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Acute Glomerulonephritis

Acute Glomerulonephritis Syndrome

Acute glomerulonephritis (AGN) is an immune-mediated inflammation and destruction of the glomeruli and peri-glomerular tissues including the basement membrane, mesangium, and the capillary endothelium.


Presentation

AGN is asymptomatic in approximately 50% of patients. In those who present with symptoms, the initial presentation is peripheral edema, low urine volume, and dark-colored urine due to hematuria.The reduction in GFR coupled with the salt and water retention in the distal tubule results in an increased intravascular volume, edema, and systemic hypertension. Edema appears as facial and periorbital swelling initially, before becoming obvious in the lower extremities. Elevated blood pressure progresses with the kidney damage. Non-specific symptoms are also common and include nausea, malaise, and dizziness.

Fever and fatigue are the most frequent presentations of rapidly progressive glomerulonephritis. Other symptoms include nausea, anorexia, vomiting, arthralgia, and abdominal pain. Furthermore in these cases, hypertension is usually absent or mild.

The symptoms of acute post-streptococcal glomerulonephritis include passage of coke-colored or dark brown urine, hypertension, facial puffiness and pedal edema, and proteinuria on urinalysis [11]. Occasionally, the complications of hypertension such as seizures and persistent headaches may be the only presentations of the patient.

