Acute Glomerulonephritis - CECitycecity.com/acp_pier/pdfs/PCD638.pdf · Acute Glomerulonephritis...

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Acute Glomerulonephritis View online at http://pier.acponline.org/physicians/diseases/d638/d638.html

Module Updated: 2013-03-05

CME Expiration: 2016-03-05

Author

Nadia Bennett, MD

Table of Contents

1. Diagnosis ..........................................................................................................................2

2. Consultation ......................................................................................................................7

3. Hospitalization ...................................................................................................................9

4. Therapy ............................................................................................................................10

5. Patient Counseling ..............................................................................................................14

6. Follow-up ..........................................................................................................................15

References ............................................................................................................................16

Glossary................................................................................................................................18

Tables ...................................................................................................................................20

Figures .................................................................................................................................31

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Acute Glomerulonephritis


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1. Diagnosis Top

Base the diagnosis on clinical findings of acute nephritis or the presence of inflammatory changes in the glomeruli on kidney biopsy.

1.1 Recognize the broad spectrum of symptoms that can be associated with

acute glomerulonephritis.

Recommendations

• Appreciate the broad spectrum of clinical presentations of acute glomerulonephritis, ranging from

minor symptoms to symptoms of acute kidney injury, including:

Fever

Dark urine

Local or generalized swelling

Nausea and vomiting

Decreased urine output

Confusion

• Look for clues suggesting a specific underlying diagnosis of acute glomerulonephritis, such as the

presence of:

Rash

Sore throat

Joint pain

History of hepatitis or endocarditis

• See table History and Physical Examination Elements for Acute Glomerulonephritis.

Evidence

• A large outbreak of acute glomerulonephritis in Nova Serrana, Brazil, was caused by group C

Streptococcus; of 134 patients identified, 48% had broad symptomatology ranging from fever and

dark urine to nausea, vomiting, and confusion (1).

• Reviews show that PSGN, the prototype of acute glomerulonephritis, classically presents with

symptoms of acute glomerulonephritis 7 to 21 days after the streptococcal pharyngitis (2; 3; 4; 5).

• Although acute glomerulonephritis occurs more commonly in children and young adults, a review at

a hospital in Uberaba, Brazil, found that 82 patients between the ages of 14 and 64 developed

acute glomerulonephritis after an upper airway or skin infection. This study revealed the varied age

of disease presentation (6).

Rationale

• Acute nephritis is an inflammatory state in the kidneys and can often be associated with fever,

particularly when the acute glomerulonephritis is due to infection (e.g., PSGN) or associated with

an autoimmune disease (e.g., SLE).

• Acute glomerulonephritis may also present with dark urine (because of hematuria or decreased

free water clearance).

• Nausea, vomiting, and confusion are symptoms of acute kidney injury that may be associated with

acute glomerulonephritis.

• Autoimmune diseases associated with systemic manifestations, such as rashes or joint pain, can

also cause acute glomerulonephritis.



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Comments

• Recognize that the diagnosis of acute glomerulonephritis begins with a broad differential diagnosis

(e.g., the etiology of edema); when further information is obtained (e.g., elevated creatinine,

hematuria/proteinuria) the diagnosis can be narrowed.

• Juvenile acute nonproliferative glomerulonephritis is a clinicopathological entity that is

distinguished from acute PSGN by the presence of normal serum complement and the absence of

diffuse proliferation of mesangial cells in the glomeruli (7).

1.2 Perform a detailed physical exam to look for signs of acute nephritis and

the specific etiology of the acute glomerulonephritis.

Recommendations

• Look for signs of acute nephritis:

High BP

Edema

Asterixis, pericardial rub, and encephalopathy, suggesting acute kidney injury

• Look for signs that suggest a specific etiology of acute glomerulonephritis:

Infection:

o Fever

o Heart murmur

o Malaise

o Sore throat

Systemic vasculitis:

o Fever

o Rash

o Arthritis

o Scleritis

o Uveitis

o Saddle-shaped nose

o Mononeuritis multiplex

Liver disease:

o Icterus

o Jaundice

o Hepatomegaly

• See table History and Physical Examination Elements for Acute Glomerulonephritis.

Evidence

• Consensus.

Rationale

• Many systemic diseases can cause acute glomerulonephritis, and a detailed physical exam may

uncover a specific etiology or narrow the list of potential etiologies.

1.3 Obtain lab data to support the diagnosis of acute glomerulonephritis.

Recommendations

• Look for hematuria, with or without proteinuria, on urine dipstick.

• Obtain fresh urine for phase-contrast microscopy to look for erythrocyte casts.



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• Quantify proteinuria either with a spot urine test for protein/creatinine ratio (if >2 is significant) or

24-hour urine collection (if >2 g/24 hours is suggestive of glomerular pathology).

• Obtain serial serum creatinine measurements and estimated GFR (MDRD formula) to detect the

presence of and any worsening renal insufficiency.

• See table Laboratory and Other Studies for Acute Glomerulonephritis and Underlying Disease in

Acute Glomerulonephritis.

• See figure Erythrocyte Cast.

• See figure Normal Glomerular Capillary Diagram.

Evidence

• In multiple studies correlating initial urinalysis findings with the subsequent kidney biopsy results,

the presence of erythrocyte casts or dysmorphic urinary erythrocytes corresponded to a glomerular

origin of the hematuria (13; 14; 15).

• Dysmorphic erythrocytes are a sensitive but not specific marker of hematuria of glomerular origin.

In a review of the urine microscopy of 27 normal volunteers, 31 patients undergoing kidney biopsy,

and 28 patients with lower GI bleeding, dysmorphic erythrocytes in the urine strongly suggested

glomerular etiology (14).

• A study evaluated midstream urine samples from 88 patients evaluated for hematuria. Fifty-eight

of the patients were diagnosed with a glomerular source of hematuria, and 55 of those had

dysmorphic erythrocytes. None of the 30 patients diagnosed with nonglomerular hematuria had

dysmorphic erythrocytes (13).

• In an older cohort study of 30 patients with kidney disease from varying causes, high urinary

albumin excretion (and high total urinary protein) was found in patients with glomerular disease

(16).

• A retrospective study of 112 patients in China with acute PSGN found that children had a higher

incidence of macroscopic hematuria than adults (58.3% vs. 32.7%, P<0.05) (17).

• A 2012 review provides an excellent summary of the pathophysiology and causes of MPGN (18).

Rationale

• Dysmorphic erythrocytes and erythrocyte casts in the urine suggest acute glomerulonephritis;

however, dysmorphic erythrocytes are difficult to appreciate.

