Before the diagnosis with cryoglobulinemic glomerulonephritis, the patient needed hemodialysis twice

Before the diagnosis with cryoglobulinemic glomerulonephritis, the patient needed hemodialysis twice. the human body, temperatures below Sulfasalazine normal body temperature cause them to accumulate in various Sulfasalazine organs (1); this Sulfasalazine is a disease state known as cryoglobulinemia. The clinical manifestations of cryoglobulinemia are hyperviscosity syndrome and systemic vasculitis. Renal involvement is usually common and manifests as rapidly progressive glomerulonephritis with membranous proliferative glomerulonephritis as the characteristic histological obtaining (1). Decades ago, treatments for cryoglobulinemia were similar to those for other forms of systemic vasculitis; in 1991, however, it was shown that about 90% of cases of mixed cryoglobulinemia are associated with hepatitis C virus (HCV) Sulfasalazine contamination (2) and that chronic HCV contamination triggers B-cell expansion, which results in the production of cryoglobulins (3). Rituximab was reported as an efficacious treatment in 2003 (4,5) and became the recommended immunosuppressive treatment for patients with histologically active HCV-associated glomerular disease who do not respond to antiviral therapy according to the Kidney Disease Improving Global Outcomes (KDIGO) guidelines in 2018 (6). In addition, direct-acting antiviral brokers (DAAs) have been used for the last decade to improve the clearance of HCV (7). Although these treatments Rabbit polyclonal to ADI1 are expected to improve the clinical outcomes of cryoglobulinemia, several cases of treatment failure or relapse after rituximab and DAAs have recently been reported (8,9). We herein report a case of serologically persistent cryoglobulinemia in which glomerulonephritis was successfully treated with rituximab, DAAs, occasional plasmapheresis and long-term steroid. Case Report A 68-year-old man was referred to our nephrology department because of progressive renal insufficiency and proteinuria. He had been diagnosed with chronic hepatitis C in his teens but had not been treated for it. He had been diagnosed with diabetes mellitus at 55 years old. He had a history of myocardial infarction at 59 and 63 years old. In addition, one year previously, he had been hospitalized due to worsening depression. One month before the present admission, his serum creatinine level had increased from 1.61 to 2.11 mg/dL. At that time, he had noted bilateral leg edema. He was admitted to our hospital to investigate the cause of his worsening renal function and edema. On admission, his height and weight were 160.7 cm and 61.7 kg, respectively. He did not notice any weight gain because he did not weigh himself regularly. His vital signs were as follows: blood pressure 153/89 mmHg, pulse 63 beats/min and temperature 36.3C. A physical examination revealed bilateral leg pitting edema, no purpura, no cutaneous ulcer and no paresthesia, with otherwise normal findings. A Sulfasalazine complete blood count revealed a hemoglobin concentration of 8.8 g/dL. A laboratory examination showed aspartate aminotransferase of 44 U/L, alanine transaminase of 46 U/L, lactate dehydrogenase of 268 U/L, total protein of 5.0 g/dL, albumin of 2.3 g/dL, creatinine of 2.45 mg/dL and total cholesterol of 213 mg/dL (Table). Occult blood and proteinuria were positive on a urinalysis, and the 24-hour urinary protein excretion was 7.4 g/day. Hemoglobin A1c was 5.9%. Immunological assessments revealed negative results for anti-nuclear antibody, anti-DNA antibody, proteinase-3 antineutrophil cytoplasmic antibody (ANCA), myeloperoxidase ANCA and anti-glomerular basement membrane antibody. Cryoglobulins were detected through a qualitative analysis, and cryocrit was 5%. Immunoglobulin M (IgM) was elevated to 692 mg/dL (reference range: 27-205 mg/dL). Rheumatoid factor (RF) was also elevated to 2018 IU/mL (reference range: 0-15.0 IU/mL). Complements were suppressed, as follows: complement C3 at 56.3 mg/dL (reference range: 70.5-125.6 mg/dL) and complement C4 at 2.6 mg/dL (reference range: 10.6-33.0 mg/dL). A virologic test showed serotype 1 HCV RNA of 7.0 LogIU/mL. Table. Laboratory Data on Admission, at Discharge and 27 Months after Discharge. thead style=”border-top:solid thin; border-bottom:solid thin;” th valign=”middle” align=”center” rowspan=”1″ colspan=”1″ Laboratory test /th th valign=”middle” align=”center” rowspan=”1″ colspan=”1″ At diagnosis /th th valign=”middle” align=”center” rowspan=”1″ colspan=”1″ At discharge /th th valign=”middle” align=”center” rowspan=”1″ colspan=”1″ 27 months after.