Thus, we considered that secukinumab had little harmful effect on his nephropathy

Thus, we considered that secukinumab had little harmful effect on his nephropathy. In summary, we present the case of a patient with psoriasis and remission of secondary IgA nephropathy undergoing treatment with secukinumab. common treatment for psoriasis is usually topical therapy, such as steroid ointment or systemic immunosuppressive drugs. Psoriasis is also known to be associated with kidney dysfunction. It is reported that defects in T cell function or increased immune complexes play a role [2], and the association between this activity and increased risk for kidney disease has also been reported [3]. Inflammatory diseases, such as psoriasis, are exacerbating factors of IgA nephropathy [4]. In recent years, biological drugs, such as adalimumab or secukinumab, have been reported to be effective for the treatment of resistant cases [5, 6]; however, the association between biologics treatment and the clinical course of nephritis has rarely been reported. Moreover, the underlying mechanisms of kidney injury in psoriasis remain unclear. Here, we describe the case with psoriasis who Eprosartan developed secondary IgA nephropathy during treatment with secukinumab and discuss some potential underlying relationships. Case presentation A 60-year-old man was diagnosed with psoriasis 4?years ago. Treatment was initiated with steroid ointment, but his psoriasis did not improve. His psoriasis area and severity index (PASI, range 0C72) score was 40. Treatment with adalimumab, a monoclonal anti-TNF- antibody, was initiated, and psoriasis improved with treatment. The patient designed hypertension, and antihypertensive drugs including angiotensin II receptor blockers were started. Even though psoriasis was well controlled for 3?years, it relapsed (month 0). The patients PASI score was 40 (Fig.?1). Symptoms of peripheral edema, fever, anorexia, and difficulty walking arose. The patient was hospitalized and diagnosed with secondary failure of adalimumab. He also developed nephritis with severe kidney dysfunction [estimated glomerular filtration rate (eGFR) 26?mL/min/1.73?m2], proteinuria, and hematuria. Adalimumab was discontinued, and treatment with a steroid ointment, ultraviolet therapy, etretinate, and systemic antibiotics was started. The psoriasis improved and the patients PASI score was 2.8 (Fig.?1). Treatment with secukinumab, a human monoclonal antibody for interleukin (IL)-17A, was launched to maintain remission. As psoriasis improved, nephritis improved gradually, and remission was achieved in a few weeks (Fig.?2). The patient was in remission with treatment of secukinumab and was regularly followed up in our outpatient clinic. After the induction phase, treatment with an injection of secukinumab changed from once a week to once every 4?weeks. Open in a separate windows Fig.?1 Clinical course of the patient. ARBs, Angiotensin II Receptor Blockers; CTRX, ceftriaxone; PASI, Psoriasis Area and Severity Index; eGFR, estimated glomerular filtration rate Open in a separate windows Fig.?2 Photographs of the skin lesion. Upon recurrence of psoriasis (month 0), the PASI Eprosartan score was 40 (a). After 3?months of treatment with secukinumab (month 5), the PASI score was 0.8 (b) Five months later (month 6), pitting edema in the lower legs appeared and worsened. The patient was diagnosed with nephrotic syndrome and admitted to our hospital for further investigation. On admission, his height was 164.8?cm and excess weight was 74.9?kg, which increased by 13?kg within 5?months. A CT scan demonstrated an increased visceral excess fat. His waist circumference was 92?cm. The patient experienced hypertension and dyslipidemia and he met the diagnostic criteria for metabolic syndrome. The patients blood pressure, heart Eprosartan rate, and body temperature were 134/76?mmHg, 75?bpm, and 36.4?C, respectively. A moderate psoriasis lesion was Eprosartan observed in the extensor surfaces of extremities. Laboratory data were as follows: proteinuria, 7.2?g/g Cr; hematuria, 3+; reddish blood cell casts, 1+; hemoglobin level, 14.8?g/dL; BUN, Eprosartan 18?mg/dL; serum Cr level, 1.15?mg/dL; eGFR, 49.8?mL/min/1.73?m2; total protein PRF1 level, 5.9?g/dL; serum albumin level, 3.2?g/dL; IgG level, 777?mg/dL; IgA level, 844?mg/dL; IgM level, 43?mg/dL; C3, 98?mg/dL; C4, 17?mg/dL; CH50, 55 U/mL; ASO,? ?70?IU/mL; ASK, 40 occasions; and C-reactive protein level, 0.2?mg/dL. We could not detect antinuclear antibodies, anti-double stranded DNA antibodies, proteinase-3 antineutrophil cytoplasmic antibodies (PR3-ANCA), myeloperoxidase-ANCA (MPO-ANCA), anti-glomerular basement membrane (GBM) antibodies, or cryoglobulin. An immunofixation electrophoresis test showed the presence of IgG kappa monoclonal protein. No evidence of amyloidosis or bone marrow disease was found after examination of the serum-free light-chain ratio and bone marrow examination. Treatment continued with secukinumab and telmisartan, an angiotensin II receptor blocker. After 1?week on a sodium-restricted diet with bed rest,.