2016年 · 第32卷第12期

Renal anemia is one of the most common complications in patients with chronic kidney disease (CKD) and an independent risk factor for cardiovascular events in patients with CKD^[1]。 Early application of erythropoietin (EPO) and iron can effectively treat renal anemia^[2]。 Current diagnostic criteria for renal anemia are based on the general population^[3]。 However, whether this standard is applicable to CKD patients who have been in high altitude areas for a long time has not been reported yet. We conducted a cross-sectional survey of CKD patients in Tibet to understand the hemoglobin levels of CKD patients in high altitude areas, evaluate the prevalence of renal anemia in Tibet and its related risk factors, and provide a basis for further research and formulation of diagnostic criteria for renal anemia suitable for high altitude areas.

It is well known that measuring the blood pressure before, during and after dialysis of hemodialysis (HD) patients is the basic monitoring method to ensure the safety of patients on dialysis. Due to the influence of ultrafiltration of water during dialysis, changes of plasma osmotic pressure, clearance of antihypertensive drugs and vasoactive substances, vascular sclerosis and dysfunction of autonomic nerve function, the blood pressure of HD patients during dialysis showed many different fluctuations^[1,2]。 Studies have shown that changes in blood pressure during dialysis not only affect fluctuations in blood pressure between dialysis periods^[3]and is a strong predictor of prognosis in HD patients^[4]。 However, at present, there are few studies on the influencing factors of blood pressure fluctuation in dialysis at home and abroad. Since volume is one of the key factors affecting blood pressure in HD patients, this study aims to measure the characteristics of body fluid distribution before and after dialysis in HD patients by bioelectric impedance, and compare the characteristics and changes of body fluid distribution under different blood pressure fluctuation forms during dialysis.

A 69-year-old male was admitted to the hospital on September 19, 2016 due to "dysuria for half a year and fever for 1 d". Six months ago, the patient underwent "posterior lumbar 4-5 pedicle screw fixation, spinal canal incision and decompression, intervertebral discectomy, and intervertebral bone grafting fusion" in the Department of Orthopedics, Zhongda Hospital affiliated to Southeast University due to "lumbar disc herniation". Postoperatively, he developed dysuria and oliguria. He was catheterized and 800 ml of urine was discharged. Gross hematuria appeared in the catheter. Emergency B-ultrasound: substantial hypoechoic mass in the bladder (considering the possibility of blood clot accumulation), bilateral upper ureteral dilatation with double renal pelvic effusion. Then he was transferred to the urology department to undergo cystoscopic "electrocoagulation and hemostasis of bladder mucosal hemorrhage and cystostomy". Two weeks ago, the cystostomy tube was removed at the patient's strong request. After extubation, the urination was inexhaustible and there was incontinence from time to time. One day ago, the patient developed chills and fever, with the highest body temperature of 38.9℃, so he was admitted to the nephrology department of our hospital. The patient underwent "radical rectal cancer surgery" for "rectal cancer" 15 years ago, and now he often has fecal incontinence. Other medical history is denied. Physical examination: T 37.9℃, R 20 times/min, BP 157/80 mmHg. Clear, poor spirit, anemic appearance, no abnormalities in heart and lungs; Soft abdomen, tenderness in ureteral point and bladder area, and light percussion pain in kidney area; Moderate depressed edema of both lower limbs. Laboratory test: Blood routine WBC 12.2×10⁹/L, N 79.1%, Hb 97 g/L; Urine routine: turbidity, nitrite (+), WBC 544/μ L, white blood cells (3+), protein (+), occult blood test (3+). CT scan of abdomen and pelvis showed perirenal exudation, full dilatation of renal pelvis and ureter on both sides, and diffuse thickening of bladder wall. Immediately after admission, catheterization was performed, blood and urine specimens were collected for culture, and hematuria occurred when 300 ml of drainage was performed; Temporary intravenous infusion of piperacillin and tazobactam sodium 4.5 g, 3 times/d, blood culture and urine culture on the second day showed Gram-negative bacterial infection. Two days later, the patient continued to have fever, with a maximum body temperature of 40.1℃. The antibiotic was adjusted to biapenem on day 3; On the 6th day, the patient's body temperature was normal. On the same day, the blood anaerobic bacteria culture and urine culture of upper and lower limbs showed that Citrobacter freundii was positive, and he was sensitive to antibiotics such as acamicin, ciprofloxacin, ertapenem, cefepime, gentamicin, nitrofurantoin, imipenem, levofloxacin, moxifloxacin, compound trimoxazole and tobramycin. On the 9th day, the patient's urine color was normal, bladder irrigation was stopped, and the urinary catheter was removed. On the 14th day, the urinary tract ultrasonography was re-examined: the volume of both kidneys increased, and the bladder wall was uneven and diffuse thickened. Reexamination of blood and urine routine was normal; C-reactive albumin 9.11 mg/L. After stopping the drug and discharging from the hospital, he was instructed to review the middle urine culture half a month later to determine whether the infection was completely controlled.

Phosphorus is a macroelement in human body, not only as an important body tissue component, but also participates in many physiological processes, such as energy metabolism, cell signal transduction, nucleic acid metabolism, regulation of protein synthesis, maintenance of cell membrane integrity and bone mineralization. In order to ensure the normal progress of these physiological processes, the phosphorus concentration of extracellular fluid and intracellular fluid must be maintained within a narrow range. The maintenance of phosphorus homeostasis involves the absorption of dietary phosphorus by the small intestine, the reabsorption and secretion of phosphorus by the kidney, and the exchange of phosphorus in extracellular fluid with stored phosphorus in bone. We know less about intestinal phosphorus regulation than we know about kidney phosphorus regulation. This review aims to provide an overview of recent advances in the intestinal regulation of phosphorus absorption and the role of the intestinal-renal axis for phosphorus homeostasis.

