BACKGROUND: There are increasing reports of glomerular disease (GD) following COVID-19 infection and vaccination. Current evidence on the possible link between COVID-19 infection or vaccination and GD is conflicting.
OBJECTIVE: The present study undertakes a scoping review of research to describe the relationship between COVID-19 infection and vaccination with GD and the common management strategies and overall outcomes of the disease to identify knowledge gaps and guide further research.
METHODS: All original research studies published in English until 5th September 2022 were considered for inclusion in the review. Exclusion criteria were animal studies, autopsy studies, and data involving patients who were paediatric patients (< 16 years), were transplant recipients, had a recurrence of glomerular disease, had concomitant cancer or non-COVID-19 infection which may cause glomerular disease, or did not receive a renal biopsy.
METHODS: The five electronic databases searched were MEDLINE, PubMed, Scopus, EMBASE, and Cochrane.
METHODS: Two separate search strings related to COVID-19, and glomerular disease were combined using the Boolean operator \'AND\'. Filters were used to limit publications to original research studies published in English. Search results from each database were imported into Covidence software ( www.covidence.org ) and used for de-duplication, article screening, and data extraction. Descriptive analyses were used to summarise demographics, diagnoses, and treatment outcomes.
RESULTS: After removing duplicates, 6853 titles and abstracts were screened. Of the 188 studies included, 106 studies described 341 patients with GD following COVID-19 infection and 82 described 146 patients with GD following a COVID-19 vaccination. IgA nephropathy was the most common GD pathology reported following COVID-19 vaccination with GD most common following mRNA vaccines. Collapsing focal segmental glomerulosclerosis was the most common GD following COVID-19 infection. Immunosuppressive treatment of GD was more common in the vaccine cohort than in the infection cohort.
CONCLUSIONS: Despite the significant number of COVID-19 infections and vaccinations around the world, our understanding of GD associated with COVID-19 infection and vaccination remains poor, and more research is needed to understand the possible relationship better.

BACKGROUND: People with Tuberculosis (TB) infection may present with glomerulonephritis (GN). The range of presentations, renal pathologies, and clinical outcomes are uncertain. Whether clinical features that establish if GN etiology is medication or TB related, and possible benefits of immunosuppression remain uncertain.
METHODS: A scoping review was completed, searching MEDLINE, EMBASE, Cochrane Central Register of Controlled Trials, Web of Science and Conference Abstracts from Inception to December, 2023. The study population included patients with TB infection who developed GN and underwent renal biopsy. All data regarding presentation, patient characteristics, renal pathology, management of TB and GN, and outcomes were summarized.
RESULTS: There were 62 studies identified, with 130 patients. These cases included a spectrum of presentations including acute kidney injury, nephrotic syndrome and hypertension, and a range of 10 different renal pathology diagnoses. Cases that included immunosuppression and outcomes ranged from complete remission to long-term dialysis dependence. The presence of granulomas (4/4, 100%), anti-glomerular basement membrane disease (3/3, 100%), amyloidosis (75/76, 98.7%), and focal segmental glomerulosclerosis (2/2, 100%) were specific for GN being TB-infection related. On the other hand, minimal change disease was specific for anti-TB therapy related (7/7, 100%). While patients with more aggressive forms of GN commonly were prescribed immunosuppression, this study was unable to confirm efficacy. Only rifampin or isoniazid were implicated in drug-associated GN.
CONCLUSIONS: This study provides a clear rationale for renal biopsy in patients with TB and GN, and outlines predictors for the GN etiology. Thus, this study establishes key criteria to optimize diagnosis and management of patients with TB and GN.

OBJECTIVE: As obesity and chronic kidney disease (CKD) remain a public health issue, we aim to elaborate on their complex relationship regarding pathogenetic mechanisms and therapeutic potential as well. The purpose of this review is to enhance our understanding of the interplay between obesity and CKD in order to timely diagnose and treat obesity-related CKD.
RESULTS: Obesity and CKD pose significant intertwined challenges to global health, affecting a substantial portion of the population worldwide. Obesity is recognized as an independent risk factor, intricately contributing to CKD pathogenesis through mechanisms such as lipotoxicity, chronic inflammation, and insulin resistance. Recent evidence highlights additional factors including hemodynamic changes and intestinal dysbiosis that exacerbate kidney dysfunction in obese individuals, leading to histologic alterations known as obesity-related glomerulopathy (ORG). This narrative review synthesizes current knowledge on the prevalence, pathophysiology, clinical manifestations, and diagnostic strategies of obesity-related kidney disease. Furthermore, it explores mechanistic insights to delineate current therapeutic approaches, future directions for managing this condition and controversies. By elucidating the multifaceted interactions between obesity and kidney health, this review aims to inform clinical practice and stimulate further research to address this global health epidemic effectively.

