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Objective To investigate the clinical significance and level changes of uric acid (UA)/albumin(ALB) ratio (UAR) in patients with chronic kidney disease (CKD) complicated with coronary heart disease (CHD). Methods A total of 175 patients with CKD were divided into the simple CKD group (control group, n=94) and the CKD complicated with CHD group (experimental group, n=81). The differences of blood routine, blood lipid, renal function and UAR were compared between the two groups. The influencing factors of CKD complicated with CHD were analyzed by binary Logistic regression. Receiver operating characteristic (ROC) curve was used to analyze the predictive value of each index for CKD complicated with CHD. Results There were no significant differences in white blood cell count (WBC), monocytes (Mon), total cholesterol (TC), total triglyceride (TG), high-density lipoprotein (HDL-C) and low-density lipoprotein (LDL-C) between the two groups. The levels of neutrophils (Neu), red cell distribution width variation coefficient (RDW-CV), blood urea nitrogen (BUN), creatinine (Cr), UA and UAR levels were higher in the experimental group than those in the control group (R＜0.05). The levels of lymphocyte (Lym), red blood cell count (RBC), mean corpuscular hemoglobin concentration (MCHC), platelet (PLT), estimated glomerular filtration rate (eGFR) and albumin (Alb) were lower in the experimental group than those in the control group (R＜0.05). Logistic regression analysis showed that lower levels of RBC and MCHC, and higher levels of UAR were independent risk factors for CKD complicated with CHD. ROC curve showed that the area under the UAR curve was the largest in RBC, MCHC and UAR detection, which was 0.912 (95%CI: 0.870-0.953), the sensitivity was 90.10%, the specificity was 77.70%, the Yoden index was 0.678 and the cutoff value was 10.935. The AUC of combined detection of RBC, MCHC and UAR was 0.987 (95%CI: 0.974-0.999), the sensitivity was 93.80% and the specificity was 97.90%. Conclusion The increased serum UAR level in patients with CKD is a predictor of CHD. The combined detection of UAR, RBC and MCHC has higher prediction efficiency. [ABSTRACT FROM AUTHOR]

BACKGROUND Minimal change disease is a common cause of nephrotic syndrome in adults. There are few reported cases of vaccine-related podocytopathy with nephrotic-range proteinuria in the setting of a minimal change disease history. There have been rare reports of acute renal damage following vaccination to prevent COVID-19 and some cases of exacerbation of ongoing nephropathy. This report is a 33-year-old man with a 22-year history of nephrotic syndrome due to minimal change disease which exacerbated following a third dose of an mRNA SARS-CoV-2 vaccine for COVID-19. CASE REPORT We report a case of nephrotic syndrome after the third dose of the BNT162b2 mRNA COVID-19 vaccine. The patient presented with mild edema in the bilateral lower extremities and sacrum. Laboratory investigations confirmed nephrotic-range proteinuria and hypoalbuminemia. A kidney sonogram demonstrated mild renal parenchymal disease and a small non-obstructing right renal calculus. Renal biopsy revealed diffuse podocyte foot process effacement, punctuate IgG podocyte cytoplasmic staining, and minimal global glomerulosclerosis, consistent with a diagnosis of a diffuse podocytopathy with a minimal change disease phenotype. The patient was started on oral prednisone treatment, which led to remission of his symptoms and normalization of lab test results with normal BUN and Cr and resolution of proteinuria. Treatment was tapered off over the course of 28 weeks. CONCLUSIONS We presents a case of longstanding minimal change disease that showed exacerbation following a third dose of an mRNA vaccine for SARS-CoV-2. Although this may be a rare association, this case supports that patients with chronic glomerulonephritis need to be monitored.

Background/Purpose: Congenital nephrotic syndrome (CNS) is one of the important causes of end-stage kidney disease in children. Studies on the genotype, phenotype, and clinical outcome in infants with CNS caused by genetic mutations are scarce. Methods: We analyzed the genetic background, clinical manifestations, treatment response, and prognosis of pediatric patients with CNS in Taiwan. Results: Fifteen infants with CNS were enrolled, and 11 patients of median age 21 (interquartile range 3∼44) days caused by genetic mutations from 10 unrelated families were included in the study. Of the eleven patients, 9 had extra-renal manifestations including microcephaly, facial dysmorphism, and skeletal anomalies. More than two-thirds of the patients had disease onset before 1 month of age. Diffuse meningeal sclerosis was the most common histological characteristic. Whole exome sequencing followed by direct Sanger sequence revealed mutations in OSGEP (R247Q), WT1 (R366H and R467Q), LAMB2 (Q1209∗ and c. 5432–5451 19 bp deletion), NUP93 (D302V), and LAGE3 (c.188+1G > A). Three of the variants were novel. Corticosteroids and/or immunosuppressants were administered in 2 patients, but both were refractory to treatment. During the mean 3.5 years of follow-up, all but two died of uremia and sepsis. The two survivors reached end-stage kidney disease and required peritoneal dialysis, and one of them underwent uneventful renal transplantation. Conclusion: The majority of patients with CNS in Taiwan were caused by OSGEP followed by WT1 mutation. R247Q is the hotspot mutation of OSGEP in Taiwan. CNS patients in Taiwan suffer from significant morbidity and mortality.

