Post Streptococus GN

7/30/2019 Post Streptococus GN

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Background

Acute glomerulonephritis is characterized by the sudden appearance ofhematuria,proteinuria,

red blood cell casts in the urine, edema, andhypertensionwith or without oliguria. It can followstreptococcal infections. This illness was first recognized as a complication of the convalescence

period ofscarlet feverin the 18th century.[1] A link between hemolytic streptococci andacuteglomerulonephritiswas recognized in the 20th century.

Diagram of a nephron.

Although the incidence ofpoststreptococcal glomerulonephritishas declined in the UnitedStates, it continues to have high incidence in other parts of the world, especially in areas with

tropical climates where skin infections are common.[2, 3]

Recent studies

In a study of leukocytes and glomeruli obtained from 22 pediatric patients with acute

poststreptococcal glomerulonephritis (APSGN), Wu et al found evidence that in cases ofnephritis, the 15-lipoxygenase derivatives lipoxin A 4 (LXA 4 ) and 15-S-hyroxyeicosatetraenoic

acid (15-S-HETE) have anti-inflammatory effects.

The authors found up-regulation of LXA 4 and 15-LO expression in patients' leukocytes and

glomeruli during the acute phase of glomerulonephritis and for 6-8 weeks after the disease's

onset. Moreover, blood and urinary concentrations of leukotriene B 4 (LTB 4 ) peaked during theacute phase of glomerulonephritis and fell during the disease's resolution phase, with the number

of glomerular polymorphonuclear leukocytes also rising and falling during the acute and

resolution phases, respectively.

In addition, the investigators found that in vitro, the introduction of 15-S-HETE and LXA 4inhibited LTB 4 -induced chemotaxis of polymorphonuclear leukocytes; inhibition of LTB 4production from the leukocytes of patients with APSGN was also noted.

[4]

Pathophysiology
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Poststreptococcalglomerulonephritisfollows infection with only certain strains of streptococci,

designated as nephritogenic. The offending organisms are virtually alwaysgroup A streptococci.

Acute poststreptococcalglomerulonephritis(APSGN) follows pyodermatitis with streptococci Mtypes 47, 49, 55, 2, 60, and 57 and throat infection with streptococci M types 1, 2, 4, 3, 25, 49,

and 12.

Although many morphologic, clinical, and serologic features suggest that APSGN is an immune

complex disorder, the precise nature of the antigen-antibody interaction is undefined. APSGN is

believed to be an immune-mediated disease, in which an immune complex containing astreptococcal antigen is deposited in the affected glomeruli. The size of glomerular basement

membrane (GBM) pores and the molecular size of the streptococcus-Ig complex are also

important determinants. The molecular size of the streptococcus-Ig complex is about 15 nm (10

nm for streptococcus group A and 5 nm for immunoglobulin). The GBM pore sizes in childrenand adults are 2-3 nm and 4-4.5 nm, respectively. Therefore, the immune complex molecule can

be more easily rodded into the glomerulus in children than in adults and, thus, may explain the

increased frequency of APSGN in children compared to that in adults.

The 2 antigens isolated from nephritogenic streptococci are under investigation in APSGN.

These include the cationic cysteine protease streptococcal pyrogenic exotoxin B and nephritis-associated streptococcal plasmin receptor, which is a plasmin-binding protein with

glyceraldehyde phosphate dehydrogenase (also known as presorbing antigen or PA-Ag).[5]

These

fractions have an affinity for glomeruli and have been shown to induce specific, long-lasting

antibody responses in biopsy specimens from patients with APSGN. The relevance of exotoxin Band glyceraldehyde phosphate dehydrogenase was evaluated in the same renal biopsy and serum

samples of patients with well-defined APSGN. Glomerular deposits of and antibody response to

exotoxin B were more consistently present in APSGN than were deposits of and antibodyresponse to glyceraldehyde phosphate dehydrogenase.

Antibodies to exotoxin B and PA-Ag are elevated in the majority of patients with APSGN.Intravenous injections of PA-Ag produce acute glomerulonephritis in animals. Antibodies to PA-

Ag are found in 30 of 31 patients with APSGN but are low or absent in those with uncomplicated

streptococcal infection or in patients with rheumatic fever.

PA-Ag is also known to activate the alternate pathway of the complement cascade, which

happens to be preferentially activated in persons with APSGN. The observation that somepatients may only have C3 deposition may relate to this mechanism.