Fever
  • Familial Mediterranean fever (FMF) is an inherited auto-inflammatory disorder. Secondary AA amyloidosis is the most devastating complication of FMF.[ncbi.nlm.nih.gov]
  • This report highlights the occurrence of acute glomerulonephritis in a 7-year-old girl who presented with fever and vomiting. Peripheral smear examination demonstrated ring forms of P. vivax.[ncbi.nlm.nih.gov]
  • Keywords: Acute glomerulonephritis, dengue hemorrhagic fever, glomerular cast, hypertension, hematuria How to cite this article: Meena K R, Kumar P, Anita, Paul P. Acute glomerulonephritis in dengue hemorrhagic fever: A rare case report.[atmph.org]
  • It is generally assumed that acute tubular necrosis is the etiology of renal failure that can occur during the course of Rocky Mountain spotted fever (RMSF).[ncbi.nlm.nih.gov]
  • Abstract We report a case of acute glomerulonephritis associated with acute Q fever.[ncbi.nlm.nih.gov]
Rapidly Progressive Glomerulonephritis
  • AGN due to these autoimmune diseases is most likely associated with rapidly progressive glomerulonephritis.[symptoma.com]
  • The postinfectious form of rapidly progressive glomerulonephritis with crescents is a form of immune complex glomerulonephritis which seem to have a better prognosis.[doi.org]
  • progressive glomerulonephritis, 1 - 2% develop chronic glomerulonephritis Poor prognosis more likely if massive proteinuria and abnormal GFR; 2 - 5% die from pulmonary edema, hypertensive encephalopathy or crescentic glomerulonephritis; children with[pathologyoutlines.com]
  • Rarely, PSAGN can present with severe acute kidney injury with rapidly progressive glomerulonephritis.[clinicaladvisor.com]
  • Renal biopsy When in doubt about the diagnosis or if there is suspicion of rapidly progressive glomerulonephritis, a renal biopsy is the gold standard for diagnosis. Prognosis The prognosis of post-streptococcal glomerulonephritis is good.[myvmc.com]
Congestive Heart Failure
  • She was referred by her primary care physician for suspected congestive heart failure but she had an elevated creatinine level and an abnormal urinalysis. Renal biopsy showed diffuse endocapillary proliferative glomerulonephritis.[ncbi.nlm.nih.gov]
  • IN acute glomerulonephritis the systemic manifestations of hypertension, edema and congestive heart failure result, in large part, from salt and water retention whereas hematuria and proteinuria are direct expressions of the inflammatory process in the[nejm.org]
  • heart failure, acute or chronic renal failure, and end-stage renal disease.[medi-info.com]
  • This is secondary to congestive heart failure and azotemia. Congestive heart failure is more common in adults (43%) than in children ( 5%). Nephrotic-range proteinuria is also more common in adults (20%) than in children (4-10%).[emedicine.com]
Malaise
  • Among the signs and symptoms of acute proliferative glomerulonephritis are the following: Hematuria Oliguria Edema Hypertension Fever (headache, malaise, anorexia, nausea.)[en.wikipedia.org]
  • […] pulmonary edema, hypertensive encephalopathy or crescentic glomerulonephritis; children with obesity may have greater renal injuries ( Clin Nephrol 2009;71:632 ) Children age 6 - 10 : nephritic presentation with abrupt onset of hematuria, oliguria, fever, malaise[pathologyoutlines.com]
  • Non-specific symptoms are also common and include nausea, malaise, and dizziness. Fever and fatigue are the most frequent presentations of rapidly progressive glomerulonephritis.[symptoma.com]
  • 2011; 195: 150-152) Clinical record A 10-year-old boy from a remote village in Western Province, Papua New Guinea (PNG), presented to Saibai Island Primary Health Centre in the northern Torres Strait, Queensland, with a 4-year history of intermittent malaise[mja.com.au]
  • […] that may occur include: Blurred vision, usually from burst blood vessels in the retina of the eye Cough containing mucus or pink, frothy material from fluid buildup in the lungs Shortness of breath, from fluid buildup in the lungs General ill feeling (malaise[nlm.nih.gov]
Weight Gain
  • Body weight gain ranged from 3 to 10 kg. Three of the patients had contact with erythema infectiosum simultaneously with or within 10 days before development of flu-like symptoms.[ncbi.nlm.nih.gov]
  • Symptoms PSGN Onset of symptoms occurs 1 to 6 weeks after infection; symptoms include hypertension, headache, edema, oliguria, dark urine, reduced urine output, flank pain, weight gain, fever, chills, nausea, and vomiting; about half of cases are asymptomatic[medi-info.com]
  • The most important symptoms noted were weight gain, edema, dyspnea, oliguria and red or smoky urine. The most prominent physical signs were elevated blood pressure, edema, abnormalities in the chest and fever of over 100 F.[ncbi.nlm.nih.gov]
  • gain is the earliest sign of fluid retention): use same standing scale every day.[registerednursern.com]
  • Despite corticosteroids being effective, in many patients high doses for prolonged periods can have significant side affects including: weight gain, hyperglycemia, destruction of bones, easy bruising, and thinning of the skin.[nephrocor.com]
Vomiting
  • Post-infectious acute glomerulonephritis with hypertensive encephalopathy is characterized by episodic hypertension with headache, vomiting, and hematuria.[ncbi.nlm.nih.gov]
  • This report highlights the occurrence of acute glomerulonephritis in a 7-year-old girl who presented with fever and vomiting. Peripheral smear examination demonstrated ring forms of P. vivax.[ncbi.nlm.nih.gov]