• The frequency of serum creatinine measurements may vary between days to weeks, depending on

the presence of acute kidney injury and the degree of renal function loss.

Comments

• Acute glomerulonephritis is suspected by the presence of an active urine sediment (the presence of

hematuria, proteinuria, erythrocyte casts) in the appropriate clinical setting (hypertension, edema,

renal insufficiency). Urine dipstick and urine microscopy can detect blood and protein in the urine.

• Urine microscopy should only be done by experienced clinicians.

• Creatinine clearance calculated from equations such as the Cockcroft-Gault and MDRD may not be

accurate if kidney function is not in steady state.

1.4 Obtain additional lab tests to help determine the etiology of acute

glomerulonephritis.

Recommendations

• Based on clinical suspicion of specific underlying diseases, obtain additional studies, including:

Cultures of possible sources of infection, such as blood or throat



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Complement levels (C3, C4, and CH50)

Serologic tests for hepatitis B and C

ASO titers and anti-DNAse antibodies for PSGN

ANA and anti-dsDNA for SLE

Mixed cryoglobulins for cryoglobulinemic glomerulonephritis or MPGN

pANCA and cANCA antibodies for vasculitis and anti-GBM antibodies for Goodpasture's disease

• Consider a skin biopsy of any purpuric rash to confirm leukocytoclastic vasculitis.



Evidence

• Reviews stress that documentation of a streptococcal throat infection in the setting of acute

glomerulonephritis would increase suspicion for PIGN. PIGN, lupus nephritis, cryoglobulinemic

glomerulonephritis, and MPGN are associated with low complement levels (19; 20).

• Many forms of acute glomerulonephritis are associated with specific serologic markers, such as

anti-GBM antibody for Goodpasture's disease, pANCA, cANCA for systemic vasculitis, and

cryoglobulins for cryoglobulinemia (21).

• A retrospective study in Taiwan identified 20 adults with infection-associated glomerulonephritis. All

of these patients developed acute renal failure and most of them required dialysis support.

Staphylococcus was identified as the infectious agent most frequently, in 60% of the cases (22).

Rationale

• Many different infections can cause acute glomerulonephritis.

• Hepatitis B and C are associated with acute glomerulonephritis, specifically cryoglobulinemic

glomerulonephritis and MPGN; SLE, small vessel vasculitis, and anti-GBM disease (Goodpasture's

disease) can also cause acute glomerulonephritis.

• Complement levels may help narrow the differential diagnosis of acute glomerulonephritis.

• Acute glomerulonephritis can be classified based on low complement levels (PIGN, lupus nephritis,

cryoglobulinemic glomerulonephritis, MPGN) or normal complement levels (IgA nephropathy,

ANCA-associated glomerulonephritis, anti-GBM disease, fibrillary glomerulonephritis).

Comments

• Results from many of these serologic tests can take more than 1 day to obtain. Depending on

clinical suspicion, some or all of the tests might be sent at the initial evaluation to help expedite

the diagnosis of acute glomerulonephritis.

1.5 Make an early referral for a kidney biopsy if there is a high index of suspicion for acute glomerulonephritis to enable initiation of appropriate

treatment.

Recommendations

• Obtain early referral to a nephrologist for a kidney biopsy if there is a high index of suspicion for

acute glomerulonephritis, especially if there is evidence of systemic vasculitis (with or without

ANCA or lupus serology positivity) or anti-GBM positivity, or worsening of renal function,

hypertension, or proteinuria.



Evidence



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• As in most glomerulopathies, patients who develop progressive disease typically have elevated

serum creatinine, hypertension, or proteinuria at diagnosis (23).

Rationale

• Early treatment is more likely to result in preservation of or improvement in renal function. Specific

treatment may be indicated, depending on disease.

• Patients with glomerular disease may benefit from long-term follow-up with a nephrologist.

Comments

• A kidney biopsy is done to help diagnose the etiology of acute glomerulonephritis, guide treatment,

and provide prognostic information. Common complications of kidney biopsy include bleeding or

hematuria, which may require close observation; blood transfusion; and, rarely,

embolization/nephrectomy and death.

1.6 Recognize that several conditions can have clinical features that mimic acute glomerulonephritis.

Recommendations

• Classify glomerulonephritis into infectious or noninfectious processes based on history and physical

exam.

• Recognize that several other conditions may present with acute kidney injury, hematuria,

proteinuria, and hypertension.

• Use history, physical exam, and urinalysis to differentiate acute glomerulonephritis from other

conditions that present similarly and to classify acute glomerulonephritis by its etiology.

• See table Differential Diagnosis of Acute Glomerulonephritis.

• See table Etiologies of Acute Glomerulonephritis.

• See module Acute Kidney Injury.

Evidence

• Consensus.

Rationale

• Elements in the history, physical exam, and urinalysis may individually suggest a diagnosis of acute

glomerulonephritis, but when evaluated further they often implicate another diagnosis.




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2. Consultation Top

Consult appropriate specialists for help in diagnosing acute glomerulonephritis. Consult appropriate specialists for help in managing patients with acute glomerulonephritis.

2.1 Consult a nephrologist when the diagnosis is suspected, and consider

consulting other appropriate specialists if acute glomerulonephritis is suspected as a manifestation of a systemic disease.

Recommendations

• Consult a nephrologist to help with the diagnostic work-up, including a kidney biopsy; do so

urgently if there is evidence of ongoing loss of renal function as manifested by an increasing

creatinine level or a decreasing estimated GFR (MDRD formula).

• Consult other specialists, such as a rheumatologist, depending on the suspected etiology of

underlying systemic disease.

Evidence

• Acute glomerulonephritis can present as an RPGN with rapid loss of renal function, requiring

expeditious diagnosis and kidney biopsy (2).

Rationale

• Acute glomerulonephritis can result in a rapid decline in renal function; a timely diagnosis, often

requiring a kidney biopsy, allows appropriate treatment that can spare renal function and even

reverse renal injury.

• Rheumatologists can help diagnose patients with systemic disease, such as vasculitis, causing

glomerulonephritis.

2.2 Consult a nephrologist for patients with acute glomerulonephritis who

develop acute kidney injury and other specialists as needed.

Recommendations

• Consult a nephrologist for management of acute kidney injury and complications, such as:

Severe hypertension

Oliguria

Fluid overload

Atypical course or failure of expected resolution of clinical signs of acute glomerulonephritis

Uremia or chronic kidney disease

Electrolyte abnormalities (e.g., severe hyperkalemia)

Acid-base abnormalities (e.g., severe metabolic acidosis)

• Consult a nephrologist or rheumatologist to manage immunosuppressive therapy, depending on the

underlying etiologies.

