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Acute glomerulonephritis refers to 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. Hippocrates originally described the manifestation of back pain and hematuria, which lead to oliguria or anuria. With the development of the microscope, Langhans was later able to describe these pathophysiologic glomerular changes. Most original research focuses on the poststreptococcal patient. Acute glomerulonephritis is defined as the sudden onset of hematuria, proteinuria, and red blood cell casts. This clinical picture is often accompanied by hypertension, edema, and impaired renal function. As will be discussed, acute glomerulonephritis can be due to a primary renal or systemic disease.

Pathophysiology Glomerular lesions in acute glomerulonephritis are the result of glomerular deposition or in situ formation of immune complexes. On gross appearance, the kidneys may be enlarged up to 50%. Histopathologic changes include swelling of the glomerular tufts and infiltration with polymorphonucleocyte. Immunofluorescence reveals deposition of immunoglobulins and complement. With the exception of poststreptococcal glomerulonephritis, the exact triggers for the formation of the immune complexes are unclear. In streptococcal infection, involvement of derivatives of streptococcal proteins has been reported. A streptococcal neuramidase may alter host immunoglobulin G (IgG). IgG combines with host antibodies. IgG/anti-IgG immune complexes are formed and then collect in the glomeruli. 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.

Medical Care Treatment of acute PSGN is mainly supportive because there is no specific therapy for renal disease. Treat the underlying infections when acute GN is associated with chronic infections.

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Antimicrobial therapy o Antibiotics (eg, penicillin) are used to control local symptoms and to prevent spread of

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infection to close contacts. Antimicrobial therapy does not appear to prevent the development of GN, except if

given within the first 36 hours. Loop diuretic therapy o Loop diuretics may be required in patients who are edematous and hypertensive in

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order to remove excess fluid and to correct hypertension. Relieves edema and controls volume, thereby helping to control volume-related

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elevation in BP. Vasodilator drugs (eg, nitroprusside, nifedipine, hydralazine, diazoxide) may be used

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if severe hypertension or encephalopathy is present. Glucocorticoids and cytotoxic agents are of no value, except in severe cases of PSGN.

Consultations Nephrologist

Diet

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Sodium and fluid restriction - For treatment of signs and symptoms of fluid retention (eg,

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edema, pulmonary edema) Protein restriction for patients with azotemia - If no evidence of malnutrition

Activity Recommend bed rest until signs of glomerular inflammation and circulatory congestion subside. Prolonged inactivity does not benefit in the patient recovery process.

Medication The goals of pharmacotherapy are to reduce morbidity, to prevent complications, and to eradicate the infection.

Antimicrobials (antibiotics) In streptococcal infections, early antibiotic therapy may prevent antibody response to exoenzymes and render throat cultures negative, but may not prevent the development of PSGN.

Penicillin V (Pen VEE K, V-Cillin K)

More resistant than penicillin G to hydrolysis by acidic gastric secretions and is absorbed rapidly after oral administration. 250 mg of penicillin V = 400,000 U of penicillin.

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Dosing Interactions Contraindications Precautions

Adult

500,000 U PO q6-8h Pediatric

25,000-90,000 U/kg/d PO in 3-6 divided doses

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Loop diuretics

Decrease plasma volume and edema by causing diuresis. The reduction in plasma volume and stroke volume associated with diuresis decreases cardiac output and, consequently, BP.

Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, inhibiting sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule. Rapidly absorbed from the GI tract. The diuretic effect is apparent within 1 h of PO administration, peaks by second h and effect lasts for 4-6 h. Following IV administration diuresis occurs within 30 min; duration of action is about 2 h; 66% of dose is excreted in the urine.

