Acute Glomerulonephritis
View online at http://pier.acponline.org/physicians/diseases/d638/d638.html
Module Updated:
CME Expiration:
2013-03-05
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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level 1 studies, which meet all of the evidence criteria for that study type;
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of the CME activity, participants should be able to demonstrate an increase in the skills and knowledge required to maintain competence, strengthen
their habits of critical inquiry and balanced judgement, and to contribute to better patient care. Disclosures: Nadia Bennett, MD, current author of this
module, has no financial relationships with pharmaceutical companies, biomedical device manufacturers, or health-care related organizations.
Deborah Korenstein, MD, FACP, Co-Editor, PIER, has no financial relationships with pharmaceutical companies, biomedical device manufacturers, or
health-care related organizations. Richard B. Lynn, MD, FACP, Co-Editor, PIER, has no financial relationships with pharmaceutical companies,
biomedical device manufacturers, or health-care related organizations.
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Acute Glomerulonephritis
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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Acute Glomerulonephritis
• 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.
• See table Laboratory and Other Studies for Acute Glomerulonephritis and Underlying Disease in
Acute Glomerulonephritis.
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.
• See table Laboratory and Other Studies for Acute Glomerulonephritis and Underlying Disease in
Acute Glomerulonephritis.
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
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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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Top
References
1. Pinto SW, Sesso R, Vasconcelos E, Watanabe YJ, Pansute AM. Follow-up of patients with epidemic poststreptococcal
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2. Hricik DE, Chung-Park M, Sedor JR. Glomerulonephritis. N Engl J Med. 1998;339:888-99. (PMID: 9744974)
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2001;63:1557-64. (PMID: 11327431)
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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
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21. Mason PD, Pusey CD. Glomerulonephritis: diagnosis and treatment. BMJ. 1994;309:1557-63. (PMID: 7819900)
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23. D’Amico G. Influence of clinical and histological features on actuarial renal survival in adult patients with idiopathic IgA
nephropathy, membranous nephropathy, and membranoproliferative glomerulonephritis: survey of the recent literature. Am J
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27. Orth SR. Smoking—a renal risk factor. Nephron. 2000;86:12-26. (PMID: 10971149)
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28. Kidney Disease: Improving Global Outcomes (KDIGO) Glomerulonephritis Work Group. KDIGO Clinical Practice Guideline for
Glomerulonephritis. Kidney inter., Suppl. 2012; 2:139–274.
29. Toto RD, Mitchell HC, Lee HC, Milam C, Pettinger WA. Reversible renal insufficiency due to angiotensin converting enzyme
inhibitors in hypertensive nephrosclerosis. Ann Intern Med. 1991;115:513-9. [Full Text] (PMID: 1883120)
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)
31. Lai KN, Lai FM, Ho CP, Chan KW. Corticosteroid therapy in IgA nephropathy with nephrotic syndrome: a long-term controlled
trial. Clin Nephrol. 1986;26:174-80. (PMID: 3536231)
32. Donadio JV Jr, Bergstralh EJ, Offord KP, Spencer DC, Holley KE. A controlled trial of fish oil in IgA nephropathy. Mayo
Nephrology Collaborative Group. N Engl J Med. 1994;331:1194-9. (PMID: 7935657)
33. Hogg RJ, Lee J, Nardelli N, Julian BA, Cattran D, Waldo B, et al. Clinical trial to evaluate omega-3 fatty acids and alternate day
prednisone in patients with IgA nephropathy: report from the Southwest Pediatric Nephrology Study Group. Clin J Am Soc
Nephrol. 2006;1:467-74. (PMID: 17699247)
34. Nolin L, Courteau M. Management of IgA nephropathy: evidence-based recommendations. Kidney Int Suppl. 1999;70:S56-62.