  • A three-year-old boy presented with high grade fever, a seven-day history of the progressive swelling of his body and a one-day history of vomiting. An examination revealed hypertension ( 95th percentile), pallor and hepatosplenomegaly.[ncbi.nlm.nih.gov]
  • Its clinical features include headache, decreased alertness, mental abnormalities, such as confusion, diminished spontaneity of speech, changed behavior ranging from drowsiness to stupor, seizures, vomiting, and abnormalities of visual perception like[ncbi.nlm.nih.gov]
  • A 3-year-old boy presented with fever, vomiting and oliguria. He had hypertension, deranged renal function and low serum complement (C3), and urine microscopy showed red blood cells and granular casts.[ncbi.nlm.nih.gov]
Nausea
  • Among the signs and symptoms of acute proliferative glomerulonephritis are the following: Hematuria Oliguria Edema Hypertension Fever (headache, malaise, anorexia, nausea.)[en.wikipedia.org]
  • Amlodipine: edema, headache, fatigue, palpitations, nausea. Labetalol: bradycardia, bronchospasm, headache, nausea, arrhythmia.[clinicaladvisor.com]
  • Other symptoms include nausea, anorexia, vomiting, arthralgia, and abdominal pain. Furthermore in these cases, hypertension is usually absent or mild.[symptoma.com]
  • […] hypertensive encephalopathy or crescentic glomerulonephritis; children with obesity may have greater renal injuries ( Clin Nephrol 2009;71:632 ) Children age 6 - 10 : nephritic presentation with abrupt onset of hematuria, oliguria, fever, malaise and nausea[pathologyoutlines.com]
  • Symptoms PSGN Onset of symptoms occurs 1 to 6 weeks after infection; symptoms include hypertension, headache, edema, oliguria, dark urine, reduced urine output, flank pain, weight gain, fever, chills, nausea, and vomiting; about half of cases are asymptomatic[medi-info.com]
Abdominal Pain
  • pain Chronic Glomerulonephritis Prevention There is no known way to prevent chronic glomerulonephritis.[healthcommunities.com]
  • Other symptoms include nausea, anorexia, vomiting, arthralgia, and abdominal pain. Furthermore in these cases, hypertension is usually absent or mild.[symptoma.com]
  • Nausea, vomiting, and abdominal pain can occur but are more common in children than in adults.[web.archive.org]
  • pain Blood in the vomit or stools Cough and shortness of breath Diarrhea Excessive urination Fever General ill feeling, fatigue, and loss of appetite Joint or muscle aches Nosebleed The symptoms of chronic kidney disease may develop over time.[mountsinai.org]
Loss of Appetite
  • […] of appetite; overall itching; headache; easy bruising; frequent hiccups or bleeding; and impaired vision Increased pigmentation of the skin Abdominal pain Chronic Glomerulonephritis Prevention There is no known way to prevent chronic glomerulonephritis[healthcommunities.com]
  • […] of appetite and vomiting.[yourkidshealth.net]
  • This can lead to nausea, loss of appetite, and fatigue Chronic glomerulonephritis: It develops slowly over years, as the kidneys are not effectively filtering blood.[dovemed.com]
  • […] of appetite Joint or muscle aches Nosebleed The symptoms of chronic kidney disease may develop over time.[mountsinai.org]
  • When kidney failure is severe or near end stage, symptoms include: confusion decreased urination fatigue headache high blood pressure itchy skin loss of appetite muscle twitching or cramping nausea and vomiting nosebleeds puffy eyes, hands, and feet ([medbroadcast.com]
Hypertension
  • Post-infectious acute glomerulonephritis with hypertensive encephalopathy is characterized by episodic hypertension with headache, vomiting, and hematuria.[ncbi.nlm.nih.gov]
  • Reversible posterior leukoencephalopathy syndrome is an increasingly recognized brain disorder most commonly associated with hypertension, toxemia of pregnancy, or the use of immunosuppressive agents.[ncbi.nlm.nih.gov]
  • Abstract Acute glomerulonephritis (AGN) manifests with abrupt onset of hematuria, facial edema, hypertension and impairment of renal function.[ncbi.nlm.nih.gov]
  • In some cases, even with nephrotic syndrome, and hypertension, especially in adults over 30 years (group 3), being the least frequent finding of gross hematuria, and rarely, acute renal failure.[ncbi.nlm.nih.gov]
  • A 44-year-old woman with no relevant past medical history suffering from obesity and hypertension well controlled with metoprolol without hypertensive retinopathy was admitted to our hospital as a donor of PBSC.[ncbi.nlm.nih.gov]
Back Pain
  • Learn about this topic in these articles: description In Bright disease Acute glomerulonephritis is characterized by severe inflammation, renal (kidney) insufficiency, swelling, increased blood pressure, and severe back pain.[britannica.com]
Facial Edema
  • Abstract Acute glomerulonephritis (AGN) manifests with abrupt onset of hematuria, facial edema, hypertension and impairment of renal function.[ncbi.nlm.nih.gov]
  • Facial edema, or swelling, is common which tends to be more prominent in the morning. This edema tends to spread to the extremities and the abdomen during the day.[yourkidshealth.net]
Facial Swelling
  • We used these data to categorise children by history during the epidemics: The PSGN group had documented oedema (facial swelling or dependent oedema) or hypertension (diastolic pressure 80 mmHg if aged 2-12 years and 85 mmHg if over 12, levels corresponding[mja.com.au]
Headache
  • Post-infectious acute glomerulonephritis with hypertensive encephalopathy is characterized by episodic hypertension with headache, vomiting, and hematuria.[ncbi.nlm.nih.gov]
