6/8 UWorld Flashcards
Where are immune complex depositions in Post-strep glomerulonephritis
Type 3 HSR
Immune complex deposition sub-epithelially
Where are immune complex depositions in IgA nephropathy
Aka Berger disease (Henoch Schonlein purpura)
IgA immune complex deposits in mesangium
What is the cause of Alport syndrome
- Due to defect in Type IV collagen (basement membrane)
- Leads to splitting of the basement membrane longitudinally
Presentation of Alport syndrome
Presents as isolated hematuria, sensory hearing loss, and ocular disturbances
“Can’t see, can’t pee, can’t hear high C”
Where are immune complex depositions seen in diffuse proliferative glomerulonephritis
DPGN seen in Lupus
Immune complexes seen subendothelially and within the mesangium
Describe light microscopy of lupus nephritis (DPGN)
- Light microscopy – deposits make basement membrane look thick – “wire looping” of capillaries
- THINK: wire lupus
Describe the mechanism behind the following in nephrotic syndrome:
- Edema
- Increased risk of infection
- Increased risk of thrombosis
- Hyperlipidemia
- Proteinuria > 3.5 g/day
- Hypoalbuminemia – protein lost in urine
- Edema – decreased oncotic pressure due to hypoalbuminemia
- Increased risk of infection – loss of immunoglobulin in urine
- Increased risk of thrombosis – loss of antithrombin III
- Hyperlipidemia – liver tries to make more lipoproteins in order to make up for decreased oncotic pressure
What are the types of nephritic syndrome
Post-strep glomerulonephritis
Alport Syndrome
IgA Nephropathy
Diffuse proliferative glomerulonephritis
What are the types of nephrotic syndrome
Foot process effacement: Minimal change disease, focal segmental glomerulosclerosis
Immune deposition: Membranous nephropathy, Membranoproliferative glomerulonephritis
Other: Diabetes, Amyloidosis
What is a trigger for minimal change disease
- Triggered by infections or immunizations
- Most common cause of nephrotic syndrome in children
Where are the immune complex deposits in membranous nephropathy
subepithelial
- H&E – thickening of basement membrane
- EM – “spike and dome” appearance with subepithelial deposits (IgG and C3)
- IF – granular
Describe biopsy of Diabetic nephropathy
- Will show sclerosing of the mesangium with Kimmelstie-Wilson nodules (round acellular nodules)
Where in the glomerulus will you find amyloid depositis in Amyloid nephropathy
In the mesangium
What type of stone is a struvite stone?
Ammonium magnesium phosphate stone
- Major risk factor = Urease + bacteria
- Recall:
- Urea is broken down by urease into NH3 and CO2
- NH3 converted to NH4+ which can combine with magnesium and phosphate
What is the other symptom associated with Henoch Schonlein purpura other than palpable purpura and IgA nephropathy
Arthralgias
What are the radioopaque (seen in XR) vs. radiolucent kidney stones
Radiopaque = calcium and struvite
Radiolucent = uric acid and cystine
Describe histology of renal cell carcinoma
- Will see polygonal clear cells filled with accumulated lipids and carbohydrates
Horomones secreted by RCC
- Hormones secreted by renal cell carcinoma:
- Erythropoietin - polycythemia
- ACTH - Cushing
- PTH-related peptide - Hypercalcemia
- Prolactin - hypogonadism, decreased libido, galactorrhea
What is WAGR complex
- Wilms tumor, Aniridia (absence of iris), Genitourinary malformation, mental/motor Retardation
What disease is associated with thyroidization of the kidney
- Chronic pyelonephritis
- Eosinophilic casts dilate the tubules, causing the tubules to have a colloid/thyroid-like appearance
What disease is associated with eosinophils in urine
- Acute interstitial nephritis
- Acute interstitial renal inflammation that results in acute renal failure
- Presentation:
- Fever, rash, eosinophilia, azotemia
Describe BUN/Cr and FENa in pre-renal, intrinsic, and post-renal azotemia
- (1) Pre-renal azotemia:
- BUN/Creatinine > 20
- BUN is reabsorbed, creatinine is not
- FENa (fractional excretion of sodium) < 1%
- Tubular function intact so Na+ can still be reabsorbed
- BUN/Creatinine > 20
- (2) Intrinsic renal failure:
- BUN/Creatinine < 15
- Tubular dysfunction = decreased reabsorption of BUN
- FENa > 2%
- Tubular dysfunction = decreased reabsorption of Na+
- BUN/Creatinine < 15
- (3) Post-renal azotemia:
- Early stage
- BUN/Cr > 20
- FENa < 1%
- Late stage - tubular damage occurs
- BUN/Cr < 15
- FENa > 2%
- Early stage
Consequences of chronic renal failure
- Inability to produce urine = water retention:
- Peripheral edema, heart failure, pulmonary edema, HTN
- Hyperkalemia (due to decreased renal excretion)
- Metabolic acidosis
- Uremia
- Anemia (decreased erythropoietin production)
- Hypocalcemia (due to decreased Vitamin D active form)
- Renal osteodystrophy (due to decreased Vitamin D active form)