Evidence

• KDIGO's 2012 guideline is available to help guide management for acute glomerulonephritis (28).

• In 2002, K/DOQI issued guidelines for the management of chronic kidney disease (37), a possible

sequelae of acute glomerulonephritis.

Rationale

http://www.kdigo.org/clinical_practice_guidelines/pdf/KDIGO-GN-Guideline.pdf



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• Nephrologists can help manage the complications of acute kidney injury (anemia, bone disease,

hyperphosphatemia, acidosis) and help prepare the patient for renal replacement therapy if

needed.

• A specialist may have more experience with the clinical course of the disease, with titration of

immunosuppressive medications to manage the disease, and with the side effects of the

immunosuppressive medications.

Comments

• There is no definitive rule for when a patient should see a nephrologist. The threshold of a GFR of

30 mL/min does not take into account the rate of fall of GFR, patient preferences, or the familiarity

of the patient's primary physician with managing chronic kidney disease.



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3. Hospitalization Top

Hospitalize patients with acute glomerulonephritis and worsening renal function and its complications.

3.1 Hospitalize patients with acute glomerulonephritis and a decline in renal function, acute kidney injury, complications of acute kidney injury, or a severe

manifestation of the underlying systemic disease.

Recommendations

• Admit a patient with an increasing creatinine level for complete evaluation of acute kidney injury

and to determine and initiate the appropriate treatment based on the diagnosis.

• Admit a patient with complications of acute kidney injury (volume overload, electrolyte

abnormalities, hypertension) for management of these complications, which may include

medications, dialysis, or both.

Evidence

• A 1996 review discussed the management of acute kidney injury and dialysis (25).

Rationale

• Renal function can deteriorate rapidly in the setting of acute glomerulonephritis.

• Other serious electrolyte abnormalities can occur with acute kidney injury and be life threatening.

• Inpatient hospitalization allows a more efficient evaluation and monitoring of the condition;

procedures and tests, such as dialysis or a kidney biopsy, can be done more efficiently while the

patient is hospitalized.



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4. Therapy Top

Provide supportive therapy in the initial management of patients with acute glomerulonephritis and dialysis for severe cases of acute kidney injury. Initiate drug therapy based on the specific diagnosis.

4.1 Provide supportive therapy in the initial management of patients with

acute glomerulonephritis and other measures, depending on the etiology.

Recommendations

• In patients with edema:

Restrict sodium intake to 100 mmol (2.3 g)/d

Restrict fluid intake

• Encourage smoking cessation.

• Consider the need for dialysis in patients with severe kidney injury.

• Consider referral to a renal dietitian for patients with hyperkalemia or hyperphosphatemia.

• Consider plasma exchange in patients with Goodpasture's syndrome and ANCA vasculitis.

• See module Smoking Cessation.

Evidence

• Acute glomerulonephritis is a salt-retaining state, likely due to a renal response to the decreased

GFR (2).

• Salt restriction is helpful for volume management, particularly in patients with nephrotic-range

proteinuria (21).

• In a retrospective multicenter case-control study, smoking increased the risk for end-stage renal

disease in men with inflammatory renal disease. In men with IgA nephropathy, smoking was found

to increase the risk for progressing to acute kidney injury in a dose-dependent manner (26).

• Smoking has been implicated in the progression of autosomal dominant polycystic kidney disease

(26) and in diabetic nephropathy (27).

Rationale

• Acute glomerulonephritis is a salt-retaining state; limiting salt intake should decrease salt

retention, decrease edema, and help to improve BP control.

• Acute dialysis helps correct the metabolic abnormalities associated with acute kidney injury, such

as hyperkalemia, acidosis, and volume overload.

• Smoking is associated with a faster progression of kidney disease.

Comments

• Salt restriction and diuretics have complementary mechanisms of action in the management of

volume overload.

4.2 Treat the clinical manifestations of acute glomerulonephritis regardless of etiology.

Recommendations

• Treat edema with a loop diuretic if needed.

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• Treat hypertension with appropriate antihypertensive agents, such as β-blockers, centrally acting

agents, and calcium-channel blockers.

• Avoid ACE inhibitors and angiotensin-receptor blockers early in the course of acute

glomerulonephritis.

• Correct:

Acidosis with oral sodium bicarbonate

Anemia with erythropoietin

Hypocalcemia and hyperphosphatemia with alfacalcidol and phosphate binders

• See table Drug Treatment for Acute Glomerulonephritis.

Evidence

• KDIGO's 2012 guideline is available to help guide management of acute glomerulonephritis (28).

• ACE inhibitors can cause a decrease in GFR by altering renal hemodynamics (29; 30). This

decrease can confuse clinicians who are following a patient with acute glomerulonephritis and are

monitoring for acute kidney injury.

Rationale

• The use of ACE inhibitors or angiotensin-receptor blockers in the early stages of acute

glomerulonephritis may cause worsening renal function through decreasing effective renal blood

flow.

4.3 Treat the underlying etiology of acute glomerulonephritis.

Recommendations

• Use appropriate antibiotics.

• Use corticosteroids, cyclophosphamide, or mycophenolate mofetil alone or in combination to treat

patients with autoimmune-mediated glomerulonephritis (i.e., SLE, ANCA vasculitis, anti-GBM,

cryoglobulinemic glomerulonephritis).

• Use corticosteroids, fish oil, or mycophenolate mofetil in patients with IgA nephropathy.

• Use steroids, dipyridamole, or ASA to treat MPGN and any underlying infectious disease that may

be a contributing factor, such as hepatitis C.

• Consider immunosuppression therapy after a histologic diagnosis of acute glomerulonephritis is

confirmed, recognizing that the type and duration of immunosuppression also depends on the

histologic findings.

• For hepatitis C-infected patients with chronic kidney disease, stage 1 or 2, and glomerulonephritis,

consider combined antiviral treatment using pegylated interferon and ribavirin as in the general

population.

• For hepatitis C-infected patients with chronic kidney disease, stage 3, 4, or 5, and

glomerulonephritis, not yet on dialysis, consider monotherapy with pegylated interferon, with doses

adjusted to the level of kidney function.

• For patients with hepatitis C and mixed cryoglobulinemia (IgG/IgM) with nephrotic proteinuria or

evidence of progressive kidney disease or an acute flare of cryoglobulinemia, consider

plasmapheresis, rituximab, or cyclophosphamide, in conjunction with iv methylprednisolone and

concomitant antiviral therapy.

• For patients with hepatitis B infection and glomerulonephritis, treat with interferon-α or with

nucleoside analogues as recommended for the general population by standard clinical practice

guidelines for hepatitis B infection.