  • Its clinical features include headache, decreased alertness, mental abnormalities, such as confusion, diminished spontaneity of speech, changed behavior ranging from drowsiness to stupor, seizures, vomiting, and abnormalities of visual perception like[ncbi.nlm.nih.gov]
  • […] or other symptoms of high blood pressure In severe cases, symptoms of kidney failure, including fatigue; seizures; nausea and vomiting; loss of appetite; overall itching; headache; easy bruising; frequent hiccups or bleeding; and impaired vision Increased[healthcommunities.com]
  • Among the signs and symptoms of acute proliferative glomerulonephritis are the following: Hematuria Oliguria Edema Hypertension Fever (headache, malaise, anorexia, nausea.)[en.wikipedia.org]
  • Symptoms PSGN Onset of symptoms occurs 1 to 6 weeks after infection; symptoms include hypertension, headache, edema, oliguria, dark urine, reduced urine output, flank pain, weight gain, fever, chills, nausea, and vomiting; about half of cases are asymptomatic[medi-info.com]
Papilledema
  • Other signs and symptoms were fever 19%, arthralgia 4%, epistaxis 6% and bilateral papilledema 1% (Figure 3). Laboratory investigations Urinalysis showed haematuria in 90% and atleast 1 proteinuria in 77% of patients.[jpma.org.pk]
Guillain-Barré Syndrome
  • To our knowledge this is the first report of an association between ex novo episodes of acute glomerulonephritis and Guillain-Barré syndrome.[ncbi.nlm.nih.gov]
Hematuria
  • Post-infectious acute glomerulonephritis with hypertensive encephalopathy is characterized by episodic hypertension with headache, vomiting, and hematuria.[ncbi.nlm.nih.gov]
  • Although his hematuria and hypocomplementemia spontaneously subsided within a month, proteinuria remained.[ncbi.nlm.nih.gov]
  • Abstract Acute glomerulonephritis (AGN) manifests with abrupt onset of hematuria, facial edema, hypertension and impairment of renal function.[ncbi.nlm.nih.gov]
  • In some cases, even with nephrotic syndrome, and hypertension, especially in adults over 30 years (group 3), being the least frequent finding of gross hematuria, and rarely, acute renal failure.[ncbi.nlm.nih.gov]
  • These findings suggest that filgrastim may induce transient urinary excretion of protein and hematuria in PBSC donors as the symptoms of acute GN without adversely affecting renal function.[ncbi.nlm.nih.gov]
Oliguria
  • We report the case of a 10-year-old boy with acute glomerulonephritis who presented with gross hematuria, headache, vomiting, and oliguria, and developed transient cortical blindness as a complication of hypertensive encephalopathy.[ncbi.nlm.nih.gov]
  • The patient showed acute onset of heavy proteinuria, microscopic hematuria and kidney dysfunction with arthralgia and oliguria after close contact with a person suffering from erythema infectiosum.[ncbi.nlm.nih.gov]
  • Poststreptococcal gomerulonephritis • Onset abrupt with – Puffness of face – Oliguria – Smoky urine – Reddish urine – Hypertension – Oedema 16.[slideshare.net]
  • A 3-year-old boy presented with fever, vomiting and oliguria. He had hypertension, deranged renal function and low serum complement (C3), and urine microscopy showed red blood cells and granular casts.[ncbi.nlm.nih.gov]
  • Acute postinfectious (poststreptococcal) diffuse proliferative glomerulonephritis is a primary glomerulonephritis, which produces nephritic syndrome (hematuria, oliguria, uremia, hypertension and mild proteinuria).[pathologyatlas.ro]
Dark Urine
  • Symptoms PSGN Onset of symptoms occurs 1 to 6 weeks after infection; symptoms include hypertension, headache, edema, oliguria, dark urine, reduced urine output, flank pain, weight gain, fever, chills, nausea, and vomiting; about half of cases are asymptomatic[medi-info.com]
  • However, those who come down with symptoms may present with swelling of the face and legs, reduced urine volume, passage of coke-colored or dark urine, urine frothiness and a high blood pressure.[symptoma.com]
  • If symptoms appear, they can include swelling around the feet, ankles, lower legs, and eyes, reduced urination and dark urine (due to the presence of red blood cells in the urine).[drugs.com]
  • The dark urine is due to the oxidation of hemoglobin that turns brown after a prolonged time in an acidic environment. Gross hematuria may last up to 10 days and recur after a febrile illness.[emedicine.medscape.com]
Macroscopic Hematuria
  • The macroscopic hematuria and proteinuria occurred on 5th day of G-CSF administration. Due to mobilization and collection of stem cells, proteinuria was becoming more intense and reached the nephrotic range.[ncbi.nlm.nih.gov]
  • Source: Public Health Image Library, CDC Clinical Features The clinical features of acute glomerulonephritis include: Edema (often pronounced facial and orbital edema, especially on arising in the morning) Hypertension Proteinuria Macroscopic hematuria[cdc.gov]
  • Nephrotic syndrome was present in one patient with HBV-PIGN and two patients with non-HBV associated PIGN and was treated with glucocorticoid. 4 patients with HBV-PIGN and 6 patients with non-HBV associated PIGN had macroscopic hematuria.[journals.plos.org]
Smoky Urine
  • Poststreptococcal gomerulonephritis • Onset abrupt with – Puffness of face – Oliguria – Smoky urine – Reddish urine – Hypertension – Oedema 16.[slideshare.net]
  • The most important symptoms noted were weight gain, edema, dyspnea, oliguria and red or smoky urine. The most prominent physical signs were elevated blood pressure, edema, abnormalities in the chest and fever of over 100 F.[ncbi.nlm.nih.gov]

