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ESSENTIALS OF DIAGNOSIS

ESSENTIALS OF DIAGNOSIS

  • Mild cases: Asymptomatic glomerular hematuria

    • –Hematuria with dysmorphic RBCs

    • –Proteinuria typically < 1 g/day

  • More severe cases: nephritic syndrome

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

    • –Proteinuria typically 1–3.5 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 typically 1–3.5 g/day

    • –Systemic symptoms

General Considerations

“Glomerulonephritis” is a term given to nephritic diseases and usually signifies an inflammatory process causing kidney dysfunction. Glomerulonephritis is further classified according to one of five subtypes: immune-complex (eg, lupus nephritis), pauci-immune, anti-GBM, C3 glomerulopathy, or monoclonal immunoglobulin–mediated. Presentation may be acute (developing over days to weeks), with or without resolution, or may be chronic and indolent with progressive scarring. As noted above, nephritic diseases may present with glomerular hematuria and proteinuria, with nephritic syndrome, or with RPGN.

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 (“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 include C3 and C4 complement levels, ANA, cryoglobulins, hepatitis serologies, serum/urine protein electrophoreses and immunofixation, serum free light chains, ANCAs, anti-GBM antibodies, and anti-pathogen antibodies (eg, antistreptolysin O titers) (Table 24–8).

2. UA

The urine dipstick is positive for protein and blood. Urinary microscopy reveals RBCs that are 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 3.5 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 or inform prognosis; 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. Contraindications include a bleeding diathesis, thrombocytopenia, and uncontrolled hypertension.

Treatment

General measures include treatment of hypertension and 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 ...

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