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• Initiate antiretroviral therapy in all patients with biopsy-proven HIV-associated nephropathy,

regardless of CD4 count.

• See module Vasculitis.

• See module Systemic Lupus Erythematosus.

• See module Cryoglobulinemia.

• See module Hepatitis B.

• See module Hepatitis C.

• See module HIV Disease.

Evidence

• KDIGO's 2012 practice guideline for glomerulonephritis provides specific recommendations

regarding the treatment of GN due to many causes (28).

• A study on patients with IgA nephropathy compared 4 months of oral steroids to placebo in

patients with nephritic syndrome, with 17 patients in each group. There was no difference in GFR

between the groups, but the steroid-allocated patients had a higher rate of remission of nephritic

syndrome (31).

• Studies have shown that patients with IgA nephropathy who were treated with fish oil were less

likely to have worsening renal function (32; 33).

• A review article discussed the role of steroids, fish oil, tonsillectomy, and ACE inhibitors in the

management of IgA nephropathy (34).

• Two small randomized trials assessed the effects of dipyridamole and aspirin in MPGN (35; 36).

One study had nine patients in each arm and found a reduction in proteinuria in the treatment

group as compared to control (35). The other study found that the patients in the treatment group

had slower decline of GFR compared to control (36). The control group did have a rapid rate of GFR

decline, and the study has been criticized for perhaps having unequal comparison groups and

therefore exaggerating the benefit of treatment with dipyridamole and aspirin.

Rationale

• Corticosteroids and cyclophosphamide have been shown to improve the outcomes of autoimmune

diseases in general and nephritis in particular.

• Treating an underlying infection is part of the management of these patients.

• Removal of the infection (and the immune response to the infection) is thought to help in the

treatment of PIGN.

4.4 Vaccinate patients against pneumonia and influenza.

Recommendations

• Administer pneumonia vaccine to patients with glomerulonephritis and nephrotic syndrome.

• Administer influenza vaccination annually.

Evidence

• KDIGO's 2012 practice guideline for glomerulonephritis recommends vaccination for pneumonia

and influenza (28).

Rationale

• Patients with glomerulonephritis and nephrotic syndrome are at increased risk for invasive

pneumococcal infection and should therefore receive the pneumonia vaccination along with an

annual influenza vaccination.











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5. Patient Counseling Top

Educate patients about the overall approach to acute glomerulonephritis.

5.1 Educate patients about the cause, course, management, and complications of acute glomerulonephritis.

Recommendations

• Educate patients about the underlying disease that has caused acute glomerulonephritis, its course,

and the prognosis.

• Instruct patients about measures of kidney function, such as creatinine or GFR.

• Make patients aware of the need to take medication dosages based on kidney function.

• Educate patients about potential nephrotoxins, such as NSAIDs and intravenous contrast dye.

• Educate patients to identify clinical symptoms and signs of renal insufficiency, such as:

Swelling

Shortness of breath

Weight gain

Severe hypertension

Confusion

• Inform patients with systemic forms of glomerulonephritis, such as SLE, about the nature of their

underlying disease, other organ-system involvement, and symptoms or signs to watch for that may

represent a recurrence or exacerbation of the underlying systemic disease.

Evidence

• Medications are a common cause of worsening renal function in patients with underlying kidney

disease (25).

Rationale

• Glomerulonephritis can cause permanent kidney damage.

• The dosages of some medicines need to be adjusted in renal insufficiency.

• Common medicines (e.g., NSAIDs, ACE inhibitors, contrast dyes) can affect renal function.



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6. Follow-up Top

Monitor patients with acute glomerulonephritis regularly for recurrence or worsening renal function.

6.1 Schedule regular follow-up for patients with acute glomerulonephritis based on the severity and activity of their disease.

Recommendations

• Depending on clinical stability, follow-up at 1 to 10 weeks as necessary to document improvement

in:

Hypertension

Proteinuria

Edema

Azotemia

Serum complement levels if PSGN is the diagnosis

• Follow-up at 3, 6, 9, and 12 months to document improvement in or resolution of proteinuria and

hematuria.

Encourage smoking cessation

• Follow patients more frequently (every week) if they:

Do not show signs of improved clinical course

Have an exacerbation of the underlying disease necessitating hospitalization to manage their condition

• Ask about nausea, vomiting, weight loss, swelling, itching, and confusion.

• Ask about symptoms of systemic disease, such as arthralgia, skin rash, and dyspnea.

• Examine patient for asterixis, encephalopathy and signs of systemic diseases.

Evidence

• KDIGO's 2012 guideline is available to help guide management for acute glomerulonephritis (28).

• K/DOQI guidelines for management of chronic kidney disease resulting from any etiology were

published in 2002 (37).

Rationale

• Glomerulonephritis may cause kidney damage leading to renal insufficiency, which needs to be

followed closely.

• Glomerulonephritis may be a recurrent disease; therefore, routine evaluation for symptoms and

signs of recurrence is necessary.

Comments

• The follow-up interval is determined by the clinical situation. Initially, patients are usually followed

more frequently to insure that the kidney function and disease course is stable. As the patient

shows clinical stability over time, the interval between appointments can be increased. Specific

serologic markers of underlying systemic disease, such as complement levels and anti-dsDNA

titers, may need to be checked regularly.




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References Top

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2. Hricik DE, Chung-Park M, Sedor JR. Glomerulonephritis. N Engl J Med. 1998;339:888-99. (PMID: 9744974)

3. Hayes CS, Williamson H Jr. Management of Group A beta-hemolytic streptococcal pharyngitis. Am Fam Physician. 2001;63:1557-64. (PMID: 11327431)

4. Pichichero ME. Group A streptococcal tonsillopharyngitis: cost-effective diagnosis and treatment. Ann Emerg Med. 1995;25:390-403. (PMID: 7864482)

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6. Marques Vde P, Neves PD, Mendonça HM, Fugikaha I, Fernandes EL. Acute glomerulonephritis after upper airway or skin infection: descriptive analysis of 82 cases between 14 and 64 years-old. J Bras Nefrol. 2010;32:237-41. (PMID: 21103685)

7. Marina VP, Tarabishi R, Malhotra D. A rare case of juvenile acute non-proliferative glomerulonephritis with a 6-year follow-up experience. Int Urol Nephrol. 2013;45:917-20. (PMID: 22297470)

8. Snow V, Mottur-Pilson C, Cooper RJ, Hoffman JR, et al. Principles of appropriate antibiotic use for acute pharyngitis in adults. Ann Intern Med. 2001;134:506-8. [Full Text] (PMID: 11255529)

