Patients suffering from acute glomerular nephritis may initially present with sudden facial edema and puffiness. Their urine may dark and output decreased. Urinary sediment contains red blood cells, red cell casts, white cells and protein [14].

They may also have a new onset hypertension. Other nonspecific symptoms such as weakness, fever, abdominal pain, and malaise may occur. Onset is generally abrupt.

Regardless of the type of acute glomerulonephritis, the clinical presentation is similar. Symptoms include the following [14]:

• Hematuria
• Oliguria
• Edema (peripheral or periorbital) 
• Headache
• Hypertension
• Dyspnea or shortness of breath with exertion
• Flank pain
• Weight gain
• Abdominal pain
• Anorexia
• Sexual dysfunction and loss of libido
• Nephrotic syndrome

Complications of an acute case of glomerular nephritis include [12] [14]:

• Nephrotic syndrome and sclerosis
• Acute renal failure
• Decreased in glomerular filtration rate 
• Pulmonary edema
• Severe proteinuria with ascites
• Malignant hypertension with cardio and/or cerebrovascular damage
• Hypertensive retinopathy
• Hypertensive encephalopathy
• Chronic renal failure
• End-stage renal failure

Post infectious glomerulonephritis usually occurs 1-3 weeks or longer after infection. It is important to identify and treat the causative agent. In these cases there may be a history of recent fever, sore throat, joint pains, hepatitis, travel outside the country, valve replacement, and/or intravenous drug use [4].

Urinalysis and examination of urine for protein, blood, red blood cells, white blood cells, red blood cell casts, granular casts, and oval fat bodies is essential. The presence of red blood cell casts is diagnostic of glomerulonephritis [3]. The urine is usually dark with a specific gravity greater than 1020 [3] [14].

Other tests should include the following [2] [14]:

• Complete blood count
• Blood urea nitrogen and serum creatinine 
• Serum electrolytes, especially serum potassium
• Glomerular filtration rate
• Erythrocyte sedimentation rate
• Complement levels (C3, C4, CH50) [2]
• Streptozyme testing
• 24-hour urine study

Patients with acute post-streptococcal glomerulonephritis low C3 levels are found and C4 levels may be slightly low. Blood and tissue cultures to rule out or identify infectious agents should also be done [2].

Imaging studies may be required in some patients. These include [14]:

• Computed tomography of kidney
• Chest radiography
• Ultrasonography of kidney 
• Echocardiography in patients with new cardiac symptoms
• Renal biopsy

There is no specific treatment for renal disease. Treatment of acute glomerulonephritis is mainly supportive. In post-infection cases the underlying infections must be identified and treated first [2] [14]. In all other forms of the disease treatment and control of comorbid conditions is needed to slow the progress of kidney dysfunction and prevent cardiovascular injury [3] [14].

Supportive treatment is aimed at the control of inflammation[1], and then to treat hypertension, infection, and underlying conditions (cardiovascular disease, diabetes) [14]. After these interventions monitoring of the progression of kidney status and treatment of the complications is essential [14]. Once the acute disease has progressed to chronic renal disease the goal of treatment is to delay progression to end-stage renal disease and preparation dialysis or renal replacement therapy [14].

Pharmacologic therapy for glomerular nephritis includes [1] [8] [15]:

• Antibiotics and antimicrobials
• Loop diuretics in patients with edema 
• Anti-hypertensive medications
• Vasodilator drugs
• Glucocorticoids [1] 
• Bicarbonate supplementation may preserve renal function in chronic kidney disease [8]
• Cytokine-based therapies [15]

Diet

Sodium and fluid restriction should be advised when fluid retention is severe or pulmonary edema is present.
Protein restriction may be needed in patients with.

Activity

Bed rest may be recommended in the acute phase or until symptoms of inflammation subsides. After this, regular activity should be resumed.

Most cases of infectious glomerulonephritis result in complete recover. The highest mortality rate occurs in the pediatric population and is reported at 0-7% [14]. More than 98% of individuals are asymptomatic after 5 years, with chronic renal failure reported 1-3% of the time [13]. Most patients have spontaneous improvement in a week, with resolution of fluid retention and hypertension. Proteinuria and microscopic hematuria can persist for 6 months to 1 year. Recurrent episodes of post infectious glomerulonephritis are unusual. 

