Renovascular disorders

By: Dr./ Sahar H. Mostafa
El-Mataria Teaching Hospital- Cairo- Egypt
January, 2017
Renovascular
Disorders

Introduction To Renovascular Disease
(RVD)
 The Kidneys depend on systemic blood pressure
(SBP) to maintain adequate RBF and hence
adequate GFR, tubular function and overall salt
and water balance
 This explains the vulnerability of kidneys to
diseases involving the renal vasculature
 Vascular injury to kidneys is usually a
manifestation of generalized vascular pathology

Classification of RVD according to
anatomic location of vasculopathy
Renal Arteries Renal Arterioles and
microvasculature
Renal Veins
Thromboembolic
occlusion
Atheroembolic Disease
(cholesterol embolism
syndrome CES)
Renal Vein
Thrombosis (RVT)
Renal Artery Stenosis
(RAS), and
Ischemic renal
disease
Hypertensive arteriolar
Nephrosclerosis
Thrombotic
Microangiopathies:
1. Hemolytic Uremic
Syndrome (HUS)
2. Thrombotic
Thrombocytopenic
Purpura (TTP)
Scleroderma
Sickle cell nephropathy

Thromboembolic Occlusion of Renal
Arteries
Causes:
►►Intrinsic pathology in renal vessels:{In situ
thrombosis}
 Post-traumatic.. Young patients (blunt trauma, deceleration injury,..)
 Atherosclerotic.. Old patients
 Dissection/Aneurysm/Arteriography
 Inflammatory: Takayasau, syphilis, systemic vasculitis,
thrombangitis obliterans
►► Embolization: {originating in distant vessels};
much more common (90%) and usually unilateral
 Tumor/Fat emboli
 Emboli from left heart (most common), as left mural thrombus
following MI or AF, or bacterial endocarditis, septic/aseptic
valvular vegetations..
►► Paradoxical emboli, passing through patent foramen
ovale or ASD

Clinical Manifestations Of
Thromboembolism
 Difficult to diagnose, require high index of
suspicion
 Variable, depend on: extent/time course of occlusion
and state of pre-existing renal circulation
 Acute renal thrombosis/infarction ---------->
o Sudden onset of flank pain/tenderness (? absent in
55 %)
o Fever/nausea/vomiting
o Hematuria (microscopic)
o Deteriorated renal function: transient (unilateral), or
severe (bilateral)
o Hypertension, usually transient (renin release in peri-
infarction zone)
o Elevated TLC, AST, LDH, ALP (renal enzymes in
infarction)

Clinical Manifestations Of
Thromboembolism
 Gradual unilateral occlusion --> may go
undetected
Patients with RAS & established collateral
circulation have no symptoms (little/no
infarction)
----------------------
** Thus, the spectrum of clinical manifestations lies
between some extremes in different occasions:
 ARF
 Unexplained Progressive Azotemia (old patient ±
refractory HTN)
 HTN + Azotemia (renal transplant)

Diagnosis and Treatment Of
Thromboembolism
 Diagnosis:
 MRA
 Spiral CT
 Duplex U/S
 Renal Arteriography
 Renal Scintigraphy
 ± Echocardiography
 TTT:
 Surgical revascularization (for traumatic renal A. thrombosis),
mortality rate:11-25%
 Intra-arterial thrombolytic (for iatrogenic occlusion of renal As,
as a result of angiography or angioplasty)
 Adequate hydration/HTN Control
 Anticoagulation
 Renal replacement therapy (RRT)
N.B. The warm ischemia time beyond which recovery of renal
function would not be anticipated, is several hours..!!

