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Small vessel vasculitis
Published in Biju Vasudevan, Rajesh Verma, Dermatological Emergencies, 2019
Renu George, Ankan Gupta, Aswin M. Nair
Renal manifestations vary from isolated hematuria with or without proteinuria to hypertension. The more severe cases may manifest as nephrotic syndrome with significant proteinuria or as acute glomerulonephritis. Nephritis occurs within a mean period of 2 weeks after the diagnosis of HSP is made and usually within a month in the majority of cases. The risk factors for developing nephritis are age older than 8 years, abdominal pain, and recurrence of HSP disease. It is recommended that weekly urine analysis be done for the first 2 months [62]. The prognosis of HSP is dependent on the severity of renal involvement. This can lead to chronic kidney disease in a small proportion of patients, even as late as 20 years after diagnosis [63]. Renal disease can mimic poststreptococcal glomerulonephritis or SLE nephritis. The C3 levels are normal in HSP nephritis as opposed to those of SLE with nephritis. The rare complications of HSP include cerebral vasculitis [64], scrotal or testicular hemorrhage [65], and interstitial pulmonary hemorrhage [66]. HSP nephritis with pulmonary findings may mimic AAV.
The Urinary System and Its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
Glomerulonephritis may present with an abrupt onset, often as a result of immune-complex disease following an infection. Termed acute, postinfectious, or poststreptococcal glomerulonephritis (PSGN), the disorder causes edema, oliguria (decreased urine output, technically less than 500 ml per day), hematuria (blood in the urine), proteinuria(protein in the urine), and even headaches and visual disturbances secondary to hypertension if fluid retention is severe enough. With a more insidious onset is subacute glomerulonephritis, also called rapidly progressive glomerular disease or RPGN. Although fairly rare, subacute glomerulonephritis presents with hematuria, proteinuria, and RBC casts in the urine and often progresses to total, irreversible anuria (an- = without; -uria = urine production: production of less than 100 ml of urine per day) of terminal renal failure. Chronic glomerulonephritis is a syndrome characterized by slow, progressive loss of renal function and is often asymptomatic for years before it is detected. Pathologically, chronic glomerulonephritis produces sclerosis of glomeruli; and the clinical presentation includes proteinuria, cylindruria (the presence of cylindrical casts in the urine), and usually hematuria.
Epidemiology and Clinical Characteristics of Henoch–Schönlein Purpura Associated with Streptococcal Infection in 217 Children in Hubei Province, China
Published in Fetal and Pediatric Pathology, 2022
Jun Chen, Jian-gang Wu, Ying Cheng, Hong-bo Hu
There was a significantly higher frequency of renal involvement in the infectious group than in the noninfectious group (p = 0.048). An important finding in the present study is a possible association between infection with GABHS and renal involvement among HSP patients. Oda T. et al. showed that nephritis associated plasmin receptor (group A streptococcal antigen) may play a pathogenic role in patients with acute post-streptococcal glomerulonephritis [14]. In recent years, the pathogenesis model of post-streptococcal glomerulonephritis has been proposed from the perspective of humoral and cellular immunity. Delayed hypersensitivity is also associated with glomerular manifestations of the disease. Given the small number of children involved in this study, contingency cannot be excluded as an explanation for this link. This possible relationship needs further study.
Immune-mediated organ pathologies of vital organs
Published in International Reviews of Immunology, 2021
Blood filtration is an essential physiological process for a mammal’s survival and it takes place in a specialized organ known as the kidney. Glomerulonephritis is a condition in which the function of the kidney is compromised, resulting in the accumulation of fluid, electrolytes and metabolic waste, which eventually affects vital parameters and other vital organs of the body. Glomerulonephritis can be caused by microbial or parasitic infection. It can also occur as a consequence of an autoimmune disease such as systemic lupus erythematosus or the presence of a tumor. Streptococcus pyogenes is a Group A streptococcus and its infection causes immune-mediated acute post-streptococcal glomerulonephritis (APSGN). The first review article in this issue by Mosquera et al. sheds light on the biology of APSGN. The article also discusses host–streptococcus interaction and the factors involved in glomerulonephritis [1]. The article enriches knowledge by providing a fundamental understanding of bacteria-induced glomerulonephritis and will be of interest to fundamental and clinical immunologists (Figure 1).
Acute renal failure with need for renal replacement therapy as a complication of zoonotic S. zooepidemicus infection: case report and review of the literature
Published in Acta Clinica Belgica, 2018
Laurens Veldeman, Katrien De Wilde, Dirk Vogelaers, Evelyne Lerut, An Vonck, Dien Mertens, Annelies Koch, Jan Beckers
Post-Streptococcal Glomerulonephritis (PSGN) is a non-suppurative, immunologically mediated complication of streptococcal infection.1 The classical clinical presentation of PSGN in children comprises a triad of edema, hematuria (with tea- or cola-colored urine) and arterial hypertension, manifesting in the weeks following upper respiratory or cutaneous infection.1,2 Scarlatina or scarlet fever, an acute pharyngitis with fever, swollen tonsils and characteristic ‘strawberry’ tongue as well as an exanthemous skin eruption, caused by a Lancefield group A β-hemolytic streptococcus (S. pyogenes) is the best known infection preceding PSGN in children.1 In children there is a latency period between infection and onset of the acute glomerulonephritis syndrome, averaging one to two weeks in throat infection and somewhat longer, four to six weeks, after skin infection with S. pyogenes.1,3As compared to children, PSGN in adults has a different spectrum of causal pathogens, sites of preceding infection and duration of the latency period. In adults, staphylococcal infections are as common as streptococcal infections, and the sites of infection are more heterogeneous and not only limited to throat and skin. In a significant percentage of adults the triggering infection is only discovered at the onset of glomerulonephritis, so that the underlying and triggering infection may go unrecognized for some time. For this reason, the term infection-related glomerulonephritis (IRGN) has been proposed.4