Workup

No symptom or sign is pathognomonic of AGN. Laboratory tests are, therefore, necessary to confirm a suspected case of AGN.

Urinalysis is necessary and may reveal red blood cell and white blood cell casts. Red blood cell casts are indicative of glomerular damage while the white cell casts are indicative of infection or inflammation of the nephron. Urinalysis also reveals proteinuria. Blood investigations necessary for diagnosis are tests for creatinine and urea levels.

Imaging studies such as abdominal plain radiographs, ultrasonography, and computed tomography (CT) scans may be necessary. However, a kidney biopsy is the definitive diagnostic modality to confirm AGN [12].

Creatinine Increased
  • Her course was prolonged with serum creatinine increased from the baseline level of 1.1 mg/dl to 2.2 mg/dl, returning toward the baseline level (1.2 mg/dl) after one month. Serum creatinine then started to increase again.[ncbi.nlm.nih.gov]
Uric Acid Increased
  • On follow-up, it was confirmed that as serum C3 level returned to normal, urinary excretion of uric acid increased and serum uric acid level decreased, thereby resolving the burning pain of the left big toe.[ncbi.nlm.nih.gov]

Treatment

The management of AGN involves treatment of the underlying trigger, supportive care, and conservative management of the complications of the disease.

Diuretics are necessary to resolve the edema and antihypertensives are equally vital [13]. Furthermore, dietary modifications should consist of low protein diet and salt restriction. Antibiotics are administered in cases of infectious AGN, however, antibiotics may be ineffective since the nephritis occurs 1 to 6 weeks after the inciting infection. Typically, the infection resolves before the onset of the nephritis, however, if the infection still persists, antibiotics can be administered.

Corticosteroids are administered in cases of AGN triggered by autoimmune disease and in rapidly progressive glomerulonephritis. High dose corticosteroids are administered intravenously for up to 7 days after which they are switched to oral forms. Immunosuppressants may also be beneficial for these patients [14]. Plasmapheresis may also be a beneficial procedure to clear off antibodies from the blood. 

Generally, prompt diagnosis and treatment prevents progression of the disease to ESRD. Renal transplantation is the definitive treatment for ESRD; however, rapidly progressive glomerulonephritis may reappear in the transplanted kidney.

Prognosis

Post-streptococcal glomerulonephritis and IgA nephropathy have a minimal risk of progressing to chronic kidney disease if the underlying pathology is treated well in time. Complete resolution of symptoms is observed in most patients, especially children.

