scholarly journals Collapsing Focal Segmental Glomerulosclerosis in Viral Infections

2022 ◽  
Vol 12 ◽  
Author(s):  
Anne K. Muehlig ◽  
Sydney Gies ◽  
Tobias B. Huber ◽  
Fabian Braun
Keyword(s):  
Acute Kidney Injury ◽  
Focal Segmental Glomerulosclerosis ◽  
Viral Infections ◽  
Current Knowledge ◽  
Parvovirus B19 ◽  
Kidney Injury ◽  
Hemodynamic Instability ◽  
Rapid Progression ◽  
Special Focus ◽  
Segmental Glomerulosclerosis

Collapsing glomerulopathy represents a special variant of the proteinuric kidney disease focal segmental glomerulosclerosis (FSGS). Histologically, the collapsing form of FSGS (cFSGS) is characterized by segmental or global condensation and obliteration of glomerular capillaries, the appearance of hyperplastic and hypertrophic podocytes and severe tubulointerstitial damage. Clinically, cFSGS patients present with acute kidney injury, nephrotic-range proteinuria and are at a high risk of rapid progression to irreversible kidney failure. cFSGS can be attributed to numerous etiologies, namely, viral infections like HIV, cytomegalovirus, Epstein–Barr-Virus, and parvovirus B19 and also drugs and severe ischemia. Risk variants of the APOL1 gene, predominantly found in people of African descent, increase the risk of developing cFSGS. Patients infected with the new Corona-Virus SARS-CoV-2 display an increased rate of acute kidney injury (AKI) in severe cases of COVID-19. Besides hemodynamic instability, cytokine mediated injury and direct viral entry and infection of renal epithelial cells contributing to AKI, there are emerging reports of cFSGS associated with SARS-CoV-2 infection in patients of mainly African ethnicity. The pathogenesis of cFSGS is proposed to be linked with direct viral infection of podocytes, as described for HIV-associated glomerulopathy. Nevertheless, there is growing evidence that the systemic inflammatory cascade, activated in acute viral infections like COVID-19, is a major contributor to the impairment of basic cellular functions in podocytes. This mini review will summarize the current knowledge on cFSGS associated with viral infections with a special focus on the influence of systemic immune responses and potential mechanisms propagating the development of cFSGS.

Viral Nephropathies

2017 ◽  
Author(s):  
Kar Neng Lai ◽  
Andrew SH Lai ◽  
Sydney CW Tang
Keyword(s):  
Hepatitis C ◽  
Hepatitis B ◽  
Hiv Infection ◽  
Focal Segmental Glomerulosclerosis ◽  
Viral Infections ◽  
Parvovirus B19 ◽  
Laboratory Data ◽  
Molecular Testing ◽  
Segmental Glomerulosclerosis ◽  
Bk Polyomavirus

Viral infections are important causative agents in renal disease and are responsible for significant morbidity and mortality. The diagnostic criteria for virus-related nephropathy include detailed clinical and laboratory data and tissue molecular analysis. Possible pathogenetic mechanisms include kidney tropism of the virus, induction of abnormal immune complexes, direct cytopathogenic effects, and multiorgan failure. Hepatitis B virus is associated with membranous nephropathy and mesangiocapillary glomerulonephritis in endemic areas. Hepatitis C virus causes various forms of glomerulonephritis, including cryoglobulinemia-mediated glomerulonephritis. HIV infection is associated with a collapsing focal segmental glomerulosclerosis, a distinctive disease that mainly affects Africans and African Americans. In the course of HIV infection, other types of immune complex glomerulonephritis may occur. Recent reports indicate a role for parvovirus B19 in idiopathic collapsing focal segmental glomerulosclerosis. Acute kidney injury occurs in hantavirus and coronavirus-associated severe acute respiratory syndrome. Of particular interest are those viral infections with productive replication in the kidney, which often occur in immunocompromised hosts, such as renal allograft recipients. Epstein-Barr virus, cytomegalovirus, adenovirus, and BK polyomavirus are prominent members of this group causing specific diseases. Renal biopsy followed by appropriate serologic and molecular testing is essential for defining virus-related nephropathies and guiding prognostic and therapeutic evaluation. This review contains 4 figures, 3 tables, and 90 references. Key words: BK polyomavirus, cytomegalovirus, glomerulonephritis, hepatitis B, hepatitis C, HIV-associated nephropathy, viral infection

scholarly journals Infection-Related Focal Segmental Glomerulosclerosis in Children

