Acute Glomerulonephritis

Definition
According to Porth (2009), Glomerulonephritis is characterized by hematuria with red cell
casts, a diminished glomerular filtration rate (GFR), azotemia (presence of nitrogenous wastes
in the blood), oliguria, and hypertension. It is caused by diseases that provoke a proliferative
inflammatory response of the endothelial, mesangial, or epithelial cells of the glomeruli. The
inflammatory process damages the capillary wall, permitting red blood cells to escape into the
urine and producing hemodynamic changes that decrease the GFR. The nephritic syndromes
include acute proliferative glomerulonephritis and rapidly progressive glomerulonephritis.
According to Smeltzer (2010), Glomerulonephritis is an inflammation of the glomerular
capillaries that can occur in acute and chronic forms.
According to Davidson (2010), Glomerulonephritis refers to an inflammation of the
glomerulus, which is the unit involved in filtration in the kidney. This inflammation typically
results in one or both of the nephrotic or nephritic syndromes. (Davidson's principles and
practice of medicine. (21st ed. ed.). Edinburgh: Churchill Livingstone/Elsevier. 2010. ISBN 9780-7020-3084-0.)
Incidence
National: In 1998, 26% of the 5861 admissions recorded in a 6-year review was caused
by acute glomerulonephritis. (Avner E, Harmon W. Niaudet P, 2004. Pediatric Nephrology
Lippincott Williams and Wilkins)
International: (Worldwide Study). The incidence of primary glomerulonephritis
worldwide: a systematic review of the literature. This study found that incidence rates of
primary GN vary between 0.2/100,000/year and 2.5/100,000/year. The incidence of IgA
nephropathy is at least 2.5/100,000/year in adults; this disease can exist subclinically and is
therefore only detected by chance in some patients. In addition, referral policies for diagnostic
biopsy vary between countries. This will affect the incidence rates found. (McGrogan A,
Franssen CF, de Vries CS. 2010 Nov 10. Nephrol Dial Transplant. 2011 Feb;26(2):414-30. doi:
10.1093/ndt/gfq665.)

Etiology:
The causal factors that underlie acute GN can be broadly divided into infectious and
noninfectious groups.

Infectious
The most common infectious cause of acute GN is infection by Streptococcus species
(ie, group A, beta-hemolytic). Two types have been described, involving different
serotypes:
Serotype 12 - Poststreptococcal nephritis due to an upper respiratory
infection, occurring primarily in the winter months
Serotype 49 - Poststreptococcal nephritis due to a skin infection, usually
observed in the summer and fall and more prevalent in southern regions
of the United States
PSGN usually develops 1-3 weeks after acute infection with specific nephritogenic
strains of group A beta-hemolytic streptococcus. The incidence of GN is approximately
5-10% in persons with pharyngitis and 25% in those with skin infections.
Nonstreptococcal postinfectious GN may also result from infection by other bacteria,
viruses, parasites, or fungi. Bacteria besides group A streptococci that can cause acute
GN include diplococci, other streptococci, staphylococci, and mycobacteria. Salmonella
typhosa, Brucella suis, Treponema pallidum, Corynebacterium bovis, and actinobacilli
have also been identified.
Cytomegalovirus (CMV), coxsackievirus, Epstein-Barr virus (EBV), hepatitis B virus
(HBV), rubella, rickettsiae (as in scrub typhus), and mumps virus are accepted as viral
causes only if it can be documented that a recent group A beta-hemolytic streptococcal
infection did not occur. Acute GN has been documented as a rare complication of
hepatitis A.
Attributing glomerulonephritis to a parasitic or fungal etiology requires the exclusion of a
streptococcal infection. Identified organisms include Coccidioides immitis and the

following parasites: Plasmodium malariae, Plasmodium falciparum, Schistosoma

mansoni, Toxoplasma gondii, filariasis, trichinosis, and trypanosomes.

