Question 1
Which of the following is NOT an extra-renal manifestation of polycystic kidney disease?
(A) hepatic cysts
(B) hepatic fibrosis
(C) mitral valve prolapse
(D) Aortic stenosis
(E) intracranial aneurysms
D: PEP lectures 2014.
Question 2
What treatment is not considered helpful in the management of cystic kidney diseases?
(A) tolvaptan in ADPKD
(B) everolimus in cystic kidney disease secondary to tuberous sclerosis complex
(C) everolimus in autosomal polycystic kidney disease
(D) ACE-inhibitors in proteinuria (>1g/24h) associated with chronic kidney disease
(E) Renal transplantation
C: No change in creatinine or reduction in progression to renal failure in ADPKD, but some evidence for slowing of increase in renal volume - only for evorolimus not sirolimus. However there is some evidence in cystic diseases secondary to tuberous sclerosis complex. Tolvaptan may be used, however the absolute benefit in decreasing the rate of increase in cyst size and creatinine is small and the drug would have to be used for 30 - 40 years for a good benefit. N Engl J Med 2010; 363:830-840, N Engl J Med 2010; 363:820-829, N Engl J Med 2012; 367:2407-2418
Question 3
15% of creatinine is secreted from proximal tubular cells into the tubular lumen to be excreted in urine. Which of the following drugs do not cause a rise in serum creatinine by either interfering with the assay or decreasing creatinine secretion?
(A) cimetidine
(B) trimethoprim
(C) dronedarone
(D) flucytocine
(E) amiloride
E: Cimetidine, trimethoprim and dronedarone decrease creatinine secretion into the urine. Flucytosine is an anti fungal agent that interferes with the creatinine serum assay, which is a calorimetric assay. Acetoacetate is also recognised through the calorimetric assay. Ann Intern Med. 1980;93(2):280. JAMA. 1982;247(2):205. Nephron. 1989;53(3):218, Ann Intern Med. 1984;101(2):278. Clin Nephrol. 1984;22(4):214. Nephrol Dial Transplant. 2010;25(4):1285
Question 4
A 34 year old female has resistant hypertension. An angiogram of the renal arteries is shown below
Which of the following is NOT an extra-renal manifestation of polycystic kidney disease?
(A) hepatic cysts
(B) hepatic fibrosis
(C) mitral valve prolapse
(D) Aortic stenosis
(E) intracranial aneurysms
D: PEP lectures 2014.
Question 2
What treatment is not considered helpful in the management of cystic kidney diseases?
(A) tolvaptan in ADPKD
(B) everolimus in cystic kidney disease secondary to tuberous sclerosis complex
(C) everolimus in autosomal polycystic kidney disease
(D) ACE-inhibitors in proteinuria (>1g/24h) associated with chronic kidney disease
(E) Renal transplantation
C: No change in creatinine or reduction in progression to renal failure in ADPKD, but some evidence for slowing of increase in renal volume - only for evorolimus not sirolimus. However there is some evidence in cystic diseases secondary to tuberous sclerosis complex. Tolvaptan may be used, however the absolute benefit in decreasing the rate of increase in cyst size and creatinine is small and the drug would have to be used for 30 - 40 years for a good benefit. N Engl J Med 2010; 363:830-840, N Engl J Med 2010; 363:820-829, N Engl J Med 2012; 367:2407-2418
Question 3
15% of creatinine is secreted from proximal tubular cells into the tubular lumen to be excreted in urine. Which of the following drugs do not cause a rise in serum creatinine by either interfering with the assay or decreasing creatinine secretion?
(A) cimetidine
(B) trimethoprim
(C) dronedarone
(D) flucytocine
(E) amiloride
E: Cimetidine, trimethoprim and dronedarone decrease creatinine secretion into the urine. Flucytosine is an anti fungal agent that interferes with the creatinine serum assay, which is a calorimetric assay. Acetoacetate is also recognised through the calorimetric assay. Ann Intern Med. 1980;93(2):280. JAMA. 1982;247(2):205. Nephron. 1989;53(3):218, Ann Intern Med. 1984;101(2):278. Clin Nephrol. 1984;22(4):214. Nephrol Dial Transplant. 2010;25(4):1285
Question 4
A 34 year old female has resistant hypertension. An angiogram of the renal arteries is shown below
What is the most appropriate management?
