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Pediatric Clinics of North America Dec 2022Postinfectious glomerulonephritis (PIGN) is a leading cause of acute glomerulonephritis in children. The presentation of PIGN can vary from asymptomatic microscopic... (Review)
Review
Postinfectious glomerulonephritis (PIGN) is a leading cause of acute glomerulonephritis in children. The presentation of PIGN can vary from asymptomatic microscopic hematuria incidentally detected on routine urinalysis to nephritic syndrome and a rapidly progressive glomerulonephritis. Treatment involves supportive care with salt and water restriction, and the use of diuretic and/or antihypertensive medication, depending on the severity of fluid retention and the presence of hypertension. PIGN resolves completely and spontaneously in most children, and the long-term outcomes are typically good with preserved renal function and no recurrence.
Topics: Child; Humans; Glomerulonephritis; Antihypertensive Agents; Diuretics; Hematuria; Hypertension
PubMed: 36880922
DOI: 10.1016/j.pcl.2022.08.001 -
Pediatrics in Review Jan 2015On the basis of strong research evidence, the prevalence of poststreptococcal glomerulonephritis (PSGN) is decreasing worldwide, although it still remains the leading... (Review)
Review
On the basis of strong research evidence, the prevalence of poststreptococcal glomerulonephritis (PSGN) is decreasing worldwide, although it still remains the leading cause of glomerulonephritis in children. The overall decrease in prevalence of PSGN has been mainly driven by a significant decrease in pyoderma seen in the last half-century, such that postpharyngitic PSGN is most commonly seen in developed nations. On the basis of primarily consensus because of a lack of relevant clinical studies, the latency period between streptococcal infection and the development of nephritis is a hallmark of PSGN, with this period lasting 1 to 2 weeks with pharyngeal infections or 2 to 6 weeks with skin infections. Concurrent infectious and nephritis symptoms should elicit further suspicion of other causes of glomerulonephritis. On the basis of expert opinion, PSGN is one of a handful of nephritic disorders with hypocomplementemia (low C3 level). The decrease in C3 is found in more than 90% of PSGN cases and is typically seen earlier than an increase in antistreptolysin O titers. Measuring C3 and C4 may also be helpful in the evaluation of other causes of acute nephritis. On the basis of primarily consensus because of a lack of relevantclinical studies, the main sequelae of PSGN (hypertension, edema,gross hematuria, and impaired renal function) are greatest in thefirst 7 to 10 days of disease. Therefore, this period requires themost vigilance for adverse effects. On the basis of some research evidence and consensus, the most effective treatment of hypertension and edema in PSGN is loop or thiazide diuretics, which may also address hyperkalemia. Angiotensin-converting enzyme inhibitors or angiotensin receptor blockers may be effective in hypertension control but carry the risk of hyperkalemia and temporarily impairing recovery of renal function. On the basis of some research evidence and consensus, the prognosis for PSGN, even long term, is good. Despite being the most prevalent of the childhood glomerulonephritides, it often does not cause chronic kidney disease, but persistent microscopic hematuria and proteinuria may be seen in less than 10% of patients.
Topics: Acute Disease; Anti-Bacterial Agents; Child; Child, Preschool; Diagnosis, Differential; Glomerulonephritis; Humans; Male; Streptococcal Infections; Streptococcus pyogenes
PubMed: 25554106
DOI: 10.1542/pir.36-1-3 -
Postgraduate Medical Journal Apr 2003Glomerulonephritis is an important cause of renal failure thought to be caused by autoimmune damage to the kidney. While each type of glomerulonephritis begins with a... (Review)
Review
Glomerulonephritis is an important cause of renal failure thought to be caused by autoimmune damage to the kidney. While each type of glomerulonephritis begins with a unique initiating stimulus, subsequent common inflammatory and fibrotic events lead to a final pathway of progressive renal damage. In this article the different forms of inflammatory glomerulonephritis and their diagnosis are discussed. In a review of therapy both immediate life saving treatment given when glomerulonephritis causes acute renal failure and more specific treatments designed to modify the underlying mechanisms of renal injury are considered.
