Acute glomerulonephritis requires prompt diagnosis, as it can rapidly progress to permanent kidney disease if left undiagnosed. Glomerulonephritis is the third most common cause of end-stage renal disease, following diabetes mellitus and hypertension,  and is responsible for about 15% of cases of end-stage renal disease. 
The emergency physician must consider acute glomerulonephritis in the differential diagnosis for patients that present with hypertension, hematuria, proteinuria, peripheral edema, and/or acute pulmonary edema. Acute glomerulonephritis is defined as inflammation and subsequent damage of the glomeruli leading to hematuria, proteinuria, and azotemia; it may be caused by primary renal disease or systemic conditions. The glomerular filtration rate is decreased, leading to activation of the renin-aldosterone system and subsequent salt and water retention, resulting in edema and hypertension.
Most intrinsic causes of acute glomerulonephritis fall under the classification of nephritic syndromes. Nephritic syndromes are classified by hematuria, proteinuria, and red blood cell casts with hypertension and decreased urine production. Nephrotic syndromes are due to impaired filtration of the glomeruli secondary to loss of function of the electrical barrier in the basement membrane, leading to loss of protein (primarily albumin) in large amounts (>3.5 g/day). The loss of albumin results in generalized edema from the loss of oncotic pressure that typically holds the fluid within the intravascular space.
The diagnosis of acute glomerulonephritis is usually made on the basis of urinary findings, especially the presence of red blood cell casts. One of the most important tests is the complement C3 level, with hypocomplementemia being the most characteristic of poststreptococcal acute glomerulonephritis; normocomplementemia is most often seen with IgA nephropathy. 
Rapidly progressive glomerulonephritis (RPGN) can lead to a necrotizing destruction of glomeruli causing irreversible kidney damage within several months or even weeks. Proteinuria greater than 3 g/day is diagnostic for a glomerular damage. The elimination of a specific cause for a given glomerulonephritis or vasculitis, such as an infection, a malignancy or a drug-related side-effect, remains the key principle in management. 
This article concentrates on the emergency management of acute glomerulonephritis. For more detailed information, refer to Acute Glomerulonephritis.
Emergency Department Care
Patients with acute glomerulonephritis may present anywhere along a wide spectrum of chief complaints, ranging from asymptomatic hematuria to respiratory distress from acute pulmonary edema and altered mental status.
The patient may report gross hematuria, dark or tea-colored urine, or have been referred from clinic for blood found on urinalysis. Emergency department workup should initially include urinalysis to look for hemoglobin, red blood cells, markers of urinary tract infection, and cellular casts. Cystitis can cause gross or microscopic hematuria.
Treatment of the urinary tract infection with antibiotics should resolve the hematuria, but the patient must be instructed to return for follow-up urinalysis after completion of treatment. If a patient reports flank pain, nephrolithiasis should be considered as the cause of hematuria. If the urinalysis is positive for hemoglobin but no red blood cells are present, the patient may have rhabdomyolysis. The most common worldwide cause of glomerulonephritis is immunoglobulin A (IgA) nephropathy, which presents as recurrent gross or microscopic hematuria.  If the patient is otherwise well and other laboratory tests do not suggest acute kidney injury, patient may follow up for further workup of hematuria as an outpatient.
Patients with pulmonary edema from acute glomerulonephritis present in respiratory distress with hypertension. They also may have an altered mental status if they have developed hypertensive encephalopathy. The differential diagnosis for acute pulmonary edema should include acute exacerbation of heart failure, new-onset heart failure secondary to acute coronary event, and fluid overload in end-stage renal disease (ie, dialysis patients). A urinalysis must be included in the workup for these patients, because if acute glomerulonephritis is not considered, the diagnosis will be missed. Some patients may require intubation or noninvasive ventilation in cases of severe pulmonary edema.
The initial management should be tailored to treatment of hypertension with reduction of afterload (nitroglycerin) and diuresis to decrease preload (loop diuretics, such as furosemide).  If the patient has developed renal failure, electrolyte abnormalities may be present and should be corrected. Some patients may require dialysis, so early renal consultation is important.