Gitelman Syndrome (GS; OMIM 263800) is a group of hereditary salt-loss nephropathies with hypokalemic metabolic alkalosis, activation of the renin-angiotensin Ⅱ-aldosterone system (RAAS), normotension or low blood pressure, mainly caused by mutations in the SLC12A3 gene encoding the Na-Cl co-transporter (NCC) of the renal distal convoluted tubules^[1]。 The prevalence of the disease in western countries is 1 in 40 000, while in Asian populations it has increased by 4 to 9 times^[2]。 The traditional view is that the main characteristics of clinical manifestations of GS patients are low magnesemia and low calciuria, which are different from those of Bartter Syndrome (BS). However, with the establishment of the gold standard of genetic examination, there have been reports of normal blood magnesium in GS patients^[3,4,5,6]。 In several large sample GS studies published in recent years, the proportion of normal blood magnesium patients is about 8% to 22% (8% of Taiwan Three Military General Hospital, China^[3]Ruijin Hospital11.1%^[7]Qingdao Medical College 11.9%^[8]Peking Union Medical College Hospital16.7%^[9]and 21.8%^[10]etc.), suggesting that normal blood magnesium may be a subtype of GS. Hypomagnesemia is a risk factor for poor prognosis in chronic kidney disease and cardiovascular disease^[11]However, since there are no large sample long-term follow-up GS prognosis reports, there is insufficient evidence to prove the difference in long-term prognosis between normagnesemia and hypomagnesemia patients^[12]。 However, the clinical manifestations and NCC functional impairment of patients with hypomagnesemia are more serious than those of patients with normomagnesia, and magnesium supplementation in patients with normomagnesia also benefits. Therefore, the clinical significance of distinguishing normomagnesia subtypes mainly lies in identifying more atypical GS patients, improving the diagnosis rate of GS and improving the treatment effect.

end-stage renal disease (ESRD) has become a global public health problem^[1]。 According to statistics, there are about 100,000 ESRD patients in China, and the number is increasing year by year^[2]。 At present, the treatment methods of ESRD mainly include hemodialysis, peritoneal dialysis and kidney transplantation^[3]。 Because peritoneal dialysis has little effect on hemodynamics, can effectively protect residual renal function, and is easy to operate, it has been widely used in the treatment of clinical ESRD patients^[4]。 However, long-term peritoneal dialysis, high-glucose peritoneal dialysate stimulation and inflammatory reaction can induce peritoneal fibrosis, which in turn leads to the loss of peritoneal ultrafiltration function and the failure of transport function, and eventually patients are forced to withdraw from peritoneal dialysis treatment. Recent studies have found that epigenetic modification can regulate the occurrence and development of fibrosis^[5,6,7,8]； Our research group has been devoted to the research on the mechanism of peritoneal fibrosis and new prevention and treatment targets for a long time^{[11,12,13,14]}Some studies have also shown that histone acetylation and histone methylation modification can lead to the activation of renal interstitial fibroblasts and promote the occurrence and development of renal interstitial fibrosis^[5,9,10]。 Therefore, this article will review the role and mechanism of epigenetic alterations in regulating peritoneal fibrosis.

Diabetic nephropathy (DN) is one of the common microvascular complications in diabetic patients. The incidence rate is as high as 20% to 40% in patients with type 2 diabetes mellitus (T2DM). The main features are progressive impairment of glomerular filtration function, Kimmelstiel-Wilson lesions and proteinuria, which can eventually lead to the development of end-stage renal disease (ESRD)^[1]。 In recent years, the prevalence of DN in chronic kidney disease (CKD) has gradually increased. Ranking of DN among ESRD causes reported in the literature: the United States ranked first, China and the United Kingdom both ranked second^[2]。 The latest statistical report shows that the prevalence of DN in China has exceeded that of chronic glomerulonephritis, and has become the first cause of urban hospitalized CKD patients. It is estimated that there are 24.3 million diabetes-related CKD patients nationwide^[3]。 The number of deaths caused by DN worldwide also increased from 463,000 in 1990 to 1.731 million in 2013, an increase of 3.8 times, the fastest growth among chronic diseases. Moreover, the socio-economic burden caused by DN is heavy. In 2012 alone, the global medical expenses for treating diabetic complications such as DN reached 471 billion US dollars, and the proportion of DN in the total medical and health expenses in China is also increasing year by year. However, the pathogenesis of DN is complex and has not yet been thoroughly explored. Glycosylation end products, activated polyol metabolism pathway, protein kinase activity, lipid metabolism abnormalities and hemodynamic changes are the hot topics in early years; In recent years, many non-genetic factors such as immune inflammatory response, autophagy and podocyte transdifferentiation have been reported. RNA-binding protein Tristetraprolin (TTP), kidney damage molecule (KIM-1), glycogen synthase kinase 3 β (GSK-3 β), 1,25-dihydroxyvitamin D₃And its receptor (VDR) play important roles in immune inflammatory response, autophagy, podocyte transdifferentiation, etc^{[4,5,6,7,8,9]}。 However, the research on genetic factors such as gene polymorphism and epigenetics has also made new breakthroughs, which has become a new hot spot in current research. This paper mainly reviews the research achievements of genetic factors in recent years, and provides reference for further exploring the pathogenesis and treatment direction of DN.