Topics: Acute Disease; Acute Kidney Injury; Glomerulonephritis; Glomerulonephritis, IGA; Glomerulonephritis, Membranoproliferative; Humans; IgA Vasculitis; Lupus Nephritis; Staphylococcal Infections
PubMed: 12743337
DOI: 10.1136/pmj.79.930.206 -
Pediatric Clinics of North America Feb 2019Acute postinfectious glomerulonephritis or infection-related glomerulonephritis has been associated with several viral or bacterial infections. Group A beta-hemolytic... (Review)
Review
Acute postinfectious glomerulonephritis or infection-related glomerulonephritis has been associated with several viral or bacterial infections. Group A beta-hemolytic streptococcal infection is the prototypical cause of postinfectious glomerulonephritis and the main focus of this discussion. The clinical spectrum can vary widely, from asymptomatic microscopic hematuria incidentally detected on routine urinalysis to rapidly progressive glomerulonephritis with acute kidney injury requiring emergent dialysis. Other important causes include glomerulonephritis associated with endocarditis and ventriculoatrial shunt infections. Multiple renal pathologic conditions have been associated with hepatitis B and C infections.
Topics: Acute Disease; Bacterial Infections; Glomerulonephritis; Humans; Risk Factors; Virus Diseases
PubMed: 30454751
DOI: 10.1016/j.pcl.2018.08.005 -
Paediatrics and International Child... Nov 2017Post-infectious glomerulonephritis (PIGN) is one of the most common causes of acute glomerulonephritis in children. Although post-streptococcal glomerulonephritis (PSGN)... (Review)
Review
Post-infectious glomerulonephritis (PIGN) is one of the most common causes of acute glomerulonephritis in children. Although post-streptococcal glomerulonephritis (PSGN) is still common, there is a wide spectrum of causative agents of PIGN. Non-streptococcal organisms are emerging as the main aetiological agents in high-income countries. Nephritis-associated plasmin receptor (NAPlr) and streptococcal pyrogenic exotoxin B (SPeB) are the two common antigens implicated in the pathogenesis of PSGN. Both NAPlr and SPeB activate the alternative complement pathway, resulting in low serum complement levels, and have an affinity to plasmin and glomerular proteins. The clinical presentation of PIGN varies from a benign asymptomatic condition to rapidly progressive glomerulonephritis requiring dialysis. In most cases, PIGN is self-limiting and the evidence base for the treatments used is quite weak. Renal biopsy is indicated when there are atypical features, rapid progression or inadequate recovery, or where an alternative diagnosis has to be considered. IgA-dominant nephritis, endocarditis-associated nephritis and shunt nephritis are special sub-subtypes of PIGN. The prognosis is generally excellent, although long-term follow-up may be needed.
Topics: Antigens, Bacterial; Bacterial Proteins; Exotoxins; Glomerulonephritis; Humans; Receptors, Cell Surface; Streptococcal Infections
PubMed: 28891413
DOI: 10.1080/20469047.2017.1369642 -
Indian Journal of Pediatrics 1999Acute glomerulonephritis (AGN) manifests with abrupt onset of hematuria, facial edema, hypertension and impairment of renal function. The commonest form of AGN in... (Review)
Review
Acute glomerulonephritis (AGN) manifests with abrupt onset of hematuria, facial edema, hypertension and impairment of renal function. The commonest form of AGN in developing countries is that following a beta hemolytic streptococcal infection where the glomerular injury is mediated by deposition of immune complexes. In the usual patient with moderately severe poststreptococcal AGN (PSAGN) the above-mentioned features are present However, gross or microscopic hematuria may be the only abnormality. A similar picture may occasionally be produced by a variety of infections (when GN is referred to as post-infectious and the mechanism of glomerular damage and the renal histology are similar to that in PSAGN), primary renal glomerular disorders (e.g. membranoproliferative GN, IgA nephropathy), collagen vascular diseases (systemic lupus erythematosus), systemic vasculitis (Henoch Schonlein purpura) and hereditary nephritis and some nonglomerular conditions. PSAGN may also present with one or more of its complications such as profound volume expansion with heart failure and hypertensive encephalopathy. PSAGN resolves rapidly and has an excellent prognosis. Patients with severe renal involvement and life threatening complications need expert supportive management. AGN with associated systemic features or very pronounced azotemia, nonstreptococcal AGN and unresolving GN need prompt, appropriate evaluation that often includes a renal biopsy. If extensive crescentic changes are found (crescentic GN), aggressive immunosuppression will be necessary.