Noninfectious
Noninfectious causes of acute GN may be divided into primary renal diseases, systemic
diseases, and miscellaneous conditions or agents.
Multisystem systemic diseases that can cause acute GN include the following:
Vasculitis (eg, Wegener granulomatosis) - This causes glomerulonephritis
that combines upper and lower granulomatous nephritides).
Collagen-vascular diseases (eg, systemic lupus erythematosus [SLE])
This causes glomerulonephritis through renal deposition of immune
complexes).
Hypersensitivity vasculitis This encompasses a heterogeneous group of
disorders featuring small vessel and skin disease.
Cryoglobulinemia This causes abnormal quantities of cryoglobulin in
plasma that result in repeated episodes of widespread purpura and
cutaneous ulcerations upon crystallization.
Polyarteritis nodosa - This causes nephritis from a vasculitis involving the
renal arteries.
Henoch-Schnlein purpura This causes a generalized vasculitis
resulting in glomerulonephritis.
Goodpasture syndrome This causes circulating antibodies to type IV
collagen and often results in a rapidly progressive oliguric renal failure
(weeks to months).
Primary renal diseases that can cause acute GN include the following:
Membranoproliferative glomerulonephritis (MPGN) - This is due to the
expansion and proliferation of mesangial cells as a consequence of the
deposition of complements. Type I refers to the granular deposition of C3;
type II refers to an irregular process.
Berger disease (IgG-immunoglobulin A [IgA] nephropathy) - This causes
GN as a result of diffuse mesangial deposition of IgA and IgG.
Pure mesangial proliferative GN[1]

 Idiopathic rapidly progressive glomerulonephritis - This form of GN is

characterized by the presence of glomerular crescents. Three types have
been distinguished: Type I is an antiglomerular basement membrane
disease, type II is mediated by immune complexes, and type III is
identified by antineutrophil cytoplasmic antibody (ANCA).
Miscellaneous noninfectious causes of acute GN include the following:

Guillain-Barr syndrome
Irradiation of Wilms tumor
Diphtheria-pertussis-tetanus (DPT) vaccine
Serum sickness
Epidermal growth factor receptor activation and possibly to its inhibitor
cetuximab

References
1. Wen YK, Chen ML. The significance of atypical morphology in the changes of spectrum
of postinfectious glomerulonephritis. Clin Nephrol. Mar 2010;73(3):173-9. [Medline].

2. Oda T, Yoshizawa N, Yamakami K, Sakurai Y, Takechi H, Yamamoto K, et al. The role of

nephritis-associated plasmin receptor (NAPlr) in glomerulonephritis associated with
streptococcal infection. J Biomed Biotechnol. 2012;2012:417675. [Medline]. [Full Text].

3. Nasr SH, Markowitz GS, Stokes MB, et al. Acute postinfectious glomerulonephritis in the
modern era: experience with 86 adults and review of the literature. Medicine (Baltimore).
Jan 2008;87(1):21-32. [Medline].

4. Safadi R, Almog Y, Dranitzki-Elhalel M, Rosenmann E, Tur-Kaspa R. Glomerulonephritis

associated with acute hepatitis B. Am J Gastroenterol. Jan 1996;91(1):138-9. [Medline].

5. Aggarwal A, Kumar D, Kumar R. Acute glomerulonephritis in hepatitis A virus infection: a

rare presentation. Trop Doct. Jul 2009;39(3):186-7. [Medline].

6. Tang J, Liu N, Zhuang S. Role of epidermal growth factor receptor in acute and chronic
kidney injury. Kidney Int. Jan 16 2013;[Medline].

7. Sasaki

K,

Anderson

E,

Shankland

SJ,

Nicosia

RF.

Diffuse

Proliferative

Glomerulonephritis Associated With Cetuximab, an Epidermal Growth Factor Receptor

Inhibitor. Am J Kidney Dis. Mar 6 2013;[Medline].