For other glomerular pathologies, the outcome is generally better if the patient presents with asymptomatic hematuria open link and proteinuria and in those with focal instead of diffuse glomerular changes on renal biopsy. Patients with diffuse glomerular involvement usually have a poorer prognosis.

Generally, poor prognostic factors include severe proteinuria, severe renal dysfunction, unresponsiveness to treatment, and extensive fibrotic changes in the glomeruli such as glomerulosclerosis.

If patients having membranoproliferative disease remain untreated, 50-60% of them will lead to ESRD in a period of 10-15 years. The situation in case of Wegener granulomatosis is different because about 20-25% are at risk of leading to ESRD [9] [10]. 

Etiology

The etiological factors responsible for AGN may be classified into infectious and non-infectious causes. The commonest infections responsible for AGN are streptococcal infections, particularly strep pharyngitis.

Noninfectious causes of AGN are mostly autoimmune diseases and include systemic lupus erythematosus (SLE), goodpasture's syndromeamyloidosis, Wegener granulomatosis, and polyarteritis nodosa [3].

Prolonged and heavy use of nonsteroidal anti-inflammatory drugs (NSAIDs) have also been suggested as a risk factor for AGN.

Epidemiology

AGN accounts for 10-15% cases of glomerular diseases in the United States. However, the incidence rates have been variable, partially because of the asymptomatic nature of this condition in more than 50% of patients. Generally, statistics reveal a decline in the incidence of post-streptococcal glomerulonephritis in the United States. This decline is attributable to improved healthcare delivery and socioeconomic conditions.

In the United States, AGN is responsible for 25-30% of cases of ESRD. In about 25% of cases, the disease progresses to an acute nephritic syndrome. Acute nephritic syndrome, in turn, progresses to end-stage renal failure after several weeks or months.

Worldwide, the commonest cause of AGN is Berger disease or IgA nephropathy. Post-streptococcal glomerulonephritis open link is most commonly seen in Africa, the Caribbean, India, South America, Malaysia, and Pakistan.

In Nigeria's Port Harcourt city, the incidence of AGN in children between the ages of 3 to 16 years was 15.5 cases per year. Furthermore, the incidence of the disease was higher among males than females with a ratio of 1.1:1. However, currently the difference in incidence among males and females is not so significant [4].

Generally, there are more marked variations in geographic and seasonal incidence rates of post-streptococcal glomerulonephritis following pharyngeal infections than those which follow streptococcal skin infections [4] [5].

Sex distribution
Age distribution

Pathophysiology

AGN presents with both morphological and functional changes in the kidneys. There is cellular proliferation in the glomerular tufts as a result of the excess proliferation of the mesangial, epithelial, and endothelial cells triggered by the immune-complex deposition [6]. The cellular proliferation may be confined to the glomerular capillary, in what's described as endocapillary proliferation. Alternatively, it may occur in the Bowman's capsule beyond the glomerular cells and it is referred to as extra capillary proliferation. Accompanying this cellular proliferation is neutrophilic and monocytic infiltration of the glomerular capillary lumen.

On light microscopy, the glomerular capillary walls appear thickened. A study using electron microscopy clearly shows the basement membrane as thickened due to the deposits of electron-dense particles on the subendothelial, mesangial, and subepithelial parts of the basement membrane. The structural changes in the kidneys may be focal, segmental, diffuse, or global. Morphologically the kidneys appear grossly enlarged as a result of swelling effect in the glomerular tufts.

The main feature of AGN is the deposition or formation of immune complexes in the glomerulus. The deposition of complement factors and immunoglobulins is demonstrable by immunofluorescence.

The triggers for the formation of immune complexes in the glomerulus are largely unclear, except in cases of post-streptococcal glomerulonephritis. In post-streptococcal glomerulonephritis, a streptococcal neuraminidase alters the host immunoglobulin G (IgG) which combines with the host antibodies forming IgG/anti-IgG complexes which subsequently deposit in the glomeruli. Furthermore, the presence of high titers of antistreptolysin O or antihyaluronidase, streptokinase, and DNAase-B strongly suggest a preceding streptococcal infection. Specific antibodies may combine with these antigens to form immune complexes.

