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.