DIT review - Renal 3 Flashcards
1
Q
Describe histology of renal cell carcinom
A
- Will see polygonal clear cells filled with accumulated lipids and carbohydrates
2
Q
Presentation of RCC
A
- Hematuria, palpable mass, polycythemia
3
Q
Hormones secreted by RCC
A
- Erythropoietin - polycythemia
- ACTH - Cushing
- PTH-related peptide - Hypercalcemia
- Prolactin - hypogonadism, decreased libido, galactorrhea
4
Q
Common metastasis of RCC
A
- Invades the renal vein then IVC and spreads hematogenously
- Metastasizes to lung and bone
5
Q
Describe Wilms tumor and associated genetic defect
A
- Most common renal malignancy in children aged 2-4
- Contains embryologic glomerular structures
- Loss of function mutation of tumor suppressor gene WT1 or WT2
6
Q
Presentation of Wilms tumor
A
- Hematuria, large flank mass
7
Q
Describe WAGR syndrome
A
- Wilms tumor, Aniridia (absence of iris), Genitourinary malformation, mental/motor Retardation
8
Q
Describe location and presentation of Transitional cell carcinoma
A
- Most common tumor of the urinary tract
- Can occur in renal calyces, renal pelvis, ureters, and bladder
- Painless hematuria suggests bladder cancer
9
Q
Risk factors for Transitional cell carcinoma
A
- Cyclophosphamide, Smoking, Aniline dye
10
Q
Describe presentation of acute pyelonephritis
A
- White blood cells/casts
- Presentation:
- Fever, painful urination, urgency, AMS (elderly), CVA tenderness
11
Q
Describe histology of chronic pyelonephritis
A
- Associated with thyroidization of kidney
- Eosinophilic casts dilate the tubules, causing the tubules to have a colloid/thyroid-like appearance
- WBC casts
12
Q
What is the common presentation of drug-induced (acute) interstitial nephritis
A
- Acute interstitial renal inflammation that results in acute renal failure
- Presentation:
- Fever, rash, eosinophilia in urine, azotemia
13
Q
Common causes of acute interstitial nephritis
A
- NSAIDs, Penicillin, Cephalosporin, Sulfonamides, Ciprofloxacin, Cimetidine, Allopurinol, PPIs, Indinavir, Mesalamine
- REMEMBER the P’s:
- Pee (diuretics), Pain-free (NSAIDs), Penicillin and Cephalosporins, PPIs, rifamPin
14
Q
Describe diffuse cortical necrosis and its cause
A
- Acute generalized cortical infarction of both kidneys
- Likely due to a combination of vasospasm and DIC
- Multiorgan failure
- ARDS
- DIC
- Septic shock
15
Q
Describe acute tubular necrosis and its causes
A
- Injury and necrosis of tubular epithelial cells that line the renal tubules
- Necrotic cells plug the tubules and obstruction leads to decreased GFR
- Will see granular “muddy brown” casts
- Most common cause of acute kidney injury in hospitalized patients
- Causes:
- Ischemia
- Decreased renal blood flow (hypotension, shock, sepsis, hemorrhage, heart failure)
- Nephrotoxic injury
- Drugs: aminoglycosides, cephalosporins, polymyxins
- Radiograph contrast dye – prevent with fluids
- Rhabdomyolysis/myoglobinura
- Muscle breakdown (seizure disorder, cocaine, crush injury) causes myoglobin to be released, which will eventually block up the kidney
- Ischemia
16
Q
Presentation of renal papillary necrosis
A
- Sloughing off of necrotic renal papilla (where tips of pyramids empty into renal calyces)
- Presentation:
- Gross hematuria, flank pain, protein in urine
17
Q
Causes of renal papillary necrosis
A
- Any condition that causes ischemia (sickle cell, NSAIDs, acetaminophen, diabetes, pyelonephritis)
18
Q
Describe BUN/Cr and FENa in pre-renal, intrinsic, and post-renal azotemia
A
- (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
19
Q
Causes of prerenal azotemia
A
- Decreased renal blood flow = decreased GFR
- Hypovolemia, shock, hypotension, renal vasoconstriction with NSAIDs
20
Q
Causes of intrinsic renal failure
A
- Acute interstitial necrosis, glomerulonephritis, acute tubular necrosis, DIC, acute pyelonephritis
21
Q
Causes of post-renal azotemia
A
- Outflow obstruction
- Stones, BPH, Neoplasia, Congenital abnormalities
22
Q
Consequences of chronic renal failure
A
- 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)
23
Q
Describe the pathogenesis of renal osteodystrophy
A
- Recall:
- Kidneys promote conversion of calcidiol to calcitriol (active form of Vitamin D)
- Chronic renal disease = Vitamin D deficiency = hypocalcemia + hyperphosphatemia = secondary hyperparathyroidism = increased degradation of bone
24
Q
Presentation of Autosomal dominant polycystic kidney disease (ADPKD)
A
- Mutation in PKD1 or PKD2
- Numerous cysts in cortex and medulla
- Presentation:
- Flank pain, hematuria, UTIs, renal failure
25
Disorders associated with ADPKD
* Associated with cysts in the liver, berry aneurysms, mitral valve prolapse
26
Presentatino of autosomal recessive polycystic kidney disease
* Presents in infants
* Cystic dilation of collecting ducts
* Can presents as oliguria/Potter sequence in utero
27
Differentiate between simple vs. complex cysts
* Simple
* Anechoic (dark) on ultrasound
* Common and asymptomatic
* Complex
* Have solid components on imagine
* Require removal due to risk of renal cell carcinoma
28
Describe medullary cystic disease
* Can lead to fibrosis and progressive renal insufficiency
* Will present as cysts in the collecting ducts and shrunken kidney due to fibrosis