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Anne Katrin Dettmar ◽  
Jun Oh
Keyword(s):  
Focal Segmental Glomerulosclerosis ◽  
Viral Infections ◽  
Parvovirus B19 ◽  
Systemic Infection ◽  
Human Immune Deficiency Virus ◽  
Steroid Resistant ◽  
Pediatric Nephrologist ◽  
Segmental Glomerulosclerosis ◽  
B Virus ◽  
Viral Components

Focal segmental glomerulosclerosis (FSGS) is the most common cause of steroid resistant nephrotic syndrome in children. It describes a unique histological picture of glomerular damage resulting from several causes. In the majority of patients the causing agent is still unknown, but in some cases viral association is evident. In adults, the most established FSGS causing virus is the human immune-deficiency virus, which is related to a collapsing variant of FSGS. Nevertheless, other viruses are also suspected for causing a collapsing or noncollapsing variant, for example, hepatitis B virus, parvovirus B19, andCytomegalovirus. Although the systemic infection mechanism is different for these viruses, there are similarities in the pathomechanism for the induction of FSGS. As the podocyte is the key structure in the pathogenesis of FSGS, a direct infection of these cells or immediate damage through the virus or viral components has to be considered. Although viral infections are a very rare cause for FSGS in children, the treating pediatric nephrologist has to be aware of a possible underlying infection, as this has a relevant impact on therapy and prognosis.

scholarly journals Current Concepts of Pediatric Acute Kidney Injury—Are We Ready to Translate Them into Everyday Practice?

2021 ◽  
Vol 10 (14) ◽  
pp. 3113
Author(s):  
Kinga Musiał
Keyword(s):  
Acute Kidney Injury ◽  
Surrogate Marker ◽  
Kidney Injury ◽  
Tubuloglomerular Feedback ◽  
Everyday Practice ◽  
Special Focus ◽  
Functional Reserve ◽  
Renal Functional Reserve ◽  
Acute Kidney Disease ◽  
Pediatric Acute Kidney Injury

Pediatric acute kidney injury (AKI) is a major cause of morbidity and mortality in children undergoing interventional procedures. The review summarizes current classifications of AKI and acute kidney disease (AKD), as well as systematizes the knowledge on pathophysiology of kidney injury, with a special focus on renal functional reserve and tubuloglomerular feedback. The aim of this review is also to show the state-of-the-art in methods assessing risk and prognosis by discussing the potential role of risk stratification strategies, taking into account both glomerular function and clinical settings conditioned by fluid overload, urine output, or drug nephrotoxicity. The last task is to suggest careful assessment of eGFR as a surrogate marker of renal functional reserve and implementation of point-of-care testing, available in the case of biomarkers like NGAL and [IGFBP-7] × [TIMP-2] product, into everyday practice in patients at risk of AKI due to planned invasive procedures or treatment.

scholarly journals Mechanical challenges and cytoskeletal impairments in focal segmental glomerulosclerosis

2018 ◽  
Vol 314 (5) ◽  
pp. F921-F925 ◽  
Author(s):  
Di Feng ◽  
Clark DuMontier ◽  
Martin R. Pollak
Keyword(s):  
Blood Flow ◽  
Focal Segmental Glomerulosclerosis ◽  
Kidney Injury ◽  
Future Research ◽  
Disease States ◽  
Filtration Barrier ◽  
Segmental Glomerulosclerosis ◽  
The Face ◽  
Foot Process ◽  
Future Research Directions

Focal segmental glomerulosclerosis (FSGS) is a histologically defined form of kidney injury typically mediated by podocyte dysfunction. Podocytes rely on their intricate actin-based cytoskeleton to maintain the glomerular filtration barrier in the face of mechanical challenges resulting from pulsatile blood flow and filtration of this blood flow. This review summarizes the mechanical challenges faced by podocytes in the form of stretch and shear stress, both of which may play a role in the progression of podocyte dysfunction and detachment. It also reviews how podocytes respond to these mechanical challenges in dynamic fashion through rearranging their cytoskeleton, triggering various biochemical pathways, and, in some disease states, altering their morphology in the form of foot process effacement. Furthermore, this review highlights the growing body of evidence identifying several mutations of important cytoskeleton proteins as causes of FSGS. Lastly, it synthesizes the above evidence to show that a better understanding of how these mutations leave podocytes vulnerable to the mechanical challenges they face is essential to better understanding the mechanisms by which they lead to disease. The review concludes with future research directions to fill this gap and some novel techniques with which to pursue these directions.

scholarly journals Principles of Drug Dosing in Sustained Low Efficiency Dialysis (SLED) and Review of Antimicrobial Dosing Literature

