1. An 18-year-old white man presents to your office after developing gross hematuri a. Your physical examination reveals some
papules on his face and neck. They are 1- 3 mm in size and are nontender. BP is normal , and serum creatinine is 1.2. Urinalysis
reveals a pattern of uniformly shaped red blood cells in greater than 100 cells per high power field. The patient has completed high
school, but he was known as a very slow learn er and a poor student. Imaging of his kidneys reveals some cystic change in both
kidneys and a solid-looking vascular mass in the ri ght kidney.
What is the MOST likely diagno sis?
A. Renal cell carcinoma
B. ADPKD
C. Autosomal recessive PKD
D. Tuberous sclerosis
E. Von Hippel-Lindau syndrome
Answer: D
Explanation:
The patient described has the skin lesions and renal find ings of tuberous sclerosis. The renal lesions are typically
angiomyolipomas and can bleed. Although mental retardation is common in this autosomal dominant disorder, it is not inevitable.
Von Hippel-Lindau syndrome is a possibility based on the renal fi nding, but this would not explain the skin lesions. ADPKD is
unlikely with this imaging picture and again would not explain the skin lesions. A renal cell carcinoma is possible but at his age is
unlikely and is unaccompanied by some genetic syndrome with skin lesions.
2. On ult rasound images, the norm al kidney should have w hich characteristic?
A. Larger than 14 cm in length
B. Have wedge-shaped areas of low blood flow in the cortex on Power Doppler
C . Be equal or less echogenic than the liver
D. Have symmetric bilateral effacement of the renal sinus echo-complex with dilated calyces
Answer: C
Explanation:
The echogenicity of normal kidneys is less than that of pancreas and equal or less than that of liver and spleen. Increased renal
echogenicity indicates renal disease. Normal kidneys measure 9- 13 cm on ultrasound exams; A is incorrect. Normal kidneys have
no low flow areas on Doppler exams, and wedge-shaped deficiencies are indicative of infarcts; B is incorrect. Dilated calyces
should not be present in normal kidneys, and these suggest obstruction or ectasia from pri or disease; D is incorrect.
3. A 49-year-old morbidly obese man with a history of hypertension (HTN), metabolic syndrome,
osteoarthritis, and gout undergoes a Roux-en-Y bypass procedure . Medications include
lisinopril, furosemide, ibuprofen, and glyburide . The patient presents 4.5 weeks later with
weakness and fatigue. Labs reveal a serum creatinine of 3.7 mg/dL. Urin e sediment
demonstrates 1- 3 RBCs/HPF, 0- 1 WBCs/HPF, 2- 5 renal tubular cells/ HPF, and the crystals
seen in the figu re.
Whic h BEST describes the crystals?
A. Calcium phosphate crystals
B. Uric acid crystals
C . Cystine crystals
D. Calcium oxalate crystals
E. Sulfonamide crystals
Answer: D
Explanation:
The patient developed kidney injury after the gastric bypass procedure. The urine microscopy reveals calcium oxalate crystals,
which reflect the enteric hyperoxaluria that has developed following the malabsorption induced by the weight loss procedure . With
fat malabsorption, calcium is saponified by the fat, allowing free oxalate to be reabsorbed. This leads to increased serum oxalate
with subsequent hyperoxaluria and acute oxalate nephropathy. The other crystals are incorrect.
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,ASN BRCU Virtual 2021 Practice Questions
4. Which statement is TRUE about women who donate a kidney before becoming pregnant?
A. They are at increased risk for progression of kidney disease postpartum .
B. They are at increased risk for adverse outcomes during pregnancy including preeclampsia.
C . They are NOT at increased risk for adverse outcomes during or after pregnancy if their kidney function is normal and they
have no proteinuria.
D. They are at increased risk for progression of kidney disease but not adverse outcomes during pregnancy.
Answer: B
Explanation:
Kidney donation is associated with increased risk for adverse outcomes DURING pregnancy. The other answers are incorrect and
not observed in the described scenari os.
References:
Garg AX, Nevis IF, McArthur E, Sontrop JM, Koval JJ, Lam NN, Hildebrand AM, Reese PP, Storsley L, Gill JS, Segev DL,
Habbous S, Bugeja A, Knoll GA, Dipchand C, Monroy-Cuadros M, Lentine KL; DONOR Network. Gestational hypertension and
preeclampsia in living kidney donors. N Engl J Med 372: 124- 133,20 15.
5. Whic h statement is TRUE about the use of ACE inhibitors during pregnan cy?
A. Contraindicated, but only in the second and third trimesters.
B. Contraindicated, but only in the first trimester.
C. Contraindicated, but they can be used during breastfeeding postpartum .
D. Contraindicated, they are contraindicated durin g pregnancy and during breastfeeding.
Answer: C
Explanation:
ACE inhibitors are contraindicated during pregnancy but can be used in the postpartum period durin g infant breastfeeding.