Renal Artery Stenosis (RAS) and
Ischemic Renal Disease
RAS Ischemic Renal
Disease
Prevalence:
2-4 % in general population
30-40 % in accelerated HTN
and renal insufficiency
Causes:
Atherosclerosis:(ARV
D)
o90 %
oElderly
Fibromuscular
Dysplasia:
o5-10 %
oYoung
Atherosclerosis of 1 or both renal
As
 Elderly male
± HTN
Often with atherosclerotic PVD
(68%)
IHD (45%)
CHF (33%)
History of stroke (28%)
Progressive loss of renal function

Atherosclerotic Renovascular
disease(ARVD)
 It accounts for >90% of all RVD, in patients > 55, or < 30
Ys of age
 Lesions of RAS are 90% ostial (within the1st one cm of
renal artery origin)
 It can be demonstrated in:
o >10% of patients undergoing coronary angiography
o >40% with peripheral vascular disease (PVD), with > 5 vessels
involvement
o 30% with congestive cardiac failure (CCF), aged >70 years
o 15-20 % with ESRD
 It is increased with aging and is associated with common
atherogenic risk factors:
o Hypertension
o Hypercholesterolemia
o Smoking
o Diabetes

Clinical Presentations of ARVD
 Hypertension (HTN), with Chronic Kidney Disease (CKD),
a pro-atherogenic state make the incidental finding of
ARVD, rather than being the cause of it..?
 Epigastric bruit
 Hypokalemia and metabolic alkalosis
 Flash pulmonary edema(5%):
o Sudden onset of acute heart failure in absence of myocardial
ischemic event
o Commonly at night(due to posture-related redistribution of fluid
or may be due to diurnal variations of vasoactive peptides)
o Mechanism may be due to reduced natriuretic ability, coupled
with LVH and severe HTN in patients with severe bilateral
RAS
 Acute Kidney Injury (AKI), due to arterial occlusion
 Ischemic ATN, or related to ACE-I (after 1-14 days)

Prognosis of ARVD
 Renal outcome is determined by the presence of
parenchymal disease giving the picture of
ischemic nephropathy (intrarenal atheroma, or
cholesterol embolization)
 The correlation between the severity of proximal
lesions(degree of stenosis or occlusion) and renal
function is poor.. (?? Variable outcome for
revascularization)
 Poor prognosis (5-year survival<20 %)

Fibromuscular Dysplasia (FMD)
 It accounts for 10% of all RVD
 Most commonly in young women (20-35 Ys)
 The stenotic lesions are distal and appear like
“string of beads”, at angiography
 Clinically, presented with severe HTN, but renal
failure is unusual
 It is usually associated with other arterial
lesions (carotid stenosis in 10% of cases)
 Revascularization cure the HTN and restores
the kidney function completely; because the
kidney beyond the FMD, is usually healthy

Radiological Diagnosis of RAS
 MRA:
o Optimum, non-invasive
o 3-D phase contrast
o Safe in CKD stages 3 and 4
 Gadolinium-based MRI: ? Fear of related Nephrogenic systemic
fibrosis (NSF)
 Duplex /Color Doppler U/S:
o Disparate kidney size (> 1.5 cm in bipolar length)
o Can be combined with measurement of proximal renal blood flow velocity,
with intrarenal resistive index
o Accurate for detection of ARVD and for assessment of severity of RAS
o Time-consuming/Highly operator-dependent
 Captopril renal Scintigraphy: if unilateral disease and S. creat
< 2 mg/dl
 CT-angiography, can be complicated by radiocontrast
nephropathy
 Conventional intra-arterial arteriography:
o Reserved for patients with complex anatomy
o For confirmation of RAS prior to revascularization

Treatment of RAS
 Conservative medical management:
• Cessation of smoking/weight loss/exercise
• Strict Control of HTN
• Lipid lowering agents
• Aspirin
 Revascularization, especially successful in significant RAS
associated AKI, or with flash pulmonary edema:
o Percutaneous Transluminal Renal Angioplasty (PTRA), with
stenting (PTRAS), in >95% of cases
o Surgical reconstruction: celiac, or mesenteric –to- Renal
Bypass, in remainder of cases
 Balloon angioplasty:
o Uncontrolled HTN
o FMD (less effective in ARVD, recoil after dilatation can occur because
of the rigid lesions or because of dissection)
o Success rate:82-100 %
o Recurrence rate: 10 % (follow-up with duplex U/S)

