Introduction Vaccination against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can upregulate the immune system and may contribute to glomerular disease (GD). Here, we describe a spectrum of GD that manifested following vaccination against SARS-CoV-2 (COVID-19 vaccinations). Material and methods This was a descriptive study of 10 cases enrolled between January 2021 and January 2023. Patients with biopsy-proven GD that manifested following COVID-19 vaccinations were included. Results We found 10 cases of biopsy-proven GD following the COVID-19 vaccination. This included five cases of minimal change disease (MCD), three cases of focal segmental glomerulosclerosis (FSGS), one case of C3 glomerulonephritis (C3GN), and one case of IgA nephropathy (IgAN). The pre-existing disease was found in the last two patients (IgAN and C3GN) who got unmasked following vaccination. We did not observe any relation between vaccine type (Covisheld; six cases vs. Covaxin; four cases) and GD. In most cases (8/10 cases, 80.0%), GD developed after a repeat dose (second or booster dose). The onset time following vaccination was typically less than a week, and even less following a repeat dose. Conclusion Post-vaccination GD can be either de novo or a flare-up of a pre-existing one. The onset time following vaccination was typically less than a week for both Covishield and Covaxin.

Cancer immunotherapy represents a giant leap forward in the management of malignant diseases. An optimal anti-tumor immune response requires cancer antigen recognition by T-cells followed by an effector immune response. Suppression of T-cell activation prevents cancer cell clearance resulting in tumor proliferation. Recent clinical successes of immune checkpoint inhibitors and chimeric antigen receptor T cell therapies has transformed the landscape of cancer immunotherapy. The goal of immunotherapy is to boost host-protective anti-tumor immunity without concomitantly causing immune-related adverse events. However, immunotherapies can cause multiorgan dysfunction including acute kidney injury. Prompt recognition and management of immunotherapy-associated kidney injury is critical in preserving kidney function and improving patient outcomes.

Paraproteinemias are a group of complex diseases associated with an overproduction of a monoclonal immunoglobulin that can cause a diversity of kidney disorders and end-organ damage. In this review, we focus on paraprotein-mediated glomerular diseases. Kidney biopsy plays a crucial role in diagnosing these disorders, enabling the identification of specific histological patterns. These lesions are categorized into organized (such as amyloidosis, immunotactoid glomerulopathy, fibrillary glomerulonephritis, cryoglobulinemic glomerulonephritis, and monoclonal crystalline glomerulopathies) and nonorganized deposits (such as monoclonal Ig deposition disease and proliferative glomerulonephritis with monoclonal Ig deposits) based on the characteristics of immunofluorescence findings and the ultrastructural appearance of deposits on electron microscopy. This review aims to provide an update, highlight, and discuss clinicopathological aspects such as definition, epidemiology, clinical manifestations, mechanisms of kidney injury, histological features, and diagnostic procedures.

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Accumulating evidence indicates that inflammatory and immunologic processes play a significant role in the development and progression of glomerular diseases. Podocytes, the terminally differentiated epithelial cells, are crucial for maintaining the integrity of the glomerular filtration barrier. Once injured, podocytes cannot regenerate, leading to progressive proteinuric glomerular diseases. However, emerging evidence suggests that podocytes not only maintain the glomerular filtration barrier and are important targets of immune responses but also exhibit many features of immune-like cells, where they are involved in the modulation of the activity of innate and adaptive immunity. This dual role of podocytes may lead to the discovery and development of new therapeutic targets for treating glomerular diseases. This review aims to provide an overview of the innate immunity mechanisms involved in podocyte injury and the progression of proteinuric glomerular diseases.

Antibrush border antibody (ABBA) disease is a rare cause of kidney disease characterized by progressive renal tubular injury associated with immune complex deposition along the basement membranes of the proximal tubule and circulating autoantibodies to brush border antigens. Several antigens have been identified as targets of autoantibodies in this disease, including low-density lipoprotein receptor related protein 2 (LRP2), cubilin, and amnionless proteins. We present 9 patients from 2 academic medical centers and describe the clinicopathologic characteristics and outcome data. All patients presented with acute kidney injury and proteinuria. Pathology confirmed immune complex deposition along proximal tubular basement membranes in all patients, but the majority (6/8) also showed segmental glomerular subepithelial immune complexes. Two of 3 patients treated with rituximab demonstrated stabilization of kidney function; 1 of these patients had mantle cell lymphoma. One patient with lung cancer showed stabilization of disease after treatment of the malignancy. The remaining patients progressed to end-stage kidney disease with either conservative therapy (3 patients) or immunosuppression with glucocorticoids (2 patients). This series highlights the poor prognosis of ABBA disease, but a potential benefit of anti-B cell therapy or treatment of an underlying malignancy in some cases.

