2018年 · 第34卷第10期

Secondary hyperparathyroidism (SHPT) is one of the common complications in patients with end-stage kidney disease, and its incidence is increasing year by year. Studies have shown that about 70% of patients with stage IV chronic kidney disease (CKD) have SHPT^[1]。 At present, relevant guidelines recommend vitamin D receptor activators (VDRAs) as the first choice drug for the treatment of SHPT. However, there are many types of VDRAs, and the choice of drug types has become a hot spot for scholars at present^[2]。 Because calcitriol can cause disorder of calcium and phosphorus metabolism in the body, its wide application is limited. Paricalcitol is a selective vitamin D analogue that has less effect on intestinal reabsorption of calcium as well as bone remodeling. This study is a randomized controlled phase III clinical trial to compare the efficacy and safety of paricalcitol and calcitriol in patients with SHPT secondary to CKD for the first time in Xinjiang.

Polycythemia vera (true red) is a chronic myeloproliferative disease with abnormal increase of clonal red blood cells as the main manifestation. Korean scholars report that the prevalence of true red is 2.8~5.4 cases/100,000^[1]。 True red can cause thromboembolic events and cardiovascular disease, with a high risk of death. Blood cell lowering therapy and oral aspirin to prevent thromboembolism can improve the prognosis of patients^[2]。 We report a case of peritoneal dialysis (PD) combined with true red and ischemic bowel disease secondary to true red, in order to attract the attention of peers to this disease.

Peritonitis is one of the most common complications in peritoneal dialysis (PD) patients. Although the improvement of PD connection pipeline has significantly reduced the incidence of peritonitis, peritonitis is still the main cause of PD failure and withdrawal from PD treatment, and it is also the main risk factor for death in PD patients. In recent years, Gram-negative (G^-The prevalence of bacteria-related peritonitis is increasing, which has attracted more and more clinical attention. In G^-Peritonitis caused by Salmonella in bacteria is rare. Two cases of Salmonella-related peritonitis have been treated in our center in the past 5 years, which are reported as follows.

Patients with human immunodeficiency virus (HIV) infection are at high risk of chronic kidney disease. Common kidney pathological types are divided into HIV-related nephropathy (HIVAN), HIV immune complex-related nephropathy (HIVICK), drug-induced tubulointerstitial damage, thrombotic microangiopathy, etc.^[1]。 With the emergence of anti-retrotranscriptional drugs, the renal pathology of HIV-infected patients has changed significantly. In the United States, 80% of HIV-infected patients with renal pathology were reported to be HIVAN in 1997 and 20% in 2004^[2]； HIVAN accounted for 27% and HIVICK 21% in South Africa in 2006^[3]。 There are not many cases of renal biopsy in HIV infected patients in China. A total of 12 cases were retrieved, including 5 cases of IgA nephropathy, 2 cases of lupus nephritis, 2 cases of focal segmental glomerulosclerosis (non-collapsed), 1 case of collapsed focal segmental glomerulosclerosis, 1 case of membranous nephropathy and 1 case of purpura nephritis^[4,5,6,7,8]。 HIV infection complicated with minimal lesion nephropathy (MCD) has not been reported in China.