Nephritis-associated plasmin receptor (NAPlr) has been described as a glyceraldehyde-3-phosphate dehydrogenase which functions a plasminogen receptor. NAPlr deposition was demonstrated in the initial stages of post-streptococcal glomerulonephritis in immunofluorescence staining of renal biopsy specimens with anti-NAPlr antibodies. This finding links NAPlr with the pathogenesis of post-streptococcal glomerulonephritis [7].

A study conducted among adults revealed that the two commonest infectious triggers of AGN were streptococci and staphylococci, occurring in 27.9% and 24.4% of cases, respectively [8]. In infections of groups A, C, and G streptococcus associated with glomerulonephritis, titers of antibodies against nephritis-associated protease (NAPR) are significantly elevated. Anti-NAPR antibodies persist for several years and have been suggested to help prevent further episodes of post-streptococcal glomerulonephritis.

Prevention

Prevention of AGN may include routine urinalysis done for patients with autoimmune diseases such as SLE.

Summary

Acute glomerulonephritis (AGN) is inflammation of the glomeruli which occurs as a result of autoimmune response to an infection or immune complex depositions occurring in autoimmune pathologies. AGN may also affect the various parts of glomerulus such as mesangium, the capillary endothelium and basement membrane.

Generally, the causes of AGN may be infectious or autoimmune diseases. AGN often occurs sequel to a streptococcal infection open link, usually strep throat or strep cutaneous infections [1]. This post-streptococcal glomerulonephritis is often commonly seen in children between 2 and 10 years. Noninfectious causes of AGN include autoimmune diseases such as IgA nephropathy, systemic lupus erythematosus, cryoglobulinemia, goodpasture syndrome, and Wegener granulomatosis [2]. AGN due to these autoimmune diseases is most likely associated with rapidly progressive glomerulonephritis.

The characteristic features of AGN are the formation and deposition of immune complexes in the glomerular tufts, accompanied by polymorphonuclear cellular infiltrates. Functionally, AGN results in hematuria, proteinuria, facial or pedal edema, and systemic hypertension. Nonspecific symptoms are also common in this disease.

Disease prognosis becomes poor due to severe proteinuria, hematuria, and renal damage on presentation, unresponsiveness to appropriate therapy, and the presence of extensive renal fibrosis or sclerosis on biopsy. The main complication of AGN is the end-stage renal disease (ESRD).

Renal biopsy is the main diagnostic tool of choice to confirm AGN. However, other investigations including bloodwork, urinalysis, and imaging studies provide details to corroborate the diagnosis.

Management of AGN comprises of symptomatic control and treatment of the underlying disorder. Antibiotics and corticosteroids are administered for infectious and autoimmune-associated AGN, respectively. Additionally, diuretics are necessary to relieve the edema. 

Patient Information

Overview

The kidney is an organ of waste excretion in the form of urine. However, the process of waste excretion is very complex involving several small structures within each kidney. The first stage of urine production is the filtration of the waste products from the blood. Some useful products are also filtered, but are later reabsorbed into the blood. The units which filter the blood are called the glomeruli (singular: glomerulus).

Acute glomerulonephritis (AGN) is an inflammation and consequent destruction of the glomeruli and adjacent tissues. This, in turn, would lead to reduced urine production as well as salt and water retention in the body.

Etiology

AGN may be caused by infections or certain noninfectious diseases called autoimmune diseases in which the body's antibodies attack certain normal tissues in the body confusing them for foreign harmful substances. The commonest infectious causes of AGN are infections caused by the bacterium streptococcus, which are mostly are responsible for sore throat and skin infections. The common autoimmune diseases which cause AGN includes systemic lupus erythematosus (SLE), Wegener granulomatosis, and Berger disease.

Pathophysiology

AGN develops when antibodies formed in the body against certain components of the bacterium or infectious agents bind with these agents and deposit in the glomeruli causing destruction of the glomeruli and surrounding tissues.

Presentation

More than half of the patients with this disease may not show any symptoms. However, those who come down with symptoms may present with swelling of the face and legs, reduced urine volume, passage of coke-colored or dark urine, urine frothiness and a high blood pressure.

