Glomerulopathies

Glomerulopathies is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

  • Classically, the presentation of glomerular diseases have been described as existing on a continuum with the nephrotic syndrome on one end, characterized by proteinuria >3.5 g/d and accompanied by hypoalbuminemia, hyperlipidemia, and edema, and the nephritic syndrome on the other end, characterized by hematuria, hypertension, edema, and renal insufficiency. However, disease entities typically present somewhere in between with overlapping features. Specific disease do present with a tendency to feature one syndrome over the other, related to the predominant site of glomerular injury.
  • Nephrotic diseases typically show injury along the filtration barrier, with thickening of the glomerular basement membrane (GBM) or fusion of the podocyte foot processes. By comparison, nephritic diseases generally show varying degrees of mesangial cell proliferation and mesangial deposition and, with more aggressive disease, may reveal crescent formation.
  • When a glomerular process is suspected, it may be useful to check antinuclear antibodies (ANA), complement levels (C3, C4), cryoglobulins, and viral (HIV, hepatitis B and C) serologies. A serum protein electrophoresis (SPEP) and urine immunofixation can be performed in proteinuric patients to evaluate for a monoclonal gammopathy and may be suspected by a large protein–albumin gap.
  • When a nephritic process is suspected by the clinical presentation, testing for anti-GBM antibodies, antineutrophil cytoplasmic antibodies (ANCA), and anti-streptolysin-O (ASO) titers may be helpful in narrowing the differential diagnosis.
  • Nephrotic diseases are more likely to be minimal change disease (MCD), membranous nephropathy (MN), focal segmental glomerulosclerosis (FSGS), diabetic nephropathy (DN), and deposition dysproteinemias.
  • Nephritic syndromes are more likely to be membranoproliferative glomerulonephropathy (MPGN), IgA nephropathy/Henoch–Schönlein purpura, postinfectious glomerulonephritis, lupus nephritis (LN), anti-GBM disease, and granulomatosis with polyangiitis.

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General Principles

  • Classically, the presentation of glomerular diseases have been described as existing on a continuum with the nephrotic syndrome on one end, characterized by proteinuria >3.5 g/d and accompanied by hypoalbuminemia, hyperlipidemia, and edema, and the nephritic syndrome on the other end, characterized by hematuria, hypertension, edema, and renal insufficiency. However, disease entities typically present somewhere in between with overlapping features. Specific disease do present with a tendency to feature one syndrome over the other, related to the predominant site of glomerular injury.
  • Nephrotic diseases typically show injury along the filtration barrier, with thickening of the glomerular basement membrane (GBM) or fusion of the podocyte foot processes. By comparison, nephritic diseases generally show varying degrees of mesangial cell proliferation and mesangial deposition and, with more aggressive disease, may reveal crescent formation.
  • When a glomerular process is suspected, it may be useful to check antinuclear antibodies (ANA), complement levels (C3, C4), cryoglobulins, and viral (HIV, hepatitis B and C) serologies. A serum protein electrophoresis (SPEP) and urine immunofixation can be performed in proteinuric patients to evaluate for a monoclonal gammopathy and may be suspected by a large protein–albumin gap.
  • When a nephritic process is suspected by the clinical presentation, testing for anti-GBM antibodies, antineutrophil cytoplasmic antibodies (ANCA), and anti-streptolysin-O (ASO) titers may be helpful in narrowing the differential diagnosis.
  • Nephrotic diseases are more likely to be minimal change disease (MCD), membranous nephropathy (MN), focal segmental glomerulosclerosis (FSGS), diabetic nephropathy (DN), and deposition dysproteinemias.
  • Nephritic syndromes are more likely to be membranoproliferative glomerulonephropathy (MPGN), IgA nephropathy/Henoch–Schönlein purpura, postinfectious glomerulonephritis, lupus nephritis (LN), anti-GBM disease, and granulomatosis with polyangiitis.

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