2018年 · 第34卷第11期

The prevalence of chronic kidney disease (CKD) in Tibet is about 19.1%^[1]Significantly higher than the national level of 10.8%^[2]。 Because of its unique geographical and environmental factors, patients in the Tibetan plateau are in a long-term hypoxia state, and the incidence of tuberculosis and other infectious diseases is high. Therefore, there may be clinical characteristics different from IgA nephropathy (IgAN) in the plain area. This study retrospectively analyzed the data of 27 patients with IgAN in our hospital, aiming at summarizing the clinical and pathological characteristics of IgAN patients in Tibet, and providing scientific basis for guiding clinical diagnosis and treatment and judging prognosis.

The 25-year-old female was admitted to the hospital on October 16, 2017 due to "finding elevated blood sugar for 18 years, edema with oliguria for more than 2 months". The patient was diagnosed with type 1 diabetes for 18 years, and his blood glucose was controlled with insulin. It was found 3 years ago that urine protein was 5 g/L, urine red blood cells were negative, and serum albumin was 24.0 g/L. Fundus examination revealed diabetic retinopathy. 2 months ago, 2 weeks after cold, facial and lower limb edema with decreased urine output and no macroscopic hematuria. Urinary protein was 6 g/L and erythrocytes 428.4/μ L in other hospitals; Urinary protein quantification 11.8 g/24 h; Urine erythrocyte phase: erythrocytes 512 500/ml, G1 10%; Hemoglobin 98 g/L; Serum creatinine was 362.8 μ mol/L and serum albumin was 22.1 g/L. Consider "nephrotic syndrome with acute kidney injury" to be admitted to the local hospital. Check: Blood complement C3 0.09 g/L, C4 0.22 g/L; Serum anti-streptolysin "O" (ASO) 1390.3 IU/ml (0-200 IU/ml). Methylprednisolone was given 40 mg/d, and antihypertensive, hypoglycemic and symptomatic supportive therapy was given. Diagnosis by renal biopsy: diffuse intracapillary proliferative IgA nephropathy. Continue treatment with methylprednisolone 40 mg/d. Because of the patient's low urine output and aggravated edema, internal jugular vein catheterization and single ultrasound treatment were performed one by one. After 22 days, the patient developed chills and fever, and the catheter blood culture was Klebsiella pneumoniae. Considering "hemodialysis catheter-related infection", the patient was extubated and treated with anti-infection. Methylprednisolone was reduced to 24 mg/d. After 12 days of treatment, the patient's body temperature was normal, and the serum creatinine was 156.9 μ mol/L and the serum albumin was 24.5 g/L. Blood complement C3 0.85 g/L, C4 0.13 g/L; ASO 692.6 IU/ml, He got better and was discharged. The edema gradually worsened 4 days after discharge, so the addition of neosespin 25 mg, q12 h, after the medication, the patient developed sore throat, and was admitted to our hospital for further diagnosis and treatment. Previous history of hyperthyroidism for 3 years, I¹³¹Hypothyroidism occurred after treatment, and he was now treated with Euthyrol; History of hypertension and thalassemia for 3 years. Physical examination: T 36.7℃, BP 132/79 mmHg, general condition OK, mild anemia, no abnormalities in heart, lung and abdomen, mild depressed edema of both lower limbs. Laboratory test: white blood cells 13.35×10⁹/L, neutrophils 89.4%, hemoglobin 101 g/L, platelets 366×10⁹/L; Urinary specific gravity 1.020, protein 3+, red blood cell 2+; Urinary protein quantification 13.5 g/24 h; Urinary erythrocyte phase: protein 4+, 0 orthomorphic erythrocytes/ml, 76,000 abnormal erythrocytes/ml; Serum creatinine 175 μ mol/L, albumin 21 g/L; Blood complement C3 0.8 g/L and C4 0.15 g/L; ASO 73.9 IU/ml; No abnormalities were found in preoperative screening; Antinuclear antibody, anti-double-stranded DNA, ANCA, anti-DNase B, cryoglobulin and immunofixation electrophoresis were all negative. Ultrasound examination showed increased echogenicity in both kidneys. Fundus examination revealed diabetic retinopathy (ou).

Membranous nephropathy is the most common pathological type of adult nephrotic syndrome, with circulating antibodies against M-type phospholipase A2 receptor (PLA2R) on glomerular podocytes present in approximately 75% of patients with membranous nephropathy. At present, it is believed that this antibody is related to the pathogenesis of idiopathic membranous nephropathy, and clearing antibody is a new treatment direction of membranous nephropathy. In recent years, studies have shown that rituximab can achieve good results, and a few cases have been reported in China. Individual cases of bortezomib in the treatment of membranous nephropathy have been reported abroad, but none have been reported in China. We treated a case of membranous nephropathy with rituximab combined with bortezomib, which is reported below and reviewed in the literature.

In recent years, the epidemiological data and evidence-based medical evidence on the treatment of renal anemia are gradually increasing at home and abroad. In order to adapt to the development and changes of clinical diagnosis and treatment in China and standardize the management of renal anemia, it is necessary to update the expert consensus on clinical diagnosis and treatment of renal anemia in chronic kidney disease (CKD) according to China's situation and international guidelines. To this end, the Consensus Expert Group on the Diagnosis and Treatment of Renal Anemia of the Nephrology Branch of the Chinese Medical Association launched the consensus revision work in early 2017, aiming to provide guiding suggestions for the standardized diagnosis and treatment of renal anemia in CKD patients in China.