9. Bisno AL, Gerber MA, Gwaltney JM Jr, Kaplan EL, Schwartz RH. Diagnosis and management of group A streptococcal pharyngitis: a practice guideline. Infectious Diseases Society of America. Clin Infect Dis. 1997;25:574-83. (PMID: 9314443)

10. Donadio JV, Grande JP. IgA nephropathy. N Engl J Med. 2002;347:738-48. (PMID: 12213946)

11. Galla JH. IgA nephropathy. Kidney Int. 1995;47:377-87. (PMID: 7723227)

12. Whitley K, Keane WF, Vernier RL. Acute glomerulonephritis. A clinical overview. Med Clin North Am. 1984;68:259-79. (PMID: 6369024)

13. Fairley KF, Birch DF. Hematuria: a simple method for identifying glomerular bleeding. Kidney Int. 1982;21:105-8. (PMID: 7077941)

14. Pollock C, Liu PL, Györy AZ, Grigg R, Gallery ED, Caterson R, et al. Dysmorphism of urinary red blood cells—value in diagnosis. Kidney Int. 1989;36:1045-9. (PMID: 2689749)

15. Fassett RG, Horgan BA, Mathew TH. Detection of glomerular bleeding by phase-contrast microscopy. Lancet. 1982;1:1432-4. (PMID: 6123721)

16. Peterson PA, Evrin PE, Berggård I. Differentiation of glomerular, tubular, and normal proteinuria: determinations of urinary excretion of beta-2-macroglobulin, albumin, and total protein. J Clin Invest. 1969;48:1189-98. (PMID: 4978446)

17. Luo C, Chen D, Tang Z, Zhou Y, Wang J, Liu Z, et al. Clinicopathological features and prognosis of Chinese patients with acute post-streptococcal glomerulonephritis. Nephrology (Carlton). 2010;15:625-31. (PMID: 20883283)

18. Sethi S, Fervenza FC. Membranoproliferative glomerulonephritis--a new look at an old entity. N Engl J Med. 2012;366:1119-31. (PMID: 22435371)

19. Jennette JC, Falk RJ. Diagnosis and management of glomerulonephritis and vasculitis presenting as acute renal failure. Med Clin North Am. 1990;74:893-908. (PMID: 2195260)

20. Madaio MP, Harrington JT. The diagnosis of glomerular diseases: acute glomerulonephritis and the nephrotic syndrome. Arch Intern Med. 2001;161:25-34. (PMID: 11146695)

21. Mason PD, Pusey CD. Glomerulonephritis: diagnosis and treatment. BMJ. 1994;309:1557-63. (PMID: 7819900)

22. Wen YK. Clinicopathological study of infection-associated glomerulonephritis in adults. Int Urol Nephrol. 2010;42:477-85. (PMID: 19669926)

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30. Bakris GL, Weir MR. Angiotensin-converting enzyme inhibitor-associated elevations in serum creatinine: is this a cause for concern? Arch Intern Med. 2000;160:685-93. (PMID: 10724055)

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Glossary Top

ACE angiotensin-converting enzyme

AIN acute interstitial nephritis

ANA antinuclear antibody

ANCA antineutrophil cytoplasmic antibody

anti-dsDNA anti-double-stranded deoxyribonucleic acid

anti-GBM

antiglomerular basement membrane

ASA acetylsalicylic acid

ASO antistreptolysin O

ATN

acute tubular necrosis

bid twice daily

BP blood pressure

BUN blood urea nitrogen

C3 third component of complement

C4 fourth component of complement

cANCA reacts with proteinase 3

CH50

(total serum) hemolytic activity

CMV cytomegalovirus

DNA deoxyribonucleic acid

DNAse

deoxyribonuclease

dsDNA double-stranded deoxyribonucleic acid

ENT ear, nose, and throat

GFR glomerular filtration rate



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GI

gastrointestinal

HIV human immunodeficiency virus

HUS hemolytic-uremic syndrome

IgA

immunoglobulin A

IgG immunoglobulin G

IgM immunoglobulin M

IMPD inosine-5’-monophosphate dehydrogenase

iv intravenous

K/DOQI Kidney/Dialysis Outcomes Quality Initiative

KDIGO Kidney Disease: Improving Global Outcomes

MDRD

Modification of Diet in Renal Disease

MPGN membranoproliferative glomerulonephritis

NSAID nonsteroidal anti-inflammatory drug

pANCA

reacts with myeloperoxidase

PIGN postinfectious glomerulonephritis

po orally

PSGN poststreptococcal glomerulonephritis

qd every day

RNA ribonucleic acid

RPGN rapidly progressing glomerulonephritis

SLE

systemic lupus erythematosus

TTP thrombotic thrombocytopenic purpura



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Tables Top

History and Physical Examination Elements for Acute Glomerulonephritis

Category Element Notes

History Sore throat Development of acute glomerulonephritis within 7-21 d after the

onset of streptococcal pharyngitis is typical of PSGN. There is no

conclusive evidence indicating that antibiotic treatment of acute pharyngitis reduces the risk of developing PSGN (3; 8; 9). Note

that up to 50% of patients with IgA nephropathy present with one

episode or recurrent episodes of gross hematuria 5-10 d after

bacterial tonsillitis (synpharyngitic hematuria) or viral upper

respiratory infections (10; 11)

History Cough, dyspnea, hemoptysis Acute glomerulonephritis can present with respiratory symptoms

(vasculitis, respiratory tract infections, or pulmonary

edema/uremia)

History Dark or bloody urine The urine is frequently described as cola colored, tea colored, or

rusty

History Swelling Acute glomerulonephritis can present with edema, either local or

generalized

History Fever Fever could be associated with PIGN or autoimmune diseases

History Oliguria Decreased urine output is usually noticed in severe forms of acute

glomerulonephritis

History Nausea/vomiting Acute glomerulonephritis can present with symptoms of acute

kidney injury, such as nausea or vomiting

History Confusion or encephalopathy Confusion may be the initial presentation of acute

glomerulonephritis associated with acute kidney injury

History Dermatologic symptoms, such as pruritus, rash, bruising, jaundice Acute glomerulonephritis can present as acute kidney injury; the

pruritus may be a uremic manifestation. Hepatitis B or C may cause

acute glomerulonephritis. A rash from a systemic disease may provide clues to a specific autoimmune disease (e.g., SLE) as the

underlying cause of acute glomerulonephritis

History Joint aches, arthritis Autoimmune diseases can cause arthritis and acute

glomerulonephritis

History History of hepatitis Viral hepatitides are associated with secondary forms of acute

glomerulonephritis, usually as a chronic complication (2; 12)

History History of endocarditis Endocarditis can be associated with acute glomerulonephritis (12)