In addition to streptococcal antigens, rheumatoid factor, cryoglobulins, and antineutrophilcytoplasmic serum antibodies are present in some of these patients. The pathogenic significance

of this autoimmune response is not defined.

There are also host susceptibility factors. In one study, HLA-DRB1*03011 was reported to be

found at a significantly higher frequency in 32 unrelated patients with APSGN as compared to

380 healthy individuals.[6]

Epidemiology
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Frequency

United States

The incidence of clinically detectable glomerulonephritis during an epidemic is up to 10% of

children with pharyngitis and 25% of children with impetigo. One study reported a change in theepidemiology of APSGN and found that pharyngitis has replaced impetigo as the predominant

cause of APSGN.[7]

International

APSGN can occur sporadically or epidemically.

Incidence seems to be decreasing in the United States and Europe, but sporadic cases ofthe disease continue to be reported from all over the world. The prevalence of nephritisvaries considerably among persons with sporadic infections with nephritogenic

streptococci. The reason for this variability is not known. Epidemic poststreptococcal glomerulonephritis occurs mainly in developing countries in

areas such as Africa, the West Indies, and the Middle East. Reasons for this changing

epidemiology relate to the nutritional status of the community, the more liberal use of

antibiotic prophylaxis, and possibly, the change in the nephritogenic potential of

streptococci. Among epidemic infections with nephritogenic streptococci, the apparentclinical attack rate is 10-12%.

[2, 3]

Mortality/Morbidity

Early death is extremely rare in children (< 1%) but is significantly more common in adults

(25%). This is secondary to congestive heart failure and azotemia.

Congestive heart failure is more common in adults (43%) than in children (< 5%). Nephrotic-range proteinuria is more common in adults (20%) than in children (4-10%). Approximately 83% of adults have azotemia, compared to 25-40% of children.

Race

No racial predilection is recognized.

Sex

Clinical cases of APSGN are twice as common in males than in females. If subclinical disease is

considered, both sexes are affected equally. The familial incidence rate is nearly 40%, but no

genetic marker has been identified.

Age


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This condition typically affects children aged 2-12 years. A large series reported that 5% are

younger than 2 years and 10% are older than 40 years.

History

A history suggestive of preceding streptococcal infection may include a preceding infectiveepisode such as pharyngitis, tonsillitis, or pyoderma. This is the sine qua non for the diagnosis of

APSGN.

Latent periodo A latent period always occurs between the streptococcal infection and the onset of

signs and symptoms of acute glomerulonephritis.

o In general, the latent period is 1-2 weeks after a throat infection and 3-6 weeksafter a skin infection.

o The onset of signs and symptoms at the same time as pharyngitis (also calledsynpharyngitic nephritis) is more likely to be immunoglobulin A (IgA)

nephropathy rather than APSGN. Dark urine (brown-, tea-, or cola-colored)

o This is often the first clinical symptom.o Dark urine is caused by hemolysis of red blood cells that have penetrated the

glomerular basement membrane and have passed into the tubular system.

Periorbital edemao The onset of puffiness of the face or eyelids is sudden. It is usually prominent

upon awakening and, if the patient is active, tends to subside at the end of the day.

o In some cases, generalized edema and other features of circulatory congestion,such as dyspnea, may be present.

o Edema is a result of a defect in renal excretion of salt and water.o The severity of edema is often disproportionate to the degree of renal impairment.

Nonspecific symptomso These can include general malaise, weakness, and anorexia and are present in

50% of patients.

o Approximately 15% of patients complain of nausea and vomiting.

Physical

Acute nephritic syndromeo Acute nephritic syndrome presenting as edema, hematuria, and hypertension with

or without oliguria is the most frequent presentation of APSGN.

o Approximately 95% of clinical cases have at least 2 manifestations, and 40% havethe full-blown acute nephritic syndrome.

Edemao Edema is present in 80-90% of cases, and it is the presenting complaint in 60% of

cases.


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Poststreptococcal glomerulonephritis follows infection with only certain strains ofstreptococci designated as nephritogenic.

The offending organisms are virtually always group A streptococci. APSGN follows pyodermatitis with streptococci M types 47, 49, 55, 2, 60, and 57 and

throat infection with streptococci M types 1, 2, 4, 3, 25, 49, and 12.

