Pathology Flashcards
Significance of casts in urine
Indicates hematuria/pyuria is of glomerular or renal tubular in origin
Type of casts seen in glomerulonephritis and malignant HTN
RBC casts
Type of casts seen in tubulointerstitial inflammation
WBC casts
Type of casts seen in acute pyelonephritis
WBC casts
Type of casts seen in transplant rejection
WBC casts
Type of casts seen in nephrotic syndrome
Fatty casts (oval fat bodies)
Type of casts seen in acute tubular necrosis
Granular, muddy brown casts
Type of casts seen in end-stage renal disease or chronic renal failure
Waxy casts
Significance of hyaline casts
Non-specific normal finding seen in concentrated urine
Mechanism of nephrotic syndrome
Podocyte disruption leads to charge barrier impairment
Findings in nephrotic syndrome
Proteinuria > 3.5 g/day Hypoalbuminemia Hyperlipidemia Edema Fatty casts in urine (oval fat bodies)
Mechanism of nephritic syndrome
GBM disruption
Findings in nephritic syndrome
HTN Proteinuria < 3.5 g/day BUN and Creatine increased Oliguria Hematuria RBC casts in urine
LM findings in PSGN
Enlarged hypercellular glomeruli
IF findings in PSGN
“Starry sky”, granular appearance and “lumpy-bumpy”
Type of deposits seen in PSGN
IgG, IgM and C3 deposits along GBM and mesangium
EM findings in PSGN
Subepithelial immune complex humps (look like camel humps)
Type III hypersensitivity reaction seen in children after group A strep infection affecting glomerulus presenting with peripheral and periorbital edema, coca-colored urine and hypertension
Post-Streptococcal Glomerulonephritis (PSGN)
Which plasma protein is deficient in PSGN
C3
LM and IF show crescent moon shape consisting of fibrin and C3b proteins with glomerular parietal cells, monocytes and macrophages with doubling of creatinine in < 3 months
Rapidly progressive glomerulonephritis (RPGN)
Treatment for PSGN
Supportive
Type II hypersensitivity reaction affecting glomerulus presenting with hematuria and pulmonary symptoms with doubling of creatinine in < 3 months
Goodpasture syndrome
IF findings in Goodpasture RPGN
Linear pattern of antibodies to GBM
Type II hypersensitivity reaction affecting glomerulus presenting with hematuria, sinus symptoms, PR3-ANCA/c-ANCA positive with doubling of creatinine in < 3 months
Granulomatosis with polyangiitis (Wegener)
Type II hypersensitivity reaction affecting glomerulus presenting with hematuria and MPO-ANCA/p-ANCA positive with doubling of creatinine in < 3 months
Microscopic polyangiitis
Presents with malar rash and has nephrotic and nephritic symptoms
Diffuse proliferative glomerulonephritis
LM findings in diffuse proliferative glomerulonephritis
Wire looping of capillaries
EM findings in diffuse proliferative glomerulonephritis
Subendothelial and/or intramembranous IgG-C3 immune complex deposits
IF findings in diffuse proliferative glomerulonephritis
Granular pattern
Glomerular disease presenting with episodic gross hematuria with RBC casts after respiratory or GI tract infection
IgA nephropathy
LM findings in IgA nephropathy
Mesangial proliferation
EM findings in IgA nephropathy
Mesangial immune complex deposits
IF findings in IgA nephropathy
IgA-based immune complex deposits in mesangium
Glomerular disease presents with sensory hearing loss, ocular disturbances and hematuria with basket-weave appearance on EM
Alport syndrome
Inheritance pattern of Alport syndrome
X-linked dominant
Mutation in Alport syndrome
Type IV collagen causing thinning and splitting of GBM
Hepatitis B patient presents with hematuria and has subendothelial immune complex deposits with granular IF - diagnosis
Membranoproliferative glomerulonephritis type I
Description of PAS stain and H and E stain findings
Tram-track appearance due to GBM splitting from mesangial ingrowth
Glomerular disease presents with decreased C3 levels and granular IF from immune complex deposition
Membranoproliferative glomerulonephritis type II
Mechanism of decreased C3 levels in membranoproliferative glomerulonephritis
IgG antibody stabilizes C3 convertase leading to persistent compliment activation
LM findings in minimal change disease
Normal glomeruli
IF findings in minimal change disease
No findings
EM findings in minimal change disease
