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Glomerulonephritis (GN) is not a specific disease, but rather an inflammatory state within the renal glomerulus. This inflammation causes glomerular injury and results in impaired glomerular filtration with subsequent abnormal urinary sediment and possibly decreased renal function. It is often associated with edema and hypertension. Clinically, GN spans a wide spectrum of disease from a fairly benign, self-limited condition to an aggressive systemic disease that can lead to rapid loss of renal function. This chapter focuses on the four common presentations of GN that are most likely to be found in hospitalized patients: asymptomatic hematuria, acute GN, rapidly progressive GN (RPGN), and chronic GN.


The causative mechanism of glomerulonephritis is not entirely understood, but scientific literature supports an immunologic mechanism as the pathogenesis of glomerular inflammation.1 The triggering of an autoimmune rather than the direct immune response to foreign antigens is likely responsible.2,3 Humeral and cellular mediated responses as well as a variety of host factors play a role in the development of glomerulonephritis.3



Asymptomatic hematuria can be either microscopic or macroscopic and is not associated with hypertension, impaired renal function, or proteinuria. Asymptomatic isolated microscopic hematuria, defined as hematuria unaccompanied by proteinuria or pyuria, can be the result of many different conditions other than GN such as fever, gastrointestinal disturbances, and bladder catheterization. Because this presentation may frequently be misdiagnosed as a urinary tract infection, urine culture is imperative. In cases of asymptomatic isolated microscopic hematuria, experts recommend at least two of three urinalyses show microhematuria over 2 to 3 weeks before further evaluation is performed.4 Outpatient follow-up is appropriate in these patients. The combination of hematuria, either microscopic or gross, and proteinuria is concerning for possible GN, and diagnostic evaluation is therefore indicated.


Acute GN is characterized by an abrupt onset of gross hematuria, azotemia, and hypertension. Proteinuria is common, although it is rarely within the nephrotic range (nephrotic range is >40 mg urinary protein/m2/hr or a urinary protein/creatinine ratio >2.0). Edema is also common and is usually due to renal sodium retention secondary to an abrupt decrease in renal function, not from hypoalbuminemia. Post-infectious glomerulonephritis (PIGN) is caused by an immunologic response of the kidney to infection.5 It is the most common cause of acute GN, but rates of PIGN are declining in most industrialized countries.5 Post-streptococcal glomerulonephritis (PSGN) is a common form of PIGN. In its classic form, there is a sudden onset of painless gross hematuria (often described as “tea colored”) 14 to 21 days after a streptococcal infection. Only nephritogenic streptococcal infections cause PSGN, and host and microbial factors determine susceptibility.6

PIGN occurs most frequently in children between 4 and 10 years of age. Physical examination often reveals pallor, mild ...

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