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14th - 16th March, 2005
Department of Pathology
Sanjay Gandhi Postgraduate
Institute of Medical Sciences
Lucknow- 226014, INDIA
Coordinator:
R.K. Gupta
Professor & Head
Department of Pathology
SGPGIMS, Lucknow, India
US Coordinator:
Surya V. Seshan
Professor of Pathology
Chief, Renal Pathology
Weill Medical College of
Cornell University
New York, NY
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Slide Seminar – III
Pathology of Renovascular
& Tubulo-interstitial Diseases
Sharda Sabnis
Lorraine Racusen
Chief,
Division of Renal Pathology
Armed Forces
Institute of Pathology
Washington DC
Prof. of Pathology
Johns Hopkins Medical
School
Baltimore, MD
International CME on Renal Pathology, Department of Pathology , SGPGI, Lucknow, INDIA
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Slide Seminar- III
Pathology of Renovascular
& Tubulo-interstitial Diseases
•
•
•
•
•
•
Case 1: 33 years gravida III with hypertension and generalized edema
Case 2: 71 yrs female with hypertension, renal crisis, tight skin
Case 3: 52 yrs male with flank pain, red urine, proteinuria
Case 4: 52 yrs male with chronic eye problems and NSAID intake
Case 5: 60 yrs female with atrial fibrillations and red urine
Case 6: 33 yrs old female on anti-retroviral therapy
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 1
Case 1
H/O
• 33 yrs gravida III, abortion I and para 1 presented at 24
weeks of pregnancy with elevated BP 160-170/100 mm Hg.
• Was normotensive during previous pregnancy.
• At 7 weeks patient had baseline hypertension with urinary
protein of 111mg/day and normal LFTs.
• After 20 week gestation she noticed headache, followed by
nausea, vomiting and neck discomfort. She had pleuritic chest
pain, sore throat and diarrhea. A week later she noted
significant generalized edema.
• She had significant proteinuria and positive ANA test.
• No H/O visual disturbances, current headaches, nausea,
vomiting, abdominal pain, vaginal bleeding, joint pains,
rashes, oral ulcerations.
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Case 1
P/E:
• BP 182/118 mm Hg, generalized edema, shortness of breath,
genital herpes, abdominal exam normal for gestation, no
tenderness or other findings.
Laboratory findings:
• CBC: Hb 11.7, HCT 34, platelets 212000, white cell count
12.2
• U/A: >300mg/dl protein (> 9gms/day), 10-25 RBCs/hpf with
casts, 5-10 WBCs/hpf, urine output 30 cc/ hour
• BUN 19, Creatinine 0.9, bicarb 21, Glucose 118, albumin 2.3,
total protein 5.1, ALT 51, AST41, Alk Phos 155, uric acid 7.6,
anti-DNA antibody negative, complement levels-pending
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 1
Case 1
? Diagnosis
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 1
Case 1
Light Microscopy Diagnosis:
• In view of clinical history the above changes by
light microscopy are consistent with probable
pre-eclampsia. However, changes associated
with lupus nephritis (positive ANA test) cannot be
excluded
without
electron
and
immunofluorescence microscopy.
• Paraffin embedded tissue for electron microscopy was
available. Tissue for IF was not available.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 1
Case 1
Electron Microscopy
• The paraffin embedded tissue yielded eleven (11)
glomeruli.
• By electron microscopy: Glomerular capillary basement
membranes of normal thickness.
• Swollen endothelial and mesangial cells obliterate most
capillary lumina and some also contain foamy material.
• Fibrin tactoids are present in some capillary lumina.
• Along some capillaries electron dense material is noted;
however, immune-complex type deposits are absent.
Epithelial foot processes, in general, are slender.
