2015年 · 第31卷第01期

Glomerular diseases (GN) are a group of diseases caused by multiple etiologies and pathogenesis. Because of their different pathological types and overlapping clinical manifestations, the diagnosis is relatively difficult. Renal puncture biopsy can mostly confirm the diagnosis, but as an invasive examination, there are certain risks. This study mainly investigated whether the number of podocytes in urine can be used to judge the type and prognosis of kidney disease.

Purpura nephritis (HSPN) is one of the common secondary kidney diseases in pediatrics^[1]Its etiology and pathogenesis have not been fully defined. Studies have shown that cellular immunity and humoral immunity are involved in the acute phase of HSPN^[2]。 Macrophage migration inhibitory factor (MIF) is a cytokine mainly secreted by activated T cells and macrophages, which is involved in immune and inflammatory responses. MIF-173 gene polymorphism is closely related to immune and inflammatory diseases^[3], HSPN has certain genetic susceptibility, with different genetic backgrounds among different races and ethnic groups^[4]。 This study investigated whether MIF-173 C allele is a susceptible gene for HSPN in Mongolian and Han children, and the gene polymorphism among Mongolian and Han children with HSPN.

tubulointerstitial nephritis and uveitis syndrome (TINU) is a clinical syndrome of acute tubulointerstitial nephritis (ATIN) combined with ocular uveitis, which is independent and associated with immune disorders. At present, there are few reported TINU in China, and peers' understanding of the disease is insufficient, which easily leads to misdiagnosis and missed diagnosis. A case of TINU diagnosed in our hospital is reported as follows.

The patient, a 50-year-old male, was admitted to the hospital because of "hypertension for more than 20 years, dizziness and headache for 10 days". Physical examination of the patient more than 20 years ago showed elevated blood pressure, up to 210~220/110~120 mmHg. No dizziness, headache, blurred vision and other discomfort symptoms. Long-term administration of metoprolol succinate sustained-release tablets (Betaloc), valsartan, furosemide, spironolactone, nifedipine controlled-release tablets and other drugs, blood pressure fluctuation is 150~170/90~100 mmHg. 10 days ago, the patient had dizziness and headache symptoms without obvious reason and came to the hospital for treatment. Previous history of diabetes for 3 years, diet control plus irregular use of acarbose tablets (Baitangping) to control blood sugar, current blood sugar control is stable; Smoking and drinking history for more than 20 years; Has a family history of hypertension.

A 61-year-old male was admitted to our hospital with the main complaint of "facial and lower extremity edema for more than 4 months and abnormal urine test for more than 1 month". The patient developed facial and lower limb edema without obvious trigger more than 4 months ago, and was not treated. One month ago, due to the aggravation of edema, I went to the local hospital for treatment. Serum albumin was 20.5 g/L, serum creatinine was 99 μ mol/L, total cholesterol was 7.43 mmol/L, and 24-h urine protein was 4.73 g. Color ultrasound: polycystic kidney. Urinary protein 3+ was re-examined 2 days ago. Past physical health, denied family genetic history. Physical examination: blood pressure 135/89 mmHg, no abnormalities in cardiopulmonary auscultation, unpalpable liver and spleen, soft abdomen without resistance, no tenderness, rebound pain, ascites sign (+), no percussion pain in renal area, palpable enlarged kidneys on both sides, depressed edema in both lower limbs. Auxiliary examination: urine routine: urine protein 3+, red blood cells 0~1/HR, blood routine: white blood cells 6.8×10⁹/L, red blood cells 3.56×10¹²/L, hemoglobin 111 g/L, platelets 90×10⁹/L, hematocrit 0.33, serum albumin 14.1 g/L, total cholesterol 7.02 mmol/L, triacylglycerol 1.57 mmol/L, urea nitrogen 9.3 mmol/L, serum creatinine 100 μ mol/L, uric acid 268 μ mol/L, 24-h urine protein 11.6 g, urine volume 1.7 L/24 h, serum immunofixation electrophoresis was not abnormal, urine protein electrophoresis this week was negative, ANA, ds-DNA, p-ANCA, c-ANCA, MPO-ANCA were all negative, hepatitis B surface antigen, antibody, hepatitis B e antigen, antibody, hepatitis B core antigen, antibody, hepatitis c antibody were all negative; Color ultrasound: the size of both kidneys was increased, the left kidney was 135 mm ×56 mm ×70 mm, and the right kidney was 163 mm ×72 mm ×85 mm. The surface was uneven, and multiple echoes of different sizes could be seen inside, the larger one was about 66 mm ×61 mm, and multiple cystic echoes could be seen in the liver, the larger one was about 15 mm ×14 mm, suggesting multiple cysts, polycystic kidney, and massive peritoneal effusion in the liver; CT: Polycystic kidney and liver multiple cysts. To confirm the pathological diagnosis, renal puncture biopsy under CT was performed, seeFigure 1。 Pathological findings, seeFigure 2。 Immunofluorescence: IgG (+ ~2+), C3 (+ ~2+) and IgM (2+) were deposited in granular form on the capillary wall and mesangial region. Light microscopy: Diffuse thickening of the glomerular basement membrane, formation of segmental nail processes and deposition of complexoglobin under the epithelium; Renal tubules: epithelial cells vacuolated, granular degeneration, focal lumen dilatation, low and flat cells, brush-shaped margin shedding, small focal atrophy, renal interstitium: focal lymphoid, monocyte infiltration with fibrosis, no obvious lesions in small arteries. Electron microscopy: One glomerulus, the epithelial foot process of the glomerular visceral layer was extensively fused, most massive electron density was deposited under the epithelium, the lysosomes of the renal tubular epithelium increased, and there was no obvious lesion in the renal interstitium. The pathological diagnosis was stage I ~ II membranous nephropathy. According to the examination results, secondary membranous nephropathy such as systemic lupus erythematosus, hepatitis B-related nephropathy, and tumor were excluded, and idiopathic membranous nephropathy was diagnosed. Prednisone 60 mg qd was administered orally. After 1 month, the outpatient review showed that serum albumin was 19.8 g/L, urine protein was 2+, 24 h urine protein was 5 g, and serum creatinine was 86 μ mol/L. The patient's condition was partially relieved.