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Dosing Interactions Contraindications Precautions

Adult

Edema: Initial: 40-80 mg PO, titrate to satisfactory diuresis in 20- to 40-mg increments q6h; not to exceed 200 mg per dose; once effective single dose determined, may repeat qd/tid Hypertension: 20-40 mg PO bid; titrated to desired response; if 40 mg PO bid does not lead to clinically significant response, add another antihypertensive agent rather than increasing the dose Pediatric

0.5-1 mg/kg PO/IV; not to exceed 2 mg/kg PO qd or 1 mg/kg IV qd; in newborn and premature babies, daily dose should not exceed 1 mg/kg

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Vasodilators Reduce SVR, which, in turn, may allow forward flow, improving cardiac output.

Sodium nitroprusside (Nitropress)

Potent, rapidly acting IV antihypertensive agent. Effect is immediate and usually ends as soon as infusion is stopped because of its rapid biotransformation. Produces vasodilation and increases

inotropic activity of the heart. At higher dosages may exacerbate myocardial ischemia by increasing heart rate. Use only for treatment of acute severe hypertension or malignant hypertension refractory to standard therapy.

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Dosing Interactions Contraindications Precautions

Adult

0.5-8 mcg/kg/min IV infusion Pediatric

Not established

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Calcium channel blockers In specialized conducting and automatic cells in the heart, calcium is involved in the generation of the action potential. The calcium channel blockers inhibit movement of calcium ions across the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.

Nifedipine (Adalat, Adalat CC, Procardia, Procardia XL)

A dihydropyridine calcium channel blocker. The specific mechanisms by which nifedipine reduces BP have not been fully determined but are believed to be brought about largely by its vasodilatory action on peripheral blood vessels. Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery.

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Dosing Interactions Contraindications Precautions

Adult

10-30 mg IR cap PO tid; not to exceed 120-180 mg/d 30-60 mg SR tab PO qd; not to exceed 90-120 mg/d

Pediatric

Not established

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Hydralazine (Apresoline)

Lowers BP by exerting a peripheral vasodilating effect through direct relaxation of vascular smooth muscle. Sodium retention and excessive sympathetic stimulation of the heart may be precluded by coadministration of a thiazide diuretic and a beta-blocker.

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Dosing Interactions Contraindications Precautions

Adult

10 mg PO qid, gradually titrate to 25-50 mg qid; alternatively, 5-10 mg slow IV initially; repeat dose after 20-30 min if necessary Maintenance dose: 50-200 mg PO qd in divided doses Pediatric

Not established

GASTROENTERITIS Gastroenteritis (also known as gastro, gastric flu, tummy bug in the United Kingdom, and stomach flu, although unrelated to influenza) is inflammation of the gastrointestinal

tract, involving both the stomach and the small intestine (see also gastritis and enteritis) and resulting in acute diarrhea

Prevention Main article: Rotavirus vaccine Because improved sanitation does not decrease the prevalence of rotaviral disease, and the rate of hospitalisations remains high, despite the use of oral rehydrating medicines, the primary public health intervention is vaccination.[81] In 2006, two vaccines against Rotavirus A infection were shown to be safe and effective in children: Rotarix by GlaxoSmithKline[82] and RotaTeq by Merck.[83] Both are taken orally and contain disabled live virus. Rotavirus vaccines are available in Australia,[84] Europe, Canada,[85] Brazil,[86] Egypt, India,[87] Israel, Taiwan, South Africa,[88] Panama, Argentina and the United States.[89] The Rotavirus Vaccine Program is a collaboration between PATH, the World Health Organization, and the U.S. Centers for Disease Control and Prevention, and is funded by the GAVI Alliance. The Program aims to reduce child morbidity and mortality from diarrhoeal disease by making a vaccine against rotavirus available for use in developing countries.[90] On June 5, 2009, WHO announced that clinical trials of Rotarix vaccine “in highmortality, low-socioeconomic settings of South Africa and Malawi, found that the vaccine significantly reduced severe diarrhoea episodes due to rotavirus.” WHO now recommends that rotavirus vaccine be included in all national immunization programs.[91]