random renal facts

Question 1

Which stones are radiolucent?

Answer 1

Uric acid

Question 2

Which stones precipitate with acid?

Answer 2

Cystine, uric acid, and calcium oxalate

Question 3

What can be used to prevent kidney stones?

Answer 3

For all stones: dilute urine. Decrease or chelate calcium for oxalate and phosphate stones - use citrate and thiazides Alkalinize urine, for cystine and uric acid stones - use citrate Acidify urine, for phosphate, struvite stones

Question 4

Na and K in DKA? NH3?

Answer 4

K is high (intracellular K low). Na is low due to osmotic activity of glucose and osmotic diuresis. NH3 increased due to proteolysis (due to conterregulatory glucagon et al).

Question 5

Compare and contrast MCD with FSGS

Answer 5

MCD: T-cell mediated damage, responds to steroids. Prevalent in children.

FSGS: Idiopathic. Poor steroid response. Prevalent in African-Americans and Hispanics, HIV+, heroin users.

Both present with proteinuria, hypogammaglobulinemia, hypercoag, hyperlipidemia. Both have effacement of foot processes. No deposits

Question 6

Compare and contrast membranous nephropathy with membranoproliferative glomerulonephritis

Answer 6

Membranous nephropathy:

• spike and dome subepithelial deposits
• prevalent in caucasians
• may be associated with Hep B, C, tumors, SLE, or drugs (NSAIDs, penicillamine)
• thickening of BM only

Membranoproliferative glomerulonephritis

• Type I: subendothelial deposits - associated with Hep B, Hep C
• Type II: intramembranous “dense deposit disease” - associated with C3 nephritic factor
• thickening of mesangium and BM

Both:

• poor response to steroids
• granular staining pattern

Question 7

Compare and contrast PSGN vs IgA nephropathy

Answer 7

PSGN

• Occurs 2-3 weeks after streptococcal skin or pharynx infection
• subepithelial deposits - hence will self-limit

IgA nephropathy

• Occurs few days after viral mucosal infection (eg gastroenteritis)
• mesangial deposits - may progress to renal failure
• maybe HSP also

Question 8

Which are the diseases with subendothelial deposits?

Answer 8

• MPGN type I - recall type II is intramembranous (DD)
  
  • subendothelial, nephrotic (sometimes also nephritic) presentation
  • tram-tracking due to reduplication of BM caused by mesangial ingrowth
  • associated with HBV, HCV
• DPGN
  
  • subendothelial (sometimes also mesangial), nephritic (sometimes also nephrotic)
  • wire looping due to endothelial and mesangial proliferation

Question 9

Compare and contrast:

Bartter, Liddle, Gitelman syndromes

Answer 9

• Bartter - defect in the NKCC transporter of the TAL
  
  • like taking lots of furosemide - contraction alkalosis
  • hyponatremia, hypokalemia, hypocalcemia, hypomagnesemia
  • hypercalciuria, stones, polyuria, polydypsia
• Gitelman - defect in the NaCl transporter of the DCT
  
  • like taking lots of thiazide - contraction alkalosis
  • hyponatremia, hypokalemia, hypercalcemia, hypomagnesemia (?)
• Liddle - activating mutation of ENaC
  
  • pseudohyperaldosteronism - low RAA levels
  • hypertension, hypernatremia, hypokalemia, alkalosis
  • Tx: triamterene and amiloride, not *lactone

Question 10

Red currant jelly stools: infant and adult

Answer 10

Infant: intusussception

Adult: ischemic bowel