2018年 · 第34卷第06期

The medical term "chronic kidney disease (CKD)" has been widely used for 16 years since 2002, when it was proposed by the National Kidney Foundation (NKF) Kidney Disease Outcomes Quality Initiative (KDOQI). With the popularization and application of "CKD", the detection rate of "CKD" in all parts of the world has increased significantly, which suggests from some aspects that this definition has improved people's understanding of "CKD" and promoted the development of nephrology, which is worthy of recognition. However, as the term "CKD" is widely used in clinical practice, some problems gradually appear, and some different views have emerged in academic circles, which are not quoted here.

The maintenance of the special structure of podocytes depends on the actin-dominated cytoskeletal system. Alpha-actinin-4 is only specifically expressed in glomerular podocytes. Crosslinked actin filaments play a role in stabilizing the cytoskeletal structure and foot process morphology of podocytes by regulating the polymerization and depolymerization of actinin. The damage and exfoliation of podocyte are closely related to the occurrence of glomerular proteinuria and glomerulosclerosis. The purpose of this study was to investigate the correlation between α-actinin-4 expression in renal tissue and the number of podocyte in kidney and urine in patients with primary glomerular disease.

peritoneal dialysis (PD) has now become the preferred treatment for patients with end-stage renal disease^[1]。 With the continuous progress of dialysis technology, the survival time of patients is significantly longer than before, and the number of patients requiring surgery due to concomitant diseases is increasing day by day. At present, there is still a lack of uniform standards for the selection of dialysis protocols for perioperative PD patients. Compared with hemodialysis, PD has lower toxin clearance efficacy, so most patients often need to choose hemodialysis or continuous renal replacement therapy (CRRT) temporarily during surgery, which increases the pain and financial burden of patients. Current studies have shown that automated peritoneal dialysis (APD) is useful in abdominal wall hernia repair^[2]Severe heart failure^[3]And new catheterization^[4]All patients with PD have good curative effect, but there are few reports of application in the perioperative period of PD patients. The center began to use APD treatment in the perioperative period of PD patients in 2015, which is now reported below.

glomerulopathy with fibronectin deposits (GFND) is a rare hereditary disease with different degrees of proteinuria, hematuria, deterioration of renal function, and pathological manifestations of renal tissue as glomerular nodular changes. At present, it is believed that the genetic mode of this disease is autosomal dominant inheritance, and it has been found that the mutation of FN1 gene located at chromosome 2q35 is related to the pathogenesis of GFND. This study aims to further explore the pathogenic mechanism of GFND by analyzing the mutation sites of FN1 gene in patients with GFND and their family members.

The patient, a 62-year-old male, was admitted to the hospital on July 20, 2017 due to "abdominal distension for 1 month, chest tightness, shortness of breath, confusion, and high creatinine for 20 days". The patient took herbal medicine 1 month ago (self-reported as herbal medicine for diabetes for 5 days, twice daily, specific herbal medicine cannot be provided). After taking the herbal medicine for 5 days, the patient began to have abdominal distension, decreased food appetite, and self-complained urine output began to decrease. The daily urine output was about 700~900 ml. There was no abdominal pain and diarrhea, no fear of cold and fever, no macroscopic hematuria, no foamy urine, and no edema of both lower limbs. After taking the herbal medicine for 8 to 9 days, the patient's abdominal distension aggravated, lack of appetite, chest tightness and shortness of breath after activity, which can be improved after rest, and the daily urine output is about 400 to 500 ml. Twenty days ago, after lunch at home, I developed chest tightness and shortness of breath, and abdominal distension aggravated, so I went to the local hospital for treatment. On the way, I had difficulty breathing, which gradually aggravated. When I went to the emergency department, I was confused, and my blood white blood cells were checked for 19.22×10.⁹/L, serum creatinine 1069.49 μ mol/L, serum potassium 7.18 mmol/L, BNP 615 ng/L. Cardiac ultrasound in local hospital: small amount of tricuspid regurgitation; Chest CT: A little infection in both lower lungs, coronary artery calcification, and a little pleural effusion on both sides. After admission to ICU for oxygen inhalation, continuous renal replacement therapy (CRRT), lowering blood potassium, and improving heart failure, the patient's consciousness recovered and his physical condition improved compared with before. After 4 days of treatment, he was transferred to the nephrology ward for treatment, and was given treatment such as kidney protection, microcirculation improvement and blood pressure reduction. Hemodialysis was continued twice. The patient's urine output gradually increased to about 1000 ml per day, so hemodialysis was stopped. However, the serum creatinine decreased slowly. On July 17, 2017, the serum creatinine was 631 μ mol/L. Now, for further treatment, go to our hospital for treatment, and plan to be admitted to the Department of Nephrology of our hospital with "acute renal failure, hypertension and diabetes".