Approximately 30% of adult patients and 10% of pediatric patients with any form of glomerulonephritis progress to chronic renal disease [14]. It is the most common cause of chronic renal failure (25%) [14] .

Long-term prognosis is not necessarily benign in patients who recover. Some patients experience hypertension, proteinuria, and renal insufficiency for the rest of their lives [14].

Prognosis is worse in patients with significant proteinuria, severe hypertension, and elevated creatinine levels [14]. Outcomes vary from complete recovery to complete renal failure. It depends on the overall health of the individual, especially underlying cardiopulmonary, neurologic, and diabetic conditions.

Glomerulonephritis is characterized by inflammation of the glomeruli of the kidney [16]. These structures are responsible for the primary function of filtration by the kidney.

Symptoms include proteinuria, hematuria, reduction in glomerular filtration rate, oliguria, red blood cells and red blood cell casts in the urine [16]. The decreased glomerular filtration rate results in an increased intravascular volume, edema, and, frequently, systemic hypertension [1]. Many patients with glomerulonephritis may have microscopic hematuria without proteinuria [13].

Glomerulonephritis is defined as either acute or chronic. The acute form is of short duration and usually resolves without sequelae. All forms of acute glomerulonephritis may progress to the chronic form which is characterized by irreversible and progressive glomerular and tubular renal fibrosis [1] [2]. This ultimately leads to a decreased glomerular filtration rate and an increase in uremic toxins systemically. Eventually chronic kidney disease (CKD), end-stage renal disease (ESRD), and cardiovascular disease result [1] [2] [9] [13]. The progression from acute glomerulonephritis to chronic glomerulonephritis depends on the etiology [17].

Acute glomerulonephritis can be divided into infectious and noninfectious groups [17]. The most common cause of infectious acute glomerulonephritis is an infection by group A, beta-hemolytic streptococcus bacteria. Post-streptococcal glomerulonephritis develops 1-3 weeks after the infection. The incidence of glomerulonephritis is in individuals with pharyngitis is approximately 5-10% and 25% in those with skin infections [17].

Determining that an episode of acute infectious glomerulonephritis is due to any other organism first requires the exclusion of streptococci as the precipitating agent [5] [17]. Complete recovery of renal function occurs in most patients with post-streptococcal glomerulonephritis and other infectious forms. Post-infectious glomerulonephritis may occur after infections by other bacteria, viruses, parasites, or fungi [5] [17]. Bacteria include diplococci, other streptococci, staphylococci, and mycobacteria. Viruses include cytomegalovirus, coxsackie virus, Epstein-Barr virus, and hepatitis B virus [5].

Noninfectious causes of acute glomerulonephritis include the following [6] [7]:

• Guillain-Barré syndrome
• Irradiation of Wilms tumor
• Diphtheria-pertussis-tetanus (DPT) vaccine
• Serum sickness

Chronic glomerulonephritis is divided into primary renal diseases, systemic diseases, chronic disease, or those of unknown etiology [17].

Primary renal diseases that can cause glomerulonephritis include the following [1] [14]:

• Membrano-proliferative glomerulonephritis with the expansion and proliferation of mesangial cells
• Immunoglobulin A nephropathy [10]
• “Pure” mesangial proliferative glomerulonephritis
• Idiopathic rapidly progressive glomerulonephritis

Multisystem systemic diseases that can cause glomerulonephritis include the following [11]:

• Vasculitis, like Wegener granulomatosis
• Collagen-vascular diseases, such as systemic lupus erythematosus
• Hypersensitivity vasculitis
• Cryoglobulinemia
• Polyarteritis nodosa
• Henoch-Schönlein purpura
• Goodpasture syndrome

Glomerulonephritis may also occur as a result of other chronic diseases such as diabetes, cardiovascular disease, and atherosclerosis.

The National Kidney Foundation defines chronic kidney disease by the following criteria [14]:

• Evidence of kidney damage: proteinuria or hematuria and/or structural abnormalities seen on ultrasound
• Glomerular Filtration Rate (GFR) less than 60 mL/min for 3 or more months.