Chronic kidney disease (CKD) is associated with renal lipid dysmetabolism among a variety of other pathways. We recently demonstrated that oxysterol-binding protein like 7 (OSBPL7) modulates the expression and function of ATP Binding Cassette Subfamily A Member 1 (ABCA1) in podocytes, a specialized type of cell essential for kidney filtration. Drugs that target OSBPL7 lead to improved renal outcomes in several experimental models of CKD. However, the role of OSBPL7 in podocyte injury remains unclear. Employing mouse models and cellular assays, we investigated the influence of OSBPL7 deficiency on podocytes. We demonstrated that reduced renal OSBPL7 levels as observed in two different models of experimental CKD are linked to increased podocyte apoptosis, primarily mediated by heightened endoplasmic reticulum (ER) stress. While as expected the absence of OSBPL7 also resulted in lipid dysregulation (increased lipid droplets and triglycerides content), OSBPL7-deficiency related lipid dysmetabolism did not contribute to podocyte injury. Similarly, we demonstrated that the decreased autophagic flux we observed in OSBPL7-deficient podocytes was not the mechanistic link between OSBPL7-deficiency and apoptosis. In a complementary zebrafish model, osbpl7 knockdown was sufficient to induce proteinuria and morphological damage to the glomerulus, underscoring its physiological relevance. Our study shed new light on the mechanistic link between OSBPL7 deficiency and podocyte injury in glomerular diseases associated with CKD, and it strengthen the role of OSBPL7 as a novel therapeutic target.

To date, approximately 500 monogenic inherited kidney diseases have been reported, with more than 50 genes associated with the pathogenesis of monogenic isolated or syndromic nephrotic syndrome. Most of these genes are expressed in podocytes of the glomerulus. Neurological symptoms are common extrarenal manifestations of syndromic nephrotic syndrome, and various studies have found connections between podocytes and neurons in terms of morphology and function. This review summarizes the genetic and clinical characteristics of monogenic inherited diseases with concomitant glomerular and central nervous system lesions, aiming to enhance clinicians\' understanding of such diseases, recognize the importance of genetic diagnostic techniques for comorbidity screening, and reduce the rates of missed diagnosis and misdiagnosis.
至今为止，已报道约500种单基因遗传性肾脏病，其中50多个基因与单基因孤立性或综合征性肾病综合征的发病相关，这些基因大多在肾小球足细胞中表达。神经系统症状为综合征性肾病综合征常见的肾外表现，各种研究发现足细胞和神经元在形态和功能方面存在联系。该综述总结了同时出现肾小球和中枢神经系统病变的单基因遗传病的遗传学进展及临床特点，有助于提高临床医生对该类疾病的了解，认识基因诊断技术对共病筛查的重要性，降低漏诊、误诊率。.

Podocyte health is vital for maintaining proper glomerular filtration in the kidney. Interdigitating foot processes from podocytes form slit diaphragms which regulate the filtration of molecules through size and charge selectivity. The abundance of lipid rafts, which are ordered membrane domains rich in cholesterol and sphingolipids, near the slit diaphragm highlights the importance of lipid metabolism in podocyte health. Emerging research shows the importance of sphingolipid metabolism to podocyte health through structural and signaling roles. Dysregulation in sphingolipid metabolism has been shown to cause podocyte injury and drive glomerular disease progression. In this review, we discuss the structure and metabolism of sphingolipids, as well as their role in proper podocyte function and how alterations in sphingolipid metabolism contributes to podocyte injury and drives glomerular disease progression.

The case study aims to describe the nephrotic syndrome (NS) in a castrated 3-year-old male Cocker Spaniel dog. The patient arrived at the hospital with a loss of appetite and weakness. Skin oedema with ascites was observed along with hypoalbuminaemia, hypoproteinaemia, hyperlipidaemia, hypercholesterolaemia, and proteinuria (urine protein to creatinine ratio = 22.4). Based on these findings, the patient was diagnosed with NS, although a renal biopsy was not conducted. Prednisolone (1 mg/kg, p.o. q12 h) and mycophenolate mofetil (10 mg/kg, p.o. q12 h) were prescribed as the immunosuppressive drugs, and previously cryopreserved allogeneic adipose tissue-derived mesenchymal stem cells (2 × 107 cells/kg) were injected intravenously. After several weeks of treatment, the patient recovered from NS. This is the first case report on immunosuppressive drugs and allogeneic mesenchymal stem cells being used to treat a dog with NS.