Acute poststreptococcal glomerulonephritis results from the entrapment and collection of antigen-antibody complexes (produced as an immunologic mechanism in response to a group A beta-hemolytic streptococcus) in the glomerular capillary membranes, inducing inflammatory damage and impeding glomerular function. The immune complement occasionally further damages the glomerular membrane. The damaged and inflamed glomeruli lose the ability to be selectively permeable, allowing red blood cells (RBCs) and proteins to filter through as the glomerular filtration rate (GFR) falls. Uremic poisoning may result.

Renal function progressively deteriorates in 33% to 50% of adults who contract sporadic acute poststreptococcal glomerulonephritis, usually in the form of glomerulosclerosis accompanied by hypertension. The more severe the disorder, the more likely it is that complications will follow.

In most cases, acute poststreptococcal glomerulonephritis begins within 1 to 3 weeks after an untreated streptococcal infection
in the respiratory tract. The patient—or the patient’s parents—may report decreased urination, dark brown or rust-colored urine, and fatigue. The patient may also experience shortness of breath, dyspnea, and orthopnea. These symptoms of pulmonary edema point to heart failure resulting from hypervolemia.

Assessment findings may show oliguria (with output less than 400 ml/24 hours) and mild to moderate periorbital edema. Findings may also reveal mild to severe hypertension resulting from either sodium or water retention (caused by decreased GFR) or inappropriate renin release.

The elderly patient may complain of vague, nonspecific symptoms, such as nausea, malaise, and arthralgia. Auscultation reveals bilateral basilar crackles if heart failure is present.