NP23 Nephrology

Parenchymal Kidney Diseases

Essential Med Notes 2015

Clinical/Lab Features
fibrous crescents typically present on renal histopathology
RBC casts and/or dysmorphic RBCs in urine
classified by immunofluorescence staining
Type I: Anti-GBM mediated (15% of cases)
Type II: Immune Complex Mediated (24% of cases)
Type III: Non-Immune Mediated (60% of cases)
Type IV: Double Antibody Positive
treatment: underlying cause for postinfectious; corticosteroids + cyclophosphamide or other
cytotoxic agent + plasmaphoresis in select cases
prognosis: 50% recovery with early treatment, depends on underlying cause
3. NEPHROTIC SYNDROME
Clinical/Lab Features
heavy proteinuria (>3.5 g/1.73m2/d)
hypoalbuminemia
edema
hyperlipidemia (elevated LDL cholesterol), lipiduria (fatty casts and oval fat bodies on
microscopy)
hypercoagulable state (due to antithrombin III, Protein C, and Protein S urinary losses)
patient may report frothy urine
glomerular pathology on renal biopsy
minimal change disease (or minimal lesion disease or nil disease) e.g. glomeruli appear
normal on light microscopy
membranous glomerulopathy
focal segmental glomerulosclerosis (FSGS)
membranoproliferative GN
nodular glomerulosclerosis
each can be idiopathic or secondary to a systemic disease or drug (sirolimus can cause
proteinuria without obvious glomerular pathology)
Table 10. Nephrotic Syndrome
Minimal
Change

Membranous
Glomerulopathy

Focal Segmental
Membranoproliferative
Glomerulosclerosis Glomerulonephritis

Nodular
Glomerulosclerosis

Secondary
Causes

Hodgkins
lymphoma

HBV, SLE, solid

tumors (lung,
breast, GI)

Reflux nephropathy,
HIV, HBV, obesity

HCV, malaria, SLE, leukemia,

lymphoma, infected shunt

DM, amyloidosis

Drug Causes

NSAIDs

Gold, penicillamine Heroin

Therapy

Steroids

Reduce BP, ACEI,

steroids

Aspirin, ACEI, dipyridamole

(Persantine) controversial

Treat underlying
cause

Steroids, ACEI/ARB
for proteinuria

4. END STAGE RENAL DISEASE

refer to section End Stage Renal Disease, NP35
INVESTIGATIONS FOR GLOMERULAR DISEASE
blood work
first presentation: electrolytes, Cr, urea, albumin, fasting lipids
determining etiology: CBC, ESR, serum immunoelectrophoresis, anti-GBM, C3, C4, ANA,
p-ANCA, c-ANCA, cryoglobulins, HBV and HCV serology, ASOT (anti-streptolysin titres),
VDRL, HIV
urinalysis: RBCs, WBCs, casts, protein
24 h urine for protein and CrCl
radiology
CXR (infiltrates, CHF, pleural effusion)
renal U/S
renal biopsy (percutaneous or open) if heavy proteinuria or renal insufficiency and cause is not
obviously diabetic nephropathy
urine immunoelectrophoresis
for Bence-Jones protein if proteinuria present
SECONDARY CAUSES OF GLOMERULAR DISEASE
Amyloidosis
nodular deposits of amyloid in mesangium, usually related to amyloid light chain (AL)
presents as nephrotic range proteinuria with progressive renal insufficiency
can be primary or secondary
secondary causes: multiple myeloma, TB, rheumatoid arthritis, malignancy

Presentation of Nephrotic Syndrome

HELP
Hypoalbuminemia
Edema
Lipid abnormalities
Proteinuria