Chronic renal disease is classified into 5 stages [3] [12] [14]:

• Stage 1: Kidney damage with a normal glomerular filtration rate (≥ 90 mL/min).
• Stage 2: Kidney damage with a mild decrease in the glomerular filtration rate (60-90 mL/min).
• Stage 3: Moderately decreased glomerular filtration rate (30-59 mL/min).
• Stage 4: Severe decrease in the glomerular filtration rate (15-29 mL/min).
• Stage 5: Renal failure; glomerular filtration rate <15.

Glomerulonephritis accounts for 10 to 15% of renal disease [1]. The incidence of post-streptococcal glomerulonephritis has fallen over the past few decades due to better diagnosis and treatment of streptococcal infections. Post-infectious glomerulonephritis is most common in children but may occur at any age. Only 10% occur in patients older than 40 years of age [17].

Other forms of acute glomerulonephritis may occur at any age, including infancy [1]. Acute glomerulonephritis affects males more frequently than females (2:1 male-to-female ratio) [17]. Incidence of glomerulonephritis does not change due to race or socioeconomic factors [1] [2].

Chronic glomerulonephritis is the third leading cause of end-stage renal disease in the United States and accounts for 10% of patients on dialysis [16]. In some Asian countries, chronic glomerulonephritis accounts for 28 to 40% of patients on dialysis [4]. Diabetic nephropathy is found in approximately 40% of patients on dialysis [16].

The exact triggers for most forms of glomerulonephritis are unknown, except for post streptococcal glomerulonephritis whose trigger is a streptococcal infection.

Damage and complications in acute glomerulonephritis are the result of glomerular inflammation [1] [12] [14]. The kidney is especially vulnerable to inflammatory injury [16]. Cytokine production by mesegial cells occurs in response to injury to renal tissue stimulating the inflammatory process [15] [16]. Glomerular basement membranes and capillary walls thicken [14].

The nephrotic syndrome refers to a group of symptoms that occur with glomerular inflammation and includes edema, proteinuria, hypoproteinemia, and hyperlipidemia. Inflammation surrounding the glomerulus increases its permeability by the glomerular endothelium to proteins [14] [15]. When the liver is unable to compensate for the excreted proteins, serum protein levels, particular albumin and globulin, are decreased. With hypo-proteinemia there is a decreased circulating osmotic pressure resulting in fluid moving into the tissue. The body secretes aldosterone in response to the decrease blood volume and the retention of sodium and water [12].

The other complications of nephritic syndrome include hematuria, oliguria, and hypertension as a result of inflammation of the glomerulus and capillaries of the kidneys [14]. Renal filtration and circulation are altered [15]. Decreased renal profusion results in decreased urine production. Increased circulating toxins, blood urea nitrogen and creatinine, and activation of the renin-angiotensin system occur resulting in hypertension [12].
Metabolic acidosis (MA), low plasma bicarbonate levels, is common in late stage chronic kidney disease (CKD) with glomerular filtration rate below 30 ml/min. This may cause stunted growth in children, loss of bone and muscle mass, negative nitrogen balance, and possible acceleration of progression of renal failure [8].

The reduction in the glomerular filtration rate results in the following [12] [14]:

• Decreased production of erythropoietin and anemia.
• Decreased production of vitamin D [6], hypocalcemia, secondary hyperparathyroidism, and loss of bone density.
• Reduction in excretion of acids, potassium, salts, and water, resulting in acidosis, hyperkalemia, hypertension, and edema.
• Platelet dysfunction and increased bleeding.

All organ systems are affected by the accumulation of uremic toxins. These toxins include blood urea nitrogen, creatinine, phenols, and guanidines [16].

Hypertension itself can cause damage in the glomeruli and tubules of the kidney [13]. More than half the patients with malignant hypertension have an underlying renal cause [13].

