java barcode scanner library Studies have shown that nephrology referral improves outcome in acute renal failure in Objective-C

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Studies have shown that nephrology referral improves outcome in acute renal failure
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Admission is appropriate when a patient has signs or symptoms of acute renal failure that require immediate intervention, such as intravenous fluids, dialytic therapy, or a team approach that cannot be coordinated as an outpatient
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Fever Transient maculopapular rash Acute renal insufficiency Pyuria (including eosinophiluria), white blood cell casts, and hematuria
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Hematuria, dysmorphic red cells, red cell casts, and mild proteinuria Dependent edema and hypertension Acute renal insufficiency
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Acute interstitial nephritis accounts for 10 15% of cases of intrinsic renal failure An interstitial inflammatory response with edema and possible tubular cell damage is the typical pathologic finding Cell-mediated immune reactions prevail over humoral responses T lymphocytes can cause direct cytotoxicity or release lymphokines that recruit monocytes and inflammatory cells Although drugs account for over 70% of cases, acute interstitial nephritis also occurs in infectious diseases, immunologic disorders, or as an idiopathic condition The most common drugs are penicillins and cephalosporins, sulfonamides and sulfonamide-containing diuretics, NSAIDs, rifampin, phenytoin, and allopurinol More recently, protonpump inhibitors have also been recognized as a cause of acute interstitial nephritis Infectious causes include streptococcal infections, leptospirosis, cytomegalovirus, histoplasmosis, and Rocky Mountain spotted fever Immunologic entities are more commonly associated with glomerulonephritis, but systemic lupus erythematosus, Sj gren s syndrome, sarcoidosis, and cryoglobulinemia can cause interstitial nephritis Acute glomerulonephritis is a relatively uncommon cause of acute renal failure, accounting for about 5% of cases of intrinsic renal failure Pathologically, inflammatory glomerular lesions are seen These include mesangioproliferative, focal and diffuse proliferative, and crescentic lesions The larger the percentage of glomeruli involved and the more severe the lesion, the more likely it is that the patient will have a poor clinical outcome Categorization of acute glomerulonephritis can be done by serologic analysis Markers include antineutrophil cytoplasmic antibodies (ANCA), anti-GBM antibodies, and other immune markers of disease Immune complex deposition usually occurs when moderate antigen excess over antibody production occurs Complexes formed with marked antigen excess tend to remain in the circulation Antibody excess with large antigen antibody aggregates usually results in phagocytosis and clearance of the precipitates by the mononuclear phagocytic system in the liver and spleen Causes include IgA nephropathy (Berger s disease), peri-infectious or postinfectious glomerulonephritis, endocarditis, lupus nephritis, cryoglobulinemic glomerulonephritis (often associated with hepatitis C virus), and membranoproliferative glomerulonephritis Anti-GBM associated acute glomerulonephritis is either confined to the kidney or associated with pulmonary hemorrhage The latter is termed Goodpasture s syndrome Injury is related to autoantibodies aimed against type IV collagen in the GBM rather than to immune complex deposition Pauci-immune acute glomerulonephritis is a form of small-vessel vasculitis associated with ANCA, causing primary and secondary renal diseases that do not have direct immune complex deposition or antibody binding Tissue injury is believed to be due to cell-mediated immune processes An example is Wegener s granulomatosis, a systemic necrotizing vasculitis of small arteries and veins associated with intravascu-
Clinical Findings
Clinical features can include fever (> 80%), rash (25 50%), arthralgias, and peripheral blood eosinophilia (80%) The urine often contains red cells (95%), white cells, and white cell casts Proteinuria can be a feature, particularly in NSAIDinduced interstitial nephritis, but is usually modest Eosinophiluria can be detected by Wright s or Hansel s stain
Treatment & Prognosis
Acute interstitial nephritis often carries a good prognosis Recovery occurs over weeks to months, but acute dialytic therapy may be necessary in up to one-third of all patients
Kidney Disease
lar and extravascular granuloma formation In addition to glomerulonephritis, these patients can have upper airway, pulmonary, and skin manifestations of disease Cytoplasmic ANCA (C-ANCA) is a common pattern Microscopic polyangiitis is another pauci-immune vasculitis causing acute glomerulonephritis Perinuclear staining (P-ANCA) is the common pattern ANCA-associated and anti-GBM-associated acute glomerulonephritis can evolve to crescentic glomerulonephritis and often have poor outcomes unless treatment is started early Both are described more fully below Other vascular causes of acute glomerulonephritis include malignant hypertension and the thrombotic microangiopathies such as hemolytic-uremic syndrome (see 11) and thrombotic thrombocytopenic purpura (see 13)
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