A 53-year-old female was admitted for "fever with chest tightness, fatigue and facial edema for 1 month". Past history: Anemia for more than 20 years, untreated. Family history is not special. Physical examination: body temperature 38℃, severe anemia, no yellowing stain of skin and sclera, dry rales can be heard in the right lung, low breathing sounds in both lower lungs, no abnormalities in the physical examination of the heart and abdomen, and mild edema in both lower limbs. Laboratory tests: blood routine: hemoglobin 55 g/L, mean red blood cell volume 86.6 fL, white blood cell 2.4×10⁹/L, platelets 85×10⁹/L. Urinary routine: urinary protein 3+, urinary occult blood 3+, urinary protein amount 8.06 g/24 h. Blood biochemistry: serum creatinine 141 μ mol/L, serum albumin 16.4 g/L, globulin 29 g/L, direct bilirubin 1.7 mmol/L, indirect bilirubin 2 mmol/L, lactate deacidase 396 IU/L (normal reference value 120~250 IU/L). Coagulation function test: Activated partial thromboplastin time (APTT) 53 s (normal reference value 29.2~41.2 s). Antinuclear antibody profile: ANA positive (1:100), anti-double stranded DNA antibody, anti-SSA antibody, anti-nucleosome antibody positive. Erythrocyte sedimentation rate (ESR) 70 mm/h; C-reactive protein (CRP) 3.4 mg/L (normal reference value 0-5.0 mg/L), complement C3 266 mg/L (normal value 790-1520 mg/L), complement C4 100 mg/L (normal reference value 160-38 330 mg/L), anti-phospholipid antibody negative. CT of the lung showed exudative changes in the right lung, pericardial and pleural effusion. Diagnosis: Systemic lupus erythematosus (SLE) (involving blood system, kidney, serous cavity), lupus nephritis, acute kidney injury. Methylprednisolone 240 mg/d was administered intravenously. Double plasma exchange (20% albumin and Ringer's solution) was performed on the 5th, 7th and 9th days after admission, with an exchange volume of 3.5 L/time and unfractionated heparin anticoagulation. On the 10th day of admission, the patient had sudden severe pain in the right lower abdomen. Physical examination: Right lower abdominal midline protuberance with tenderness. Emergency hemoglobin 59 g/L, platelet 39×10⁹/L, activated partial thromboplastin time (APTT) 180 s, prothrombin time (PT) 33.9 s (normal range 11.4 to 14.5 s). The changes of platelets and hemoglobin during hospitalization and the intervention measures are shown inFigure 1。 A plain CT scan of the abdomen showed swelling of the right rectus abdominis muscle, considering a hematoma (seeFIG. 2A）。 Immediately stop plasma exchange, give human immunoglobulin, blood transfusion and other treatments, and local pressure dressing at the same time. Multiple reexaminations of B-ultrasound and abdominal enhanced CT showed that the hematoma was larger than before (seeFigure 2B), right external iliac artery angiography was performed on the 18th day of admission, and plaque contrast spillage of the right inferior abdominal artery was observed during the operation (seeFigure 2C), suggesting active bleeding. Abdominal wall artery embolization was administered (seeFigure 2D）。 Intraoperative reimaging showed disappearance of active hemorrhage, postoperative reexamination of hemoglobin increased, and abdominal CT scan showed disappearance of rectus abdominis hematoma (seeFigure 2E）。 Two months later, the patient was re-admitted to the hospital for renal biopsy, and the pathological diagnosis was lupus nephritis (type V + III), and the treatment regimen of glucocorticoid plus cyclophosphamide continued. At present, his condition is stable and he is still being followed up.

Infection is the second leading cause of death in hemodialysis (HD) patients after cardiovascular disease^[1]According to the literature, approximately 31% of HD patients develop blood stream metastatic infection, and 5.7% of them develop suppurative spondylitis^[2]。 In the past 5 years, we have found that suppurative spondylitis, which was originally rare in HD patients, has occurred one after another. Therefore, this article aims to summarize and analyze the clinical characteristics of 15 HD patients complicated with suppurative spondylitis in our hospital, so as to improve clinicians' awareness and attention.

Heart and kidney are two important blood-rich organs of human body. Through the innervation of sympathetic and parasympathetic nerves, they play a role in maintaining blood pressure, vascular tension and peripheral tissue perfusion. The two organs interact with each other through complex pathophysiological mechanisms. The heart depends on the balance of water and sodium metabolism in the kidney to ensure the stability of effective circulating blood volume, while the physiology of the kidney depends on the maintenance of cardiac blood pressure and stable blood supply. Due to the interdependence of heart and kidney, when one organ is dysfunctional, another organ will be involved, thus triggering a vicious cycle.

Diabetic nephropathy (DN) is one of the most important causes of end-stage renal disease (ESRD). Previous clinical interventions targeting the traditional pathogenesis of DN include: inhibition of the production of inflammatory-related factors, increased advanced glycation end products (AGEs), and abnormal activation of the renin-angiotension system (RAS)^[1]。 However, none of these measures can effectively prevent DN. In recent years, a large number of studies have found that mitochondrial biosynthesis, energy metabolism, kinetic abnormalities and autophagy dysfunction of renal innate cells exist in the progression of DN^[2,3,4]It suggests that mitochondrial structural and functional damage may play a role in the pathogenesis and progression of DN. At the same time, mitochondrial targeting drugs have also opened up new ideas for the clinical diagnosis and treatment of DN.