2017年 · 第33卷第03期

antiphospholipid syndrome (APS) is a disease with repeated arterial or venous thrombosis, pathological pregnancy, and continuous positive anticardiolipin or lupus anticoagulant tests. The disease mainly occurs in middle-aged and young people, and is more common in women. It can be secondary to systemic lupus erythematosus (SLE) or other autoimmune diseases, or it can appear alone. antiphospholipid syndrome nephropathy (APSN) is a renal vascular disease caused by APS. A case of SLE combined with APSN diagnosed in our hospital is reported as follows.

encapsulating peritoneal sclerosis (EPS) is a rare and serious complication that may occur in patients with long-term peritoneal dialysis (PD). Once it occurs, the prognosis is poor and the mortality rate is high. About 50% of them usually die within 12 months after diagnosis^[1]。 Its pathogenesis is still unclear, and intestinal obstruction is its basic diagnostic feature. Clinically, there may be no obvious symptoms in the early stage, and partial or complete intestinal obstruction may occur with progressive fibrous thickening of the peritoneum, resulting in intestinal encapsulation^[2]。 In recent years, there have been reports about EPS in various countries in the world, but EPS has not been widely recognized in China, and there are no related reports. A case of peritoneal dialysis complicated with EPS diagnosed and treated in our hospital is summarized and reported as follows, and the literature is reviewed in combination with the case.

A 65-year-old female was admitted with "elevated Scr for 16 years, hemodialysis for 3 years, left fingertip ulcer for 2 months". The patient had an elevated Scr 16 years ago, underwent arteriovenous fistuloplasty of the deep perforator vein of the brachial artery of the left upper limb 3 years ago, and started hemodialysis treatment after the fistula matured. Thereafter, the patient gradually felt a chill in his left hand. Pain in my left hand occurred 3 months ago, especially during dialysis, and it gradually worsened. Ulcer of left middle finger and ring finger with swelling of finger tip appeared 2 months ago. Previous history of diabetes for 30 years; History of hypertension 3 years. Admission physical examination: An old longitudinal surgical scar of about 4 cm in length was seen on the left forearm, with local palpable tremor and vascular murmur. The left finger tip is cyanotic and swollen, the skin temperature is lower than that of the right hand, and the middle finger and ring finger are ulcerated and necrotic. The skin temperature measuring instrument showed that the left side of the tiger's mouth area on the back of the hand was 33.1℃ and the right side was 34.7℃. Upper limb Doppler segmental pressure: left brachial artery 172 mmHg, radial artery 63 mmHg, ulnar artery 57 mmHg; Right brachial artery 161 mmHg, radial artery 157 mmHg, ulnar artery 157 mmHg. All fingerpressures were measured by photoplethysmography (PPG). Basic acupressure (BDP): 45 mmHg in left thumb, 42 mmHg in index finger, 0 mmHg in middle finger, ring finger and pinky finger, and no wave shape in 3 ulnar fingers; The right thumb is 101 mmHg, the index finger is 101 mmHg, the middle finger is 97 mmHg, the ring finger is 95 mmHg, and the little finger is 100 mmHg. The waveforms are all high and pointed. Compression of internal fistula: left radial artery 185 mmHg, ulnar artery 195 mmHg, thumb 61 mmHg, index finger 55 mmHg, middle finger, ring finger and little finger all 0 mmHg. Change of fistula pressure (CDP): 122 mmHg in left radial artery, 138 mmHg in ulnar artery, 16 mmHg in thumb, 13 mmHg in index finger, and 0 mmHg in middle finger, ring finger and pinky finger. Calculation of digital brachial index (DBI): 0 for left middle finger, 0 for ring finger; The right middle finger is 0.60 and the ring finger is 0.59. Diagnosis: chronic renal failure uremic stage, renal hypertension, maintenance hemodialysis; Sign of distal limb ischemia caused by dialysis access after arteriovenous fistula of left upper limb; Type 2 diabetes mellitus, diabetic nephropathy stage V. The blood flow at dialysis was 200 ml/min, the dialysate flow was 500 ml/min, and the on-line urea clearance was 1.09. Closure of left upper extremity arteriovenous fistula was performed to relieve ischemic signs. On the postoperative day, the patient complained that the pain in the left fingertip improved and the chill disappeared. The temperature measurement results of skin temperature measuring instrument showed that the left side was 34.1℃ and the right side was 33.5℃. Acupressure 1 day after surgery: left middle finger 51 mmHg, short and blunt wave; The right middle finger was 143 mmHg with a high blunt waveform and a left DBI of 0.27. Two weeks after surgery, the reexamination complained that the pain was significantly improved, and there was no obvious chill at the fingertips. The reexamination of acupressure: right thumb 142 mmHg, index finger 135 mmHg, middle finger 125 mmHg, ring finger 117 mmHg, little finger 142 mmHg; The left thumb is 101 mmHg, the index finger is 68 mmHg, the middle finger is 90 mmHg, the ring finger is 85 mmHg, and the little finger is 68 mmHg. The left wave shape is higher and sharper than the front. DBI: Left thumb 0.48, index finger 0.32, middle finger 0.43, ring finger 0.40, little finger 0.32.