Immunotactoid glomerulopathy (ITG) is a rare glomerular disease that typically presents with proteinuria, hematuria, and kidney dysfunction. A kidney biopsy is essential to establish the diagnosis of ITG. ITG is characterized by glomerular electron-dense immunoglobulin deposits with hollow-cored microtubules. ITG is classified as either monoclonal or polyclonal based on immunofluorescence staining of the immunoglobulin deposits. Monoclonal ITG is associated with an underlying hematologic disorder in two-thirds of the cases, lymphoma and plasma cell dyscrasias being the most common. Polyclonal ITG is associated with autoimmune diseases but can be seen with hematologic disorders and chronic infections. Due to the preponderance of hematologic disorders in both monoclonal and polyclonal ITG, a thorough hematologic workup must be performed in all cases of ITG. In monoclonal ITG with a detectable clone, clone-directed therapy is administered to achieve hematologic remission, as the renal response is highly dependent on the hematologic response. In clone-negative monoclonal ITG, anti-B cell therapy is often used as a first-line therapy. Management of polyclonal ITG without an underlying hematologic disorder is poorly defined. Compared to monoclonal ITG, patients with polyclonal ITG have a higher risk of progression to end-stage kidney disease. Recurrence of ITG following kidney transplantation is common and is often associated with hematologic relapse.

Defects in the mitochondrial tRNA genes cause a group of highly clinically and genetically heterogeneous disorders, which poses a challenge for clinical identification and genetic diagnosis. Here, we present a pre-school boy with a novel MT-TD variant m.7560T>C at the heteroplasmy level of 76.53% in blood, 93.34% in urine sediments, and absent in the healthy mother\'s blood and urine. Besides convulsions, brain magnetic resonance imaging abnormalities and high plasma lactate, the boy presented with the prominent extra-neurologic phenotype including steroid-resistant nephrotic syndrome associated with focal segmental glomerulosclerosis characterized by abnormal mitochondria in podocytes, cortical blindness, and pancreatitis. To our knowledge, this is the unique case with MT-TD m.7560T>C-related multi-organ impairments, which expands the phenotypic and mutational spectrum of primary mitochondrial diseases.

Utilizing ultrasound radiomics, we developed a machine learning (ML) model to construct a nomogram for the non-invasive evaluation of glomerular status in diabetic kidney disease (DKD).
Patients with DKD who underwent renal biopsy were retrospectively enrolled between February 2017 and February 2023. The patients were classified into mild or moderate-severe glomerular severity based on pathological findings. All patients were randomly divided into a training (n =79) or testing cohort (n = 35). Radiomic features were extracted from ultrasound images, and a logistic regression ML algorithm was applied to construct an ultrasound radiomic model after selecting the most significant features using univariate analysis and the least absolute shrinkage and selection operator algorithm (LASSO). A clinical model was created following univariate and multivariate logistic regression analyses of the patient\'s clinical characteristics. Then, the clinical-radiomic model was constructed by combining rad scores and independent clinical characteristics and plotting the nomogram. The receiver operating characteristic curve (ROC) and decision curve analysis (DCA), respectively, were used to evaluate the prediction abilities of the clinical model, ultrasound-radiomics model, and clinical-radiomics model.
A total of 114 DKD patients were included in the study, including 43 with mild glomerulopathy and 71 with moderate-severe glomerulopathy. The area under the curve (AUC) for the clinical model based on clinical features and the radiomic model based on 2D ultrasound images in the testing cohort was 0.729 and 0.761, respectively. Further, the AUC for the clinical-radiomic nomogram was constructed by combining clinical features, and the rad score was 0.850 in the testing cohort. The outcomes were better than those of both the radiomic and clinical single-model approaches.
The nomogram constructed by combining ultrasound radiomics and clinical features has good performance in assessing the glomerular status of patients with DKD and will help clinicians monitor the progression of DKD.

