. Neurological examination was otherwise normal.

The white cell count was 6.6 x 109/L (60.4% granulo-cytes), platelets were 299 x 109/L, and erythrocyte sedimentation rate was 115 mm/h. Liver chemistries were abnormal, with an alanine aminotransferase of 140 U/L (normal range, 0-45), gamma glutamyl transpeptidase 341 U/L (normal range, 11-85) and the alkaline phosphatase was 372 U/L (normal range, 41-117). Serological tests for hepatitis B surface antigen, antibodies to hepatitis B core antigen, and hepatitis A IgM were negative. Antibodies to brucella and leptospira were not detected. Anti-nuclear antibodies were not detected. Angiotensin converting enzyme level was normal. Anti-double stranded DNA antibodies and anti-neutrophil cytoplasmic antibodies were not detected. A liver biopsy was normal.

The cerebrospinal fluid was sterile with a moderate Iymphocytosis of 49/uL. CSF protein was 1.8 glL and glucose 4.2 mmol/L. Examination of CSF for Mycobacterium tuberculosis by Ziehl-Neelsen stain and culture were negative. Oligoclonal bands which were not matched on a simultaneous serum sample, were detected on isoelectric focusing of CSF. A mantoux test was negative and a Tensilon test was normal.

Urinalysis showed sterile pyuria, with proteinuria. Renal function was impaired with a blood urea of 29.7 mmol/L (normal range, 2.8-6.8) and a serum creatinine of 462 umol/L (normal range, 62-150). Renal biopsy showed mesangiocapillary (membranoproliferative) glomerulonephritis. The immunofluorescence staining pattern showed linear positivity for IgG, IgA and C3, and was consistent with type 1 disease (see figures 1, 2 & 3). Electron microscopy was not performed. C3 nephritic factor and serum cryoglobulins were not measured, but C3 and C4 levels were within the normal range.

During the hospital admiss-ion the sixth cranial nerve palsy became bilateral. A computed tomography scan of the brain was normal. Magnetic resonance imaging of the brain and ventricular system showed no abnorm-ality. Temporal artery biopsy was not performed.

Antibodies to Borrelia burgdurferii were detected at 35.25 units by ELlSA (>30 units is construed a strong positive). IgG immunoblot was performed to confirm serological reactivity with specific Borrelia burgdorferi antigens and was interpreted as indicating present or past Lyme disease.

Treatment was commenced with intravenous methy-lprednisolone in a dosage of 500 mgs daily for three days. There was a prompt improvement of the headache. He was discharged on a reducing dose of oral prednisolone, and intramuscular ceftriaxone (2 grams daily) for three weeks, which was tolerated for ten days. The cranial nerve palsies resolved.

On follow-up at one month renal function had improved with a urea of 12.7mmol/L and serum creatinine of 134 umol/L. ESR was 33 mm/h. On follow up at twelve months he remained well with no evidence of neurological or renal sequelae.

Based on the clinical and laboratory findings in this case a diagnosis of membranoproliferative glomerulonephritis and cranial arteritis secondary to Lyme disease was made.

Discussion

A link between Borellia burgdorferi and cranial arteritis has been reported previously¹. It has been shown that Borrelia burgdorferi can cause membranoproliferative glomerulonephritis in dogs², which is manifested clinically as a rapidly progressive and fatal glomerular disease. A variety of infectious agents have been implicated in causation but, to our knowledge, there have been no previous reports of an association with B. burgdorferi or Lyme disease in man.

The pathogenesis of membranoproliferative glomerulonephritis is not completely understood³, but there is considerable evidence that it is immune complex mediated⁴. In patients with chronic hepatitis B infection and membranoproliferative glomerulonephritis, hepatitis B surface antigen has been demonstrated in mesangial deposits⁵. It has been proposed that chronic hepatitis B infection causes a state of chronic antigenemia, with the formation of circulating immune complexes which are deposited in the glomeruli, causing type 1 or atypical membranoproliferative glomerulonephritis⁴.

We suggest that the pathogenesis of membranoproliferative glomerulonephritis in this man with Lyme disease is similar to that proposed in chronic hepatitis B infection.

Correspondence:

P Finnegan,
Dept. of Medicine,
University College Hospital,
Galway.

References

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