Diet for acute glomerulonephritis
Go to Emergent Management of Acute Glomerulonephritis and Acute Poststreptococcal Glomerulonephritis for complete information on these topics. Acute proliferative glomerulonephritis is a disorder of the glomeruli ( glomerulonephritis ), or small blood vessels in the kidneys. These structural changes can be focal, diffuse or segmental, or global. When acute GN is associated with chronic infections, the underlying infections must be treated. Bacteria besides group A streptococci that can cause acute GN include diplococci, other streptococci, staphylococci, and mycobacteria. Histopathologic changes include swelling of the glomerular tufts and infiltration with polymorphonucleocytes (see Histologic Findings). Identified organisms include Coccidioides immitis and the following parasites: Plasmodium malariae, Plasmodium falciparum, Schistosoma mansoni, Toxoplasma gondii, filariasis, trichinosis, and trypanosomes. Attributing glomerulonephritis to a parasitic or fungal etiology requires the exclusion of a streptococcal infection. Acute GN can be due to a primary renal disease or to a systemic disease. Acute glomerulonephritis (GN) comprises a specific set of renal 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. With the development of the microscope, Theodor Langhans (1839 - 1915) was later able to describe these pathophysiologic glomerular changes. Functional changes include proteinuria, hematuria, reduction in GFR (ie, oligoanuria), and active urine sediment with RBCs and RBC casts. In addition, elevations of antibody titers to other antigens, such as antistreptolysin O or antihyaluronidase, DNAase-B, and streptokinase, provide evidence of a recent streptococcal infection. Three types have been distinguished: Type I is an antiglomerular basement membrane disease, type II is mediated by immune complexes, and type III is identified by antineutrophil cytoplasmic antibody (ANCA). Idiopathic rapidly progressive glomerulonephritis - This form of GN is characterized by the presence of glomerular crescents. Variable incidence has been reported, in part because of the subclinical nature of the disease in more than half the affected population. Acute GN is defined as the sudden onset of hematuria, proteinuria, and red blood cell (RBC) casts in the urine. Acute GN has been documented as a rare complication of hepatitis A. Please confirm that you would like to log out of Medscape. Glomerular lesions in acute GN are the result of glomerular deposition or in situ formation of immune complexes. Acute nephritic syndrome is the most serious and potentially devastating form of the various renal syndromes. In PSGN, involvement of derivatives of streptococcal proteins has been reported. In recent decades, however, the incidence of PSGN has fallen in the United States and other developed countries, while postinfectious GN from staphylococcal infection has risen. A streptococcal neuraminidase may alter host immunoglobulin G (IgG). In a study in adults, the two most frequently identified infectious agents were streptococci (27. Acute poststreptococcal glomerulonephritis ( PSGN ) is the archetype of acute GN. Leukocyte proliferation is indicated by the presence of neutrophils and monocytes within the glomerular capillary lumen and often accompanies cellular proliferation. Serotype 49 - Poststreptococcal nephritis due to a skin infection, usually observed in the summer and fall and more prevalent in southern regions of the United States. The pathophysiology of this disorder is consistent with an immune -complex-mediated mechanism, a type III hypersensitivity reaction. These antibodies to NAPR persist for years and perhaps are protective against further episodes of PSGN. Noninfectious causes of acute GN may be divided into primary renal diseases, systemic diseases, and miscellaneous conditions or agents. Acute GN involves both structural changes and functional changes. Electron-dense deposits can be subendothelial, subepithelial, intramembranous, or mesangial, and they correspond to an area of immune complex deposition. Multisystem systemic diseases that can cause acute GN include the following. Nonstreptococcal postinfectious GN may also result from infection by other bacteria, viruses, parasites, or fungi. Go to Acute Poststreptococcal Glomerulonephritis for complete information on this topic. Among the signs and symptoms of acute proliferative glomerulonephritis are the following.
