中华肾脏病杂志
2017年 · 第33卷第12期
中华肾脏病杂志
Female, 60 years old, went to Huashan Hospital for "frequent urination for 5 months and abnormal urine test for 2 months". Frequent urination with back pain and occasional urinary incontinence occurred 5 months ago, and abnormal urine test 2 months ago: occult blood (3+) and protein (3+); Scr 92 μ mol/L, 24 h urine protein 2.23 g. Has a history of hypertension for 3 years, oral telmisartan. Denial of history of infectious disease. Physical examination: BP 147/96 mmHg, mild anemia, no special heart, lung and abdomen, mild depressed edema of both lower limbs. Post-admission examination: urine routine: urine protein 3+, occult blood 3+; 24 h urine protein 9.8 g; Blood routine : Hb 97 g/L, WBC 8.19×109/L, PLT 384×109/L. Blood biochemistry: Albumin 32 g/L, Scr 118 μ mol/L, antinuclear antibody 1:100, anti-double-stranded DNA antibody, anti-soluble antigen antibody (ENA), anti-neutrophil cytoplasmic antibody, anti-glomerular basement membrane antibody, hepatitis markers, blood and urine immunofixation electrophoresis, complement were all negative; Middle urine culture and 24-hour urine were negative for acid-fast bacilli. CD4+T lymphocytes 40% (reference value: 30% ~60%), total blood light chain: κ light chain 2.05 g/L, λ light chain 1.24 g/L, κ/λ: 1.65 (reference value: 1.35~2.65), urine light chain: κ light chain 109 mg/L↑, λ light chain 114 mg/L↑, κ/λ: 0.96 (reference value: 0.70~4.50). Lung CT: inflammation of the basal segment of the lower lobe of the right lung, positive blood latex agglutination test (1:5), positive latex agglutination test of alveolar lavage fluid with fiberoptic bronchoscopy (1:1), considering pulmonary cryptococcosis, because cryptococcal nervous system infection is more common, so lumbar puncture was performed to rule out the possibility of concomitant central infection. Cerebrospinal fluid routine, biochemical, latex agglutination test negative. Renal biopsy pathology, light microscopy: 7 glomeruli, some glomerular segments showed obvious mesangial cell proliferation and stromal increase, a few renal tubules were slightly atrophied, interstitial edema was mild, and a few inflammatory cells infiltrated in the interstitial, mainly mononuclear cells. Immunofluorescence: lambda light chain (3+) was deposited in tubules and glomerular basement membrane, and the mesangial region of glomerulus was also deposited. The remaining IgA, IgG, IgM, C3, C1q and κ light chains were all negative. Electron microscopy: A small amount of low-density powdered electron density deposition under the endothelium in some segments, no obvious electron density deposition under the epithelium, obvious fusion of the foot processes, and no obvious deposition of the basement membrane of the tubules (see
A 44-year-old male was admitted to the hospital on 3 May 2017 due to "rash on both lower limbs with edema for half a month". Half a month ago, the patient developed symmetrical punctate rash on both lower limbs without obvious trigger, which did not fade when pressed and was distributed in clusters. He went to the local hospital, and there was no significant improvement after intravenous drip treatment with dexamethasone 5 mg/d and cimetidine 0.2 g/d, and symmetrical depressed edema of both lower limbs and face gradually appeared. Routine urine examination in other hospitals showed protein 2+, 24-h urine protein amount 5.31 g, creatinine 1092 μ mol/L, after hemodialysis treatment, the rash disappeared, and the edema was not significantly relieved. Instead, he was transferred to the outpatient clinic of our hospital, and his blood was tested for anti-glomerular basement membrane (GBM) antibody (3+), and he was admitted to hospital. The patient had no special past history, denied the history of drug and food allergy, had no special personal and family history, and had no bad habits of tobacco and alcohol. Physical examination at admission: body temperature 36.5℃, blood pressure 132/85 mmHg, breathing 20 times/min, pulse 76 times/min, consciousness, mild anemia, no obvious skin rash all over the body, mild facial edema, no special cardiopulmonary