Pharmacy ◽  
2020 ◽  
Vol 8 (1) ◽  
pp. 33
Author(s):  
Paula Brown ◽  
Marisa Battistella
Keyword(s):  
Acute Kidney Injury ◽  
Renal Replacement Therapy ◽  
Critically Ill Patients ◽  
Dose Adjustment ◽  
Kidney Injury ◽  
Hemodynamic Instability ◽  
Drug Dosing ◽  
Low Efficiency ◽  
Preliminary Recommendation ◽  
Selection Of

The use of sustained low-efficiency dialysis (SLED) as a renal replacement modality has increased in critically ill patients with both acute kidney injury (AKI) and hemodynamic instability. Unfortunately, there is a paucity of data regarding the appropriate dosing of medications for patients undergoing SLED. Dose adjustment in SLED often requires interpretation of pharmacodynamics and pharmacokinetic factors and extrapolation based on dosing recommendations from other modes of renal replacement therapy (RRT). This review summarizes published trials of antimicrobial dose adjustment in SLED and discusses pharmacokinetic considerations specific to medication dosing in SLED. Preliminary recommendation is provided on selection of appropriate dosing for medications where published literature is unavailable.

P0647ACUTE KIDNEY INJURY SECONDARY TO SUCROSE CONTAING INTAVENOUS IMMUNOGLOBULIN

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Sadiq Al Lawati ◽  
Issa Al Salmi ◽  
SUAD Hannawi
Keyword(s):  
Acute Kidney Injury ◽  
Serum Level ◽  
Kidney Function ◽  
Viral Infections ◽  
Kidney Transplant Recipient ◽  
Transplant Rejection ◽  
Organ Transplant ◽  
Vital Signs ◽  
Kidney Injury ◽  
Kaposi Sarcoma

Abstract Background and Aims Intravenous immunoglobulins (IVIG) are pooled polyvalent IgG antibodies extracted from the human plasma. While the initial indications were mainly immune deficiency states and some autoimmune diseases, the usage has been widened to include several immune mediated diseases, viral infections, and organ transplant rejection. Stabilizers in IVIG may include sugars, such as sucrose, glucose, or maltose. Sucrose in IVIG preparations may cause acute kidney injury. We report the case of a renal transplant patient who developed acute kidney injury due to sucrose nephropathy following the administration of sucrose containing IVIG. Method Four months after transplantation he was referred to our Hospital for deterioration of kidney function with eGFR (by MDRD formula) of 27ml/min. Cytomegalovirus virus (CMV) PCR turned positive (3300 copies/ml). Cyclosporine levels were high (C2: 2937 ng/ml) and hence, cyclosporine dose was adjusted. Induction therapy with Injection Ganciclovir for 2 weeks, followed by therapeutic dose of oral Valganciclovir was administered for the treatment of CMV infection. Skin examination revealed annular purple patches, suspicious of Kaposi Sarcoma, on the upper limbs. Skin biopsy confirmed the diagnosis. It was planned to give total IVIG of 2 gm/ kg in four daily divided doses. After completion of the second dose, serum creatinine increased to 370 µmol/L. He was clinically asymptomatic, euvolumic, vital signs were stable, and his urine output remained normal and his urinalysis was inactive. Results The ultrasound of the transplant kidney was normal with normal resistivity index. IVIG was stopped. He was well hydrated and underwent ultrasound guided biopsy. The graft biopsy showed acute tubular injury with flattening and vacuolation of tubular epithelial cells. Mitosis indicating tubular regeneration was seen. There was mild focal interstitial inflammation (20%) with mild lymphocytic tubulitis not amounting to graft rejection. Immunohistochemistry for C4d and polyomavirus (BKV) were both negative. The features were most consistent with sucrose induced nephropathy (Figure 1). Subsequent visits showed a decrease in BKV-PCR serum level and eventually undetected serum level of BKV-PCR at follow up about a month later. Conclusion In this paper, we presented a case of a living unrelated kidney transplant recipient who developed BKV nephropathy and developed impaired kidney function. The patient also had new onset diabetes mellitus after kidney transplantation (NODAT) but was otherwise in good general health. Treatment included sucrose containing IVIG. The patient subsequently developed acute kidney injury. The outcome was favorable with recovery of filtration rate to the baseline within 21 days without the need for dialysis. We conclude that the administration of sucrose containing IVIG may lead to acute kidney injury. We recommend the use of sucrose-free IVIG whenever possible. In all cases, caution is required when administrating IVIG.

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