10-07-2007, 03:46 PM
Take home points:
1. Don™t freak out when you have a patient with possible glomerulonephritis “ the differential diagnosis can
be straightforward if you use a systematic approach.
2. The ddx of intrinsic renal disease is: glomerular, tubular, interstitial, or vascular
3. Glomerulonephritis presents with an active sediment (RBC, protein) and
nephrotic syndrome presents
with a bland sediment (heavy protein, otherwise negative U/A).
4. The serum complements is the next step in diagnosing the cause of glomerulonephritis.
Step 1: Determine the broad cause of the acute or progressive renal failure
¢ Pre-renal, intrinsic renal, or post-renal
¢ FENa (if oliguric “ to differentiate pre-renal from ATN), U/A (to look for an active sidement),
and renal ultrasound (to rule out obstruction) can be helpful
¢ If intrinsic renal, then your differential diagnosis is:
− Glomeruli (e.g. glomerulonephritis or nephrotic syndrome or both)
− Tubules (e.g. ATN)
− Interstitium (e.g. acute interstitial nephritis (AIN))
− Vessels (e.g. atheroembolic renal disease, PAN)
Step 2: If you™ve determined it™s a glomerular cause of renal failure, differentiate a glomerulonephritis (GN) pattern from a
nephrotic syndrome pattern
¢ At this step, you must get a urinalysis, renal ultrasound, 24 hour urine protein and creatinine,
spot urine protein and creatinine (for protein:creatinine ratio)
¢ Glomerulonephritis “ look for active sediment (U/A with protein and RBCs, dysmorphic RBCs,
and/or RBC casts), 300 mg - 3.5 g/day proteinuria, HTN, edema
¢ Nephrotic syndrome “ look for anasarca, heavy proteinuria (more than 3.5 g/day), and a bland
sediment on U/A (no RBCs). Patients with true nephrotic syndrome (and not just heavy
proteinuria) will have hyperlipidemia, lipiduria, hypoalbuminemia and a hypercoagulable state
(seen most often in membranous nephropathy).
¢ Membranoproliferative glomerulonephritis (MPGN) can present as nephrotic syndrome,
glomerulonephritis or both.
Step 3: Use the serum complement levels to look help differentiate causes of GN.
¢ Normal serum complement levels indicate that the production of complement is keeping up with
consumption (normal complements doesn™t mean that complement is not involved in the
underlying disease process).
¢ Once you have the complement levels back, differentiate the GN further by looking for systemic
diseases vs. isolated renal diseases.
Low complement GN:
¢ Systemic: SLE, endocarditis, cryoglobulinemia, shunt nephritis
¢ Isolated renal: post-infectious GN, MPGN
Normal complement GN:
¢ Systemic: HSP, ANCA-associted (Wegener™s, PAN), Goodpasture™s syndrome, hypersensitivity vasculitis
¢ Isolated renal: IgA nephropathy, anti-GBM disease, RPGN
1. Don™t freak out when you have a patient with possible glomerulonephritis “ the differential diagnosis can
be straightforward if you use a systematic approach.
2. The ddx of intrinsic renal disease is: glomerular, tubular, interstitial, or vascular
3. Glomerulonephritis presents with an active sediment (RBC, protein) and
nephrotic syndrome presents
with a bland sediment (heavy protein, otherwise negative U/A).
4. The serum complements is the next step in diagnosing the cause of glomerulonephritis.
Step 1: Determine the broad cause of the acute or progressive renal failure
¢ Pre-renal, intrinsic renal, or post-renal
¢ FENa (if oliguric “ to differentiate pre-renal from ATN), U/A (to look for an active sidement),
and renal ultrasound (to rule out obstruction) can be helpful
¢ If intrinsic renal, then your differential diagnosis is:
− Glomeruli (e.g. glomerulonephritis or nephrotic syndrome or both)
− Tubules (e.g. ATN)
− Interstitium (e.g. acute interstitial nephritis (AIN))
− Vessels (e.g. atheroembolic renal disease, PAN)
Step 2: If you™ve determined it™s a glomerular cause of renal failure, differentiate a glomerulonephritis (GN) pattern from a
nephrotic syndrome pattern
¢ At this step, you must get a urinalysis, renal ultrasound, 24 hour urine protein and creatinine,
spot urine protein and creatinine (for protein:creatinine ratio)
¢ Glomerulonephritis “ look for active sediment (U/A with protein and RBCs, dysmorphic RBCs,
and/or RBC casts), 300 mg - 3.5 g/day proteinuria, HTN, edema
¢ Nephrotic syndrome “ look for anasarca, heavy proteinuria (more than 3.5 g/day), and a bland
sediment on U/A (no RBCs). Patients with true nephrotic syndrome (and not just heavy
proteinuria) will have hyperlipidemia, lipiduria, hypoalbuminemia and a hypercoagulable state
(seen most often in membranous nephropathy).
¢ Membranoproliferative glomerulonephritis (MPGN) can present as nephrotic syndrome,
glomerulonephritis or both.
Step 3: Use the serum complement levels to look help differentiate causes of GN.
¢ Normal serum complement levels indicate that the production of complement is keeping up with
consumption (normal complements doesn™t mean that complement is not involved in the
underlying disease process).
¢ Once you have the complement levels back, differentiate the GN further by looking for systemic
diseases vs. isolated renal diseases.
Low complement GN:
¢ Systemic: SLE, endocarditis, cryoglobulinemia, shunt nephritis
¢ Isolated renal: post-infectious GN, MPGN
Normal complement GN:
¢ Systemic: HSP, ANCA-associted (Wegener™s, PAN), Goodpasture™s syndrome, hypersensitivity vasculitis
¢ Isolated renal: IgA nephropathy, anti-GBM disease, RPGN