2018年 · 第34卷第09期

Case 1: A female with onset of nephrotic syndrome at 17 years old. Renal function, complement and autoantibodies were normal. Renal biopsy in outside hospital showed proliferative lesions of glomerular membrane. Renal tissues were positive for HBsAg and HBcAg, and negative for HBeAg. Blood HBV-DNA was positive and liver enzymes were high. After entecavir antiviral treatment, HBV-DNA was continuously negative and liver enzymes were normal, but urinary protein was not relieved. Following immunosuppressant therapy, urine protein was repeated. Four years later, he was admitted to our hospital for blood free light chain, immune fixation electrophoresis, cryoglobulin and rheumatoid factor, and repeated renal biopsy was performed, seeFigure 1。 Immunofluorescence: Glomerular IgG (3+), C3 (+), C1q trace, κ light chain (2+), λ light chain trace, IgG1 (2+), IgG4 trace, diffuse distribution, granular deposition in mesangial area and vascular loop, IgM, IgA, IgG2, IgG3, HBsAg, HBcAg, HBeAg were all negative. Light microscopy showed that the mesangial region of the glomerulus, more under the endothelium, and a small amount of multiphilic erythrophils were deposited on the epithelial side. Electron microscopy: More high-density electron density was deposited in the mesangial region of the glomerulus, more electron density under the endothelium, and a small amount of high-density electron density was deposited in the epithelial segment of the basement membrane and in the basement membrane. Renal tissues were negative for Congo red staining. FK506 and Tripterygium wilfordii were treated, and the urine protein was 0.83 g/24 h after 24 months follow-up. The renal function was normal, and the immune fixation electrophoresis was negative.

A 54-year-old male was admitted due to left upper abdominal discomfort for 2 years, increased nocturia for more than 1 month, and fatigue for 1 week. The patient experienced left upper abdominal discomfort, accompanied by nausea and abdominal distension without obvious trigger 2 years ago and went to the doctor. Blood biochemical test: aspartate aminotransferase (AST) 79.5 U/L (normal value 15-40 U/L); Alanine aminotransferase (ALT) 103.3 U/L (normal 9-50 U/L). Antinuclear antibody (ANA) homogeneous 1:3200 positive (normal<1∶100）； Serum IgG4 6.76 g/L (normal 0.03~2.01 g/L). No abnormalities were found in routine urine and renal function tests. Combined with the pancreatic CT findings, the clinical diagnosis was IgG4-related autoimmune pancreatitis (IgG4-RAIP). Prednisone was administered orally at 30 mg/d, then gradually reduced to 5 mg/d, and prednisone was continued for 18 months and then discontinued. One month ago, the patient developed increased nocturia with general fatigue for 1 week, Scr 321.9 μ mol/L and was readmitted. Has a history of diabetes for 3 years, and regularly uses biosynthetic human insulin injection (Novolin R) and insulin glargine to control blood sugar; History of hypertension for 1 year, oral irbesartan hydrochlorothiazide for blood pressure control. Admission physical examination: BP 131/78 mmHg, mild edema of both lower limbs. Laboratory Test: RBC 3.61×10¹²/L, Hb 107 g/L, blood BUN 17.41 mmol/L, Scr 344.2 μ mol/L, urine protein (1+) to (3+), urine protein content 0.56 g/24 h, urine glucose negative, urine specific gravity normal; Serum albumin 37.5 g/L, IgG 23.2 g/L, complement C3 0.33 g/L, C4 0.02 g/L, IgG4 3.01 g/L, glycosylated hemoglobin 6.5%; Fundus examination showed retinal hemorrhage in both eyes. Abdominal CT examination showed that both kidneys were full and the density was not uniform.