Laboratory Studies

Evidence of preceding streptococcal infectiono Antibody titers to extracellular products of streptococci are positive in more than

95% of patients with pharyngitis and 80% of patients with skin infections.

o The antistreptolysin (ASO), antinicotinamide adenine dinucleotidase (anti-NAD),antihyaluronidase (AHase), and antiDNAse B are commonly positive after

pharyngitis, and antiDNAse B and AHase titers are more often positivefollowing skin infections.

o ASO titers are frequently used to document streptococcal infection, but a moresensitive test is the streptozyme test, which tests antibodies to ASO, anti

DNAse

B, AHase, and anti-NAD.

o Studies suggest that the relatively unavailable antizymogen titer test is superior toboth antiDNAse B and ASO titers.

o Antizymogen titers that are 2 dilutions higher than the mean in healthy controlsare reported to have a sensitivity of 88% and a specificity of 85% in the diagnosis

of streptococcal infection in patients with glomerulonephritis.

o High antibody titers to glyceraldehyde phosphate dehydrogenase are also found inpersons with acute poststreptococcal glomerulonephritis (APSGN).

o In general, the antibody titers are elevated at 1 week, peak at 1 month, and falltoward preinfection levels after several months.

Elevated BUN and creatinine valueso This reflects the decrease in the glomerular filtration rate that occurs in the acute

phase.

o The elevations are usually transient.o Their failure to normalize within several weeks or months indicates that the

patient may not have a true APSGN and suggests seeking an alternative diagnosis.

o Patients who have the crescentic form of glomerulonephritis have rapiddeterioration and, often, incomplete recovery of renal function.

Serologic findingso Low serum complement levels indicative of an antigen-antibody interaction are a

universal finding in the acute phase of APSGN.

o Most patients have marked depression of serum hemolytic component CH50 andserum concentrations of C3.

o The activation of the alternative pathway of the complement system is thought tobe responsible for the hypocomplementemia.

o In some patients, the levels of C2 and C4 may also be decreased, but to a lesserextent, suggesting that both classic and alternate pathways of the complement

system are activated.


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o In most uncomplicated cases, the complement levels return to normal in 6-8weeks. Prolonged hypocomplementemia suggests an alternative diagnosis.

o Occasionally, low complement levels persist for 3 months.o The level of reduction of serum complement levels does not have any prognostic

significance.

oCirculating immune complexes and cryoglobulins are found in 60% of cases, andrheumatoid factor is found in 43% of cases.

Urinalysiso Results are always abnormal.o Hematuria and proteinuria are present in all cases.o Urine sediment has red blood cells, red blood cell casts, white blood cells,

granular casts, and, rarely, white blood cell casts.

o Dysmorphic red blood cells indicative of glomerular hematuria can usually bedetected by performing phase-contrast microscopy.

o Red blood cell casts are best detected in first, early-morning urine specimensexamined by the physician immediately after the patient voids.

oHematuria usually resolves within 3-6 months but may persist as long as 18months.

o Microscopic hematuria may be present in patients in whom the disease hasotherwise clinically resolved.

o Proteinuria may be mild or so severe that it causes nephrotic syndrome.o Approximately 5-10% of patients with APSGN have nephrotic-range proteinuria.o Proteinuria usually disappears in 6 months. A mild increase in urinary protein

excretion is present in 15% at 3 years and 2% at 10 years.

o Patients with nephrotic-range proteinuria in the acute phase or persistent heavyproteinuria have a worse prognosis. This is often associated with an evolution to a

garlandlike pattern of immune deposits as the disease progresses.

Imaging Studies

Chest radiographs may show findings of congestive heart failure. Renal ultrasound images usually reveal normal-sized kidneys bilaterally.

Procedures

APSGN is often a clinical diagnosis and requires the detection of glomerulonephritis andevidence of preceding streptococcal infection.