8. Anochie I, Eke F, Okpere A. Childhood acute glomerulonephritis in Port Harcourt, Rivers

State, Nigeria. Niger J Med. Apr-Jun 2009;18(2):162-7. [Medline].

9. Wong

W, Morris

MC,

Zwi

J.

Outcome

of

severe

acute

post-streptococcal

glomerulonephritis in New Zealand children. Pediatr Nephrol. May 2009;24(5):1021-6.

[Medline].

10. Becquet O, Pasche J, Gatti H, et al. Acute post-streptococcal glomerulonephritis in

children of French Polynesia: a 3-year retrospective study. Pediatr Nephrol. Feb
2010;25(2):275-80. [Medline].

11. Nebuloni M, Barbiano di Belgiojoso G, Genderini A, et al. Glomerular lesions in HIVpositive patients: a 20-year biopsy experience from Northern Italy. Clin Nephrol. Jul
2009;72(1):38-45. [Medline].

Pathophysiology

Oliguria and increase waste product in the blood

Muscle weakness, fatigue and poor appeti

Headache, Seizure
Hepatic encepalopathy
Accumulates in the brain

Increase creatinine and potassium

Unable to excrete wastes products

Hypertension, Cardiomegaly

Generalized edema (ANASARCA)

Periorbital edema
Facial edema
Ascites
Edema on both upper and lower extremities

Increase blood volume

Pulmonary edema
Increase pulmonary arterial pressure
Difficulty of breathing

Rupture of microvascular aneurysm

Hemoptysis

Signs and Symptoms:

The primary presenting features of an acute glomerulonephritis are hematuria, edema,
azotemia, and proteinuria. (Porth & Martin 2009). The hematuria may be microscopic (through
mcroscopic exam) or macroscopic (visible to eye). The urine appears red-tinged because of
RBCs and protein plugs or casts. RBC casts indicate glomerular injury.
Some degree of edema and hypertension is present in most patients. Marked proteinuria due to
the decreased permeability of the glomerular membrane may also occur with associated pitting
edema, hypoalbuminemia, hyperlipidemia, and fatty casts in the urine. Blood urea nitrogen and
serum creatinine levels may increase as urine output decreases. In addition, anemia may be
present.
In the more severe form of the disease, patients also complain of headache, malaise,
constipation and flank pain. Elderly patients may experience circulatory overload with dyspnea,
engorged neck veins, cardiomegaly and pulmonary edema. Atypical symptoms include
confusion, somnolence and seizures which are often confused with a primary neurologic
disorder.
Assessment and Diagnostic Findings
In acute glomerulonephritis, the kidneys become large, edematous and congested. All renal
tissues including the glomeruli, tubules and blood vessels are affected due to varying degrees.
There is a marked decrease in urine production. Furthermore, urine analysis may indicate
protein, RBCs and WBCs. Some patients progress from azotemia to uremia.

Patients with

an IgA nephropathy have an elevated serum IgA and low to normal complement levels. Electron
microscopy and immunofluorescent analysis help identify the nature of the lesion; however, a
kidney biopsy may be needed for definitive diagnosis.
Medical Management
Treatment of symptoms through medication like corticosteroids, antihypertensives and
antibacterial. Dietary restriction of protein and sodium is done if continual elevation of
nitrogenous waste and water retention continues.
Nursing Management
Providing Care in the hospital

Carbohydrates are given liberally to provide energy and reduce catabolism of protein.
Intake and output are carefully measured and recorded. Fluids are given based on the
patients fluid losses and daily body weight. Insensible fluid loss through the lungs
(300mL) and skin (600mL) is considered when estimating fluid loss. If treatment is
effective, diuresis will begin, resulting in decreased edema and blood pressure.
Proteinuria and microscopic hematuria may persist for months; in fact, 20% of patients
have some decreased GFR 1 year after presentation (Porth and Martin 2009). Other
nursing interventions focus on patient education about the disease process, and
preparation for safe and effective self-care at home.