2016年 · 第32卷第05期

Renal tubular epithelial cell apoptosis plays an important role in the progression of acute kidney injury (AKI) after ischemia-reperfusion injury^[1]。 Silencing information regulator 2-related enzyme class 1 (SIRT1) is a nicotinamide adenine dinucleotide-dependent (NAD⁺), which can regulate gene silencing, cell proliferation, differentiation, senescence, apoptosis and energy metabolism. Resveratrol, as a natural activator of SIRT1, can specifically activate the expression of SIRT1. NF-K B pathway is an important pathway to control apoptosis. It has been confirmed that resveratrol regulates apoptosis of nerve cells through NF-K B^[1,2,3]。 However, whether SIRT1 can regulate the apoptosis of rat renal tubular epithelial cells through the NF-к B pathway has not been reported. In this study, we investigated the regulatory effects of SIRT1 on apoptosis induced by hypoxia-reoxygenation injury in rat renal tubular epithelial cells, and investigated the regulatory effects of NF-κ B pathway in it, which provided theoretical basis for finding new targets for the prevention and treatment of AKI.

This article reports a case of acute renal failure due to rheumatic heart disease and paroxysmal atrial fibrillation after mechanical mitral valve replacement, which was treated with warfarin. Kidney biopsy confirmed warfarin-related nephropathy (WRN). The diagnosis and treatment of WRN were discussed to improve the understanding of WRN.

The patient, a 29-year-old male, developed dizziness and fatigue with skin ecchymosis without obvious trigger more than 10 days ago, which was not paid attention to. Three days ago, the patient felt that the symptoms did not improve, and the skin was slightly touched to produce ecchymosis. He went to another hospital, and the blood routine showed that white blood cells (WBC) were 34×10⁹/L, platelets (PLT) 17×10⁹/L, admitted to our hospital for further diagnosis and treatment. Blood routine: WBC 27.98×10⁹/L, PLT 25×10⁹/L, hemoglobin (Hb) 80 g/L, blasts 52%. The patient had high WBC, anemia, low PLT, and abnormal cells in peripheral blood. Acute leukemia was initially considered, and bone marrow examination was given to confirm the diagnosis. Renal function on admission: urea nitrogen (BUN) 9.06 mmol/L, serum creatinine (Scr) 254 μ mol/L. Urine routine: Urinary protein (2+). Blood biochemistry: Total protein was 69.2 g/L, globulin was 19.9 g/L, albumin was 49.3 g/L, and immunoglobulin was low. B-ultrasound of both kidneys: Both kidneys were enlarged, the section was about 19 mm ×16 mm, the boundary was clear, and there was no separation in the collective system, so acute kidney injury was considered. Bone marrow smears showed 26% naive plasma cells and 22% blasts. Immunotyping: Abnormal plasma cells accounted for about 75.5%. Therefore, the clinical diagnosis of primary plasma cell leukemia (PPCL) is possible. Bortezomib for injection + dexamethasone + cyclophosphamide + etoposide + arubicin was used for chemotherapy. After chemotherapy, bone marrow suppression accompanied by fever was improved after treatment with increased WBC and anti-inflammatory treatment. Lumbar puncture and intrathecal injection of chemotherapy drugs were continued, and the patient's condition was stable after one course of chemotherapy. After 1 week, blood routine showed: WBC 9.06×10⁹/L, PLT 160×10⁹/L, 1.0% blasts were seen in peripheral blood, and recurrence was considered. BUN was 5.71 mmol/L, and Scr was 210 μ mol/L. Renal puncture was given to determine the cause of renal insufficiency. Pathology of renal biopsy: Under light microscope, there were 2 cortical kidney tissues, 15 glomeruli, 1 glomerular sclerosis, the mesangial area of other glomeruli was not widened obviously, and the vascular loop was open well; The results of PASM-Masson staining were negative, about 10% of the renal tubulointerstitial mild chronic lesions, focal tubular atrophy, mild acute lesions, multifocal tubular epithelial cell swelling, a small amount of protein tubular type in the lumen, interstitial diffuse mononuclear cells, lymphocytes and plasma cell infiltration with eosinophil and neutrophil infiltration, and multiple atypical plasma cell infiltration with tubulitis formation, some of which are large and have nucleolus, seeFigure 1； Immunofluorescence was all negative; Immunohistochemical results were CD138 (+), CD79a (+), CD38 (+), MUM1 (+), CD20 (-), CD56 (-), Ki-67 (90% +), seeFigure 2； Electron microscopy, the foot process was partially fused, the basement membrane was normal, the mesangial matrix was increased, and a large number of interstitial cells infiltrated. The pathological diagnosis of renal biopsy was slight glomerular lesion and diffuse plasma cell infiltration in interstitium, which was consistent with PPCL renal damage in combination with clinical. According to the original regimen, the vital signs were stable after treatment, and the blood routine showed: WBC 2.56×10⁹/L, Hb 96 g/L, PLT 126×10⁹/L; Urinary protein (+), BUN 6.04 mmol/L, Scr 106 μ mol/L, was given to discharge.