(A) Renal artery denervation
(B) Balloon angioplasty +/- stent
(C) Stent
(D) Switch antihypertensives
(E) Early referral to hemodialysis centre
B: N Engl J Med 2004; 350:1862.
Question 5
According to the AUSDIAB study, what is the prevalence of hypertension in Australian males aged over 75?
(A) 50%
(B) 60%
(C) 70%
(D) 80%
(E) 90%
D: RPA lecture series, Ausdiab study. Australia’s Health 2006 (AIHW) pp178-179
Question 6
What is true with regards to the absolute CV mortality risk increase with each 20/10mmHg increase in blood pressure?
(A) It increases by 1.5x
(B) It increases by 2x
(C) It increases by 3x
(D) It increases by 4x
(E) It increases by 5x
B: Lewington S et al. Lancet 2002; 360: 1903–13
Question 7
What is the percentage survival 5 years following deceased donor graft for the recipient?
(A) 70%
(B) 80%
(C) 90 %
(D) 95%
(E) 100%
C: RPA Lecture 2015
Question 8
What is the percentage survival of the graft 5 years following deceased donor renal transplantation?
(A) 70%
(B) 80%
(C) 90%
(D) 95%
(E) 100%
B: RPA lecture 2015, ANZDATA
Question 9
What is the commonest cause of death with functioning graft within one year of renal transplant according to the ANZDATA compilation?
(A) Cardiac causes
(B) Vascular causes
(C) Infection
(D) Malignancy
(E) Renal failure
C: In the first year following a renal allograft, infection accounts for 42% deaths. Overall, and at anytime in the patients trajectory, malignancy is the most common cause of death, followed by cardiovascular causes. ANZDATA
Question 10
Which area of the nephron is most susceptible to renal ischaemia?
(A) Cortex
(B) Glomerular apparatus
(C) Proximal tubule
(D) Outer medulla
(E) Inner medulla
E: This is because of the distribution of blood supply, with the inner medulla only receiving 5% of renal blood flow. Cortical necrosis implies significant ATN, therefore being a bad prognostic sign - PEP lectures 2014
Question 11
Where does the macula densa lie in the kidney?
(A) Afferent arteriole
(B) Efferent arteriole
(C) Loop of Henle
(D) Distal Convuluted tubule
(E) Proximal tubule
D:
Question 12
Where is the majority of sodium reabsorbed?
(A) Proximal convuluted tubule
(B) Descending loop of Henle
(C) Ascending loop of henle
(D) Distal convuluted tubule
(E) Collecting duct
A
Question 13
What is the first inciting step in the promotion of rejection of a kidney allograft?
(A) Ischaemia-reperfusion injury causing the upregulation of HLA molecules and vascular adhesion factors
(B) Dense cellular infiltrate into the graft
(C) Presence of blood group antibodies that have not been removed
(D) Presence of anti-HLA antibodies
(E) CD8 T cell mediated cellular cytotoxicity
A: Whilst all are important mechanisms, the first event is usually due to ischaemia and reperfusion injury that triggers the upregulation of HLA molecules. N Engl J Med 2010; 363:1451-1462
Question 14
What is the major pathophysiological mechanism behind hyper-acute rejection
(A) stasis related acute thrombosis of the renal vein graft anastomosis
(B) Anti-HLA antibody mediated complement cytotoxicity
(C) Anti ABO blood group antibody mediated complement cytotoxicity
(D) CD25+ Foxp3 T Cell cytotoxicity
(E) Acute glomerulonephritis
B: N Engl J Med 2010; 363:1451-1462
Question 15
What classical histopathological marker signifies antibody mediated graft rejection?
(A) Presence of plasma cell infiltrate
(B) Vascular thrombosis
(C) Peritubular staining of C4d
(D) Peritubular staining of C1q
(E) Dendritic cellular infiltrate
C: N Engl J Med 2010; 363:1451-1462
Question 16
Following donation of a kidney, all of the following are expected changes to the donor except?
(A) Decreased probability of survival at 40 years post donation
(B) Increased systolic blood pressure
(C) Increased proteinuria
(D) Increased risk of gestational hypertension
(E) Increased risk of developing pre-eclampsia
A: According to NEJM 2009 (Ibrahim et al), eve at 40 years the probability of survival is the same. However, the cumulative incidence of end stage renal disease is increased in live kidney donors compared to matched healthy controls. References for the other data come from Garg et al. Kidney Int. 2006 Nov, N Engl J Med 2015; 372: 124 - 133
