{'fraction_non_alphanumeric': 0.03531642569329225, 'fraction_numerical': 0.015643517421189856, 'mean_word_length': 5.242603550295858, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 1, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Development of Focal segmental glomerulosclerosis 4- years following direct-acting antiviral therapy for hepatitis C virus infection: Case report

It is well celebrated that, eradication of HCV RNA from serum is commonly accompanied by clinical improvement of glomerular abnormalities. Sofosbuvir (SOF) is the only commonly used direct-acting antiviral therapies (DAAs) that is primarily cleared by kidney. The effect of sustained virologic response (SVR) on renal function is wellestablished in the setting of interferon (IFN) based regimens. Patients who achieved SVR with IFN regimens have a decreased incidence of chronic kidney disease and endstage renal disease. However this effect following DAAs therapy is scarce. There is no clinically relevant change in renal function among the majority of HCVinfected patients following completion of DAA-based treatments. During follow up of patients with SVR following DAAs therapy, we observed one patient has 4 years SVR post DAAs (Sofosbuvir plus dacklatavir) who developed resistant edema and ascites with massive proteinuria following treatment with DAAs therapies and whose kidney biopsies demonstrated focal segmental glomerulosclerosis (FSGS) hilar type and interstitial fibrosis and tubular atrophy. Introduction Direct-acting antiviral agents are now the main option therapy for chronic HCV infection with an excellent safety profile and promising clinical outcomes . There is relatively infrequent evidence suggesting DAA treatment may improve renal function. Focal segmental glomerulosclerosis (FSGS) is a histologically renal injury characterized by sclerosis, hyalinosis, foam-cell infiltration, vacuolization of podocytes, and podocyte precursor proliferation. FSCS affects only some glomeruli and only a portion of the affected glomerulus is sclerosed . Idiopathic FSGS is the commonest primary glomerular histology in the United States, and one of the principal causes of idiopathic nephrotic syndrome in adults, a main prognostic factor in the progression to end-stage renal disease (ESRD) . Previous study has shown a slight decline of estimated glomerular filtration rate (eGFR) at end of treatment of DAAs, followed by a slight rise 12 weeks after treatment. However, long-term effect of nephrontoxicity exerted by DAAs has not been well cleared . In this report, we describe a case of a severe focal segmental glomerulosclerosis 4 years post – sustained virologic response following HCV treatment with DAA in an HCVinfected patient. Case Presentations A 47 years old male with no history of renal impairment, not diabetic not hypertensive received DAAs and has SVR. After 4 years-post-SVR, during follow up, the patient presented by refractory edema and abdominal enlargement. Abdominal ultrasound reveled, average size normal liver echopattern; normal size and shape of spleen; normal size, site, shape and echopattern of both kidneys and moderate ascites. The patient has F 0/Fibroscane. Laboratory investigation showed that, ALT (30 U/L), AST (25U/L), serum bilirubin (0.9 mg/dl), serum albumin was (1.8 g/dl), AFP (1.7 IU/ml), WBC 5.3 (10/cmm), Hg 10 g/dl, platelets 174 (10/cmm) and serum creatinine (3.5 mg/dl). HIV negative, antimitochondrial antibodies (AMA) and anti-liver-kidney microsomal (ALKM) antibody were negative. Normal cardiological examination by consultation. Diagnostic paracentesis was done and revealed, ascitic protein was 2.2 gm/dl, WBC 100 (10/cmm) and SAG was less than 1.1 suggested noncirrhotic ascites. Urinalysis showed massive protein in urine in 24/ Hrs was 8.99 gm /24 hrs (normal less than 0.15). The patient was referred to nephrology department. The nephrologist suggested mostly 2ry nephrotic syndrome and advised renal biopsy. The result of pathological examination of renal tissue revealed (Focal segmental glomerulosclerosis hilar type (5/12 glom) and interstitial fibrosis and tubular atrophy about 25% (Figure 1). The patient received corticosteroid 20 mg twice day plus azathioprine 50mg twice day. Follow up after one month under treatment reveal improvement of the patient as serum albumin is 3.8 g/dl and serum creatinine is 0.9 mg/dl and abdominal ultrasonography no ascites. _