and abdominal examination, mild depressed edema of both lower limbs. Auxiliary examination: blood routine: white blood cells 17.23×109/L, hemoglobin 105 g/L, platelets 328.0×109/L. Urinary routine showed urine protein (2+), urine red blood cells 4+ /HP, and 24 h urine protein volume 22.56 g (urine volume 20 ml). Biochemistry: potassium 3.93 mmol/L, calcium 2.05 mmol/L, phosphorus 1.61 mmol/L, post-dialysis creatinine 672.0 μ mol/L, albumin 29.9 g/L, CRP 21.51 mg/L. Anti-GBM antibody (3+) (blot), anti-GBM antibody 1:32 (fluorescence). Anti-neutrophil cytoplasmic (ANCA) antibody negative. Ultrasound of both kidneys showed that the parenchymal echoes of both kidneys were slightly enhanced. Combined with the medical history and related examination results, the diagnosis was rapidly progressive renal injury, and anti-GBM nephritis was considered. After treatment with methylprednisolone 500 mg/d for 3 days, it was changed to methylprednisolone 40 mg/d for maintenance, cyclophosphamide 0.6 g was infused intravenously once, and double plasma exchange treatment was performed three times, with a plasma volume of 600 ml each time. Poststool bleeding occurred during anticoagulant therapy. Colonoscopy showed signet ring cell carcinoma in the rectum about 8 cm from the anus. Pelvic magnetic resonance imaging (MRI) showed that it was consistent with the diagnosis of rectal cancer, stage T2N0MX was considered, and the circumferential margin (CRM) was negative. Laparoscopic radical resection of rectal cancer was performed on May 24 under epidural anesthesia.
hemolytic uremic syndrome (HUS) is one of the rare acute and critical diseases in clinic. It is a syndrome characterized by intravascular hemolytic anemia, thrombocytopenia and acute renal failure. Patients with diarrhea-related HUS (D + HUS) are more common in children, less common in adults, and rarely reported in middle-aged and elderly patients. Recently, our hospital successfully treated a middle-aged and elderly patient with D + HUS. The diagnosis and treatment of the patient is summarized and reported as follows, and the literature is reviewed in combination with the case.
Hypoxia is a common physiological and pathological phenomenon. In order to cope with the hypoxic environment, the body has developed a series of regulatory mechanisms. Among them, hypoxia inducible factor (HIF) -mediated gene transcription regulation is the most important mechanism for cells to adapt to hypoxic environment. Studies have shown that the downstream pathways regulated by HIF play an important role in regulating energy metabolism, vascular regeneration, erythropoietin (EPO) synthesis, and regulating extracellular matrix (ECM). prolyl hydroxylase domain (PHD), as a key enzyme to regulate HIF, can hydroxylate HIF and lead to its degradation, which in turn affects the outcome of related diseases involved in HIF. Therefore, targeted PHD inhibitors have become a hot topic in related fields. This article reviews the pathophysiological effects of HIF and the research of PHD inhibitors in the treatment of renal anemia and organ ischemia.
obesity refers to excessive accumulation and/or abnormal distribution of fat in the body and weight gain. It is a chronic metabolic disease caused by the interaction of genetic factors, environmental factors and other factors. Nowadays, the global epidemic of obesity is the main factor that shortens human life expectancy and endangers health. The prevalence of obesity is usually related to high energy intake and lack of exercise. When energy intake exceeds the storage capacity of white adipose tissue (WAT), abnormal lipid accumulation in ectopic organs will be stimulated, resulting in metabolic disorders characterized by insulin resistance and changes in sugar and fat metabolism, and promoting the occurrence of hyperglycemia, dyslipidemia, hypertension, insulin resistance, abnormal glucose tolerance and atherosclerosis. More importantly, central obesity is a major risk factor for diabetes and hypertension, which are the main causes of end-stage renal disease (ESRD)[
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