DIT review - Renal 3

Question 1

Describe histology of renal cell carcinom

Answer 1

• Will see polygonal clear cells filled with accumulated lipids and carbohydrates

Question 2

Presentation of RCC

Answer 2

• Hematuria, palpable mass, polycythemia

Question 3

Hormones secreted by RCC

Answer 3

• Erythropoietin - polycythemia
• ACTH - Cushing
• PTH-related peptide - Hypercalcemia
• Prolactin - hypogonadism, decreased libido, galactorrhea

Question 4

Common metastasis of RCC

Answer 4

• Invades the renal vein then IVC and spreads hematogenously
  
  • Metastasizes to lung and bone

Question 5

Describe Wilms tumor and associated genetic defect

Answer 5

• Most common renal malignancy in children aged 2-4
• Contains embryologic glomerular structures
• Loss of function mutation of tumor suppressor gene WT1 or WT2

Question 6

Presentation of Wilms tumor

Answer 6

• Hematuria, large flank mass

Question 7

Describe WAGR syndrome

Answer 7

• Wilms tumor, Aniridia (absence of iris), Genitourinary malformation, mental/motor Retardation

Question 8

Describe location and presentation of Transitional cell carcinoma

Answer 8

• Most common tumor of the urinary tract
• Can occur in renal calyces, renal pelvis, ureters, and bladder
• Painless hematuria suggests bladder cancer

Question 9

Risk factors for Transitional cell carcinoma

Answer 9

• Cyclophosphamide, Smoking, Aniline dye

Question 10

Describe presentation of acute pyelonephritis

Answer 10

• White blood cells/casts
• Presentation:
  
  • Fever, painful urination, urgency, AMS (elderly), CVA tenderness

Question 11

Describe histology of chronic pyelonephritis

Answer 11

• Associated with thyroidization of kidney
  
  • Eosinophilic casts dilate the tubules, causing the tubules to have a colloid/thyroid-like appearance
• WBC casts

Question 12

What is the common presentation of drug-induced (acute) interstitial nephritis

Answer 12

• Acute interstitial renal inflammation that results in acute renal failure
• Presentation:
  
  • Fever, rash, eosinophilia in urine, azotemia

Question 13

Common causes of acute interstitial nephritis

Answer 13

• NSAIDs, Penicillin, Cephalosporin, Sulfonamides, Ciprofloxacin, Cimetidine, Allopurinol, PPIs, Indinavir, Mesalamine
• REMEMBER the P’s:
  
  • Pee (diuretics), Pain-free (NSAIDs), Penicillin and Cephalosporins, PPIs, rifamPin

Question 14

Describe diffuse cortical necrosis and its cause

Answer 14

• Acute generalized cortical infarction of both kidneys
• Likely due to a combination of vasospasm and DIC
  
  • Multiorgan failure
  • ARDS
  • DIC
  • Septic shock

Question 15

Describe acute tubular necrosis and its causes

Answer 15

• 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

Question 16

Presentation of renal papillary necrosis

Answer 16

• Sloughing off of necrotic renal papilla (where tips of pyramids empty into renal calyces)
• Presentation:
  
  • Gross hematuria, flank pain, protein in urine

Question 17

Causes of renal papillary necrosis

Answer 17

• Any condition that causes ischemia (sickle cell, NSAIDs, acetaminophen, diabetes, pyelonephritis)

Question 18

Describe BUN/Cr and FENa in pre-renal, intrinsic, and post-renal azotemia

Answer 18

• (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
• (2) Intrinsic renal failure:
  
  • BUN/Creatinine < 15
    
    • Tubular dysfunction = decreased reabsorption of BUN
  • FENa > 2%
    
    • Tubular dysfunction = decreased reabsorption of Na+
• (3) Post-renal azotemia:
  
  • Early stage
    
    • BUN/Cr > 20
    • FENa < 1%
  • Late stage - tubular damage occurs
    
    • BUN/Cr < 15
    • FENa > 2%

Question 19

Causes of prerenal azotemia

Answer 19

• Decreased renal blood flow = decreased GFR
• Hypovolemia, shock, hypotension, renal vasoconstriction with NSAIDs

Question 20

Causes of intrinsic renal failure

Answer 20

• Acute interstitial necrosis, glomerulonephritis, acute tubular necrosis, DIC, acute pyelonephritis

Question 21

Causes of post-renal azotemia

Answer 21

• Outflow obstruction
• Stones, BPH, Neoplasia, Congenital abnormalities

Question 22

Consequences of chronic renal failure

Answer 22

• 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)

Question 23

Describe the pathogenesis of renal osteodystrophy

Answer 23

• 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

Question 24

Presentation of Autosomal dominant polycystic kidney disease (ADPKD)

Answer 24

• Mutation in PKD1 or PKD2
• Numerous cysts in cortex and medulla
• Presentation:
  
  • Flank pain, hematuria, UTIs, renal failure

Question 25

Disorders associated with ADPKD

Answer 25

• Associated with cysts in the liver, berry aneurysms, mitral valve prolapse

Question 26

Presentatino of autosomal recessive polycystic kidney disease

Answer 26

• Presents in infants
• Cystic dilation of collecting ducts
• Can presents as oliguria/Potter sequence in utero

Question 27

Differentiate between simple vs. complex cysts

Answer 27

• Simple
  
  • Anechoic (dark) on ultrasound
  • Common and asymptomatic
• Complex
  
  • Have solid components on imagine
  • Require removal due to risk of renal cell carcinoma

Question 28

Describe medullary cystic disease

Answer 28

• Can lead to fibrosis and progressive renal insufficiency
• Will present as cysts in the collecting ducts and shrunken kidney due to fibrosis