Most glomerular diseases due to infection involve an antigen-antibody reaction in the circulation and glomerulus [3] [12]. Immune complements are part of the body’s immune system aiding in the body’s defense against microbial infection [16]. When these regulatory mechanisms are not functional, complements may attack host tissues such as renal basement membrane proteins [16]. The immune complexes activate white blood cell production and leukocytes and platelets accumulate in the glomerulus [12] [14]. The result is complement-mediated inflammatory injury to the kidneys [16].

Prevention of acute glomerulonephritis is not generally possible because the triggering factors are often unknown. However, the prevention of infections, especially beta hemolytic streptococcal infections, and their early treatment can be helpful in preventing the disease.

Early detection, long-term monitoring, and aggressive supportive treatment may prevent the progression of the disorder the chronic form of the disease and end-stage renal disease [14].

Glomerulonephritis refers to a group of renal diseases caused by inflammation of glomerular tissue [1] [16]. It results in damage to the basement membrane and capillary endothelium causing abnormal renal filtration, altered blood flow, and vascular obstruction within the kidney. Glomerulonephritis is one of the most common causes of chronic kidney disease and end-stage renal disease worldwide [13] [16].

Presenting symptoms of glomerulonephritis depend on the specific etiology and include back pain, hematuria, proteinuria and eventually oliguria or anuria [1]. Glomerulonephritis may be accompanied by hypertension, edema, azotemia, decreased glomerular filtration rate, and sodium and water retention [1] [13].

Glomerulonephritis can be due to primary renal disease or systemic disease. Acute post-streptococcal glomerulonephritis is the most common form of the acute form of the disease [1].

Treatment for glomerulonephritis is primarily supportive. There is no specific treatment for this renal disease. Any underlying infections or chronic diseases must be treated first [1].

What is glomerulonephritis?

Glomerulonephritis is a disorder of the kidney resulting from inflammation of the glomerulus, the cluster of small blood vessels, responsible for the filtration function of this organ. The inflammation may be the result of a variety of factors such as infections, injury, and systemic inflammatory diseases.

What are the symptoms?

The symptoms of glomerulonephritis include:

• Hematuria (blood in the urine)
• Proteinuria (protein in the urine)
• Decreased or no urine output
• Edema or swelling of feet and legs or around the eyes
• Headache
• New onset high blood pressure
• Shortness of breath with activity
• Pain in kidney area, on side between hip and rib cage
• Weight gain
• Loss of appetite

What causes glomerulonephritis?

The causes of glomerulonephritis are often not known, however, anything that causes inflammation within the kidney may cause this disorder. They can be divided into infectious and non-infectious triggers. The most common cause of glomerulonephritis has been the body’s response to infection with beta-hemolytic streptococci. The incidence of this infection and its complication has been reduced with more aggressive detection and treatment of the disease. Other bacterial, viral, and fungal infections may trigger glomerulonephritis. Non-infectious triggers of glomerulonephritis include trauma to the kidney, chronic disease (cardiovascular disease, diabetes), and systemic inflammatory diseases (lupus, vasculitis). 

Who gets glomerulonephritis?

Anyone, at any age can get glomerulonephritis. Post-infectious glomerulonephritis occurs more often in children. The form due to chronic disease is most common in older adults. The disorder occurs almost twice as often in men as in women.

How is it diagnosed?

Glomerulonephritis is suspected initially by its symptoms of hematuria, proteinuria, and facial or pedal edema. Diagnosis is made by the presence of red blood cells in the urine. Determination of the cause may be made by further tests such as testing for antibodies to streptococci bacteria and a work-up for systemic inflammatory diseases and chronic disease.
The progress of the disease may be followed by monitoring kidney function and the extent of hypertension.

How is glomerulonephritis treated?

There is no specific treatment for glomerulonephritis. Treatment is primarily supportive to prevent kidney damage and the complications of the disorder. Supportive treatments include:

• Monitoring and control of hypertension
• Treatment of underlying infections, systemic and chronic conditions
• Anti-inflammatory medications
• Monitoring of kidney function

What are the complications?

Complications of glomerular nephritis include:

• Permanent kidney damage
• Kidney failure
• Pulmonary edema
• Malignant hypertension
• Damage to blood vessels, cerebral and cardio
• Hypertensive retinopathy
• Hypertensive cerebral damage

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