Errors in First Aid for the USMLE (2007): Renal System

As always, this comes from an email sent to the First Aid team. If you find any errors, please include them in the comments.

Renal (all references from Merck Manual and Robbins Basic Pathology)

  1. P.396, Hormones acting on kidney
    1. Atrial Natriuretic Factor (ANF) is listed as Atrial Natriuretic Peptide (ANP) on the preceding page. I think one term should be used consistently.
  2. P.401, Kidney stones
    1. To help remember which stones are largely radiolucent:
      1. I can’t C U on XRay.” for Cystine and Uric acid stones.
  3. P.405, Mannitol
    1. Mannitol can be used clinically to decrease intracranial pressure (as listed). If given too rapidly, it can also cause an increase in intracranial pressure. I think this should be listed as well under the toxicities.
  4. P.405, Ethacrynic acid
    1. “Similar to furosemide; can be used in hyperuricemia, acute gout (never use to treat gout)” is not correct. This should instead say, “can cause hyperuricemia, acute gout (never use to treat gout).”
  5. P.406, ACE inhibitors
    1. One of the clinical uses for these drugs is to decrease proteinuria. In toxic doses, it can also cause proteinuria. I think this should be mentioned under clinical uses.

Return to First Aid Errors page.

8 Responses to Errors in First Aid for the USMLE (2007): Renal System

  1. John says:

    From one Carib Med Student to another –>

    Renal section p. 401 under “Transitional Cell Carcinoma”

    SCHISTOSMIASIS HAEMATOBIUM causes Squamous Cell Carcinoma of the Bladder NOT Transitional Cell Carcinoma.

  2. Ahmed says:

    pg 394, figure E – intercalated cell has K/H exchange, not Na/H (correction from official FA site).

  3. Sureshot says:

    Just an addition to what John posted above – Schistosoma hematobium can cause both transitional and squamous cell ca. However, if asked to choose between one or the other, squamous cell would be the better bet. 70% of bladder cancers from S. hematobium are squamous cell ca., and 30% are transitional cell ca.

    Reference: Goljan, RR pathology, page 432.

  4. Eric Brinton says:

    On page 400 under nephrotic syndrome, it says that there are supEPIthelial humps in SLE. This is incorrect. There are subENDOthelial humps. The immune complexes in SLE are too big to get past the basement membrane.

  5. LG says:

    This is in response to the previous correction: SLE can manifest itself in 5 different forms. For membranous lupus nephriitis, deposits can be found in the subEPIthelial space. As for “diffuse” lupus nephritis, subENDOthelial deposits can be found. Hence, the First Aid comment on “membranous glomerulonephritis pattern with wire loop lesions with subepihtelial deposits” is correct. However, if you are referring to diffuse lupus nephritis, which I believe the previous commenter was doing, it would be subENDOthelial. As a side note, you’d see mesangial deposits in both SLE forms (Type 4 and 5…I”m not quite sure about the others), allowing you to distinguish between idiopathic membranous nephritis (which is solely subEPIithelial deposits) from membranous lupus nephritis (which is both subEPIthelial AND mesangial deposits). That’s probably more than you wanted to know, but the key points are the following: there are 5 types (2 of which are probably important for the board); diffuse lupus nephritis presents with (subENDOthelial) deposits and membranous lupus nephritis presents (subEPIthelial) deposits; both diffuse and membranous have MESANGIAL deposits; distinguish between membranous lupus nephritis and idiopathic membranous nephritis (a.k.a membranous glomerulonephritis).

  6. Mark says:

    pg. 396 – Juxtaglomerular apparatus (JGA)

    The macula densa sense changes in the delivery and reabsorption of Cl-, not Na+.

    Reference: Helmut G Rennke, Renal Pathophysiology

  7. Emma says:

    Page 400: MCC nephrotic syndrome is Focal Segmental Glomerular sclerosis (see UpToDate) and second most common cause is Membranous Glomerulopathy in adults.

  8. JC says:

    p. 400 refers to “Kimmelstiel-Wilson ‘wire-loop’ lesions,” which I think conflates two distinct morphologies of glomerular disease:

    1. In DIABETES, one sees Kimmelstiel-Wilson the nodule (a globular hyaline lesions associated with non-enzymatic glycation) and
    2. In lupus nephritis, one sees the wire loop lesion (a thickening of the basement membrane on EM owing to subendothelial immune complex deposits).

    K-W nodules defined in:
    Wire loops defined in:

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