Effacement of foot processes
Most common nephrotic syndrome in children
Minimal change disease
Malignancy associated with minimal change disease
Hodgkin lymphoma
Mechanism of glomerular damage in Hodgkin lymphoma
Increases cytokines damaging epithelial cells
Treatment for minimal change disease
NSAIDs
LM findings in focal segmental glomerulonephritis
Segmental necrosis and hyalinosis
IF findings in focal segmental glomerulonephritis
Often negative but may have IgM, C3, C1 deposits
EM findings in focal segmental glomerulonephritis
Effacement of foot processes
Most common cause of nephrotic syndrome in African Americans and Hispanics
FSGS
Consequence of FSGS
Chronic renal failure if fails to respond to steroids
Common secondary causes of FSGS
HIV infection, sickle cell disease, heroin abuse
LM findings in membranous nephropathy
Diffuse capillary and GBM thickening
Nephrotic presentation of SLE
Membranous nephropathy
IF findings in membranous nephropathy
Granular as a result of immune complex deposition
EM findings in membranous nephropathy
Spike and dome appearance with subepithelial deposits
Most common cause of primary nephrotic syndrome in Caucasian adults that may progress to chronic renal failure
Membranous nephropathy
Common secondary causes of membranous nephropathy
NSAIDs, gold, penicillamine, HBV, HCV, SLE or solid tumors
Kidney is most commonly affected kidney and presents with Congo red stain showing apple-green birefringement under polarized light
Amyloidosis
Type of deposits seen in amyloidosis
Amyloid deposits in the mesangium
Disease presents with mesangial expansion, GBM thickening and eosinophilic nodular glomerulosclerosis and is the most common cause of end-stage renal disease in the U.S.
Diabetic glomerulonephritis
Mechanism of GBM thickening in diabetic glomerulonephritis
Non-enzymatic glycosylation of GBM causes increased permeability and thickening
Mechanism of hyaline arteriosclerosis in diabetic glomerulonephritis
Non-enzymatic glycosylation of efferent arterioles increases GFR causing mesangial expansion
How do ACE inhibitors affect diabetic glomerulonephritis
Slow progression of disease
Most common kidney stone with hypercalciuria and normocalcemia
Calcium oxalate stone
Treatment for calcium oxalate stones
Thiazides, citrate and low-sodium diet
Best option for treating and preventing kidney stones
Encourage fluid intake
Type of stone with increased pH and radiopaque on X-ray and CT that is wedge-shaped prism
Calcium phosphate stone
Treatment for Calcium phosphate stone
Low sodium diet and thiazides
Organisms implicated in ammonium magnesium phosphate (AMP) stones
Proteus, Staph saprophyticus, Klebsiella
Findings in AMP stones
Increased pH, radiopaque on X-ray and CT with coffin lid-shaped stones
Treatment for AMP stones
Treat underlying infection and surgical removal of stones
Radiolucent stone on X-ray with decreased pH with hyperuricemia
Uric acid stone
Treatment for uric acid stones
alkalinization of urine, allopurinol and hydration
Hexagonal-shaped radiolucent stone on X-ray
Cystine stone
Mechanism of cystine stone formation
Cystine-reabsorbing PCT transporter loses function causing cystinuria
Most common seen in children with poor reabsorption of cystine, ornithine, lysine, arginine and autosomal recessive
Cystinuria which causes cystine stones
Treatment for cystinuria
Low sodium diet, alkalinization of urine, chelating agents and hydration
Distention or dilation of renal pelvis and calyces caused by urinary obstruction, retroperitoneal fibrosis, or vesicoureteral reflux
Hydronephrosis
Area of dilation in hydronephrosis
Proximal to site of obstruction
Conditions in hydronephrosis that elevate creatinine levels
Bilateral obstruction or having only one kidney
Complications of hydronephrosis
Compression and possible atrophy of renal cortex and medulla
Conditions like renal stones, severe BPH, cervical cancer and injury to ureters can lead to what disease
Hydronephrosis
Malignancy presenting with polygonal clear cells filled with lipids and carbohydrates with golden-yellow due to increased lipid content
Renal cell carcinoma (RCC)
Population RCC most commonly affects
50 - 70 year old men
Risk factors that increase RCC
Obesity and smoking