The patient, male, 42 years old, started peritoneal dialysis (peritoneal dialysis) treatment in our hospital in January 2012 due to "chronic kidney disease stage V caused by chronic glomerulonephritis". In December 2014, I had peritoneal dialysis-related peritonitis once, and repeated peritoneal dialysis fluid culture was negative, and it improved after treatment with vancomycin + amikacin. On August 8, 2016, the patient reappeared with persistent total abdominal pain with turbidity of peritoneal dialysis fluid without obvious inducement. The peritoneal dialysis fluid was routine: 550 white blood cells/μ L, 78% neutrophils and 20% lymphocytes; Peritoneal dialysis solution was collected from the local hospital and then empirically treated with vancomycin + amikacin. The results of multiple consecutive peritoneal dialysis fluid cultures were negative, and the abdominal pain symptoms of the patient improved, but the number of white blood cells in peritoneal dialysis fluid continued to be greater than 100×10⁶/L. At the same time, the patient had systemic inflammatory manifestations such as fever. The local hospital recommended removing the peritoneal dialysis tube, but the patient refused, so he was transferred to our hospital on August 18, 2016. The patient's peritoneal dialysis regimen at admission was as follows: 1.5% dialysate 2000 ml for 6 h, 3 times a day, and 2.5% dialysate 2000 ml for 6 h, 1 time a day; The dialysate was produced by Baxter Company of the United States, and the dialysis mode was continuous ambulatory peritoneal dialysis. After admission, amikacin 200 mg was added to the peritoneal dialysis solution for 6 h, once a day, and vancomycin 500 mg was added to the peritoneal dialysis solution for 6 h, once a day. After 3 days of treatment, imipenem cilastatin sodium (Taineng needle) 500 mg was added to the peritoneal dialysis solution for 6 h, and the treatment was done once a day for 7 days. The patient's repeated peritoneal dialysis fluid culture (conventional peritoneal dialysis fluid bacterial culture, fungal culture and sediment culture after centrifugation) was still negative, the clinical symptoms did not improve significantly, and the leukocytes of the peritoneal dialysis fluid were maintained at 400×10⁶/L, so the peritoneal dialysis tube was removed on September 6, 2016. During the operation, 1 cm ×0.5 cm anterior wall peritoneal tissue was taken and sent to pathological examination. Pathological report: A large amount of Candida hyphae was seen in peritoneal tissue and fibrous necrosis exudation, seeFigure 1。 Diagnosis of "fungal peritonitis", the patient changed to hemodialysis, fluconazole needle antifungal treatment, the condition improved and discharged.

Chronic kidney disease has become an important chronic disease that threatens the health of our population. The progression process of chronic kidney disease with different etiologies is similar^[1,2]。 As a highly microvascular organ, the essence of kidney injury is microvascular injury^[3,4]But the specific mechanism is not clear^[5]。 The vascular system of the kidney includes interlobar artery, arcuate artery, interlobular artery, arterioles, capillaries and venules, among which endothelial cells and pericytes are important intrinsic cells of microvessels; Recent studies have found that its surface marker CD146 plays an important role in renal microvascularization, damage and repair. This article will review the relevant progress in this field in recent years.

Hyperphosphatemia is one of the major complications in patients undergoing maintenance hemodialysis (hemodialysis). Hyperphosphatemia increases cardiovascular calcification and accelerates aging, which is an independent risk factor for cardiovascular events and death. Traditional phosphorus-lowering treatments include hemodialysis, phosphorus-binding agents, and dietary therapy. Dietary treatment has not received sufficient attention due to the risk of malnutrition. However, recent studies have shown that choosing foods with low phosphorus bioavailability, improving cooking methods, and choosing foods with low phosphoprotein ratio can treat hyperphosphatemia without affecting nutritional status. This article will focus on the research progress of dietary treatment of hyperphosphatemia in hemodialysis patients.

diabetic kidney disease (DKD) is a serious microvascular complication of diabetes, and it is also the leading cause of end-stage renal disease (ESRD). The main mechanisms of DKD as a non-immune disease include: high glucose-induced increased activity of polyol pathway, increased formation of advanced glycation end products (AGE), activation of protein kinase C (PKC) β, δ and ε subtypes, increased activity of hexosamine pathway, activation of renin-angiotensin system in periphery and kidney, excessive production of reactive oxygen species (ROS), resulting in inherent cell damage of kidney, and finally renal insufficiency^[1]。 However, traditional treatments such as lowering blood sugar and controlling blood pressure cannot effectively delay the occurrence and progression of DKD. Recent studies have shown that macrophage (M φ) -mediated immune inflammatory response is closely related to DKD. Abnormal macrophage infiltration, recruitment and activation exist in renal tissues of DKD patients and animal models, and lead to renal immune inflammatory damage^[2,3,4]。 Therefore, the role and mechanism of macrophage-mediated immune inflammatory response in DKD are reviewed in this paper.