GLOMERULONEPHRITIS   47A

A 61-year-old woman presents to the emergency department with 3 days of shortness of breath and lower extremity swelling. She has been previously healthy with no history of heart disease. Two weeks ago, she had been treated in the hospital for pneumonia and group A streptococcus bacteremia, from which she recovered. On physical examination now, her blood pressure is 170/100 mm Hg, and she has crackles in both lower lung fields, a normal cardiac examination, and 2+ pitting edema of both lower extremities. Urinalysis shows mild proteinuria and hematuria, with many dysmorphic red blood cells (RBCs) with some RBC casts. An echocardiogram shows normal systolic function.

What are the salient features of this patient’s problem? How do you think through her problem?

Salient features: Lower extremity edema and volume overload; hypertension; mild proteinuria, hematuria and RBC casts; normal cardiac function; recent streptococcal infection suggesting possible postinfectious glomerulonephritis (GN)

How to think through: When a patient presents with new edema, it is important to consider causes other than heart failure. Fortunately, the clinician here obtained a urinalysis looking for both hematuria and proteinuria. Given the abnormal result, microscopic evaluation of urine sediment, preferably by a nephrologist, should follow. What is the most serious cause of a case such as this? (Rapidly progressive glomerulonephritis [RPGN], one cause of which is poststreptococcal glomerulonephritis [GN].) What laboratory studies help define the cause of RPGN? (Serum complement levels, ASO titer, anti-GBM antibody, antinuclear antibody [ANA] titer, antineutrophil cytoplasmic antibody [ANCA], cryoglobulins, hepatitis B surface antigen, hepatitis C antibody.) Complement levels help narrow the differential diagnosis of RPGN. Postinfectious GN, lupus nephritis, and cryoglobulinemia all consume complement by forming immune complexes. By contrast, normal complement levels are found in ANCA-associated (“pauci-immune”), anti-GBM (Goodpasture syndrome), and IgA nephropathies. Renal biopsy will demonstrate characteristic light microscopy, immunofluorescence, and electron microscopy findings but is not always performed in patients with recent streptococcal infection. However, in this severe case, it could be considered if it would change treatment. Other causes of RPGN are treated with corticosteroids or other immunosuppressive medications or, in the case of mixed cryoglobulinemia, plasmapheresis.

GLOMERULONEPHRITIS   47B

What are the essentials of diagnosis and general considerations regarding glomerulonephritis?

Essentials of Diagnosis

Hematuria, dysmorphic red cells, RBC casts, and mild proteinuria

Acute renal insufficiency, dependent edema, and hypertension

General Considerations

Postinfectious GN commonly appears 1 to 3 weeks after pharyngitis or impetigo.

Pauci-immune necrotizing GN is caused by granulomatosis with polyangiitis (formerly Wegener granulomatosis), microscopic polyangiitis, or Churg-Strauss syndrome.

Membranoproliferative GN is an idiopathic renal disease that usually presents with nephritic features ranging from asymptomatic glomerular hematuria and proteinuria to episodes of gross hematuria to the acute nephritic syndrome.

Essential (mixed) cryoglobulinemia is associated with cold-precipitable immunoglobulins (cryoglobulins) precipitating in glomerular capillaries.

Rapidly progressive acute GN requires rapid identification and treatment.

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