Physical exam BP Both systolic and diastolic hypertension may be present in patients

with acute glomerulonephritis

Physical exam Skin exam for jaundice, purpura, rash Acute glomerulonephritis can present as acute kidney injury; the

pruritus may be a uremic manifestation. Hepatitis B or C may cause



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acute glomerulonephritis. A rash from a systemic disease may

provide clues to a specific autoimmune disease (e.g., SLE) as the underlying cause of acute glomerulonephritis

Physical exam ENT exam for pharyngitis, sinusitis, hearing loss, saddle-shaped

nose

Streptococcal infection or granulomatosis with polyangiitis

(Wegener's) could be the underlying diseases in acute

glomerulonephritis

Physical exam Chest exam for decreased breath sounds Signs of consolidation and pleural effusion may be present

Physical exam Cardiac exam for pericardial rub An acute glomerulonephritis causing acute kidney injury may result

in the typical findings of uremia on physical exam, such as a

pericardial rub

Physical exam Abdominal exam for ascites Hepatitis B or C causing liver failure is associated with certain types

of acute glomerulonephritis. Ascites is a typical sign of

decompensated liver failure

Physical exam Extremity exam for edema, inflamed joints Acute glomerulonephritis causing acute kidney injury may result in

the typical findings of uremia on physical exam, such as edema.

Arthritis can be a manifestation of a systemic disease that can

cause acute glomerulonephritis

Physical exam Neurologic exam for asterixis, encephalopathy Acute glomerulonephritis causing acute kidney injury may result in

the typical findings of uremia on physical exam, such as asterixis or

encephalopathy

BP = blood pressure; ENT = ear, nose, and throat; IgA = immunoglobulin A; PIGN = postinfectious glomerulonephritis; PSGN = poststreptococcal glomerulonephritis; SLE = systemic lupus erythematosus.



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Laboratory and Other Studies for Acute Glomerulonephritis and Underlying Disease in Acute Glomerulonephritis

Test Notes

Acute glomerulonephritis

Serum creatinine Provides a rough estimate of GFR

Estimated GFR (MDRD formula) Practically the most accurate estimate of GFR

BUN Another marker of renal function that is less robust than serum creatinine because of the influence of

multiple factors, such as hydration status, catabolism, and diet

Urine microscopy for erythrocyte casts Erythrocyte casts are considered a hallmark of acute glomerulonephritis. Acute glomerulonephritis can

also be present despite a lack of erythrocyte casts in the urine sediment (13; 14). See figure

Erythrocyte Cast

Urine microscopy for dysmorphic erythrocytes Dysmorphic erythrocytes, even in the absence of erythrocyte casts, suggest glomerular pathology

Urine dipstick Active urinary sediment (microscopic hematuria with or without erythrocyte contrast) ± proteinuria

Protein/creatinine ratio in the urine Proteinuria, confirmed with a protein to creatinine ratio, suggests renal pathology. Higher amounts of

protein in the urine (>2 g/24-h period) usually indicate glomerular pathology

24-hour urine for protein Proteinuria >2 g/24 h suggests glomerular proteinuria

Electrolytes Monitored because of potential derangements due to acute kidney injury. Close attention to serum

potassium, calcium, bicarbonate, and phosphorus concentrations is needed

Ultrasound of the kidneys Often normal in patients with acute glomerulonephritis but is obtained routinely to exclude other

etiologies of acute kidney injury. Enlarged kidneys or increased echogenicity may be noted in acute

nephritis but is not a specific sign for acute glomerulonephritis

Kidney biopsy Renal histology, which includes light, immunofluorescence, and electron microscopy, is the definitive

investigation to establish the diagnosis of acute glomerulonephritis (24)

Underlying disease in acute glomerulonephritis

Throat culture To exclude streptococcal throat infection as the etiology of PIGN. Documentation of a streptococcal

throat infection in the setting of acute glomerulonephritis would increase suspicion for PIGN

Blood culture Infections, such as endocarditis, can precipitate PIGN

Serum complement Levels may help to diagnose the underlying etiology of acute glomerulonephritis by differentiating the

diseases that are associated with low complement levels (PIGN, lupus nephritis, cryoglobulinemic

glomerulonephritis, and MPGN) from those with normal complement values (19; 20)

ASO titers Measured serially, can document a streptococcal infection and, when followed serially, can help confirm the diagnosis of PSGN

Anti-DNAse If PSGN is suspected, anti-DNAse antibodies are highly specific for streptococcal infection

ANA A positive ANA result is frequently associated with SLE

dsDNA High dsDNA titers are associated with SLE activity

Mixed cryoglobulins Can be present in hepatitis C-associated MPGN



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pANCA Associated with small vessel vasculitis, which can cause acute glomerulonephritis

cANCA Associated with small vessel vasculitis, which can cause acute glomerulonephritis

Anti-GBM Anti-GBM antibody is found in Goodpasture's disease, a cause of acute glomerulonephritis

Chest radiograph May be useful to look for pulmonary manifestations of vasculitis, such as granulomas (e.g.,

granulomatosis with polyangiitis [Wegener's]) or pulmonary hemorrhage (e.g., Goodpasture's disease).

Such findings may help confirm the presence of a systemic disease that can cause acute glomerulonephritis

ANA = antinuclear antibody; anti-GBM = antiglomerular basement membrane; ASO = antistreptolysin O; BUN = blood urea nitrogen; cANCA = reacts with proteinase 3; DNAse = deoxyribonuclease; dsDNA = double-stranded deoxyribonucleic acid; GFR = glomerular filtration rate; MDRD = Modification of Diet in Renal Disease; MPGN = membranoproliferative glomerulonephritis; pANCA = reacts with

myeloperoxidase; PIGN = postinfectious glomerulonephritis; PSGN = poststreptococcal glomerulonephritis; SLE = systemic lupus erythematosus.



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Differential Diagnosis of Acute Glomerulonephritis

Disease Characteristics

Acute glomerulonephritis Symptoms and physical exam findings may reflect the underlying infectious or inflammatory cause

Kidney biopsy is often needed to confirm diagnosis

ATN and cortical necrosis ATN is a common cause of acute kidney injury. There are many causes of ATN, which can be divided

broadly into ischemic and toxic categories. Cortical necrosis is a severe, and fortunately less common,

form of ATN

ATN is differentiated from acute glomerulonephritis by a clinical history of the use of nephrotoxins

(e.g., contrast, aminoglycosides, cisplatinum) or ischemic insult to the kidneys. ATN is often associated

with dark pigmented casts on urinalysis. This finding is different from the usual predominance of

hematuria and proteinuria found in acute glomerulonephritis

AIN AIN is acute kidney injury due to allergic reaction in the kidney. The typical presentation includes flank pain, fever, renal insufficiency, and skin rash

AIN differs from acute glomerulonephritis in that a predisposing event (usually a medication) triggers

acute kidney injury. It can be associated with eosinophiluria, eosinophilia in the blood, or both

Malignant hypertension The hallmark of malignant hypertension is severe elevation of arterial BP (usually with diastolic

pressure exceeding 140 mm Hg), retinal hemorrhages, exudates, or the presence of papilledema.