Atheroembolic RVD
 Cholesterol embolisation syndrome (CES) is occurring in:
I. Elderly patients with widespread atherosclerosis (almost
exclusively)
II. As complication of abdominal aorta/renal artery manipulation or
surgery
III. As a consequence of angiography or PTRA
 Clinically:
I. Renal insufficiency &/or HTN
II. Livideo reticularis
III. Evidence of embolisation in other organs: Cerebrovascular
events, retinal artery occlusion, acute pancreatitis, ischemic
bowels, gangrene of extremities
 Urine analysis:
I. Cholesterol crystals (not usually present)
II. Increased cellularity
III. Proteinuria (mild)
IV. Eosinophiluria
 Eosinophilia: 11-16 %

Treatment of CES
 Control HTH (avoid hypotension)
 Adequate hydration
 ? Anticoagulants may delay healing of ulcerated
atherosclerotic lesions
 Dialysis may be needed

Hypertensive Nephrosclerosis
 Due to unopposed or sustained ↑ in intraglomerular
capillary hydrostatic pressure
 Great risk in African-Americans, elderly and those
with high SBP
 Pathogenesis:
o Stimulation of Renin release due to activation of
RAAS
o Reduced natriuretic capacity, due to CKD
o Disorganization of intrarenal vasculature: vascular
wall thickening and luminal obliteration
o Widespread interstitial fibrosis and
glomerulosclerosis

►► Benign nephrosclerosis:
 HTN > 10-15 Ys
 Kidneys become a victim of adverse effects --->Pronounced
medial vascular injury and progression to ESRD (2-5 %)
 Reduced kidneys size on U/S
 Unremarkable urinary sediment; except for proteinuria < 1.5
gm/day (? Asymptomatic)
 Time of initiation of effective ttt with ACE-Is/ARBs, together with
patient compliance and careful follow-up are important
 Target BP control is:
 <130/80, in patients with CKD
 <125/75, in patients with significant proteinuria

►► Malignant (accelerated) HTN:
 Abrupt ↑ of DBP > 130 mmHg  renal ischemia and renin production 
Intimal injury  Severe tubular and glomerular ischemia ARF
 Headaches, seizures/? Stroke, encephalopathy..
 Grade 3 or 4 retinopathy, with hemorrhages, exudates,
papilledema
 ? Microangiopathic hemolytic anemia
 ↑ of serum urea and creatinine
 Enlarged kidneys on U/S
 ? Active urinary sediment: Proteinuria (nephrotic range) and
hematuria (gross, or microscopic): AKI
 Emergency situation needing agressive BP control can reverse
renal functions: Parentral Na nitroprusside.. Smooth control over
36-48 Hs

Thrombotic Microangiopathies
I. Hemolytic Uremic Syndrome (HUS)
II. Thrombotic Thrombocytopenic Purpura
(TTP)
In both conditions, there is:
 Microangiopathic hemolytic Anemia (MAHA), with
anemia, RBCs fragmentation, schistocytes,
intravascular PLT clumping and hence
thrombocytopenia
 Typical renal histological lesions include
intraglomerular platelet and fibrin thrombi, with
ischemia and arteriolar lesions

Hemolytic Uremic Syndrome
(HUS)
 Commonest cause of AKI in children
 Children (< 4 years) ------> 90 % of cases
 Adults ---------> 5 cases/million/ Year

Forms of HUS
1- Typical, or Diarrhea-associated (D+ HUS):
o Onset is explosive, with AKI
o Verotoxin-producing E.Coli O157:H7 (VTEC), with damage to the
vascular endothelium(largely confined to kidneys)
o ? Associted Shigella dysentriae
o 90% ----->Good recovery
o 40% ----->Decreased GFR (long term follow-up)
o 5% ------>Mortality during acute illness
o Disease monitoring by: PLT count and RBCs fragmentation
2- Atypical, or (D-HUS):
o Older children and adults, most of them have no diarrhea
o ? Familial, associated with factor H deficiency which limit cleavage of
unusual large von Willebrand; leading to continuing platelet activation
o Poorer prognosis, death in > 50 % of cases