Previous studies on renin-angiotensin-aldosterone system (RAAS) mainly focus on renin, prorenin and prorenin receptor (PRR), which play an important role in cardiovascular, renal and other diseases. The physiological function of PRR has been widely studied. Soluble prorenin receptor (sPRR) is generated by cleavage of extracellular components of PRR by protease and secreted into extracellular space, therefore the change of sPRR level may reflect the change of RAAS in tissue. However, there are limited clinical researchs on sPRR. In recent years, increasing evidences show that sPRR has important biological functions in various pathophysiological processes. This article summarized the recent advances in sPRR in cardiovascular system, kidney diseases, respiratory diseases, endocrine and metabolic diseases, pregnancy complications and cancers, and considered that sPRR may be a new biomarker of multiple diseases, and has potential therapeutic effects on metabolic diseases.

Background: International practice guidelines advocate for the use of anti-phospholipase A2 receptor (PLA2R) antibody testing to diagnose primary membranous nephropathy (pMN). This study aimed to clarify the current status of anti-PLA2R antibody testing in the diagnosis of pMN in Japan and to scrutinize the factors associated with the implementation of this antibody test. Methods: Utilizing a web-based questionnaire for nephrologists, responses were collected from 306 facilities and 427 nephrologists between November 2021 and December 2021. Preference for anti-PLA2R antibody testing was also investigated. Factors related to the experience of quantifying anti-PLA2R antibodies were estimated by generalized estimating equations using a robust analysis of variance with clusters of facilities of affiliation. Results: Of the 427 respondents, 140 (32.8%) had previous measurement experience at their current workplace and 165 (38.6%) had previous measurement experience overall. In pMN-suspected cases without contraindications to renal biopsy, 147 (34.4%) of the respondents opted to request anti-PLA2R antibody testing. The respondents' experience with anti-PLA2R antibody quantification at their current place of work was generally higher in university hospitals and increased with the annual number of kidney biopsies and the number of years since graduation. Conclusion: The results of this study suggest that a significant proportion of nephrologists in Japan have no experience in performing anti-PLA2R antibody assays, and that the assays may be hampered by the limited capabilities of the current workplace and the financial burden on facilities and patients. [ABSTRACT FROM AUTHOR]

Congenital nephrotic syndrome (CNS) is one of the important causes of end-stage kidney disease in children. Studies on the genotype, phenotype, and clinical outcome in infants with CNS caused by genetic mutations are scarce. We analyzed the genetic background, clinical manifestations, treatment response, and prognosis of pediatric patients with CNS in Taiwan. Fifteen infants with CNS were enrolled, and 11 patients of median age 21 (interquartile range 3∼44) days caused by genetic mutations from 10 unrelated families were included in the study. Of the eleven patients, 9 had extra-renal manifestations including microcephaly, facial dysmorphism, and skeletal anomalies. More than two-thirds of the patients had disease onset before 1 month of age. Diffuse meningeal sclerosis was the most common histological characteristic. Whole exome sequencing followed by direct Sanger sequence revealed mutations in OSGEP (R247Q), WT1 (R366H and R467Q), LAMB2 (Q1209∗ and c. 5432–5451 19 bp deletion), NUP93 (D302V), and LAGE3 (c.188+1G > A). Three of the variants were novel. Corticosteroids and/or immunosuppressants were administered in 2 patients, but both were refractory to treatment. During the mean 3.5 years of follow-up, all but two died of uremia and sepsis. The two survivors reached end-stage kidney disease and required peritoneal dialysis, and one of them underwent uneventful renal transplantation. The majority of patients with CNS in Taiwan were caused by OSGEP followed by WT1 mutation. R247Q is the hotspot mutation of OSGEP in Taiwan. CNS patients in Taiwan suffer from significant morbidity and mortality. [ABSTRACT FROM AUTHOR]