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  • Asymptomatic glomerular hematuria

    • –Hematuria with dysmorphic RBCs

    • –Proteinuria < 1 g/day

  • Nephritic syndrome in more severe cases

    • –Glomerular hematuria (and RBC casts if glomerular bleeding is heavy)

    • –Proteinuria of 1–3 g/day

    • –Hypertension

    • –Edema

    • –Rising creatinine over days to months

  • Rapidly progressive glomerulonephritis in most severe cases

    • –AKI with rising creatinine over days to months

    • –Glomerular hematuria (and RBC casts)

    • –Proteinuria of 1–3 g/day

    • –Systemic symptoms

    • –Hypertension and edema uncommon

General Considerations

“Glomerulonephritis” is a term given to those diseases that present in the nephritic spectrum and usually signifies an inflammatory process causing renal dysfunction. It can be acute, developing over days to weeks, with or without resolution, or may be more chronic and indolent with progressive scarring. As noted above, diseases that cause a nephritic spectrum presentation may present with glomerular hematuria and proteinuria, with nephritic syndrome, or with RPGN (Figure 22–4). The presentation depends on the severity of the underlying inflammation and the pattern of injury caused by the disease process.

Clinical Findings

A. Symptoms and Signs

If the nephritic syndrome is present, the acute decrease in GFR leads to sodium retention. This is clinically manifested by edema, first seen in regions of low tissue pressure such as the periorbital and scrotal areas, and by hypertension. Heavy glomerular bleeding from inflammation may result in gross hematuria (smoky or cola-colored urine).

B. Laboratory Findings

1. Serologic testing

Serologic tests, including complement levels, antinuclear antibodies, cryoglobulins, hepatitis serologies, ANCAs, anti-GBM antibodies, and antistreptolysin O (ASO) titers (Figure 22–5) based on the history and physical examination help narrow the differential diagnosis of the nephritic spectrum disorder.

2. Urinalysis

The urine dipstick is positive for protein and blood. Urinary microscopy reveals red blood cells that are misshapen or dysmorphic from traversing a damaged glomerular filtration barrier. Red blood cell casts are seen with heavy glomerular bleeding and tubular stasis. When quantified, proteinuria is usually subnephrotic (less than 3 g/day).

3. Biopsy

Kidney biopsy should be considered if there are no contraindications (eg, bleeding disorders, thrombocytopenia, uncontrolled hypertension). Important morphologic information is gleaned from light, electron, and immunofluorescent microscopy.


General measures for all include treatment of hypertension and of fluid overload if present. Antiproteinuric therapy with an ACE inhibitor or ARB should be considered for those without AKI. For those with profound AKI, dialysis may be needed. The inflammatory glomerular injury may require immunosuppressive agents (see specific diseases discussed below).

When to Refer

Any patient in whom a glomerulonephritis is suspected should be referred to a nephrologist.

When to Admit


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