Treatment of HUS
Mainstay of therapy:
1. Fresh Frozen plasma (FFP) infusion
2. Plasma exchange
They are more effective in adult D+ HUS than in
childhood forms; in atypical D- form, they lower
the risk of ESRD and mortality

Thrombotic Thrombocytopenic Purpura
(TTP)
 Explosive AKI is less prominent
 Neurological abnormalities are usual
 Two main Forms:
Acute TTP Relapsing TTP
90 % Adults are usually affected,
with a chronic form of the
disease
Abrupt onset of fever,
neurological signs and purpura
Clinical condition similar to
atypical form of HU$
Survival now approaches 90 % ? Familial HU$ / TTP
Treatment: FFP infusion and plasma exchange

2ry Causes of HUS and TTP
Pregnancy-Associated Thrombotic
Microangiopathy:
TTP
HELLP
Post-partum HUS
HIV - Associated Thrombotic Microangiopathy
Cancer - Associated Thrombotic Microangiopathy
Drugs: ex: Ciclosporin

Systemic Sclerosis
 Renal involvement (50 %), in longstanding disease >
20 Ys..
 Mild proteinuria is usually present ± HTN
 Sclerodermal renal crisis, in 10-25 % of type 3
scleroderma:
o Accelerated HTN
o Microangiopathic hemolytic anemia
o AKI
 Pathology:
o Intimal proliferation of interlobular arteries, with deposition of
mucoplysaccharides: Onion-Skin appearance
o Fibrinoid necrosis of afferent arterioles  2ry Glomerular
ischemia
 Treatment: RAA-blockade, ± Non-DHPs, ±
Vasodilators (minoxidil) for HTN control.. Renal
function can recover
 Poor prognosis; because of other organ
involvement, especially restrictive cardiomyopathy

Sickle Cell Nephropathy
 Hypoxic/hypertonic medulla  Sickling  Recurrent
papillary infarction  Papillary necrosis:
o Often Silent
o ? Repeated UTI (chronic renal insufficiency)
o Hematuria (50 %)
 Vasa Recta Obliteration  Compromisation of
medullary counter-current system  ↓Urinary
concentrating ability  Volume depletion
 Nephrotic syndrome (4 %)
 Distal RTA (type 4)  ↑ K+ / ↑ Cl- metabolic
acidosis
 MPGN  FSGS

Treatment of sickle cell nephropathy
 Avoid:
 K+ supplements/K+ sparing diuretics
 NSAIDs
 TTT of volume depletion:
 Isotonic/hypotonic solutions (according to serum Na values)
 TTT of hyperkalemia:
 K+ exchange resins (Na polystyrene or kayexalate, oral or per
rectum)
 Shohl’s solution
 Na HCO3 tablets
 Loop diuretics
 TTT of hematuria:
 ɛ aminocaproic acid: in life threatening conditions, ? Fear of
thrombosis/uretral obstruction
 Mannitol/ Loop Diuretics: (reduce medullary tonicity)
 Na HCO3: (reduce medullary tonicity)

Renal Vein Thrombosis (RVT)
Causes of RVT
Nephrotic Syndrome:
(Loss of antithrombin III in urine/Protein C & S deficiency)
Renal Cell Carcinoma:
(Invasion of renal vein)
Volume Depletion:
(Impaired RBF)
Pregnancy/Estrogen therapy:
Extrinsic Compression:
{L.Ns, tumors, aortic aneurysm, retroperitoneal fibrosis or abscess,..}
(Sluggish renal venous flow)
Others:
{Sickle cell nephropathy, amyloidosis, diabetes, vasculitis, allograft
rejection}

