Anemia ; diagnosis ; etiology ; therapy ; Humans ; Multiple Myeloma ; complications ; Renal Insufficiency ; diagnosis ; etiology ; therapy

Humans ; Multiple Myeloma ; complications ; Neuritis ; etiology ; prevention & control ; therapy ; Renal Insufficiency ; etiology ; prevention & control ; therapy

No abstract available.
*Drug-Eluting Stents ; Female ; Humans ; Male ; Myocardial Infarction/*etiology/*therapy ; Renal Insufficiency, Chronic/*complications

Child, Preschool ; Humans ; Male ; Mucocutaneous Lymph Node Syndrome ; complications ; diagnosis ; Renal Insufficiency ; etiology

Cachexia ; etiology ; Cough ; Delayed Diagnosis ; Fever ; Humans ; Hypercalcemia ; etiology ; Male ; Middle Aged ; Radiography ; Renal Dialysis ; Renal Insufficiency ; etiology ; therapy ; Tuberculosis, Pulmonary ; complications ; diagnostic imaging

OBJECTIVETo understand the clinical and pathological characteristics of IgA nephropathy (IgAN) with crescentic formation in children.

METHODSClinicopathological data of 29 children with IgAN accompanied by crescents were analyzed. These patients were divided into two groups according to the percentage of glomeruli affected by crescents more or less than 50%, and their data were compared.

RESULTS(1) CLINICAL FEATURES: all the patients had hematuria and proteinuria, and macrohematuria (86%) and proteinuria were also common, protein excreted in urine was more than 1 g per day in 76% of the patients. The patients with edema, hypertension, and renal insufficiency were less than fifty percent. Nine patients in Group A (glomeruli affected by crescents > or = 50%) were crescentic IgAN. Significantly more cases in Group A had persistent macrohematuria, hypertension and renal failure than in Group B (glomeruli affected by crescents < 50%) (P < 0.05), with especially severe proteinuria (P < 0.01). It was easy to find nephritic syndrome in Group A, and asymptomatic hematuria combined with proteinuria in Group B. (2) Renal pathology: the glomeruli were affected by crescents from 5% to 85%. There were 52% to 85% in Group A, and 5% to 40% in Group B. Most crescents were cellular. All the cases had a diffuse mesangial proliferation and tubular-interstitial injury to different degree. Three cases had crescentic IgAN. Glomerulosclerosis was significantly more often seen in Group A (P < 0.05) and tuft adhesion was more frequently seen in Group B (P < 0.05). (3) Immunofluorescence: All the patients presented deposition of IgA, IgM and C3. There were 45% specimens combined with the deposition of IgG. Five cases showed 'full house' (17%), four of them were in Group A. None had IgA deposition alone.

CONCLUSIONThe main clinical feature of IgAN with crescentic formation were hematuria combined with proteinuria, especially persistent gross hematuria and severe proteinuria. All of them showed diffuse mesangial proliferation and tubular-interstitial injury in morphology of kidney. Most of them had tuft adhesion. The main type of immunofluorescence were IgA + IgM and IgA + IgM + IgG deposition. Some showed 'full house' phenomenon. The clinical manifestation and renal lesions of IgAN with diffuse crescentic formation were worse than IgAN with glomeruli affected by crescents < 50%.

Adolescent ; Biopsy ; Child ; Child, Preschool ; Female ; Glomerulonephritis, IGA ; complications ; pathology ; Hematuria ; etiology ; Humans ; Hypertension ; etiology ; Kidney ; pathology ; Kidney Function Tests ; Male ; Prognosis ; Proteinuria ; etiology ; Renal Insufficiency ; etiology

OBJECTIVETo summarize the clinical characteristics, diagnosis, treatments and outcomes of perinatal autosomal recessive polycystic kidney disease.

METHODSThe clinical data of one case with infantile polycystic kidney disease diagnosed in perinatal stage and the reports of 11 cases seen in the past 15 years searched in Pubmed, OVID and Elsevier and CNKI, Wanfang database by using the polycystic kidney disease, infant, perinatal, autosomal recessive and case report as keyword were reviewed and analyzed.