The facial and leg swelling results from the kidneys' inability to dilute the urine with water from the blood and so there is an accumulation of excess salt and water in the certain regions of the body such as the feet and face. This is also responsible for the elevated blood pressure in these patients. The dark color of the urine is due to the presence of the blood in it, and the frothiness of the urine is as a result of leakage of small proteins through the damaged glomerular filter into the urine. 

There are other non-specific symptoms of this disease which include fever, weakness, dizziness, and abdominal aches.

Diagnosis

A diagnosis of AGN is made by way of investigations which include blood tests and urinalysis: which involves examining a sample of the patient's urine and analyzing it's contents. Results of urinalysis in AGN usually show presence of white and red blood cells which indicate infective damage or inflammation of the kidney tubules and damage to the glomeruli, respectively.

The main diagnostic tool for confirming the diagnosis of AGN is kidney biopsy. This procedure involves using a big needle to take a sample of the kidney through the patient's trunk, then analyzing the sample under a microscope.

Treatment

Prompt diagnosis and treatment of AGN is necessary to avoid the major complication which is called end-stage renal disease which indicates that the kidney is too damaged to function at all.

Treatment of AGN involves treating the predisposing condition and correcting the symptoms. A class of drugs called diuretics are prescribed to remove excess fluids from the sites where they accumulate. Drugs which lower blood pressure are also necessary. If an infection is determined as the trigger of AGN, antibiotics are administered and for autoimmune-related cases, drugs called corticosteroids such as prednisolone are administered.

In cases of end-stage renal disease, kidney transplant is considered.

References

Article

  1. Tejani A, Ingulli E. Poststreptococcal glomerulonephritis: current clinical and pathological concepts. Nephron. 1990; 55:1-5.
  2. Emancipator SN. IgA nephropathy: morphological expression and pathogenesis. Am J Kidney Dis. 1994; 23:451-462.
  3. Kalluri R, Wilson CV, Weber M, et al. Identification of the α-3 chain of type IV collagen as the common autoantigen in anti-glomerular basement membrane disease and Goodpasture’s syndrome. J Am Soc Nephrol. 1995; 6:1178-1184.
  4. Anochie I, Eke F, Okpere A. Childhood acute glomerulonephritis in Port Harcourt, Rivers State, Nigeria. Niger J Med. 2009; 18(2):162-167.
  5. Wong W, Morris MC, Zwi J. Outcome of severe acute post-streptococcal glomerulonephritis in New Zealand children. Pediatr Nephrol. 2009; 24(5):1021-1026.
  6. Wen YK, Chen ML. The significance of atypical morphology in the changes of spectrum of postinfectious glomerulonephritis. Clin Nephrol. 2010; 73(3):173-179. 
  7. Oda T, Yoshizawa N, Yamakami K, et al. The role of nephritis-associated plasmin receptor (NAPlr) in glomerulonephritis associated with streptococcal infection. J Biomed Biotechnol. 2012; 2012:417675.
  8. 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). 2008; 87(1):21-32.
  9. Donadio JV Jr, Offord KP. Reassessment of treatment results in membranoproliferative glomerulonephritis, with emphasis on life-table analysis. Am J Kidney Dis. 1989; 14:445-451.
  10. Andrassy K, Erb A, Koderisch J, et al. Wegener's granulomatosis with renal involvement: patient survival and correlations between initial renal function, renal histology, therapy and renal outcome. Clin Nephrol. 1991; 35:139-147.
  11. Sad RA, Said SM. Hypertension in Jordanian children: a retrospective analysis of 70 cases Pediatr. Nephrol. 1990; 4:520-522.
  12. Nebuloni M, Barbiano di Belgiojoso G, Genderini A, et al. Glomerular lesions in HIV-positive patients: a 20-year biopsy experience from Northern Italy. Clin Nephrol. 2009; 72(1):38-45.
  13. Tapaneyaand O. AGN in children: a prospective study. J Med Assoc Thai. 1989; 72(suppl):35-38.
  14. Wong W, Morris MC, Zwi J. Outcome of severe acute post-streptococcal glomerulonephritis in New Zealand children. Pediatr Nephrol. 2009; 24(5):1021-1026.

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Last updated: 2019-07-11 20:35