2015年 · 第31卷第11期

cardiac surgery-associated acute kidney injury (CSA-AKI) is an important complication after cardiac macrovascular surgery, especially in patients undergoing cardiopulmonary bypass (CPB). It is characterized by a sharp decrease in renal function in the short term after surgery, clinically manifested by a rapid increase in serum creatinine (Scr) level and a decrease in urine output that meets the diagnostic criteria of AKI^[1,2]。 This study will analyze the epidemiological characteristics and related risk factors of CSA-AKI, and provide theoretical basis for further optimizing its prevention and control measures.

Existing studies have found that abnormal fatty acid oxidation can affect the palmitation of podocin, a marker protein of podocyte, and the lipid composition of the lipid valve, leading to renal inflammatory reaction, oxidative stress, fibrosis and even necrosis^[1]。 Our recent study found that fatty acid binding protein 3 (FABP3) present in podocytes can cause disorders in podocyte fat metabolism^[2], which is increased in podocytes of patients with obesity-associated nephropathy and is positively correlated with proteinuria levels^[3]。 This study aimed to further explore the role of FABP3 in podocyte inflammatory response and oxidative stress.

Thyroid cancer is a common malignant tumor of endocrine system, and its incidence is increasing year by year^[1]。 The incidence of thyroid cancer in patients with chronic kidney disease is rarely reported. We started parathyroidectomy earlier. Now we summarize 556 patients who underwent parathyroidectomy due to uremic secondary hyperparathyroidism (SHPT) in the past 5 years, and retrospectively analyze the clinical data of SHPT patients with thyroid cancer.

Vascular calcification is closely related to cardiovascular disease (CVD) in maintenance hemodialysis (MHD) patients, and aortic arch calcification (AoAC) is an important predictor of CVD death and all-cause death^[1]。 In recent years, the effects of fibroblast growth factor 23 (FGF-23) and Klotho protein on vascular calcification have attracted widespread attention^[2,3]。 We analyzed the relationship between AoAC and serum FGF-23, Klotho protein and other related risk factors in MHD patients to explore the possible mechanism of CVD in MHD patients.

donation after cardiac death (DCD) refers to organ donation after heartbeat and respiratory arrest and organs are in a state of no blood supply. At present, DCD is becoming one of the methods to alleviate the extreme lack of transplanted organs in the world^[1]。 The 1-year graft survival rate of DCD was similar to that of standard living donors, but the incidence of initial graft non-function and delayed recovery of graft renal function (DGF) was higher^[2]。 If the donor kidney is complicated with stones, the risk of urinary tract stones and obstruction after transplantation is significantly increased, which may become an obstacle to the recovery of transplanted kidney function. Therefore, the management of stone before and after transplantation is very critical. The clinical experience of two patients with DCD donor kidney stone transplantation in our department is reported as follows, and the perioperative management, treatment and prognosis of DCD donor kidney stone transplantation, a rare clinical type, are briefly discussed.

Oxidative stress is one of the recognized pathogenic factors in the development of diabetic nephropathy (DN)^[1]。 reactive oxygen species (ROS) in patients with diabetic nephropathy can be derived from mitochondria, reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, lipid oxidase, cytochrome P450, nitrogen oxide (NO) synthase, monoamine oxidase, and xanthine oxidase^[2]。 1961 Jensen et al.^[3]It was confirmed that mitochondria can produce ROS. Under normal physiological conditions, more than 90% of ROS in cells are produced by mitochondria, mainly by the oxidative phosphorylation of mitochondria to synthesize ATP. 0.2% ~2% superoxide anions are produced by mitochondrial respiratory electron leakage pathway^[4]。 Stimulated by high sugar, this process is continuously excessively amplified. 2005BrownLee et al.^[5]The "general theory" was put forward for the first time, and it was proposed that excess ROS produced by mitochondrial respiratory chain in high glucose environment is the initiator of diabetic nephropathy, which can activate four classical pathways causing DN, including polyol pathway, hexosamine bypass pathway, advanced glycosylation end products (AGEs) pathway and protein kinase C (PKC) pathway, and these pathways can further cause ROS accumulation, activate vascular endothelial damage pathway, lead to cell damage and apoptosis, and thus cause multiple organ damage. This theory is a milestone in the research of diabetic nephropathy. Sustained overactivation of mitochondrial-derived reactive oxygen species is thought to be a central link in initiating multiple pathophysiological processes in diabetic nephropathy^[2,3,4]。 Our review of mitochondrial-derived ROS and its role in the progression of diabetic nephropathy is presented below.

diabetic kidney disease (DKD) is one of the major complications of diabetic patients^[1], accounting for about 40% to 50% of the causes of end-stage kidney disease (ESRD)^[2]。 In patients with type 2 diabetes mellitus (T2DM) with renal insufficiency, drugs or metabolites are prone to accumulation and increase the risk of adverse reactions. Therefore, most patients with DKD were treated with insulin in the past. Recent studies have found that oral hypoglycemic therapy is also very effective for a large number of DKD patients, especially dipeptidyl peptidase-4 (DPP-4) inhibitors and SGLT-2 (sodium-glucose co-transporter 2) inhibitors and other new drugs have renal protective effects independent of hypoglycemic effects^[3]。 For patients with DKD, especially those with severe renal insufficiency, how to choose a wide variety of oral hypoglycemic drugs reasonably is a difficult point in clinical treatment^[1]All relevant guidelines have also discussed this issue in detail. This review will briefly describe the recent new knowledge about oral hypoglycemic therapy of DKD at home and abroad.

In the past, the treatment of uremic complications was very lacking, but at present, with the improvement of dialysis technology, the survival rate of patients has been greatly improved, and the treatment of uremic complications has gradually attracted people's attention. The rate of hepatitis C virus (HCV) infection in uremic patients is much higher than that in the general population, and the mortality rate of this coinfected population is higher than that of non-coinfected people. The following summarizes the latest advances in the need for treatment, the timing of treatment initiation, and the selection of treatment options and evaluation of efficacy.