Patient A, male, 21 years old. Polydipsia, polyuria, enuresis at 3 years of age. A year ago, blood creatinine was 231.7 μ mol/L. Healthy parents, no similar medical history in the family, denial of close marriage, see family genealogyFigure 1。 On admission, serum creatinine was 469 μ mol/L, urine protein (-), and urine specific gravity was 1.005. Urine β 2-mg 12.80 mg/L [normal reference value (same below): 0-0.3 mg/L], urine retinol binding protein 6.95 mg/L (0-0.75 mg/L), urine α 1-mg 80.10 mg/L (0-6 mg/L). The amount of urine protein at 24 h was 0.69 g. Urinary protein electrophoresis: renal tubular protein 31.9%, albumin 65.3%, globular protein 2.8%. No abnormalities were found in fundus, eye slit lamp and visual acuity examination. Kidney color Doppler ultrasound and CT: Both kidneys are small and multiple cysts in both kidneys.

In the past two years, our department has tried to treat the occlusion of artificial vascular fistula with ultrasound-guided intracavity therapy, and achieved good results. The report is as follows.

With the increasing prevalence of diabetes, diabetic nephropathy has become the leading cause of end-stage kidney disease (ESRD) in developed countries^[1,2]。 In 2015, diabetic nephropathy in my country has surpassed chronic glomerulonephritis and become the leading cause of chronic kidney disease in hospitalized patients^[3]。 Prevention and treatment of diabetic nephropathy is of great significance. Current strategies, such as controlling blood sugar and blood pressure, and using renin angiotensin aldosterone system (RAAS) inhibitors, cannot effectively delay the occurrence and development of diabetic nephropathy^[4,5]。 sodium-glucose co-transporter 2 (SGLT2) inhibitors are a novel class of oral hypoglycemic drugs that inhibit SGLT2 expressed in the brush margin of the proximal tubules of the kidney^[6,7]Inhibit the reabsorption of glucose, increase the excretion of urine sugar and reduce blood sugar. Representative drugs of SGLT2 inhibitors include empagliflozin, canagliflozin, dapagliflozin, etc. Recent studies have found that in addition to controlling blood sugar, SGLT2 inhibitors can bring down blood pressure^[8,9]Lose weight^[10]Reducing uric acid^[11]Reduce urine protein^[12,13]And delay the progression of kidney disease^[14]And other multiple benefits. We reviewed recent clinical studies and related mechanisms of SGLT2 inhibitors in protecting the kidney, and focused on the effects of SGLT2 inhibitors on tubuloglomerular feedback (TGF).

More than 100 years ago, nicotinamide adenine dinucleotide (NAD⁺）。 NAD⁺It was originally called coenzyme I, that is, it accepts electrons as an electron carrier, forms reduced NADH, participates in mitochondrial electron transfer, and plays an important role in metabolic processes such as tricarboxylic acid cycle and oxidative phosphorylation. Studies over the past two decades have found that NAD⁺Is a variety of NAD⁺Substrates that consume enzymes (such as SIRT1, PARP, etc.) and participate in regulating enzyme reactions. Recent studies suggest that NAD⁺It plays an important role in regulating cell senescence, apoptosis and injury response. NAD⁺The significance of being a therapeutic target for related diseases has also attracted much attention. NAD⁺Precursors have appeared on the market as nutritional products, and some clinical trials have been initiated. This article will discuss the NAD⁺The biological functions of NAD and its research in acute kidney injury (AKI), diabetic nephropathy, kidney aging, etc. are reviewed to discuss NAD⁺Perspectives of clinical application of precursor substances in the field of renal diseases.

Peritoneal dialysis (peritoneal dialysis) is one of the main alternative treatments for end-stage kidney disease (ESRD). Data show that the number of people using peritoneal dialysis in mainland China has increased by more than 10 times in the past 10 years^[1]By the end of 2016, 74,138 patients had been registered for peritoneal dialysis^[2]。 Compared with hemodialysis (hemodialysis), peritoneal dialysis has the advantages of economy, convenience and protection of residual renal function^[3,4,5,6]。 However, volume overload is a common clinical problem in patients with peritoneal dialysis. Studies have shown that the clearance of sodium in peritoneal water is related to the prognosis of patients, and adequate maintenance of fluid and sodium balance is the key to the management of patients with peritoneal dialysis. This article aims to review the principle of sodium clearance in peritoneal water and the adjustment strategy of peritoneal dialysis prescription.