Spontaneous cholesterol crystal embolism (CCE) is a disease caused by the shedding of cholesterol crystals to cause embolism of various organs in the whole body, involving many systems in the whole body, and the kidney is one of the most commonly affected organs. It has been reported at home and abroad that CCE mostly occurs after coronary angiography and/or vascular intervention^[1,2]Simple renal arteriolar cholesterol embolism is rarely reported in China. One case admitted to our hospital is reported as follows.

Acute kidney injury (AKI) is a common critical disease in clinic. It is a sudden decline of renal function caused by various causes, and its clinical manifestations are increased serum creatinine or decreased urine output. Studies have shown that the total incidence of AKI in hospital is 5.7%, and the mortality rate is as high as 60.3%^[1]。 Mitochondria is the "energy factory" of cells, which is the main place for synthesizing adenosine triphosphate, and provides energy sources for cellular life activities. Mitochondria are sensitive to various injurious stimuli, and mitochondrial dysfunction is an early event of AKI. Therefore, maintaining the integrity of mitochondrial structure and function is helpful to prevent and treat the occurrence and development of AKI. The mitochondrial permeability transition pore (MPTP), which is located between the inner and outer membranes of mitochondria, is a non-specific, voltage-dependent complex protein channel, which is the central hub of information exchange between the inner and outer mitochondria, and regulates mitochondrial function through its opening and closing state. In recent years, it has been found that the persistent and massive opening of MPTP is related to a variety of diseases, such as ischemia-reperfusion injury, aging, tumor, Alzheimer's disease, etc. And there is evidence that mitochondrial permeability transition pores also play an important role in the development of AKI. The research progress of mitochondrial permeability transition pore opening and AKI is reviewed as follows.

cardiovascular disease (CVD) is the main cause of death in patients with chronic kidney disease (CKD), and its risk is 20 to 30 times higher than that of the general population^[1]。 Coronary and aortic calcification is present in 40%-60% of patients with stage 3-5 CKD, while the calcification rate is as high as 80%-90% of patients with stage 5 CKD^[2], vascular calcification has become an independent risk factor for increased cardiovascular events in patients with CKD^[3]。 vascular calcification is not a simple passive process, but undergoes the transdifferentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells, and osteoblast-like cells secrete organic matter with calcium and phosphorus deposition and other steps are highly regulated. Many proteins have been found to be involved in the process of vascular calcification, including osteoprotegerin (OPG), alkaline phosphatase (ALP), fetuin-A, matrix-gla protein (MGP), parathyroid hormone (PTH), C-reactive protein (CRP), etc. Recently, a new protein involved in the metabolism of bone-vascular axis-sclerostin has been discovered. It has endocrine function, can enter the blood circulation, reduce the differentiation and function of osteoblasts by inhibiting Wnt pathway, and it can also be expressed at the site of vascular calcification, play a paracrine role, may have the effect of limiting vascular calcification^[4]。 This article reviews the relationship between sclerostin and vascular calcification in patients with CKD.