Atypical features in the early phase that suggest the need for renal biopsy include thefollowing:

o Absence of the latent period between streptococcal infection and acuteglomerulonephritis

o Anuriao Rapidly deteriorating renal functiono Normal serum complement levelso No rise in antistreptococcal antibodies


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o Extrarenal manifestations of systemic diseaseo No improvement or continued decrease in the glomerular filtration rate at 2 weekso Persistence of hypertension beyond 2 weeks

Atypical features in the recovery phase that mandate a renal biopsy include the following:o Failure of glomerular filtration rate to normalize by 4 weekso

Persistent hypocomplementemia beyond 6 weekso Persistent microscopic hematuria beyond 18 monthso Persistent proteinuria beyond 6 months

Histologic Findings

Pathologic findings of changes in gross appearanceo The kidneys are symmetrically enlarged to approximately 25-50% of normal.o They are pale in appearance, and the cut surfaces bulge because of interstitial

edema.

o The glomeruli may stand out as reddish or gray translucent dots.o The cut surfaces may have tiny red speckles caused by red blood cells in the

lumen of the Bowman space and tubules.

Light microscopyo The most striking finding is hypercellularity of the glomeruli. All glomeruli are

affected (diffuse) and usually to an approximately equal degree. The glomerular

tufts are larger than normal, and the cells are more numerous.

o The cell types typically present include endothelial and mesangial cells andmigrant inflammatory cells, which include polymorphonuclear leukocytes andmonocytes.

[4]

o Polymorphonuclear leukocytes are present in large numbers, hence the termexudative glomerulonephritis.

o Necrosis in the glomerular tuft is not typically found.o The individual lobules are wider than usual and may have a clubbed appearance.o Generally, the glomerular capillary walls are not thick.o In some patients, crescent formation may be found, but usually, only a small

percentage of glomeruli are affected by crescents.

o The tubules are normal in the majority of cases.o When proteinuria is present, hyaline droplets (protein reabsorption droplets) may

be present in the proximal convoluted tubules.

o In patients with severe exudative glomerulonephritis, polymorphonuclearleukocytes may be present in the lumen.

o The degree of interstitial involvement is variable. The interstitial areas showedema and infiltration with polymorphonuclear leukocytes and mononuclear cells.The arteries and arterioles are normal.

Immunofluorescenceo In biopsy samples taken in the first 2-3 weeks of illness, deposits of

immunoglobulin G and C3 in a diffuse granular pattern are present along the

glomerular capillary wall and mesangium.

o Immunoglobulin M may be present in small amounts. Significant amounts of IgAsuggest an alternative diagnosis.


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o Sorger et al have described 3 different patterns of immunofluorescence called thegarland pattern, the starry sky pattern, and the mesangial pattern.

[10]

o The starry sky pattern is an irregular, finely granular pattern with small depositsoften situated on the glomerular basement membrane overlying the mesangium.

This pattern is often seen in the early phase of the disease.

oThe starry sky pattern may turn into the mesangial pattern, which is characterizedby granular deposition of C3 with or without immunoglobulin G. It seems to bemost closely related to a resolving pattern.

o In approximately 25% of patients, the deposits are large and densely packed andaggregate into a ropelike or garlandlike pattern. These correspond to the humpson the subepithelial side of the glomerular capillary wall seen with electron

microscopy. These types of deposits may persist for months and may be

associated with the persistence of proteinuria and the development of

glomerulosclerosis.

Electron microscopyo Many of the ultrastructural changes confirm the findings from light microscopy

evaluations.o The number of endothelial, mesangial, and infiltrating inflammatory cells is

increased.

o The glomerular basement membrane is usually normal in thickness and contour,although occasionally patchy thickening may be noted.

o The most consistent and classic diagnostic finding is the presence of glomerularsubepithelial electron-dense immune-type deposits, often referred to as humps.

The deposits are discrete and are commonly found on the part of the glomerularbasement membrane overlying the mesangium.

Medical Care

Symptomatic therapy is recommended for patients with acute poststreptococcal

glomerulonephritis (APSGN), and it should be based on the clinical severity of the illness. The

major goal is to control edema and blood pressure.

During the acute phase of the disease, restrict salt and water.o If significant edema or hypertension develops, administer diuretics.o Loop diuretics increase urinary output and consequently improve cardiovascular

congestion and hypertension.

For hypertension not controlled by diuretics, usually calcium channel blockers orangiotensin-converting enzyme inhibitors are useful. For malignant hypertension,

intravenous nitroprusside or other parenteral agents are used. Indications for dialysis include life-threatening hyperkalemia and clinical manifestations

of uremia.

Restricting physical activity is appropriate in the first few days of the illness but isunnecessary once the patient feels well.