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Non-tumorlesions of the kidneys in malignant neoplasms are very diverse. They can alter the results of chemotherapy and lead to death in the long term. In this regard, the related discipline of onconephrology has increasingly begun to be identified, which emphasizes the importance of diagnosing non-tumor kidney lesions in this category of patients. This review is devoted to the classification, diagnosis, course, prevention and treatment of non-tumor kidney lesions in patients with malignant neoplasms. There are four groups of lesions: mechanical damage; nephropathy due to anticancer therapy; paraneoplastic nephropathy; lesions associated with metabolic disorders. Kidney lesions in patients with malignant neoplasms are characterized by a variable course. In some cases, acute renal failure develops. Others are characterized by an asymptomatic course with an outcome in nephrosclerosis. Timely diagnosis and treatment of kidney lesions in malignant neoplasms can improve the quality of life and prognosis of patients with malignant neoplasms.
Неопухолевые поражения почек при злокачественных новообразованиях весьма разнообразны. Они могут влиять на результаты химиотерапии и приводить в отдаленном периоде к летальному исходу. В связи с этим все чаще стали выделять смежную дисциплину — онконефрологию, что подчеркивает важность диагностики неопухолевых поражений почек у этой категории пациентов. Настоящий обзор посвящен вопросам классификации, диагностики, течения, профилактики и лечения неопухолевых поражений почек у пациентов со злокачественными новообразованиями. Выделяют 4 группы поражений: механическое поражение; нефропатии, обусловленные противоопухолевой терапией; паранеопластические нефропатии; поражения, связанные с метаболическими нарушениями. Поражения почек у пациентов со злокачественными новообразованиями характеризуются вариабельным течением. При некоторых вариантах развивается острая почечная недостаточность. Другие характеризуются бессимптомным течением с исходом в нефросклероз. Своевременная диагностика и лечение поражений почек при злокачественных новообразованиях могут улучшить качество жизни и прогноз пациентов со злокачественными новообразованиями.

Protein misfolding in the endoplasmic reticulum (ER) of podocytes contributes to the pathogenesis of glomerular diseases. Protein misfolding activates the unfolded protein response (UPR), a compensatory signaling network. We address the role of the UPR and the UPR transducer, inositol-requiring enzyme 1α (IRE1α), in streptozotocin-induced diabetic nephropathy in mice. Diabetes caused progressive albuminuria in control mice that was exacerbated in podocyte-specific IRE1α knockout (KO) mice. Compared to diabetic controls, diabetic IRE1α KO mice showed reductions in podocyte number and synaptopodin. Glomerular ultrastructure was altered only in diabetic IRE1α KO mice; the major changes included widening of podocyte foot processes and glomerular basement membrane. Activation of the UPR and autophagy was evident in diabetic control, but not diabetic IRE1α KO mice. Analysis of human glomerular gene expression in the JuCKD-Glom database demonstrated induction of genes associated with the ER, UPR and autophagy in diabetic nephropathy. Thus, mice with podocyte-specific deletion of IRE1α demonstrate more severe diabetic nephropathy and attenuation of the glomerular UPR and autophagy, implying a protective effect of IRE1α. These results are consistent with data in human diabetic nephropathy and highlight the potential for therapeutically targeting these pathways.

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Background: Lipoprotein glomerulopathy is an infrequent glomerular disorder that culminates in nephrotic syndrome and often progresses to kidney failure. Whereas most patients have been reported in Japan and China, limited reports have been documented outside these regions. This patient represents the first report of lipoprotein glomerulopathy in Pakistan. Case Presentation: A 25-year-old male patient, hypertensive for 2 years, presented with progressive body edema, frothy urine, and fatigue. Examination revealed elevated blood pressure, bilateral pedal edema, and positive shifting dullness. Laboratory results showed significant proteinuria and elevated cholesterol and triglyceride levels. Renal biopsy revealed enlarged glomeruli with a dilated capillary lumen filled with pale-staining mesh-like material \"lipoprotein thrombi.\" Mild tubular atrophy and interstitial inflammation were observed. No interstitial fibrosis was evident. Electron microscopy detailed the lipoprotein thrombi with lipid granules and vacuoles of various sizes. A diagnosis of lipoprotein glomerulopathy was rendered. Treatment with fenofibrate, rosuvastatin, and captopril led to notable improvements in symptoms, blood pressure, and lipid levels during a 6-month follow-up. Subsequent biopsy showed complete resolution of the lipoprotein thrombi and a significant reduction in subendothelial granular densities. However, the flocculent subendothelial material persisted to some extent despite the complete resolution of lipoprotein thrombi. Conclusion: This report underscores the rarity of lipoprotein glomerulopathy in Pakistan and contributes valuable insights into its histopathologic features and global epidemiology. This unique instance aims to raise awareness among healthcare professionals, aiding in improved recognition of this rare entity. The favorable response to fenofibrate treatment underscores its effectiveness in managing lipoprotein glomerulopathy.