Clinical Manifestations of RVT
 Depend on extent and rapidity of occlusion:
1. Acute:
o Nausea/vomiting
o Flank Pain
o Hematuria
o Leucocytosis
o Compromised renal functions
o Increased renal size on U/S
2. Chronic:
o Dramatic ↑ of proteinuria
o Tubular Dysfunction: Glucosuria, aminoaciduria, phosphaturia
and impaired urinary acidification

Diagnosis of RVT
 Investigations:
o MRV
o Doppler U/S: Not sensitive in “segmental” thrombosis
o Selective renal venography
o IVP: Calyceal stretch and ureteric notching
 TTT:
o Heparin, for 7-10 Ds
o Warfarin, for one year (or indefinitely)
o Fibrinolytics, for acute RVT associated with ARF

Question 1
A 38-Y-old woman was brought to the ED because
of headache, difficulty in concentration and
slurred speech. She had previously been in
excellent health. She was found to have fever,
anemia (Hb=8.4 gm/dl) and profound
thrombocytopenia (PLT=30.000). Peripheral blood
smear shows schistocytes. S. LDH was 5 times
above the normal limits. The most likely diagnosis
is:
A. ITP
B. Thalassemia major
C. TTP
D. Autoimmune hemolytic anemia
E. Aplastic anemia

Answer 1
A 38-Y-old woman was brought to the ED because
of headache, difficulty in concentration and
slurred speech. She had previously been in
excellent health. She was found to have fever,
anemia (Hb=8.4 gm/dl) and profound
thrombocytopenia (PLT=30.000). Peripheral blood
smear shows schistocytes. Serum LDH was 5
times above the normal limits. The most likely
diagnosis is:
A. ITP
B. Thalassemia major
C. Thrombotic Thrombocytopenic Purpura
(TTP)
D. Autoimmune hemolytic anemia

Question 2
A two-year-old boy with sever diarrhea, presents to the ED
with oliguria, fever, chills and pain in the flanks.
Examination revealed severe dehydration, lumbar
tenderness and the right kidney was palpable and tender.
BP was 100/40. Urine examination revealed hematuria and
proteinuria. Serum urea and creatinine were raised and
serum albumin was normal. CBC and peripheral smear
appear normal. The most probable diagnosis is:
A. Post-streptococcal GN
B. Nephrotic $
C. Hemolytic Uremic Syndrome (HU$)
D. Renal vein thrombosis (RVT)
E. Septic shock

Answer 2
A two-year-old boy with sever diarrhea, presents to the ED
with oliguria, fever, chills and pain in the flanks.
Examination revealed severe dehydration, lumbar
tenderness and the right kidney was palpable and tender.
BP was 100/40. Urine examination revealed hematuria and
proteinuria. Serum urea and creatinine were raised and
serum albumin was normal. CBC and peripheral smear
appear normal. The most probable diagnosis is:
A. Post-streptococcal GN
B. Nephrotic $
C. Hemolytic Uremic Syndrome (HU$)
D. Renal vein thrombosis (RVT)
E. Septic shock

Question 3
A 23-Y-old woman presents with marked swelling of the ankles
following a mild URT infection. Dipstick urine analysis
demonstrates: protein +++, with no hematuria.
Plasma creatinine was 68 mmol/l. Albumin 2.3 gm/dl.
Cholesterol 8.9 mmol/l (=360 mg/dl). Urinary protein
excretion 12 gm/24 Hs.
Renal biopsy was performed and shows minimal change
glomerulopathy. The patient was commenced on
prednisolone 60 mg/d and simvastatin.
Seven Days later, urine protein +++ and blood ++. She has
some loin pain and plasma creat was 106 mmol/l.
What is the most likely complication that had occurred?
A. Renal vein thrombosis
B. Interstitial nephritis 2ry to simvastatin
C. Obstruction 2ry to a sloughed papilla
D. Peri-nephric hemorrhage 2ry to renal biopsy
E. Acute crescentic change of minimal change nephropathy