Malignant hypertension can present as a thrombotic microangiopathy mimicking acute

glomerulonephritis by causing acute kidney injury and hematuria

Malignant hypertension is differentiated from acute glomerulonephritis by the history of high BP

preceding the systemic (including renal) manifestations

Atheroembolic disease Usually presents as acute kidney injury associated with blue toes, Hollenhorst plaques, and livedo

reticularis 1-2 d to a few weeks after a vascular procedure. Can be associated with low complement

levels

The history of vascular manipulation followed by acute kidney injury and embolic stigmata differentiates atheroembolic disease from acute glomerulonephritis

HUS/TTP Both TTP and HUS are thrombotic microangiopathies representing a small-vessel dysfunction that can have systemic manifestations; therefore, they can present clinically similar to a vasculitis

glomerulonephritis

TTP has a classic pentad of findings: thrombocytopenia, anemia, fever, mental status changes, and

acute kidney injury. HUS usually presents with thrombocytopenia, rash, acute kidney injury, and GI

involvement. The clinical presentation of these entities distinguishes them from acute

glomerulonephritis

AIN = acute interstitial nephritis; ATN = acute tubular necrosis; BP = blood pressure; GI = gastrointestinal; HUS = hemolytic-uremic syndrome; TTP = thrombotic thrombocytopenic purpura.




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Drug Treatment for Acute Glomerulonephritis

Drug or Drug Class Dosing Side Effects Precautions Clinical Use

Loop Diuretics Polyuria, orthostatic hypotension,

hypovolemia, hypokalemia,

hyperuricemia, ototoxicity, pancreatitis

Caution with: sulfonamide

hypersensitivity, CKD, hepatic disease

Edema

Bumetanide (Bumex) 0.5-2 mg qd Water and electrolyte depletion

Furosemide (Lasix) 10-160 mg qd Water and electrolyte depletion

Torsemide (Demadex) 5-50 mg qd Electrolyte abnormalities, leukopenia,

thrombocytopenia

β-blockers Bradycardia, hypotension, AV block,

bronchospasm, CNS side effects,

diarrhea, nausea

Avoid abrupt withdrawal. Caution

with: CKD, HF, depression,

hyperthyroidism, elderly

Hypertension

Atenolol (Tenormin) 25-100 mg qd Avoid with: pregnancy, breast-feeding.

If CrCl<35, decrease dose

Metoprolol (Lopressor) 50-100 mg bid Consider reduced dose with hepatic

disease. Substrate of CYP2D6

Dihydropyridine calcium-channel

blockers

Use slow-release or long-acting

formulations

Headache, edema Caution with: severe bradycardia, HF,

hepatic disease, reflux esophagitis,

aortic stenosis

Hypertension

Amlodipine (Norvasc) 2.5-10 mg qd

Felodipine (Plendil) 2.5-10 mg qd Reflex tachycardia

Nifedipine (Adalat CC, Procardia XL) 30-120 mg qd CNS side effects, GI side effects, rare

allergic hepatitis

Non-dihydropyridine calcium-

channel blockers

Use slow-release or long-acting

formulations

Bradycardia, hypotension, AV block,

edema, asystole, CNS side effects

Avoid with: Wolff-Parkinson-White

syndrome, advanced aortic stenosis.

Caution with: HF, hepatic disease,

reflux esophagitis. Low dose if elderly

Hypertension

Diltiazem (Cardizem CD, Dilacor XR) 90-240 mg qd GI side effects

Verapamil (Calan SR, Covera-HS,

Verelan)

120-240 mg qd Constipation, allergic-type reactions Caution with: CKD, neuromuscular

disease

Angiotensin-converting enzyme inhibitors

Hypotension, cough, hyperkalemia, angioedema, anaphylactoid reactions

Pregnancy. Avoid with: history of angioedema, renal artery stenosis

Hypertension, also to decrease proteinuria. Do not use in acute phase

of disease

Enalapril (Vasotec) 2.5-40 mg total daily dose, dosed qd or

bid

Requires hepatic activation. Decrease

dose if CrCl<30

Lisinopril (Prinivil, Zestril) 5-80 mg qd Not affected by hepatic disease.

Decrease dose if: elderly, CrCl<30

Angiotensin II receptor

antagonists

Headache, hyperkalemia. Rare:

anaphylactoid reactions, angioedema

Pregnancy. Caution with history of

angioedema

Hypertension, also to decrease

proteinuria. Do not use in acute phase



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of disease

Losartan (Cozaar) 50-100 mg total daily dose, dosed qd-

bid

Start with 25 mg with hepatic disease.

Substrate of CYPs 2C9, 3A4

Valsartan (Diovan) 40-160 mg total daily dose, dosed qd-

bid

Caution with hepatic disease. No data

with CrCl<30. Substrate of CYP2C9

Corticosteroids Long-term use can result in: HPA suppression, immunosuppression,

hypertension, adverse neurologic

effects, glucose intolerance, weight

gain, myopathy, glaucoma,

osteoporosis

Caution with hepatic disease Decrease inflammation

Prednisone 1 mg/kg qd

Methylprednisolone (A-Methapred,

Solu-Medrol)

7 mg/kg IV

Immunosuppressants Hematologic toxicity, risk of: infection,

bleeding, malignancy. Nausea,

vomiting

Avoid with pregnancy Decrease inflammation

Cyclophosphamide IV: 500-1000 mg/m2.

PO: 2-5 mg/kg

Hemorrhagic cystitis, infertility, SIADH,

severe cardiotoxicity, pulmonary

toxicity, anaphylaxis, alopecia

Consider dose reduction if CrCl<55.