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35. Zäuner I, Böhler J, Braun N, Grupp C, Heering P, Schollmeyer P. Effect of aspirin and dipyridamole on proteinuria in idiopathic
membranoproliferative glomerulonephritis: a multicentre prospective clinical trial. Collaborative Glomerulonephritis Therapy
Study Group (CGTS). Nephrol Dial Transplant. 1994;9:619-22. (PMID: 7970086)
36. Donadio JV Jr, Anderson CF, Mitchell JC 3rd, Holley KE, Ilstrup DM, Fuster V, et al. Membranoproliferative glomerulonephritis. A
prospective clinical trial of platelet-inhibitor therapy. N Engl J Med. 1984;310:1421-6. (PMID: 6371535)
37. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Guideline 5:
Assessment of Proteinuria. Kidney Disease Outcome Quality Initiative. Am J Kidney Dis. 2002;39:93-102. (PMID: 11904577)
38. Weiss PF, Feinstein JA, Luan X, Burnham JM, Feudtner C. Effects of corticosteroid on Henoch-Schönlein purpura: a systematic
review. Pediatrics. 2007;120:1079-87. (PMID: 17974746)
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Acute Glomerulonephritis
Top
Glossary
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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Acute Glomerulonephritis
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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Acute Glomerulonephritis
Top
Tables
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
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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Page 21 of 30
Acute Glomerulonephritis
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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Page 22 of 30
Acute Glomerulonephritis
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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Page 23 of 30
Acute Glomerulonephritis
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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Page 24 of 30
Acute Glomerulonephritis
Drug Treatment for Acute Glomerulonephritis
Drug or Drug Class
Dosing
Loop Diuretics
Bumetanide (Bumex)
0.5-2 mg qd
Furosemide (Lasix)
10-160 mg qd
Torsemide (Demadex)
5-50 mg qd
β-blockers
Side Effects
Precautions
Clinical Use
Polyuria, orthostatic hypotension,
hypovolemia, hypokalemia,
hyperuricemia, ototoxicity, pancreatitis
Caution with: sulfonamide
hypersensitivity, CKD, hepatic disease
Edema
Water and electrolyte depletion
Water and electrolyte depletion
Electrolyte abnormalities, leukopenia,
thrombocytopenia
Bradycardia, hypotension, AV block,
bronchospasm, CNS side effects,
diarrhea, nausea
Avoid abrupt withdrawal. Caution
with: CKD, HF, depression,
hyperthyroidism, elderly
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
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 calciumchannel blockers
Use slow-release or long-acting
formulations
Bradycardia, hypotension, AV block,
edema, asystole, CNS side effects
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
Hypotension, cough, hyperkalemia,
angioedema, anaphylactoid reactions
Pregnancy. Avoid with: history of
angioedema, renal artery stenosis
Angiotensin-converting enzyme
inhibitors
Headache, edema
Caution with: severe bradycardia, HF,
hepatic disease, reflux esophagitis,
aortic stenosis
Hypertension
Avoid with: Wolff-Parkinson-White
syndrome, advanced aortic stenosis.
Caution with: HF, hepatic disease,
reflux esophagitis. Low dose if elderly
Hypertension
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
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Page 25 of 30
Hypertension
Hypertension, also to decrease
proteinuria. Do not use in acute phase
of disease
Hypertension, also to decrease
proteinuria. Do not use in acute phase
Acute Glomerulonephritis
of disease
Losartan (Cozaar)
50-100 mg total daily dose, dosed qdbid
Start with 25 mg with hepatic disease.
Substrate of CYPs 2C9, 3A4
Valsartan (Diovan)
40-160 mg total daily dose, dosed qdbid
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
Hematologic toxicity, risk of: infection,
bleeding, malignancy. Nausea,
vomiting
Avoid with pregnancy
Decrease inflammation
Hemorrhagic cystitis, infertility, SIADH,
severe cardiotoxicity, pulmonary
toxicity, anaphylaxis, alopecia
Consider dose reduction if CrCl<55.
Requires aggressive hydration
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
Per protocol
Flatulence, abdominal pain, volume
expansion due to sodium load
Prednisone
1 mg/kg qd
Methylprednisolone (A-Methapred,
Solu-Medrol)
7 mg/kg IV
Immunosuppressants
Cyclophosphamide
IV: 500-1000 mg/m2.
PO: 2-5 mg/kg
Mycophenolate mofetil (CellCept)
Additional agent
Sodium bicarbonate
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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Page 26 of 30
Acute Glomerulonephritis
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.
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
Originally described as poststreptococcal glomerulonephritis,
postinfectious glomerulonephritis can occur after infections by
organisms other than streptococci, such as staphylococci or
meningococci
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
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)
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
Noninfectious glomerulonephritis
Primary
Secondary
SLE
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Acute Glomerulonephritis
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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Acute Glomerulonephritis
Top
Figures
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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Acute Glomerulonephritis
Normal Glomerular Capillary Diagram
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