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Nephritic syndrome is a combination of the following symptoms: blood in urine (hematuria), reduced urine output (oliguria), high blood pressure (hypertension), and edema (swelling around the eyes, on feet, ankles). Patients may also have elevated serum creatinine and variable amounts of protein in urine. Purchase a license to download a non-watermarked version of this video on AlilaMedicalMedia.com: https://www.alilamedicalmedia.com/-/g... Check out our new Alila Academy – AlilaAcademy.com - complete video courses with quizzes, PDFs, and downloadable images. Voice by: Jacob Glass ©Alila Medical Media. All rights reserved. All images/videos by Alila Medical Media are for information purposes ONLY and are NOT intended to replace professional medical advice, diagnosis or treatment. Nephritic syndrome is not a single disease, but a clinical presentation of an underlying illness, of which there are many. The syndrome can be acute or chronic, depending on how quickly symptoms develop; and primary or secondary, depending on the cause. In children, the most common cause is group A-beta streptococcal infection. Post-streptococcal nephritic syndrome typically develops a week after a strep throat or 2-3 weeks after a skin infection. In all cases, a prominent feature is inflammation of glomeruli in the kidney. A glomerulus is basically a ball of capillaries, where blood is filtered through a membrane into urine as it passes through. The filtration membrane has 3 components: the fenestrated endothelium of blood capillaries, the glomerular basement membrane, and the glomerular epithelium made of podocytes. Basically, an excessive immune response to an infection or illness activates cell-mediated and humoral pathways, as well as the complement system, in the glomeruli, resulting in: infiltration of immune cells, release of inflammatory cytokines, and formation and deposition of immune complexes. These, in turn, drive abnormal proliferation of glomerular cells in some cases. Immune deposits and proliferative cells block filtration, reducing urine output. As deposition builds up, capillary walls may rupture, releasing red blood cells into urine. The coagulation cascade may also be activated, producing tiny blood clots, further obstructing filtration. The composition and location of immune deposits and characteristics of cell proliferation vary with different causes, and can be used to identify them. For example, staphylococcal glomerulonephritis typically shows IgA and C3 complement deposits within the matrix of glomeruli. Nephritic syndrome can compromise renal function and may lead to serious complications including renal failure, uncontrolled hypertension and its consequences, electrolyte imbalances, and heart failure, among others. Diagnosis starts with patient’s history for a systemic illness and/or recent infection. Diagnostic tests include: Urinalysis for presence of red blood cells, typically including dysmorphic cells and casts; and protein content. Blood tests, for creatinine and urea levels, to assess renal functions. Blood cultures, to identify infection. and various serological tests, to determine or rule out certain causes. Renal biopsy may be performed to establish the underlying cause and assess the severity of the disease. Treatment consists of addressing the cause and managing symptoms, and may include: Corticosteroids and/or other immunosuppressive agents to treat autoimmune causes, Antibiotics to treat infectious causes, Plasma exchange, to replace the inflammatory plasma with a healthy one, Antihypertensives to lower blood pressure, Diuretics to reduce edema, Dialysis may be required with severe renal impairment. Prognosis varies depending on the cause and patient’s factors. Children with acute self-limiting disease typically have better outcome than adults with chronic disease.