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Key Clinical Updates in Nephritic Spectrum Glomerular Diseases

Prior trials suggested that corticosteroids reduced proteinuria when administered to patients with GFR > 50 mL/min/1.73 m2 and persistent proteinuria > 1 g. However, more recent data failed to demonstrate slowing of GFR loss with corticosteroid therapy compared with use of ACE inhibitor or ARB alone; enthusiasm for glucocorticoid therapy therefore has waned.

Trials using the complement inhibitor avacopan in place of glucocorticoids in cyclophosphamide- or rituximab-based regimens are ongoing and appear promising.


  • 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 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

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

B. Laboratory Findings

1. Serologic testing

Serologic tests based on the history and physical examination help narrow the differential diagnosis. These tests may include C3 and C4 complement levels, antinuclear antibodies, cryoglobulins, hepatitis serologies, serum and urine protein electrophoreses, serum free light chains, ANCAs, anti-GBM antibodies, and antistreptolysin O (ASO) titers (Figure 22–5).

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 range (less than 3 g/day).

3. Biopsy

Definitive diagnosis of the underlying glomerular disease cannot be made without a kidney biopsy. Candidates for biopsy are patients for whom test results would influence management; exceptions include those with ...

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