Steroids, immunosuppressive agents, and plasmapheresis are not generally indicated. A renal biopsy is indicated for patients with rapidly progressive renal failure. If the

biopsy findings show evidence of crescentic glomerulonephritis with more than 30% of


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the glomeruli involved, a short course of intravenous pulse steroid therapy is

recommended (500 mg to 1 g/1.73 m2

of methylprednisone qd for 3-5 d). However, no

controlled clinical trials have evaluated such therapy.

Long-term treatment with steroids or immunosuppressives is not recommended. Specific therapy for streptococcal infection is an important part of the therapeutic

regimen.o Treat patients, family members, and any close personal contacts who are infected.o Throat cultures should be performed on all these individuals. Treat with oral

penicillin G (250 mg qid for 7-10 d) or with erythromycin (250 mg qid for 7-10 d)

for patients allergic to penicillin.

o This helps prevent nephritis in carriers and helps prevent the spread ofnephritogenic strains to others.

Patients with skin infections must practice good personal hygiene. This is essential. During epidemics, recommend that high-risk individuals, including close contacts and

family members, receive empirical prophylactic treatment.

Surgical Care

Surgical care is not indicated.

Consultations

Nutritionist or dietitian Nephrologist

Diet

Low-salt diet - Two grams of sodium per day Fluid restriction - One liter per day

Activity

Restricting physical activity is appropriate in the first few days of the illness but is notnecessary once the patient feels well.

Medication Summary Therapy for patients with APSGN is symptomatic in nature and depends on the clinical

severity of the illness. The major aims are to control the edema and blood pressure. During the acute phase of the disease, salt and water should be restricted. If significant

edema or hypertension develops, diuretics should be administered. Loop diureticsincrease urinary output and consequently improve cardiovascular congestion andhypertension.

For hypertension not controlled by diuretics, calcium channel blockers or angiotensin-converting enzyme inhibitors are generally useful. For malignant hypertension,

intravenous nitroprusside or other parenteral agents are used.


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The indications for dialysis include life-threatening hyperkalemia and clinicalmanifestations of uremia. Steroids, immunosuppressive agents, and plasmapheresis are

not generally indicated. In patients with rapidly progressive renal failure, a renal biopsy isindicated. If the biopsy findings show evidence of crescentic glomerulonephritis with

more than 30% of the glomeruli involved, a short course of intravenous pulse steroid

therapy is recommended (500 mg to 1 g/1.73 m

2

of methylprednisone qd for 3-5 d).However, no controlled clinical trials have evaluated such therapy. Long-term treatmentwith steroids or immunosuppressives is not recommended.

Diuretics Class Summary Used to control edema and circulatory congestion. View full drug information Furosemide (Lasix) Increases excretion of water by interfering with chloride-binding cotransport system,

which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and

distal renal tubule. Dose must be individualized to patient. Depending on response,administer at increments of 20-40 mg, no sooner than 6-8 h after the previous dose, until

desired diuresis occurs. When treating infants, titrate with increments of 1 mg/kg/dose

until a satisfactory effect is achieved.

Calcium channel blockers Class Summary In specialized conducting and automatic cells in the heart, calcium is involved in the

generation of the action potential. Calcium channel blockers inhibit movement of calcium

ions across the cell membrane, depressing both impulse formation (automaticity) and

conduction velocity.

View full drug information Amlodipine (Norvasc) Relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn,

improves myocardial oxygen delivery. Benefits nonpregnant patients with systolicdysfunction, hypertension, or arrhythmias. Can be used during pregnancy if clinically

indicated.

Angiotensin-converting enzyme inhibitors Class Summary Decrease aldosterone secretion.

View full drug information Captopril (Capoten) Prevents conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting

in lower aldosterone secretion.