Topics: Acute Disease; Child; Glomerulonephritis; Hematuria; Humans; Immunosuppressive Agents; Kidney; Prognosis; Streptococcal Infections
PubMed: 10798062
DOI: 10.1007/BF02761208 -
Nature Reviews. Nephrology Jan 2020For over a century, acute 'post-streptococcal glomerulonephritis' (APSGN) was the prototypical form of bacterial infection-associated glomerulonephritis, typically... (Review)
Review
For over a century, acute 'post-streptococcal glomerulonephritis' (APSGN) was the prototypical form of bacterial infection-associated glomerulonephritis, typically occurring after resolution of infection and a distinct infection-free latent period. Other less common forms of infection-associated glomerulonephritides resulted from persistent bacteraemia in association with subacute bacterial endocarditis and shunt nephritis. However, a major paradigm shift in the epidemiology and bacteriology of infection-associated glomerulonephritides has occurred over the past few decades. The incidence of APSGN has sharply declined in the Western world, whereas the number of Staphylococcus infection-associated glomerulonephritis (SAGN) cases increased owing to a surge in drug-resistant Staphylococcus aureus infections, both in the hospital and community settings. These Staphylococcus infections range from superficial skin infections to deep-seated invasive infections such as endocarditis, which is on the rise among young adults owing to the ongoing intravenous drug use epidemic. SAGN is markedly different from APSGN in terms of its demographic profile, temporal association with active infection and disease outcomes. The diagnosis and management of SAGN is challenging because of the lack of unique histological features, the frequently occult nature of the underlying infection and the older age and co-morbidities in the affected patients. The emergence of multi-drug-resistant bacterial strains further complicates patient treatment.
Topics: Age Distribution; Anti-Bacterial Agents; Antihypertensive Agents; Endocarditis, Bacterial; Fluid Therapy; Glomerulonephritis; Humans; Immunosuppressive Agents; Kidney; Methicillin-Resistant Staphylococcus aureus; Staphylococcal Infections; Staphylococcus aureus; Staphylococcus epidermidis; Streptococcal Infections; Streptococcus pyogenes; Substance Abuse, Intravenous; Time Factors
PubMed: 31399725
DOI: 10.1038/s41581-019-0178-8 -
Nephrologie & Therapeutique Jul 2012Acute postinfectious glomerulonephritis are defined by an acute nonsuppurative inflammatory insult predominantly glomerular. Its current incidence is uncertain because... (Review)
Review
Acute postinfectious glomerulonephritis are defined by an acute nonsuppurative inflammatory insult predominantly glomerular. Its current incidence is uncertain because of the frequency of subclinical forms. The most common infectious agent involved is beta hemolytic streptococcus group A. Acute postinfectious glomerulonephritis is uncommon in adults, and its incidence is progressively declining in developed countries. Humoral immunity plays a key role in the pathogenesis of kidney damage. Complement activation by the alternative pathway is the dominant mechanism, but a third way (lectin pathway) has been recently identified. The classic clinical presentation is sudden onset of acute nephritic syndrome after a free interval from a streptococcal infection. Treatment is essentially symptomatic and prevention is possible through improved hygiene and early treatment of infections.
Topics: Acute Disease; Adult; Child; Complement Activation; Female; Glomerulonephritis; Humans; Kidney Glomerulus; Male; Streptococcal Infections; Streptococcus pyogenes
PubMed: 22483748
DOI: 10.1016/j.nephro.2011.11.011 -
Pediatrics in Review Jul 1995
Review
Topics: Child; Glomerulonephritis; Humans; Streptococcal Infections
PubMed: 7624281
DOI: 10.1542/pir.16-7-278 -
Pediatrics in Review Sep 2023Glomerulonephritis (GN) encompasses several disorders that cause glomerular inflammation and injury through an interplay of immune-mediated mechanisms, host... (Review)
Review
Glomerulonephritis (GN) encompasses several disorders that cause glomerular inflammation and injury through an interplay of immune-mediated mechanisms, host characteristics, and environmental triggers, such as infections. GN can manifest solely in the kidney or in the setting of a systemic illness, and presentation can range from chronic and relatively asymptomatic hematuria to fulminant renal failure. Classic acute GN is characterized by hematuria, edema, and hypertension, the latter 2 of which are the consequence of sodium and water retention in the setting of renal impairment. Although presenting signs and symptoms and a compatible clinical history can suggest GN, serologic and urinary testing can further refine the differential diagnosis, and renal biopsy can be used for definitive diagnosis. Treatment of GN can include supportive care, renin-angiotensin-aldosterone system blockade, immunomodulatory therapy, and renal transplant. Prognosis is largely dependent on the underlying cause of GN and can vary from a self-limited course to chronic kidney disease. This review focuses on lupus nephritis, IgA nephropathy, IgA vasculitis, and postinfectious GN.
Topics: Humans; Hematuria; Glomerulonephritis; Kidney; Glomerulonephritis, IGA; Inflammation
PubMed: 37653138
DOI: 10.1542/pir.2021-005259