Answer 3
A 23-Y-old woman presents with marked swelling of the ankles
following a mild URT infection. Dipstick urine analysis
demonstrates: protein +++, with no hematuria.
Plasma creatinine was 68 mmol/l. Albumin 2.3 gm/dl.
Cholesterol 8.9 mmol/l (=360 mg/dl). Urinary protein
excretion 12 gm/24 Hs.
Renal biopsy was performed and shows minimal change
glomerulopathy. The patient was commenced on
prednisolone 60 mg/d and simvastatin.
Seven Days later, urine protein +++ and blood ++. She has
some loin pain and plasma creat was 106 mmol/l.
What is the most likely complication that had occurred?
A. Renal vein thrombosis
B. Interstitial nephritis 2ry to simvastatin
C. Obstruction 2ry to a sloughed papilla
D. Peri-nephric hemorrhage 2ry to renal biopsy
E. Acute crescentic change of minimal change nephropathy

Question 4
A 33-Y-old man with hard to control HTN, is found to
have renal artery stenosis (RAS).
The following statements about RAS are true
except:
A. 80 % of cases are due to atherosclerosis
B. Fibromuscular dysplasia commonly affects
young men
C. Hypokalemia and metabolic alkalosis may occur
D. Renovascular HTN (RVH) due to Fibromuscular
dysplasia responds to revascularization in the
majority of patients
E. May produce an epigastric bruit

Answer 4
A 33-Y-old man with hard to control HTN, is found to
have renal artery stenosis (RAS).
The following statements about RAS are true
except:
A. 80 % of cases are due to atherosclerosis
B. Fibromuscular dysplasia commonly affects
young men
C. Hypokalemia and metabolic alkalosis may occur
D. Renovascular HTN (RVH) due to Fibromuscular
dysplasia responds to revascularization in the
majority of patients
E. May produce an epigastric bruit

Question 5
A 35-Y-old woman is admitted to the ER at 8.0 am, after having an
epileptic fit on the station platform.
O/E: She is confused, incontinent in urine and has a temperature of
37 o C. her husband stated that she had a diarrhea for the last few
days and she got a severe headache the evening before. She has
no previous history of epilepsy and she is taking no medications
regularly.
Hb was 8.6 gm/dl, total WBC was 12.000/l. and PLT was 23.000/l.
Retics was 4.6%. Blood film shows occasional fragmented cells.
LDH was 1300 U/l. Electrolytes were normal as well as liver
enzymes. Serum bilirubin was 1.7 mg/dl. Blood urea as 26.4 mg/dl.
Serum creatinine was 1.6 mg/dl.
Which one of the following statements is least likely to be true?
A. The clinical and pathological features may all be related to the
post-ictal state
B. Increased levels of high molecular weight von Willebrand factor
may be found in her blood
C. Enteric infection with E. Coli may be casually related to her
illness
D. The elevated LDH is likely to be of red cell origin
E. Coagulation screening tests in this disorders are usually normal

Answer 5
A 35-Y-old woman is admitted to the ER at 8.0 am, after having an
epileptic fit on the station platform.
O/E: She is confused, incontinent in urine and has a temperature of
37 o C. her husband stated that she had a diarrhea for the last few
days and she got a severe headache the evening before. She has
no previous history of epilepsy and she is taking no medications
regularly.
Hb was 8.6 gm/dl, total WBC was 12.000/l. and PLT was 23.000/l.
Retics was 4.6%. Blood film shows occasional fragmented cells.
LDH was 1300 U/l. Electrolytes were normal as well as liver
enzymes. Serum bilirubin was 1.7 mg/dl. Blood urea as 26.4 mg/dl.
Serum creatinine was 1.6 mg/dl.
Which one of the following statements is least likely to be true?
A. The clinical and pathological features may all be related to
the post-ictal state
B. Increased levels of high molecular weight von Willebrand factor
may be found in her blood
C. Enteric infection with E. Coli may be casually related to her
illness
D. The elevated LDH is likely to be of red cell origin
E. Coagulation screening tests in this disorders are usually normal

