Acute Glomerulonephritis Year 4 Paediatrics Notes OmpathStudy

Acute Glomerulonephritis Year 4 · Paediatrics Collection: 4TH YEAR ALL NOTES / PAEDS / PAEDS 4.2 / MUNGE / RENAL PAEDS -- Slide 1 Acute Glomerulonephritis Dr Rose Munge Slide 2 Introduction Acute glomerulonephritis (AGN) comprises a specific set of kidney diseases in which an immunologic mechanism triggers inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium.\n Acute nephritic syndrome is the most serious of these syndromes. AGN progresses to chronic glomerulonephritis in about 30% of patients. Slide 3 Diseases that produce GN are usually classified as primary (ie, diseases in which the kidney is the primarily affected organ)\n or\n secondary (ie, systemic disorders that involve the kidneys in addition to other organs, such as systemic lupus erythematosus [SLE]). Slide 4 Glomerulonephritis are classified as follows: Immune-complex glomerulonephritis (including infection-related glomerulonephritis, IgA nephropathy, lupus nephritis, and cryoglobulinemic glomerulonephritis) Antineutrophil cytoplasmic antibody (ANCA)–associated (pauci-immune) glomerulonephritis Anti-glomerular basement membrane glomerulonephritis C3 glomerulopathy Monoclonal immunoglobulin–associated glomerulonephritis Slide 5 AGN manifests with the sudden onset of hematuria, proteinuria, and red blood cell (RBC) casts in the urine.\n This clinical picture is often accompanied by hypertension, edema, azotemia (ie, decreased glomerular filtration rate [GFR]), and renal salt and water retention. The gold standard for the diagnosis of a glomerulonephritis is a kidney biopsy. Slide 6 In most circumstances, glomerular inflammation begins with an antigen-antibody reaction, either direct antibody binding to an antigen expressed or trapped in the glomerulus, or the localization of a circulating complex in the kidney. This incites injury by activating one or more systems of inflammatory mediators: the complement cascade, coagulation factors, cytokines, growth factors, and others.\n The inflammation is marked by proliferation of resident glomerular cells and infiltration by lymphocytes or neutrophils. Slide 7 The glomerular inflammation and expansion impairs the microcirculation, reducing the glomerular filtration rate (GFR) and usually resulting in an increase in BUN and creatinine.\n This reduction in GFR, in turn, leads to the retention of salt and water, causing fluid overload.\n In severe situations, it can be manifest by life-threatening hypertension and pulmonary edema, hypertensive encephalopathy may be the presenting complaint in some children with AGN Slide 8 Fortunately, most cases of AGN in children are either self-limited or amenable to therapy although there may be devastating complications of the illness during the acute phase.\n Less commonly, what begins as an apparent AGN may presage the development of a chronic process, which ultimately may progress into irreversible end-stage renal disease (ESRD) Slide 9 Presentation Most typically, the child with AGN will be seen because of the sudden development of change in urine color.\nOn occasion, however, the presenting complaint may relate to a complication of the disease: hypertensive seizures, edema, and so forth. Hematuria in children with AGN is typically described as “coke,” “tea,” or “smoky” colored.\nTrue bright red blood in the urine is more likely a consequence of anatomic problems such as urolithiasis than glomerulonephritis. Slide 10 Urine color in AGN is uniform throughout the stream.\nThe gross hematuria of AGN is virtually always painless; dysuria accompanying gross hematuria points to acute hemorrhagic cystitis rather than renal disease.\nA history of previous such episodes would point to an exacerbation of a chronic process such as IgA nephropathy.\nHistory of a recent documented streptococcal infection would be consistent with poststreptococcal AGN, such a history is frequently unavailable. Slide 11 It is next important to ascertain any symptoms suggestive of complications of the AGN.\nShortness of breath or exercise intolerance from fluid overload or headaches, visual disturbances, or alteration in mental status from hypertension. Since AGN may be the presenting complaint of a multisystem illness, a complete review of systems is vital- rash, joint discomfort, recent weight change, fatigue, appetite changes, respiratory complaints, and recent medication exposure. Slide 12 The family history should address the presence of any family members with autoimmune disorders, as children with both SLE and membranoproliferative glomerulonephritis (MPGN) may have such relatives.\n A family history of renal failure (specifically asking about dialysis and kidney transplantation) may be the first clue to a process such as Alport syndrome, which may initially present with an AGN picture. Slide 13 The physical examination begins with a careful assessment of vital signs, particularly blood pressure.\nBlood pr