Viral Nephropathies

2017 ◽  
Author(s):  
Kar Neng Lai ◽  
Andrew SH Lai ◽  
Sydney CW Tang

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

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Anne Katrin Dettmar ◽  
Jun Oh

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.


2007 ◽  
Vol 73 (7) ◽  
pp. 637-646 ◽  
Author(s):  
Donald E. Fry

Bloodborne pathogens continue to be a source of occupational infection for healthcare workers, but particularly for surgeons. Over 1 per cent of the U.S. population has one or more chronic viral infections. Hepatitis B is the infection that has the longest known role as an occupational pathogen, but infection with this virus is largely preventable with the use of the effective hepatitis B vaccine. Hepatitis C affects the largest number of people in the United States, and there is no vaccine available for the prevention of this infection. HIV infection still has not been associated with a documented transmission in the operating room environment, but six cases of probable occupational transmission have been reported. A total of 57 healthcare workers have had documented occupational infection since the epidemic of HIV infection began. Infection of blood-borne pathogens to patients from infected surgeons remains a concern. Surgeons who are e-antigen-positive for hepatitis B have been well documented to be an infection risk to patients in the operating room. Only four surgeons have been documented to transmit hepatitis C, although other transmissions have occurred in the care of patients when practices of infection control have been violated. No surgical transmission of HIV to a patient has been identified at this time. Prevention of occupational infection requires use of protective barriers, avoidance of exposure risk by modification of techniques, and a constant awareness of sharp instruments in the operating room. Blood exposure in the operating room carries risk of infection and should be avoided. It is likely that other infectious agents will emerge as operating room threats. Surgeons must maintain vigilance in avoiding blood exposure and percutaneous injury.


2022 ◽  
Vol 12 ◽  
Author(s):  
Anne K. Muehlig ◽  
Sydney Gies ◽  
Tobias B. Huber ◽  
Fabian Braun

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.


2011 ◽  
Author(s):  
Annika Parantainen ◽  
Minna Anthoni ◽  
America Valdes ◽  
Marie-Claude Lavoie ◽  
Ulla-Maija Hellgren ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Takaya Ozeki ◽  
Shoichi Maruyama ◽  
Toshiyuki Imasawa ◽  
Takehiko Kawaguchi ◽  
Hiroshi Kitamura ◽  
...  

AbstractFocal segmental glomerulosclerosis (FSGS) is a serious condition leading to kidney failure. We aimed to investigate the clinical characteristics of FSGS and its differences compared with minimal change disease (MCD) using cross-sectional data from the Japan Renal Biopsy Registry. In Analysis 1, primary FSGS (n = 996) were stratified by age into three groups: pediatric (< 18 years), adult (18–64 years), and elderly (≥ 65 years), and clinical characteristics were compared. Clinical diagnosis of nephrotic syndrome (NS) was given to 73.5% (97/132) of the pediatric, 41.2% (256/622) of the adult, and 65.7% (159/242) of the elderly group. In Analysis 2, primary FSGS (n = 306) and MCD (n = 1303) whose clinical diagnosis was nephrotic syndrome (NS) and laboratory data were consistent with NS, were enrolled. Logistic regression analysis was conducted to elucidate the variables which can distinguish FSGS from MCD. On multivariable analysis, higher systolic blood pressure, higher serum albumin, lower eGFR, and presence of hematuria associated with FSGS. In Japanese nationwide registry, primary FSGS patients aged 18–64 years showed lower rate of NS than those in other ages. Among primary nephrotic cases, FSGS showed distinct clinical features from MCD.


2018 ◽  
Vol 5 (5) ◽  
Author(s):  
Ralph-Sydney Mboumba Bouassa ◽  
Zita Aleyo Nodjikouambaye ◽  
Damtheou Sadjoli ◽  
Ali Mahamat Moussa ◽  
Chatte Adawaye ◽  
...  

Abstract Childbearing-aged women (n = 266) attending a gynecological clinic in Chad were subjected to multiplex immunochromatographic rapid test for HIV, hepatitis B virus (HBV), and hepatitis C virus (HCV). Ten (3.7%) and 8 (3.0%) were seropositive for HIV and HCV, respectively, and 20 (7.5%) for HBV surface antigen, allowing diagnosis of chronic viral infections in 1 of 7 (14.3%) women.


2018 ◽  
Vol 92 (7) ◽  
Author(s):  
Xiaoqiong Duan ◽  
Shilin Li ◽  
Jacinta A. Holmes ◽  
Zeng Tu ◽  
Yujia Li ◽  
...  

ABSTRACTHepatitis C virus (HCV) infection has been shown to regulate microRNA 130a (miR-130a) in patient biopsy specimens and in cultured cells. We sought to identify miR-130a target genes and to explore the mechanisms by which miR-130a regulates HCV and hepatitis B virus (HBV) replication. We used bioinformatics software, including miRanda, TargetScan, PITA, and RNAhybrid, to predict potential miR-130a target genes. miR-130a and its target genes were overexpressed or were knocked down by use of small interfering RNA (siRNA) or clustered regularly interspaced short palindromic repeat (CRISPR)/Cas9 guide RNA (gRNA). Selected gene mRNAs and their proteins, together with HCV replication in OR6 cells, HCV JFH1-infected Huh7.5.1 cells, and HCV JFH1-infected primary human hepatocytes (PHHs) and HBV replication in HepAD38 cells, HBV-infected NTCP-Huh7.5.1 cells, and HBV-infected PHHs, were measured by quantitative reverse transcription-PCR (qRT-PCR) and Western blotting, respectively. We selected 116 predicted target genes whose expression was related to viral pathogenesis or immunity for qPCR validation. Of these, the gene encoding pyruvate kinase in liver and red blood cell (PKLR) was confirmed to be regulated by miR-130a overexpression. miR-130a overexpression (via a mimic) knocked down PKLR mRNA and protein levels. A miR-130a inhibitor and gRNA increased PKLR expression, HCV replication, and HBV replication, while miR-130a gRNA and PKLR overexpression increased HCV and HBV replication. Supplemental pyruvate increased HCV and HBV replication and rescued the inhibition of HCV and HBV replication by the miR-130a mimic and PKLR knockdown. We concluded that miR-130a regulates HCV and HBV replication through its targeting of PKLR and subsequent pyruvate production. Our data provide novel insights into key metabolic enzymatic pathway steps regulated by miR-130a, including the steps involving PKLR and pyruvate, which are subverted by HCV and HBV replication.IMPORTANCEWe identified that miR-130a regulates the target genePKLRand its subsequent effect on pyruvate production. Pyruvate is a key intermediate in several metabolic pathways, and we identified that pyruvate plays a key role in regulation of HCV and HBV replication. This previously unrecognized, miRNA-regulated antiviral mechanism has implications for the development of host-directed strategies to interrupt the viral life cycle and prevent establishment of persistent infection for HCV, HBV, and potentially other viral infections.


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