References:
Cooper WO, Hernandez-Diaz S, Arbogast PG, Dudley JA, Dyer S, Gideon PS, Hall K, Ray WA. Major congenital malformations
after fi rst-trimester exposure to ACE inhibitors. N Engl J Med 2006;354:2443- 2451 .
6. A 50-year-old man was admitted to the hospital with abdominal pain and AKI.
A subsequent workup demonstrated the presence of acute pancrea titis, and an abdominal
computerized tomography (CT) scan showed multiple renal mass lesions.
A kidney biopsy revealed an extensive plasma cell infiltrate.
Laboratory results
C3: 65(nl>80 1U) Anti- nuclear antibody (ANA): positive 1:40
C4: 15 (nl >20 IU) WBC: 8500 with 10% eosinophilia
Based on this p atient' s clinical presentation, w hat is the MOST likely diagnosis?
A. Sarcoidosis with multiple renal granuloma
B. Myeloma with renal plasmacytomas
C . lgG4-related systemic disease
D. Systemic lupus erythematosus (SLE) with systemic vasculitis
E. Undocumented drug ingestion causing acute allergic interstitial nephritis
Answer: C
Explanation:
This patient presents with lgG4-related systemic disease. It is characterized by a marked plasma cell infiltrate (typically described
in a "storiform" cartwheel pattern) that produces expansile destructive lesions. Autoimmune pancreatitis is frequently seen in
conjunction with renal disease, but all maj or organs may demonstrate variable involvement. lgG4 is uniquely deposited in the
tubules. The classical complement pathway may be activated with a resul tant low C3 and C4, and there may eosinophilia and low-
grade ANA titers. A tubulointerstitial nephritis and/or membranous nephropathy is typically seen in the kidney , but obstruction can
also occur from the large plasma cell aggregates. Sarcoid and myeloma do not activate complement, nor does acute interstitial
nephritis (AIN). None of the other choices are associated with the systemic and laboratory presentation of lgG4-related systemic
disease.
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,ASN BRCU Virtual 2021 Practice Questions
7. A 38-year-old morbidly obese woman with a history of CKD, hypertension, osteoarthritis,
metabolic syndrome, and gout is started on orlistat 120 mg bid and increased to 120 mg tid
{after 1 month) for enhanced weight loss. Medications include enalapril, orlistat,
hydrochlorothiaz ide (HCTZ), naproxen, and glyburi de. The patient presents 5.5 weeks later
with anorexia, nausea, weakness, and fatigue. She describes 9 days of an exquisitely tender
left foot and ankle that are swoll en and erythematous. At the time of presenta tion, she is
fin ishing a 7-day course of trimethoprim-sulfamethoxazole for a urinary tract infection (UTI).
Serum creatinine is 3.7 mg/dL (baseline, 1.6 mg/dL). Urine sediment demonstrates red blood
cells, white blood cells, renal tubular cells, and a few crystals. A kidney biopsy is performed,
and the image is shown under polarization.
Which crystal is seen within the renal tubular lumens on renal biopsy?
A. Calcium phosphate crystals
B. Uric acid crystals
C . Calcium oxalate crystals
D. Sulfonamide crystals
Answer: C
Explanation:
The patient developed renal failure in the setting of fat malabsorption induced by the weight loss drug orlistat. The urine
microscopy reveals calcium oxalate crystals, which reflect the enteric hyperoxaluria that has developed following the malabsorption
induced by orlistat. With fat malabsorption, calcium is saponified by the malabsorbed fat, allowing free oxalate to be reabsorbed;
this leads to increased serum oxalate with subsequent hyperoxaluria and acute oxalate nephropathy. In the kidney biopsy, calcium
oxalate crystals, which polarize positively, are seen within the tubular lumens and are the cause of the AKI. Orlistat is the cause by
its mechanism to induce malabsorption. The other options are incorrect as they do not cause acute oxalate nephropathy.
8. A 50-year-old white man has been working in a fou ndry as a welder for many years . He now presents with an elevated creatinine
of 2.3 mg/dL and a urine protein/creatinine ratio of 1.2. There are no old records except for the following information:
• Medical history is positive for hypertension and gout. Smoking history is negative .
• Renal ultrasound: slightly echogenic but normal size kidneys bilaterally/no stones.
• EKG: Minimal voltage criteria for left ventricular hypertrophy (LVH).
Urinalysis
Specific gravity: 1.010
Blood: 0- 2 per high power field
WBC: 0- 2 per high power field
Protein: 1+
What is your assessment?
