Internal-Medicine

Answers and Explanations
1. (D) Urea is filtered at the glomerulus, and
thereafter, any movement in or out of tubules
is a passive process depending on gradients,
not secretion. Reabsorption of urea in the distal
tubule and collecting duct, when urine flow is
reduced, results in the disproportionate elevation
of urea nitrogen over creatinine in prerenal
azotemia. (Kasper, p. 246)
2. (D) Renal scans initially show a reduction in
excretion with cortical retention. This is the most
common type of rejection. Most acute rejections
will respond to immunosuppressive agents if
diagnosed early. In contrast, immediate nonfunction
of a graft can be caused by damage to
the kidney during procurement and storage.
Such problems are becoming less frequent.
Obstruction, vascular compression, and ureteral
compression are other causes of primary nonfunction
of a renal graft. (Kasper, p. 1672)
3. (D) Both granular and erythrocyte casts are present,
but the latter indicate bleeding from the
glomerulus and are most characteristically seen.
Red cells reach the urine probably via capillary
wall “gaps” and form casts as they become
embedded in concentrated tubular fluid with
high protein content. Proteinuria is invariably
present but is not as specific. (Kasper, pp. 250–251)
4. (E) These humps are discrete, electron-dense nodules
that persist for about 8 weeks and are highly
characteristic of the disease. Light microscopy
reveals diffuse proliferation, and immunofluorescence
reveals granular immunoglobulin
G (IgG) and C3. Most patients will recover
spontaneously. (Kasper, pp. 1680–1681)
5. (A) The urine contains large amounts of potassium,
magnesium, and sodium. The large
volume is often appropriate for preexisting
volume expansion, but careful attention to fluid
and electrolytes is important to prevent
hypokalemia, hypomagnesemia, hyponatremia
or hypernatremia, and volume depletion.
(Kasper, p. 1724)
6. (B) She has analgesic nephropathy, and chronic
analgesic ingestion may lead to papillary
necrosis and tubulointerstitial inflammation.
Complete understanding of the pathogenesis is
lacking, and may vary with different analgesics.
Depletion of reducing equivalents such
as glutathione may also play a role. (Kasper,
p. 1703)
7. (D) Although all drugs should be reassessed at
this time, and if appropriate, the dosage
adjusted, drugs with known nephrotoxicity,
such as ACE inhibitors and NSAIDs, should
be stopped. (Kasper, p. 1644)
8. (A) Diuretics are a common cause for metabolic
alkalosis since many patients take these
medications for hypertension or CHF. Diarrhea
causes a nonanion gap metabolic acidosis, and
mineralocorticoid excess leads to metabolic
alkalosis, primarily because of renal bicarbonate
generation. Other major mechanisms for
metabolic alkalosis include extracellular fluid
(ECF) volume contraction, potassium depletion,
and increased distal salt delivery. Less
common causes are Liddle syndrome, bicarbonate
loading (posthypercapnic alkalosis),
and delayed conversion of administered
organic acids. (Kasper, pp. 265, 267–268)
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