Requires aggressive hydration

Mycophenolate mofetil (CellCept) 1000-1500 mg bid Nephrotoxicity, pulmonary toxicity,

blurred vision, asthenia, insomnia,

paresthesias, rash, abdominal pain,

anorexia, diarrhea, hepatotoxicity, hypertension, edema, electrolyte

abnormalities, asthenia, headache,

hyperglycemia

Immunosuppression and risk of

infection. Risk of pregnancy loss and

teratogenicity. Caution with: hepatic

disease, CrCl<25

Additional agent

Sodium bicarbonate Per protocol Flatulence, abdominal pain, volume

expansion due to sodium load

Correct acidosis

= black box warning; AV = atrioventricular; bid = twice daily; CKD = chronic kidney disease; CNS = central nervous system; CrCl = creatinine clearance; CYP = cytochrome P450 isoenzyme; GI =

gastrointestinal; HF = heart failure; HPA = hypothalamic-pituitary-adrenal; IM = intramuscular; IV = intravenous; PO = oral; qd = once daily; qid = four times daily; SC = subcutaneous; SIADH = syndrome of

inappropriate secretion of antidiuretic hormone; tid = three times daily.

PIER provides key prescribing information for practitioners but is not intended to be a source of comprehensive drug information.



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Etiologies of Acute Glomerulonephritis

Infectious glomerulonephritis

Acute PSGN Classically, symptoms of upper respiratory infection (e.g., fever,

sore throat) precede the development of glomerulonephritis by 1-3

wk. Other streptococcal infections (e.g., skin infections) can also

precipitate PIGN.

Typically presents as an acute glomerulonephritis, manifesting as a

systemic illness, including edema, hypertension, hematuria, and

acute kidney injury.

Originally described as poststreptococcal glomerulonephritis,

postinfectious glomerulonephritis can occur after infections by

organisms other than streptococci, such as staphylococci or

meningococci

Complement levels (C3 and C4) are usually low. Anti-DNAase B is

used to document streptococcal infection with high sensitivity. ASO

titers also can be followed to document streptococcal infection and

resolution. A kidney biopsy result would show a proliferative

glomerulonephritis, possibly with crescents, and subendothelial

subepithelial deposits (humps) and mesangial deposits on electron

microscopy

Nonpoststreptococcal glomerulonephritis Infections, such as pneumonia, meningitis, endocarditis, and

ventriculoatrial shunt infections, can precipitate an immune

response resulting in acute glomerulonephritis

Complement levels (C3 and C4) are usually low and return to

baseline values after resolution of the disease

Noninfectious glomerulonephritis

Primary

IgA nephropathy Most common glomerulonephritis worldwide. The classic

presentation is hematuria 1-2 d after a sore throat (as compared to

PIGN, which causes the hematuria 1-3 wk after the sore throat).

The clinical manifestations of IgA nephropathy range from

asymptomatic microscopic hematuria to acute kidney injury

The diagnosis of IgA nephropathy is made by the predominance of

IgA deposits on the immunofluorescence staining of the kidney

biopsy

Fibrillary glomerulonephritis A rare form of acute glomerulonephritis of unknown etiology. An

abnormal protein deposition disease associated with proteinuria.

Proteinuria may be the only clinical manifestation, unless it induces

acute kidney injury

The diagnosis is made by recognizing the characteristic fibrillary

proteins on electron microscopy

Idiopathic MPGN This disease often presents as hematuria, proteinuria (often subnephrotic), and kidney injury of varying severity. It is

associated with the presence of nephritic factors, which are

autoantibodies that bind C3 convertase of the alternate

complement pathway. Many of the historical cases thought to be

“idiopathic” may have been associated with hepatitis C infection

MPGN is diagnosed by the characteristic renal biopsy findings: proliferation, thickened capillary loops on light microscopy, and

thickened glomerular basement membranes on electron microscopy

with immune deposits

Henoch-Schönlein purpura A clinical tetrad of abdominal pain, rash, arthralgia, and nephritis The diagnosis is usually made clinically. However, if there is

progressive disease in terms of worsening renal function or

proteinuria, then consider a kidney biopsy before considering

immunosuppression therapy. A skin biopsy with a combination of

leukocytoclastic vasculitis and IgA deposition is essentially

diagnostic of Henoch-Schönlein purpura. The renal histology is similar to that of IgA nephropathy (38)

Secondary

SLE SLE is a systemic disease affecting multiple organ systems and is diagnosed by the criteria described by the American College of

Rheumatology. Renal involvement is only one of the systemic

manifestations of the disease

A kidney biopsy is necessary to differentiate several patterns of renal lesions in the kidney



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Secondary MPGN A typical clinical scenario for MPGN would be the finding of

hematuria, proteinuria, or both in the setting of a patient with a chronic infection (e.g., hepatitis C, subacute endocarditis, and HIV

MPGN shows a proliferative process on light microscopy and may

present with crescents. Electron microscopy shows immune deposits in the glomerular basement membrane

ANCA-associated glomerulonephritis ANCA-associated glomerulonephritis can present as an acute

glomerulonephritis or as a subacute or even chronic

glomerulonephritis. The wide array of clinical manifestations

includes mild hematuria or proteinuria with minor renal function

abnormalities to acute kidney injury with hematuria and even

nephrotic range proteinuria

Pathology often shows a proliferative glomerulonephritis, with

crescents if the disease is aggressive, in the setting of positive

cANCA or pANCA serologic tests

Anti-GBM disease Anti-GBM disease classically presents with kidney and lung

involvement. Anti-GBM renal disease usually causes a rapidly

progressive glomerulonephritis, although it can present with more

minor renal involvement (hematuria, mild renal insufficiency)

Renal pathology shows a proliferative glomerulonephritis, often with

crescents. Anti-GBM disease is characterized by linear IgG staining

of the glomerular basement membrane on immunofluorescence

microscopy

Cryoglobulinemia Symptoms include those of both a small and medium vessel

systemic vasculitis, including palpable purpura, arthritis,

neuropathy, and distal (digital) ischemia. Renal involvement ranges from acute kidney injury to asymptomatic urinary sediment

abnormalities

Cryoglobulinemia can present with low complement levels and is

diagnosed through detection of cryoglobulins in the serum or on

kidney biopsy specimens

ANCA = antineutrophil cytoplasmic antibody; anti-GBM = antiglomerular basement membrane; ASO = antistreptolysin O; cANCA = reacts with proteinase 3; C3 = third component of complement; C4 = fourth

component of complement; HIV = human immunodeficiency virus; IgA = immunoglobulin A; IgG = immunoglobulin G; MPGN = membranoproliferative glomerulonephritis; pANCA = reacts with

myeloperoxidase; PIGN = postinfectious glomerulonephritis; PSGN = poststreptococcal glomerulonephritis; SLE = systemic lupus erythematosus.



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Figures Top

Erythrocyte Cast

A typical erythrocyte cast with densely packed erythrocytes, indicative of glomerular disease. Erythrocytes may be distinct or incorporated into a homogenous mass. The most characteristic feature of an erythrocyte cast is its orange-red appearance.



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Normal Glomerular Capillary Diagram

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