Hyperphosphatemia is a common complication of chronic kidney disease (CKD), especially in patients with end-stage renal disease undergoing dialysis, and is an independent risk factor for cardiovascular events and death in these patients^[1]Its harm cannot be ignored. In recent years, many studies have shown that abnormal phosphorus metabolism plays an important role in the pathogenesis and clinical treatment of CKD-mineral and bone disorder (CKD-MBD)^{[2,3,4,5,6,7]}。 Blood phosphorus management has become an important link to improve the prognosis of CKD patients. At present, the main treatment for hyperphosphatemia is the 3D principle, including diet, dialysis and phosphorus binding agent therapy^[8]。 However, the management of hyperphosphatemia in CKD patients in China still faces severe challenges, and there are still many difficulties in how to restrict phosphorus in reasonable diet, strengthen dialysis efficiency and correctly use phosphorus binders. A 2012 study from 28 centers in 9 provinces in my country showed that the prevalence of hyperphosphatemia (>5.5 mg/dl, 1 mg/dl =0.323 mmol/L) among hemodialysis patients in my country was as high as 57.4%, and the prevalence of hyperphosphatemia (>5.5 mg/dl, 1 mg/dl =0.323 mmol/L) among peritoneal dialysis patients was as high as 57.4%. 47.4% among peritoneal dialysis patients, but the blood phosphorus compliance rate (3.5~5.5 mg/dl) was only 38.5%, which still lags far behind the blood phosphorus management situation in developed countries^[9]。 Recently, data from the nationwide China Dialysis Calcification Study (CDCS) show that the serum phosphorus compliance rate (3.5~5.5 mg/dl) of Dialysis patients in China is still only 40.1%^[10]。 This article will focus on the role of phosphorus in the pathophysiology of CKD-MBD, the challenges faced in the management of hyperphosphatemia, and research progress.

At present, the global incidence of diabetes is rising rapidly. According to the International Diabetes Federation, there were 451 million diabetic patients in 2017, and it is expected to increase to 693 million by 2045^[1]。 With the global epidemic of diabetes, chronic kidney disease (CKD) caused by diabetes-diabetic kidney disease (DKD) has become a major public health and clinical problem all over the world. DKD is mostly a clinical diagnosis^[2], characterized by persistent albuminuria and/or progressive decline in glomerular filtration rate (GFR), while diabetic nephropathy (DN) specifically refers to glomerular disease confirmed by kidney biopsy to be caused by diabetes. Recently, according to epidemiological investigations, in patients with diabetes, especially type 2 diabetes, the incidence of chronic kidney disease with normoalbuminuria but renal function impairment is gradually increasing. This paper defines this disease as normoalbuminuric diabetic kidney disease (NADKD). The diagnostic criteria are: 1. diabetic patients who meet the diagnostic criteria of the American Diabetes Society; 2. Normal albuminuria: urinary albumin excretion rate (urine albumin excretion rate, UAER)<30 mg/24 h or urinary albumin/creatinine rate (ACR)<30 μ g/mg (two random tests over 6 months); 3. Renal function impairment: GFR<60 ml·min^-1· (1.73 m²)^-1； 4. Exclude other secondary kidney diseases. The clinical manifestations of NADKD are different from those of classical diabetic nephropathy, suggesting the complexity of the pathogenesis of DKD. This article aims to review the clinical and pathological characteristics, pathogenesis, treatment and prognosis of NADKD.

Anticoagulant therapy is critical for patients at risk of thromboembolism, with approximately 7 million patients worldwide taking oral anticoagulants (mainly warfarin or other coumarin derivatives) for the prevention and treatment of venous and arterial thromboembolism^[1]。 Warfarin, the most commonly used anticoagulant, provides reliable protection against thromboembolic events while also increasing the risk of bleeding. In recent years, some scholars have found that warfarin anticoagulation may cause a series of renal complications, including acute kidney injury (AKI)^[2,3,4]。 New research shows that taking new anticoagulants can also cause kidney damage^[5,6]。 Warfarin-related nephropathy (WRN) is one of the common complications of Warfarin anticoagulation therapy at present. Overdose Warfarin therapy [INR>3.0] can cause glomerular hemorrhage, red blood cells obstruct the renal tubules and lead to acute kidney injury^[3,4,5,6,7]。 Oral dabigatran etexilate-induced AKI cases have also been reported^[8,9]。 anticoagulation-related nephropathy (ARN) is a renal complication triggered by anticoagulants, and its occurrence is closely related to the morbidity and all-cause mortality of kidney disease^[3]。 ARN not only accelerates the progression of chronic kidney disease (CKD), but also increases short-and long-term all-cause mortality in patients^[1]So it is of great significance to discover ARN in time. Given the risk of bleeding in renal biopsies with elevated INR, the diagnosis of ARN cannot rely solely on renal biopsies with characteristic pathological changes. Currently, ARN is defined as acute kidney injury that occurs with an INR>3.0 after anticoagulation therapy, excluding other etiologies^[3]。 This review summarizes the pathogenesis, diagnostic criteria and treatment measures of anticoagulation-related nephropathy, in order to guide clinicians to optimize the treatment of patients with full consideration of the advantages and disadvantages of anticoagulation therapy.