Case Presentation:

A 61–year–old African American man with long history of diabetes and hypertension as well as end stage renal disease presented with progressive weakness of both legs for 3 months. It started as difficulty walking while carrying weights then to inability to move completely, associated with burning sensation over his bilateral foot soles. “Diabetic polyneuropathy” was initially proposed, but a diagnosis of “uremic polyneuropathy” was made after his condition worsened along with deteriorating kidney function. He started hemodialysis about 2 months earlier but no obvious improvement was observed even with more frequent daily dialysis. On presentation, patient was obese with BMI of 45.7 kg/m², vitals were normal except BP was 174/67. Physical exam revealed normal mental status and cranial nerve function. There was mild weakness over bilateral upper extremities (4/5 in strength) with thenar atrophy, and a complete loss of muscle strength (0/5) over bilateral lower extremities, which were swelling up to the thigh. No spasticity, rigidity, tremor or fasciculations were observed. The light touch, pain, vibration and temperature sensations were grossly intact except abnormal pain elicited by fine touch in the soles of both feet. The sense of position was severely impaired in the lower extremities. Notably, there was a complete loss of deep tendon reflex in all extremities. MRI without gadolinium (due to renal function) showed multiple degenerative spinal discs, but neither central canal compromise nor acute cerebral events were observed. An electromyogram and nerve conducting study revealed findings suggestive of primary demyelinating polyneuropathy with some axonal lesions. A subsequent cerebrospinal fluid analysis showed elevated protein level (85.9 mg/dl, normal: 15–45 mg/dl) with zero leukocyte count. Despite his refusal of nerve biopsy, the existence of CIDP (Chronic inflammatory demyelinating polyneuropathy) possibly on the top of diabetic or uremic polyneuropathy was thus proposed, and treatment with prednisone and intravenous immunoglobulin started. After 3 days, patient began to feel stronger subjectively, and after 5 days, he was able to move his toes. However, presumably due to preexisting axonal damage from either diabetes or uremia, and also a relatively delayed recognition of CIDP, his recovery was not complete.

Discussion:

CIDP is a chronic neuropathy of supposed immune–mediated origin. It is thought to be a common but underdiagnosed disease because the recognition can be sometimes very challenging, especially when a metabolic polyneuropathy could be a plausible explanation for neurological manifestations under conditions such as diabetes and uremia. Early diagnosis of CIDP is thus crucial as it is a potentially treatable disease.

Conclusions:

The purpose of reporting this case is to increase general awareness of CIDP, which may still exist in conditions causing metabolic polyneuropathy. Early intervention may prevent permanent nerve damage and improve the outcome.