GLF and WC made the pathological diagnosis. . Skin involvement occurs in more than 85% of lupus erythematosus (LE) cases, and the four classic presentations include malar rash, discoid rash, photosensitivity and oral mucosal lesions . Lupus-related polyneuropathy have been reported in 10C20% of patients with SLE . Many different types of neuropsychiatric symptoms occur in patients with SLE. The kidney is also one CSH1 of most frequently involved organs. The reported incidence of clinically important kidney diseases in systemic lupus varies widely, range from 12 to 69% . However, patients with SLE may present with an array of manifestations not limited to these common presentations, such as Guillan Barr syndrome (GBS), papulonodular mucinosis (PNM) and class V nephritis which are all rarer associations in SLE than describing in general about neurological, mucocutaneous manifestations and renal involvement in SLE. Awareness of the spectrum of clinical manifestations of Fosfructose trisodium SLE, especially uncommon changes, is essential for diagnosis and effective management of patients. We describe a rare case of SLE in a patient who initially had cutaneous PNM and had not been identified for 2?years until GBS and class V lupus nephritis were detected. Case presentation A 26-year-old Chinese man presented with progressive numbness, weakness and paresthesia of the extremities. One month before admission, he began to complain of mild symmetrical numbness, weakness and paresthesia of limbs (with socks and gloves distribution). Simultaneously, he was found to have transient facial erythema after exposed to ultraviolet light, which disappeared spontaneously without treatment. One week before admission, his numbness and weakness in lower extremities progressed to limit his ambulation. His medical past history was notable for isolated nodular masses twice without pain in the cheeks below the left and right earlobe in 2013 and 2014, which were 4??5?cm (left) in 2013 and 3??3?cm (right) in 2014. They were both resected with a pathological diagnosis of nodular fasciitis in his local hospital. He also complained of moderate fatigue and alopecia for 2?years. There was no family history of other connective diseases. The physical examination showed that there was motor weakness with a power of 2 of 5 in lower extremities and 3 of 5 in upper extremities. The sensory examination was normal. Deep tendon reflexes were decreased and plantar reflexes were flexor. The rest of the examination was unremarkable. Laboratory assessment indicated a erythrocyte sedimentation rate (ESR) of 79?mm/h. Urinalysis showed protein in 3+, urinary sediment 0 to 2 red cells per 10*40 field and no granular casts. Urine protein excretion was 7.00?g/24?h and serum albumin was 1.8?g/dL. The results of the blood cell count and hepatic function tests were normal. The levels of serum creatinine, and urea nitrogen were normal, respectively, 68?mol/L (range 57C97?mol/L) and 3.8?mmol/L (2.6C7.5?mmol/L). Immunological screening revealed an antinuclear antibody titer of 1 1:320, a speckled pattern and a double-stranded DNA antibody titer of 1 1:20 positive. The rest of the autoantibody profiles, including anti-smith, anti-ribonucleoprotein and antineutrophil cytoplasmic antibodies, were negative. Serum C3 Fosfructose trisodium and C4 complement factors were low, respectively, 0.43?g/L (range 0.65C1.65?g/L) and 0.07?g/L (range 0.16C0.6?g/L). The cerebrospinal fluid examination showed an increased protein concentration of 1 1.09?g/L and immunoglobulin (Ig) G level of Fosfructose trisodium 0.28?g/L with a normal number of cells (white cell count was zero). Electromyography revealed a severe demyelinating polyneuropathy and a muscle biopsy revealed neurogenic muscle damage. Kidney biopsy was performed and revealed diffuse thickening of the glomerular basement membrane with spike formation, mesangial hypercellularity and mesangial matrix expansion (Fig.?1). Immunofluorescence revealed 1 to 3+ global granular capillary wall and mesangial staining for IgG, IgA, IgM, C3, C1q, and fibrin-fibrinogen, which gave the characteristic full house immunofluorescence for lupus nephritis. The electron microscopic analyses showed numerous subepithelial and mesangial electron-dense deposits, as well as deposits within the glomerular basement membrane with extensive fusion of foot processes. The renal biopsy diagnosis was secondary membranous nephropathy and suspected lupus nephritis. Two.