A. Patient has unrecognized hypertensive nephropathy
B. Patient has beryllium nephropathy
C. Patient has cadmium nephropathy
D. Patient has lead nephropathy
E. Patient has mercury nephropathy
Answer: D
Explanation:
Working in a foundry, exposure to heavy metals is a strong consideration (option B or D). The patient could have hypertension
nephrosclerosis; but he is Caucasian, and the EKG shows minimal evidence for LVH which would be unlikely in hypertension-
induced nephroscl erosis. Cadmium exposure is more likely in a battery plant and has other associations such as bone disease and
stones. Cadmium is a well-known cause of hypertension and CKD and gives a picture of chronic tubulointerstitial nephritis with
non-nephritic proteinuria and bland urine sediment similar to lead nephropathy but is not associated with gout. Chronic lead toxicity
classically has been associated with the triad of gout, hypertension, and CKD, which this patient has. The history for mercury and
beryllium toxicity is the wrong environmental exposure.
9. A Chinese patient presented with advanced CKD . No kidney biopsy was performed, but by history, the patient routinely used a
variety of Chinese herbs for health and weight loss. He underwent a successful one-haplotype pre-emptive living related transplant
from his sister using induction therapy with an IL-2 blocker. Tacrolimus and mycophenolate were used as maintenance
immunosuppression with a steroid-free protocol. After 12 months, he now presents with painless gross hematuri a but otherwise is
afebrile and feeling well.
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Labs
Creatinine: 1.2 mg/dL
Hemoglobin: 12.3 g/dL
Platelet count: 175,000/mm3
Urinalysis: 4+ blood, 2+ albumin
Too numerous to count (TNTC) red blood cells (isomorphic)
What is the MOST likely etiology in y our differential diagnosis?
A. Acute humera l-mediated rejection
B. Renal cell carcinoma of the native kidneys as a consequence of acquired cystic kidney disease and chronic calcineurin
exposure
C. Recurrent lgA nephropathy
D. Acute BK nephropathy with hemorrhagic cystitis
E. Transitional cell carcinoma of the native urogenital tract
Answer: E
Explanation:
Patients ingesting Chinese herbs have a high chance of being exposed to Aristolochia species plant products. The derivative of
these plants, aristolochic acid, is nephrotoxic and leads to a chronic interstitial nephritis. Most importantly is the lifelong ri sk in
these patients of transitional cell carcinoma especially after transplantation, where it may occur in >30% of patients (option E). It
has been recommended that a bilateral nephrectomy be considered prior to transplant in patients with aristolochic acid
nephropathy. The norma l creatinine level and gross hematuria are inconsistent with acute humeral rejection, and the presence of a
living donor kidney also makes this less likely. The patient's ethnicity and clinical presentation suggest recurrent lgA nephropathy in
the allograft, but RBCs associated with glomerulonephritis should be dysmorphic. The isomorphic RBCs in this case suggest that
this is a urologic lesion. BK viremia is an important cause of hemorrh agic cystitis but the risk factors for BK are not present. This
patient never had a recently described rejection episode requiring an increase in immunosuppression. In addition, BK nephropathy
should be associated with allograft dysfunction. Renal cell carcinoma does occur in transplant patients , but this was a pre-emptive
transplant, and acquired cystic disease of the native kidneys is unlikely in the absence of long-term dialysis therapy. This patient
most likely has developed a transitional cell cancer of the native urogenital tract from chronic aristolochic acid exposure (option E).
10. A 45-year-old Asian woman has been ordering a variety of altern ative medicine compounds over the intern et for weight loss. You
are very concerned about the fact she takes these unknown supplements and obtain the following tests: BP, 140/90 mm Hg; pulse,
70 beats/min; temperature, 36.5°C.
Labs
Na: 140 mEq/L Urinalysis:
K: 3.0 mEq/L Albumin: negative
Cl: 95 mEq/L Blood: negative
HC03: 35 mEq/L WBC: negative
BUN : 15 mg/dL Casts: negative
Cr: 1.0 mg/dL RSC: negative
Based on the history and test results, which is MOST likely?
A. A kidney biopsy is going to show acute interstitial nephritis
B. The patient is taking star fruit
C. The patient is taking ephedra-containing compounds
D. The patient is ingesting products that contain glycerrhizic acid
E. The patient is taking high doses of Noni juice
Answer: D
Explanation:
This patient has normal kidney function and a norma l urinalysis, so acute interstitial nephritis is not likely. Star fruit is associated
with oxalate nephropathy, especially in patients with pre-existing CKD, which is not present in this patient. There are no crystal s
described in the urinalysis. Ephedra causes hypertension (HTN) and stones and, although this patient has HTN , there is also the
presence of hypokalemia . Therefore, when combining hypokalemia, HTN, and alkalosis together, this patient has an excess
mineralocorticoid-like syndrome. Although it could be an adrenal adenoma, we know that a similar condition may be present from
herbal products that use glycerrhizic acid as a sweetener (option D). This syndrome is called "apparent" mineralocorticoid excess
(AME) to differentiate it from primary hyperaldosteronism . Noni juice can cause hyperkalemia and is not relevant to this patient
presentation.
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