RESULTSThe infant was characterized by huge kidneys, severe respiratory and renal compromise. The kidneys were symmetrically enlarged and highly echogenic by ultrasonographic examination and showed high-signal intensity on T2-weighted images by MRI. Histologic analysis showed pulmonary hypoplasia, numerous dilated and elongated tubular structures in the kidney and dilated intrahepatic biliary ducts. Among the 12 cases, 8 cases' presumptive diagnosis was made by prenatal ultrasound revealed enlarged kidneys and oligohydramnios. All cases suffered respiratory distress after birth, and 5 cases complicated pneumothorax. 6 cases died in neonatal stage because of respiratory failure.1 case died 2 m after birth because of renal failure. Five cases are alive and underwent dialysis, nephrectomy or renal transplant.

CONCLUSIONNewborn infants with perinatal autosomal recessive polycystic kidney disease often have poor outcome and died from respiratory and renal failure. Aggressive respiratory support and renal replacement therapy (including nephrectomy, dialysis and transplantation) may give these infants a favorable outcome.

Bronchopulmonary Dysplasia ; etiology ; pathology ; Fatal Outcome ; Humans ; Infant, Newborn ; Infant, Newborn, Diseases ; diagnosis ; genetics ; pathology ; Kidney ; pathology ; Male ; Perinatology ; Polycystic Kidney, Autosomal Recessive ; complications ; diagnosis ; genetics ; pathology ; Renal Dialysis ; Renal Insufficiency ; etiology ; pathology ; Respiratory Insufficiency ; etiology ; pathology ; Retrospective Studies ; Ultrasonography

OBJECTIVE: To identify the main active components in Ⅲ and their targets and explore the mechanism by which Ⅲ alleviates proteinuria in chronic kidney disease (CKD) based on network pharmacology. METHODS: The active components of Ⅲ and their potential targets, along with the oral bioavailability and drug-like properties of each component were searched in the TCMSP database. The proteinuria-related targets were searched in the GeneCards database. The active component-target network was constructed using Cytoscape software, and the acquired information of the targets from ClueGO was used for enrichment analysis of the gene pathways. RESULTS: A total of 102 active components were identified from Ⅲ. These active components acted on 126 targets, among which 69 were related to proteinuria. Enrichment analysis revealed fluid shear stress- and atherosclerosisrelated pathways as the highly significant pathways in proteinuria associated with CKD. CONCLUSIONS We preliminarily validated the prescription of Ⅲ and obtained scientific evidence that supported its use for treatment of proteinuria in CKD. The findings in this study provide a theoretical basis for further study of the mechanism of Ⅲ in the treatment of proteinuria in CKD.
Biological Availability ; Drugs, Chinese Herbal ; chemistry ; pharmacokinetics ; therapeutic use ; Humans ; Proteinuria ; drug therapy ; etiology ; metabolism ; Renal Insufficiency, Chronic ; complications ; metabolism

As the incidence of diabetes mellitus is rapidly increasing worldwide,that of related complications,such as diabetic kidney disease(DKD),also increases,conferring a heavy economic burden on the patients,families,society,and government.Diabetes mellitus complicated with chronic kidney disease(CKD)includes DKD and the CKD caused by other reasons.Because of the insufficient knowledge about CKD,the assessment of diabetes mellitus complicated with CKD remains to be improved.The therapies for diabetes mellitus complicated with CKD focus on reducing the risk factors.In clinical practice,DKD may not be the CKD caused by diabetes.According to clinical criteria,some non-diabetic kidney disease may be misdiagnosed as DKD and not be treated accurately.This review summarizes the status quo and research progress in the assessment,diagnosis,and treatment of diabetes mellitus complicated with CKD and predicts the directions of future research in this field.
Humans ; Diabetes Mellitus, Type 2/complications* ; Diabetic Nephropathies/etiology* ; Renal Insufficiency, Chronic/therapy* ; Risk Factors ; Diabetes Mellitus/therapy*

Antibodies, Antineutrophil Cytoplasmic ; blood ; Child ; Female ; Hematuria ; etiology ; Humans ; Kidney ; pathology ; physiopathology ; Kidney Function Tests ; Proteinuria ; etiology ; Renal Insufficiency ; etiology ; Vasculitis ; blood ; complications ; pathology