Acute Glomerulonephritis Flashcards
What is acute glomerulonephritis?
Inflammation of the glomeruli.
sudden onset
causes: infections (strep throat) or other underlying diseases (lupus, Goodpasture’s syndrome, Wegner’s disease, and polyarteritis nodosa)
- specific set of kidney diseases
- in which immunological mechanisms trigger inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium.
What is the pathophysiology of acute glomerulonephritis (GN)?
- Glomerular lesions are the result of glomerular deposition or in situ formation of immune complexes
- Kidneys may be enlarged up to 50%
- in PSGN (streptococcal glomerulonephritis), streptococcal neuraminidase may alter host immunoglobulin G (IgG). IgG combines with host antibodies. IgG/anti-IgG immune complexes form and then collect in the glomeruli.
What are structural and functional changes in the pathophysiology of acute glomerulonephritis (GN)?
- Structure: cellular proliferation leads to an increase in the number of cells in the glomerular tuft - a proliferation of endothelial, mesangial, and epithelial cells.
- Proliferation may be endocapillary or extra capillary
- endocapillary (ie, within the confines of the glomerular capillary tufts) or extra capillary (ie, in the Bowman space involving the epithelial cells).
- In extracapillary proliferation, proliferation of parietal epithelial cells leads to the formation of crescents, a feature characteristic of certain forms of rapidly progressive glomerulonephritis.
- leukocyte proliferation may accompany cellular proliferation - neutrophils and macrophages
- Glomerular basement membrane thickening
- Hyalinization or sclerosis indicates irreversible damage
- structural changes can be diffuse, focal, or segmental, or global.
- Functional: proteinuria, hematuria, reduction of GFR (oliguria, anuria), active urine sediment with RBCs and RBC casts.
- The decreased GFR and avid distal nephron salt and water retention result in expansion of intravascular volume, edema, and, frequently, systemic hypertension.
What is the pathophysiology of poststreptococcal glomerulonephritis (GN)?
-
How are the causes of acute glomerulonephritis (GN) categorized?
infectious and non-infectious causes
What are the infectious causes of acute glomerulonephritis (GN)?
- most common: Streptococcus species - group A, beta-hemolytic
- 2 serotypes - serotype 12 & 49
- PSGN usually develops 1-3 weeks after acute
- PSGN usually develops 1-3 weeks after acute infection with specific nephritogenic strains of group A beta-hemolytic streptococcus.
- Non streptococcal infection -
postinfectious glomerulonephritis may also result from infection by other bacteria, viruses, parasites, or fungi. Bacteria other than group A streptococci that can cause AGN include the following:
Staphylococci
Diplococci
Other streptococci
Mycobacteria
Salmonella typhosa
Brucella suis
Treponema pallidum
Corynebacterium bovis
Actinobacilli
Which bacteria cause nonstreptococcal postinfectious glomerulonephritis (GN)?
Staphylococci
Diplococci
Other streptococci
Mycobacteria
Salmonella typhosa
Brucella suis
Treponema pallidum
Corynebacterium bovis
Actinobacilli
What are the viral causes of acute glomerulonephritis (GN)?
Cytomegalovirus (CMV), coxsackievirus, Epstein-Barr virus (EBV), hepatitis B virus (HBV), [11] rubella, rickettsiae (as in scrub typhus), parvovirus B19, [12] 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.
AGN has been documented as a rare complication of hepatitis A.
What are the noninfectious causes of acute glomerulonephritis (GN)?
Attributing glomerulonephritis to a parasitic or fungal etiology also requires the exclusion of a streptococcal infection. Identified organisms include Coccidioides immitis and the following parasites:
Plasmodium malariae
Plasmodium falciparum
Schistosoma mansoni
Toxoplasma gondii
Wuchereria bancrofti
Trichinella roundworms
Trypanosomes
What the multisystem systemic diseases that cause acute glomerulonephritis (GN)?
- Vasculitis
- Collagen-vascular diseases - systemic lupus erythematous
- Hypersensitivity vasculitis
- Cryoglobulinemia
- Polyarteritis nodosa
- Henoch-Schönlein 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).
What are the primary renal diseases that cause acute glomerulonephritis (GN)?
- Membranoproliferative glomerulonephritis
- Immunoglobulin A (IgA) nephropathy
- “Pure” mesangial proliferative glomerulonephritis
- ## Idiopathic rapidly progressive glomerulonephritis
What are the miscellaneous noninfectious causes of acute glomerulonephritis (GN)?
Miscellaneous noninfectious causes of acute GN include the following:
Guillain-Barré syndrome
Irradiation of Wilms tumor
Diphtheria-pertussis-tetanus (DPT) vaccine
Serum sickness
Epidermal growth factor receptor activation, [14] and possibly its inhibition by cetuximab [15]
COVID-19 vaccine
What is the global prevalence of acute glomerulonephritis (GN)?
Worldwide, IgA nephropathy (Berger disease) is the most common cause of glomerulonephritis.
Which patient groups have the highest prevalence of acute glomerulonephritis (GN)?
AGN predominantly affects males (2:1 male-to-female ratio).
Postinfectious GN has no predilection for any racial or ethnic group.
A higher incidence (related to poor hygiene) may be observed in some socioeconomic groups.
What is the prognosis of acute glomerulonephritis (GN)?
- Most epidemic cases follow a course ending in complete patient recovery (as many as 100%).
- Sporadic cases of acute nephritis often progress to a chronic form.
- Proteinuria may persist for 6 months and microscopic hematuria for up to 1 year after onset of nephritis.
- Eventually, all urinary abnormalities should disappear, hypertension should subside, and kidney function should return to normal.
What is included in patient education about acute glomerulonephritis (GN)?
Counsel patients about the need for the following measures:
Salt restriction during the acute phase to control edema and volume-related hypertension
Blood pressure monitoring at periodic intervals
Ongoing long-term monitoring of patients with persistent urinary abnormalities and elevated blood pressure
Consideration of protein restriction and angiotensin-converting enzyme (ACE) inhibitors (in patients who show evidence of persistent abnormalities or in those who develop late evidence of progressive disease)
Early antibiotic treatment of close contacts
Which clinical history findings are characteristic of acute glomerulonephritis (GN)?
- most common presentation:
- male
- 2-14 years
- puffiness of teh eyelids
- facial edema
- postrep infection
dark, scanty urine - elevated bp
- nonspecific symptoms - weakness, fever, abdominal pain, and malaise
ask patient:
- onset
- duration
What are the signs and symptoms of acute glomerulonephritis (GN)?
- hematuria
- oliguria
- edema (peripheral or periorbital)
- headache
- SOB or dyspnoea
- possible flank pain
Rash (as with vasculitis, Henoch-Schönlein purpura, or lupus nephritis)
Pallor
Renal angle (ie, costovertebral) fullness or tenderness, joint swelling, or tenderness
Hematuria, either macroscopic (gross) or microscopic
Abnormal neurologic examination or altered level of consciousness (from malignant hypertension or hypertensive encephalopathy)
Arthritis
other signs to look for:
Pharyngitis
Impetigo
Respiratory infection
Pulmonary hemorrhage
Heart murmur (possibly indicative of endocarditis)
Scarlet fever
Weight gain
Abdominal pain
Anorexia
Back pain
Oral ulcers
What are the classic presentations of acute glomerulonephritis (GN)?
Patients often have a normal physical examination and blood pressure; most frequently, however, patients present with a combination of edema, hypertension, and oliguria.