Patients may present 1-12 weeks after pharyngitis or skin infection with edema (periorbital and facial edema is common), hypertension, dark urine, and/or decreased urine output. Poststreptococcal glomerulonephritis most commonly occurs in children aged 2-12 years, and there is a male preponderance. Antibodies are formed against the exogenous streptococcal antigen that is embedded in the glomerulus at the time of infection, and symptoms usually develop after the primary infection clears.  Most cases are subclinical and self-resolving. For further information, refer to Poststreptococcal Glomerulonephritis.
The prevalence of poststreptococcal glomerulonephritis (PSGN) is decreasing worldwide, but it is still rthe leading cause of glomerulonephritis in children. PSGN is one of a handful of nephritic disorders with hypocomplementemia, which is a decrease in C3 found in more than 90% of PSGN cases. The main sequelae of PSGN are hypertension, edema, gross hematuria, and impaired renal function and are greatest in the first 7-10 days of disease. Loop or thiazide diuretics are the most effective treatment of hypertension and edema in PSGN. 
Systemic lupus erythematous (SLE) is an important cause of kidney disease, including acute glomerulonephritis. SLE must be considered in a patient who presents with any of the following symptoms: arthralgias, malar rash, photosensitive rash, pleurisy, or oral and nasal ulcers. Additional laboratory tests that can be sent from the emergency department include antinuclear antibody level (ANA), anti–double-stranded DNA, and C3 and C4 levels in addition to urinalysis with urine protein and creatinine levels. Patients with acute glomerulonephritis secondary to SLE may require therapy with high-dose steroids; consultation with a rheumatologist is recommended. 
Henoch-Schönlein purpura (HSP) may present with purpuric rash on the legs, arthralgias, and abdominal pain. HSP is small-vessel vasculitis that most commonly presents in patients younger than 20 years. Renal involvement may not be present initially, but the likelihood increases with time and is more likely in patients with persistent rash and abdominal pain.  For further information, refer to Henoch-Schonlein Purpura
Wegener granulomatosis should be considered in any patient with nonspecific complaints, such as weight loss, malaise, arthritis, and upper and/or lower respiratory tract complaints (from sinusitis to pulmonary hemorrhage). There may be cavitating lung lesions seen on chest radiographs. Wegener granulomatosis most commonly occurs in patients in their sixth to seventh decade, with equal distribution among men and women.  Any patient suspected of Wegener granulomatosis should have blood antineutrophil cytoplasmic antibody (ANCA) levels measured. Glomerulonephritis from Wegener granulomatosis may be rapidly progressive, so prompt diagnosis is critical. For further information, refer to Vasculitis and Thrombophlebitis.
Any patient suspected of having acute glomerulonephritis should have their urinary sediment evaluated by a skilled nephrologist.  Further urine and serum studies will likely be recommended by the nephrology service to help determine etiology. Urgent nephrology consultation is required if patient requires emergent hemodialysis.
If a patient is suspected to have acute glomerulonephritis or renal disease from systemic lupus erythematous (SLE), consultation with a rheumatologist is warranted. These patients may benefit from therapy with high-dose steroids (ie, pulse therapy).
Definitive diagnosis of glomerulonephritis caused by intrinsic renal disease can only be made after biopsy has been performed. Patient suspected of having acute glomerulonephritis should be admitted for further workup and possible renal biopsy, as delay in diagnosis can lead to significant morbidity.Patients who present with hematuria only, without renal impairment, severe hypertension, fluid overload, hemoptysis, or any other concerning symptoms can be sent home with thorough follow-up instructions and close follow-up with a nephrologist.
Patients discharged from the emergency department need to be counseled on the importance of outpatient follow up with a nephrologist. Patients with edema should be advised to avoid salt and to restrict fluid intake until further workup by a nephrologist.
For patient education information, see Blood in the Urine.