View full drug information Enalapril (Vasotec)
http://reference.medscape.com/drug/lasix-furosemide-342423http://reference.medscape.com/drug/lasix-furosemide-342423http://reference.medscape.com/drug/lasix-furosemide-342423http://reference.medscape.com/drug/lasix-furosemide-342423http://reference.medscape.com/drug/norvasc-amlodipine-342372http://reference.medscape.com/drug/norvasc-amlodipine-342372http://reference.medscape.com/drug/norvasc-amlodipine-342372http://reference.medscape.com/drug/norvasc-amlodipine-342372http://reference.medscape.com/drug/capoten-captoril-captopril-342315http://reference.medscape.com/drug/capoten-captoril-captopril-342315http://reference.medscape.com/drug/capoten-captoril-captopril-342315http://reference.medscape.com/drug/capoten-captoril-captopril-342315http://reference.medscape.com/drug/vasotec-enalaprilat-enalapril-342317http://reference.medscape.com/drug/vasotec-enalaprilat-enalapril-342317http://reference.medscape.com/drug/vasotec-enalaprilat-enalapril-342317http://reference.medscape.com/drug/vasotec-enalaprilat-enalapril-342317http://reference.medscape.com/drug/vasotec-enalaprilat-enalapril-342317http://reference.medscape.com/drug/vasotec-enalaprilat-enalapril-342317http://reference.medscape.com/drug/capoten-captoril-captopril-342315http://reference.medscape.com/drug/capoten-captoril-captopril-342315http://reference.medscape.com/drug/norvasc-amlodipine-342372http://reference.medscape.com/drug/norvasc-amlodipine-342372http://reference.medscape.com/drug/lasix-furosemide-342423http://reference.medscape.com/drug/lasix-furosemide-342423


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Competitive inhibitor of angiotensin-converting enzyme. Reduces angiotensin II levels,decreasing aldosterone secretion. Clinical response usually observed within 15 min of

administration.

Vasodilators Class Summary Used to treat hypertensive emergencies. Vasodilators reduce SVR, which, in turn, may

allow forward flow, improving cardiac output.

View full drug information Nitroprusside (Nitropress) Produces vasodilation and increases inotropic activity of heart. At higher dosages, may

exacerbate myocardial ischemia by increasing heart rate. Should not be used to treat

compensatory hypertension (arteriovenous shunt or coarctation of aorta).

View full drug information Hydralazine (Apresoline) Decreases systemic resistance through direct vasodilation of arterioles.

Further Inpatient Care

In the acute phase, admit for observation and treatment of hypertension and congestiveheart failure.

Admit for monitoring and to initiate dialysis (when indicated) if renal functionprogressively worsens.

Further Outpatient Care

Monitor blood pressure every month for 6 months and then every 6 months thereafter. Monitor BUN and serum creatinine levels every 3 months after the acute phase for 1 year

and then yearly after that.

Check serum complement levels at 6-8 weeks to make sure they have returned to normal. Check urine for hematuria and proteinuria every 3-6 months.

Inpatient & Outpatient Medications

Most patients do not require any medications after the acute phase. In the acute phase, diuretics may be needed to control edema and congestive heart failure. Antihypertensives may be needed in the chronic phase if the patient's blood pressure

remains high.

Transfer
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Transfer may be necessary if renal biopsy facilities are not available and the diagnosis isin doubt or if rapidly progressive renal failure develops.

Transfer may be necessary if azotemia worsens and dialysis facilities are not available onsite.

Deterrence/Prevention

The patient and any family member or close personal contact should have a throatculture.

Treatment with penicillin G or erythromycin (if allergic to penicillin) helps preventnephritis in carriers and helps prevent the spread of nephritogenic strains to others.

Patients with skin infections must pay close attention to personal hygiene. Epidemics should prompt empirical prophylactic treatment for high-risk individuals

(family and close personal contacts).

Complications Complications in the acute phase include the following:

o Congestive heart failureo Azotemiao Early death secondary to congestive heart failure and azotemia

Complications in the chronic phase include the following:o Nephrotic-range proteinuriao Chronic renal insufficiency and end-stage renal disease

Prognosis

In children, the immediate prognosis is excellent.[2] In elderly patients who have congestive heart failure or azotemia in the early phase, early

mortality rates can be as high as 25%.

The long-term prognosis is debatable.o Fewer than 1% of children have elevated serum creatinine values after 10-15

years of follow-up.

o Adults who develop massive proteinuria often have the garlandlike pattern ofimmune deposits. Their prognosis is worse; approximately 25% progress to

chronic renal failure.

Patient Education

Patients with skin infections should know the importance of personal hygiene. In epidemics, all close personal contacts and family members should be told to seek

medical attention for prophylactic treatment of streptococcal infections.


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For excellent patient education resources, visit eMedicine'sKidneys and Urinary SystemCenterandEar, Nose, and Throat Center. Also, see eMedicine's patient education articles

Blood in the UrineandStrep Throat.
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Post Streptococus GN

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