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Key Clinical Updates in Nephritic Spectrum Glomerular Diseases

SGLT2-inhibitors may be added to standard care in the well-selected patient. Corticosteroids for reducing proteinuria and slowing progression; however, may be considered for patients with GFR greater than 30 mL/min/1.73 m2 and persistent proteinuria greater than 1 g/day despite maximal ACE inhibitor or ARB.

Cheung CK et al. J Clin Med. [PMID: 34200024]


  • Asymptomatic glomerular hematuria

    • –Hematuria with dysmorphic RBCs

    • –Proteinuria < 1 g/day

  • More severe cases: nephritic syndrome

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

    • –Proteinuria of 1–3 g/day

    • –Hypertension

    • –Edema

    • –Rising creatinine over days to months

    • Most severe cases: rapidly progressive glomerulonephritis

    • –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 diseases in the nephritic spectrum and usually signifies an inflammatory process causing renal dysfunction. It may be acute (developing over days to weeks), with or without resolution, or may be chronic and indolent with progressive scarring. As noted above, diseases within the nephritic spectrum may present with glomerular hematuria and proteinuria, with nephritic syndrome, or with RPGN (Figure 22–3).

Clinical Findings

A. Symptoms and Signs

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

B. Laboratory Findings

1. Serologic testing

Serologic tests (selected based on the history and physical examination) help narrow the differential diagnosis. These 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 antipathogen antibodies (eg, antistreprolysin O titers) (Figure 22–4).

2. UA

The urine dipstick is positive for protein and blood. Urinary microscopy reveals RBCs that are misshapen or dysmorphic from traversing a damaged glomerular filtration barrier. RBC 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 advanced underlying CKD, those who cannot adhere to medical therapy, those for whom immunosuppressive therapy is not appropriate, or those for whom the presentation is “classic” for a particular disease (eg, poststreptococcal glomerulonephritis, childhood minimal change disease, and diabetic nephropathy). The major risk of biopsy is bleeding. ...

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