Renal 1

Question 1

What’s the MOA of SLE induced nephritis?

Answer 1

Immune complexes of dsDNA and anti-dsDNA Ab deposit in the mesangium and subendothelial space of the kidney&raquo_space; complement activation&raquo_space; decreased C3 and C4 levels. Immune complexes can also deposit in the subepithelial space and cause membranous glomerulonephritis&raquo_space; nephrotic syndrome.

Question 2

How would you treat a patient with hypernatremic hypovolemia?

Answer 2

Initial treatment for severe hypovolemic hypernatremia is isotonic 0.9% saline which allows you to gradually correct the hyperosmolarity and normalize volume status. Once volume deficit is restored you can switch from normal saline to 1/2 NS

** THIS IS IMPORTANT. Don’t want to correct plasma sodium greater than 1 mEq/L/h because a correction faster than this&raquo_space; cerebral edema.

Question 3

What’s the MOA of tamsulosin and what is its indicated use in removing kidney stones?

Answer 3

Tamsulosin = alpha 1 antagonist.
- You normally have alpha 1 R on distal ureter, bladder, neck, base of detrusor muscle, and urethra. Sympathetic activity&raquo_space; stimulation of alpha R to&raquo_space; contraction and maintenance of high muscular tone (to prevent incontinence). Tamsulosin and alpha 1 antagonists relax ureteral muscle and decrease intraureteral pressure.

Question 4

How does the MOA differ for bethanechol and oxybutynin in terms of their indicated use?

Answer 4

Bethanechol = cholinergic agent
Oxybutinin = anticholinergic 

You have cholinergic R on the dome of the bladder. When activated these promote contraction and bladder voiding. Bethanechol stimulates contraction and is used for atonic bladder / urinary retention.
Oxybutinin is used to decrease detrusor activity in cases of overactive bladder.

Question 5

How long does it take after a strep infection to see the presentation of PSGN?

Answer 5

10-20 days after streptococcal throat or skin infection. Presenting features include: periorbital swelling, hematuria, oliguria. Patient is likely hypertensive and urinalysis shows hematuria with RBC casts, proteinuria, and low C3 levels.

Question 6

In cases of IgA nephropathy, how long does it take between URI and renal presentation?

Answer 6

Development of glomerular disease is < 5 days after exposure. Typically present with hematuria after URI.

Question 7

If an older patient is started on an SSRI and presents weeks later with low serum osmolarity (< 275 mOsm), high urine osmolarity (>100mOsm), and increased urine sodium [ ] (>40mEq). What would be the most likely Dx?

Answer 7

SIADH. Characterized by hyptonic hyponatremic euvolemia.

Question 8

Why should you try to avoid multiple analgesic use in patients with chronic kidney disease?

Answer 8

Want to reduce the risk of tubulointerstitial nephritis and hematuria due to papillary necrosis.

Patients with multiple chronic analgesic use and CKD can present initially as asymptomatic with an elevated Cr found incidentally. Can also develop painless hematuria due to papillary ischemia from the analgesic induced vasoconstriction of medullary blood vessels (vasa recta).

Clinical Presentation:

• Elevated Cr w/UA showing hematuria or sterile pyuria
• Mild proteinuria (< 1.5 g/day)
• CT show small kidneys with bilateral renal papillary calcification

Question 9

Why do you get flank pain with renal stones?

Answer 9

Renal capsular distension

Question 10

What are 4 common cause of nephrotic syndrome in adults?

Answer 10

membranous glomerulonephropathy, FSGS, minimal change dz, amyloidosis.

** Rheumatoid arthritis is the MCC OF amyloidosis in the US

Question 11

Glomerular crescent formation on light microscopy is characteristic in what disease?

Answer 11

RPGN

Question 12

Hyalanosis of the walls of both the afferent and efferent arterioles is pathognomonic for what disease?

Answer 12

diabetic nephropathy

Question 13

Normal light microscopy findings in a patient with nephrotic syndrome usually suggests:

Answer 13

minimal change disease

Question 14

What are the three possible causes of a combined high AG and osmolol gap metabolic acidosis?

Answer 14

Acute ethanol (MCC), methanol, or ethylene glycol poisoning.

Question 15

How does a hypovolemic state in AKI result in an elevated BUN:Cr ratio?

Answer 15

Hypovolemia&raquo_space; decreased renal blood flow&raquo_space; activation of RAAS&raquo_space; increased resorption of salt and water&raquo_space; passive resorption of urea&raquo_space; elevated BUN:Cr greater than 20:1