The patient was a 69-year-old female. He was admitted to our hospital on September 21, 2017 due to "elevated Scr with hypertension for 25 years, aggravated and fever for 4 days". The patient's physical examination 25 years ago showed elevated Scr (140 μ mol/L), accompanied by elevated blood pressure. He irregularly took drugs such as nifedipine or irbesartan to control his blood pressure, and his blood pressure was controlled at about 140/90 mmHg. At that time, urine protein (+) was checked, and there was no microscopic hematuria and no leukocyturia. Clinical diagnosis of chronic renal failure; Hypertensive disease, hypertensive kidney damage. Five years ago, I came to the undergraduate outpatient clinic because of my pale face, and I was admitted to the hospital by checking Hb 87 g/L and Scr 160 μ mol/L. Urinary examination of 10 WBC/μ L (normal range 0-24); Urinary protein amount 0.65 g/24 h; Urine culture negative. Chronic kidney disease was diagnosed by B-ultrasound of both kidneys, and the right kidney was small; Magnetic resonance (MR) examination of the renal artery showed that the right renal artery was slightly slender. Discharge diagnosis: chronic renal failure; Hypertensive kidney damage, renal vascular hypertension, ischemic kidney disease may; Hypochromic microcytic anemia. After discharge, the Scr gradually increased, fluctuating from 171 to 365 μ mol/L; Multiple urine tests WBC<3/HP; Urine culture negative. 4 days ago, he came to our hospital for treatment due to mild back pain, accompanied by fatigue and poor appetite. The body temperature was 38.5℃, no frequent urination, urgency, pain in urination, and the Scr was 349 μ mol/L. After ceftriaxone treatment in the outpatient clinic, his body temperature dropped, but his renal function did not improve. He was admitted to hospital for further diagnosis and treatment. Past history: He underwent "left kidney lithotripsy" 27 years ago, and underwent surgical treatment for "right ureteral calculi" 22 years ago. Deny the history of diabetes, hepatitis, tuberculosis and other infectious diseases. Physical examination after admission: T 37.4℃, BP 129/77 mmHg, clear consciousness, fatigued face, no positive signs found in cardiopulmonary and abdominal physical examination, percussion pain in renal area (-). Blood routine: WBC 7.9×10⁹/L, Hb 74 g/L; Scr 410 μ mol/L; erythrocyte sedimentation rate 98 mm/h; CRP 51.0 mg/L. urinary osmotic concentration 388 mmol/L; Urinary retinol protein 11.9 mg/L; Urinary β 2 microglobulin 37.6 mg/L; Urinary leukocytes 10/μ L; Urine culture negative. CT of thorax and abdomen: a few inflammatory fibrous foci in both lower lungs; The right kidney is atrophic and the left kidney is small in size. Renal B-ultrasound: Two kidneys are small, the left kidney is 90 mm ×48 mm, and the right kidney is 82 mm ×33 mm. The kidney contour is unclear, the parenchyma is thinned, the echo is enhanced, and the boundary with the collective system is unclear. Admission diagnosis: chronic kidney disease with small kidneys.

With the decline of renal function in patients with chronic kidney disease (CKD), the metabolism of calcium, phosphorus and active vitamin D will be disordered, which in turn stimulates the secretion of parathyroid hormone (PTH), and eventually leads to secondary hyperparathyroidism (SHPT, referred to as secondary hyperparathyroidism) occurs. SHPT can lead to adverse outcomes such as bone disease, cardiovascular calcification and ectopic soft tissue calcification. Cardiovascular calcification is an important cause of death in patients with end-stage renal disease (ESRD).

Renal fibrosis is the main pathological basis of end-stage renal failure, and the final outcome of almost all chronic kidney diseases is renal fibrosis. In the process of renal fibrosis, a variety of signal transduction pathways are involved, such as c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) signaling pathway, TGF-β/Smad signaling pathway, Wnt/β-catenin, Jagged/Notch, epidermal growth factor receptor signaling pathway and tyrosine protein kinase/signal transduction and transcription activator signaling pathway. This review focuses on the relationship between JNK signal transduction pathway and renal fibrosis, and provides ideas for finding potential therapeutic targets for renal fibrosis.

Chronic kidney disease (CKD) is one of the major public health problems, and its incidence is high. About 5% ~10% of the global population is complicated with CKD^[1]The prevalence of CKD in China is 10.8%. CKD patients have a high percentage of end-stage renal disease (ESRD), which seriously affects the prognosis and quality of life of patients^[2]。 It is particularly important to screen CKD patients with poor prognosis early and intervene in time, but there is still a lack of clinical biomarkers that can effectively predict the progression and prognosis of CKD patients. It was found that galectin-3 (Gal-3) can regulate the progression of renal fibrosis and the occurrence of CKD complications, and is a risk factor affecting the prognosis of CKD patients. It may be a new target to delay the progression of CKD, intervene in CKD complications and improve the prognosis of CKD patients. This study will review the recent literature related to Gal-3 and CKD, and review the research progress of Gal-3 in CKD.

red blood cell distribution width (RDW) is a commonly used index to reflect different red blood cell volumes in clinic, and is usually used to identify different types of anemia. Recent studies at home and abroad have shown that elevated RDW can not only be used as a diagnostic index for many diseases, but also has important predictive value for patients' prognosis. Therefore, this article reviews the correlation between RDW and renal disease.