Question 6
A 56-Y-old white man with a history of HTN and IHD, complains
of headache and fatigue. BP was reported as 196/115 and a
normal lab. Evaluation. His physician prescribed him an
ACE-I and instructed him to return in 2-Weeks
The patient is brought to the ER five-Ds later with severe
proximal muscle weakness to the point he cannot rise from
a chair and is experiencing extreme fatigue, nausea and
vomiting.
Without other information available, which of the following
is/are possible?
A. The patient has symptomatic renal failure related to ACE-
Inhibition
B. Life-threatening Hyperkalemia is present
C. This patient has probable Renovascular HTN
D. A, B, and C are correct
E. Only A and C are correct

Answer 6
A 56-Y-old white man with a history of HTN and IHD, complains
of headache and fatigue. BP was reported as 196/115 and a
normal lab. Evaluation. His physician prescribed him an
ACE-I and instructed him to return in 2-Weeks
The patient is brought to the ER five-Ds later with severe
proximal muscle weakness to the point he cannot rise from
a chair and is experiencing extreme fatigue, nausea and
vomiting.
Without other information available, which of the following
is/are possible?
A. The patient has symptomatic renal failure related to ACE-
Inhibition
B. Life-threatening Hyperkalemia is present
C. This patient has probable Renovascular HTN
D. A, B, and C are correct
E. Only A and C are correct

Question 7
A 68-Y-old man has increasing HTN 3 weeks after an aortic angiogram and
subsequent repair of an abdominal aortic aneurysm. In the hospital, he
received brief courses of several drugs, including cephalosporins,
Cimetidine and heparin. He is currently receiving aspirin and dipyridamole.
Now BP is 170/110 mmHg. Bruits are heard on femoral arteries and there is
some mottling of the lower extremities and subungual petechiae on a lower
extremity nail bed.
Na +=142 mEq/l, and K +=5.1 mEq/l. CL -=104 mEq/l , and HCO3 - = 20
mEq/l. BUN=60 mg/dl, and S.Creat.=3.2 mg/dl. Hematocrit=35%, WBCs = 10.500
/l; PMNs=80 %, Lymphocytes=12%, Eosinophils= 8%.
Urine analysis shows: pH=5.2, protein ++, WBCs= 1-3/HPF, RBCs=10-15/HPF. Wright
stain of urine is positive for eosinophils
Choose the diagnosis most likely to explain the azotemia and HTN in
this patient
A. Nephrosclerosis
B. Atheroembolic disease
C. Drug-induced IN
D. Radio contrast-induced renal disease
E. Postoperative ATN

Answer 7
A 68-Y-old man has increasing HTN 3 weeks after an aortic angiogram and
subsequent repair of an abdominal aortic aneurysm. In the hospital, he
received brief courses of several drugs, including cephalosporins,
Cimetidine and heparin. He is currently receiving aspirin and dipyridamole.
Now BP is 170/110 mmHg. Bruits are heard on femoral arteries and there is
some mottling of the lower extremities and subungual petechiae on a lower
extremity nail bed.
Na +=142 mEq/l, and K +=5.1 mEq/l. CL -=104 mEq/l , and HCO3 - = 20
mEq/l. BUN=60 mg/dl, and S.Creat.=3.2 mg/dl. Hematocrit=35%, WBCs = 10.500
/l; PMNs=80 %, Lymphocytes=12%, Eosinophils= 8%.
Urine analysis shows: pH=5.2, protein ++, WBCs= 1-3/HPF, RBCs=10-15/HPF. Wright
stain of urine is positive for eosinophils
Choose the diagnosis most likely to explain the azotemia and HTN in
this patient
A. Nephrosclerosis
B. Atheroembolic disease
C. Drug-induced IN
D. Radio contrast-induced renal disease
E. Postoperative ATN

Renovascular disorders

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