Rapid Assessment: A Flowchart Guide to Evaluating Signs and Symptoms. The causal factors that underlie acute GN can be broadly divided into infectious and noninfectious groups. Primary renal diseases that can cause acute GN include the following. Polyarteritis nodosa - This causes nephritis from a vasculitis involving the renal arteries. Structurally, cellular proliferation leads to an increase in the number of cells in the glomerular tuft because of the proliferation of endothelial, mesangial. Miscellaneous noninfectious causes of acute GN include the following. On gross appearance, the kidneys may be enlarged up to 50%. Clinically, acute proliferative glomerulonephritis is diagnosed following a differential diagnosis between (and, ultimately, diagnosis of) staphylococcal and streptococcal impetigo. The proliferation may be endocapillary (ie, within the confines of the glomerular capillary tufts) or extracapillary (ie, in the Bowman space involving the epithelial cells). The most common infectious cause of acute GN is infection by Streptococcus species (ie, group A, beta-hemolytic). Serotype 12 - Poststreptococcal nephritis due to an upper respiratory infection, occurring primarily in the winter months. This disorder produces proteins that have different antigenic determinants, which in turn have an affinity for sites in the glomerulus. Streptococcal M-protein was previously believed to be responsible for PSGN, but the studies on which this belief was based have been discounted. On electron microscopy, this may appear as the result of thickening of basement membrane proper (eg, diabetes) or deposition of electron-dense material, either on the endothelial or epithelial side of the basement membrane. Complement activation is very important in acute proliferative glomerulonephritis. Glomerular basement membrane thickening appears as thickening of capillary walls on light microscopy. In extracapillary proliferation, proliferation of parietal epithelial cells leads to the formation of crescents, a feature characteristic of certain forms of rapidly progressive GN. Treatment of PSGN is mainly supportive, because there is no specific therapy for renal disease. PSGN usually develops 1-3 weeks after acute infection with specific nephritogenic strains of group A beta-hemolytic streptococcus. Immunofluorescence staining of renal biopsy tissues with anti-NAPlr antibody revealed glomerular NAPlr deposition in early-phase acute PSGN, and glomerular plasmin activity was almost identical to NAPlr deposition in renal biopsy tissues of acute PSGN patients. The decreased GFR and avid distal nephron salt and water retention result in expansion of intravascular volume, edema, and, frequently, systemic hypertension. The incidence of GN is approximately 5-10% in persons with pharyngitis and 25% in those with skin infections. Two types have been described, involving different serotypes. As soon as binding occurs to the glomerulus, via interaction with properdin, complement is activated. 9%) and staphylococci (24. Antibody levels to nephritis-associated protease (NAPR) are elevated in streptococcal infections (group A, C, and G) associated with GN but are not elevated in streptococcal infections without GN, whereas anti-streptolysin-O titers are elevated in both circumstances. This article addresses the aspects of GN that are relevant to its acute management. MPGN ) - This is due to the expansion and proliferation of mesangial cells as a consequence of the deposition of complements. Primary Care Medicine: Office Evaluation and Management of The Adult Patient, 6th ed. Salmonella typhosa, Brucella suis, Treponema pallidum, Corynebacterium bovis, and actinobacilli have also been identified. Factors responsible for this decline may include better health care delivery and improved socioeconomic conditions. If you log out, you will be required to enter your username and password the next time you visit. Cytomegalovirus (CMV), coxsackievirus, Epstein-Barr virus (EBV), hepatitis B virus (HBV). 4%). Richard Bright (1789- 1858) described acute GN clinically in 1827, which led to the eponymic designation Bright disease. These data suggest that NAPlr may contribute to the pathogenesis of acute PSGN by maintaining plasmin activity. Except in PSGN, the exact triggers for the formation of the immune complexes are unclear. Despite sporadic outbreaks, the incidence of PSGN has fallen over the past few decades. Hippocrates originally described the natural history of acute GN, writing of back pain and hematuria followed by oliguria or anuria. Treatment of acute proliferative glomerulonephritis consists of blood pressure (BP) control:also a renal biopsy may be needed to be performed at some point.
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