A Red Herring in the Green Grass: Syphilitic Membranous Glomerulonephritis

Physical discomfort attributed to a routine chore was actually an unusual presentation of an insidious infection. A 51-year-old man presented to the emergency department and reported 1 week of persistent, localized lower back pain that began after he had spent the day mowing his lawn. He denied any trauma, rash, dysuria, discoloration of urine, or other constitutional symptoms. His past medical history included hypertension and a seizure disorder. Approximately 2 days before presentation, he took 2 meloxicam tablets, 7.5 mg, which were acquired from a friend. The prescription drug provided no improvement in his back pain, so he sought further evaluation.

On physical examination, the patient was not in any distress. His blood pressure was 141/86 mm Hg, his pulse was 68 beats per minute, and his weight was 310 lb (140.6 kg). His cardiovascular, respiratory, neurologic, and musculoskeletal findings were all normal. He had no hepatosplenomegaly or lymphadenopathy. However, he had red lesions on the mucous membrane of his soft palate, and dark, pigmented, maculopapular rashes on the palms of his hands and the soles of his feet (Figure 1). In addition, 1+ edema was noted in his legs. Until this point, he had been unaware of the skin lesions.

Relevant electrolyte levels were as follows: sodium, 135 meq/L; potassium, 4.3 meq/L; chloride, 99 meq/L; bicarbonate, 22 meq/L; phosphorus, 6.6 mg/dL; and calcium, 7.6 mg/dL. The patient’s blood urea nitrogen level was elevated at 58 mg/dL, as was creatinine at 6.09 mg/dL (patient’s baseline, 1.0 mg/dL). His serum albumin was 2.4 g/dL; total protein was 6.7 g/dL. A complete blood count measured white blood cells at 6.3 × 103 cells/mm3, hemoglobin level at 11.1 g/dL, hematocrit at 33.5%, and platelets at 176 × 103 platelets/mm3. Urine testing identified a specific gravity of 1.025, pH of 6, protein level exceeding 300 mg/dL, and red blood cell count of 3 per high power field; no glucose, white blood cells, or casts were present in the sample.

Laboratory evaluations indicated acute kidney injury, but the patient’s relatively low creatine kinase levels of 437 U/L and 256 U/L, obtained first in the emergency department and repeated after admission, combined with sequential serum myoglobin levels of 46.4 ng/mL (reference <107 ng/mL) and 30 ng/mL and negative urine myoglobin levels, excluded exertion-related rhabdomyolysis and nonsteroidal anti-inflammatory drug-induced rhabdomyolysis as the etiology. Acute interstitial nephritis induced by use of the nonsteroidal anti-inflammatory medication was entertained as a possible cause of skin rash and acute kidney injury. Yet the patient’s urine concentrating capacity was intact, and his urine was negative for eosinophils and leukocyturia, data that rendered the diagnosis less likely without ruling it out. Viral antibody titers for exanthematous diseases were negative. A rapid plasma reagin test was ordered, because secondary syphilis was a potential cause of the patient’s palmar–plantar rash and glomerular pathology.

An investigation for possible nephrotic syndrome uncovered a 24-hour urine protein level of 4982 mg, a negative hepatitis panel, antinuclear antibody titers within normal limits, normal levels of serum C3 and C4, and normal results from serum and urine electrophoresis. Ultrasonography showed the kidneys to be of normal size. Still, the patient’s renal function failed to improve with continuous hydration. On the third day of his hospitalization, his rapid plasma reagin test proved positive with a titer of 1:512. A fluorescent treponemal antibody absorption test returned positive results, too. Testing for human immunodeficiency virus was negative.

The patient underwent a renal biopsy after confirmation of syphilis. Light microscopy demonstrated mild chronic kidney injury with approximately 15% tubular atrophy and signs of interstitial fibrosis. No evidence of acute vasculitis was present. Of 22 glomeruli, 1 was globally sclerotic, and generally the glomeruli were congested with mild ischemic changes. A slight increase in the mesangial matrix and thickening of the peripheral capillary loops was apparent (Figure 2A). Crescents, necrosis, segmental sclerosis, and hypercellularity were absent.