• Tubuloreticular inclusions cannot be evaluated due to
fixation.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 1
Case 1
Final Diagnosis
Glomerular changes
with preeclampsia
consistent
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 1
Case 1
Pregnancy and Renal Disease
• Significant glomerular changes in preeclampsia first
described in 1918 by Lohlein and in 1920 Farr called
attention to the swelling of capillary walls.
• First EM study of glomeruli in preeclampsia reported
in 1959 by Farquhar (pronounced swelling of
endothelial cells and fibrin –like material under
endothelium).
• Glomerular endotheliosis – Spargo in 1959
• Pirani in 1963 demonstrated fibrin in glomeruli by IF.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 1
Case 1
Follow up:
• Patient’s condition worsened with continued elevated
BP, generalized and pulmonary edema & oliguria
She received:
• IV Lasix and Hydralazine for hypertension
• Dexamethazone (for fetal lung maturity)
• Magnesium sulphate 4 gm load followed by 2gm /hr for
seizure prophylaxis
• Fetal assessment was normal but due to severe
preeclampsia at early gestational age she underwent
caesarean section around 26 wk of gestation. Baby
normal for gestational age.
• Post operatively urinary output increased and BP
stabilized at 149/91. She was continued on Norvasc.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 1
Case 1
Definition
• Preeclampsia is rapid development of swelling, elevated
blood pressure, and proteinuria during pregnancy. Usually
occurs after 32 weeks of pregnancy but may begin earlier in
women with pre-existing renal disease and hypertension.
Does not cause hematuria.
Causes, incidence, and risk factors
• The exact cause of preeclampsia has not been identified.
Numerous theories of potential causes exist, including
genetic, dietary, hypoperfusion with vascular endothelial
dysfunction, and autoimmune factors. None of the theories
have yet been completely proven.
• Preeclampsia occurs in approximately 8% of all pregnancies.
Increased risk is associated with first pregnancies,
advancing maternal age, African-American women, multiple
pregnancies, and women with a past history of diabetes,
hypertension or kidney disease
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 1
Case 1
Pregnancy and SLE (Reference)
•
Lockshin MD, Sammaritano LR. Lupus pregnancy.
Autoimmunity. 2003 Feb;36 (1):33-40.
Pregnant lupus patients are susceptible to preeclampsia, especially if they suffer lupus nephritis, and to
steroid-induced hypertension and hyperglycemia.
•
Julkunen H. Pregnancy and lupus nephritis.Scand J
Urol Nephrol. 2001 Sep;35(4):319-27.
The outlook of pregnancy for women with lupus nephritis is
usually favorable if the disease (both renal and non-renal)
has been quiescent for at least 6 months before pregnancy,
and if, at conception, serum creatinine is less than 140
micromol/l, proteinuria less than 3 g/24 h and blood
pressure controlled. The risk of fetal loss is, however, at
least 2-3 times higher than in the normal population and
pre-eclampsia, prematurity and fetal growth retardation
frequently complicate these pregnancies.
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Case
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I
A
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N
O • Derksen RH, Bruinse HW, de Groot PG, Kater L. Pregnancy
in systemic lupus erythematosus: a prospective study. Lupus.
S
1994 Jun;3(3):149-55.
I
The prospective study included all pregnancies between 1987
S
and 1993 in SLE patients known at least 6 months before
&
pregnancy at the Lupus Clinic of our hospital. In 25 patients there
were 35 pregnancies. Thirty-four (97%) started at sustained
D
remission of disease; 14 (40%) in women with a history of
I
biopsy-proven lupus nephritis; Pregnancy resulted in 25 (71%)
S
live births, 8 (23%) first trimester abortions, and one intrauterine
C
fetal death. One pregnancy was terminated because of
U
hydrocephalus. Nine of 25 (36%) live births were delivered by
caesarean section. For 6 of 9 (67%) caesarean sections the
S
indication was fetal distress and pre-eclampsia. In the majority of
S
patients with SLE who conceive at remission, the disease does
I
not flare in pregnancy. With optimal obstetric care, close followO
up a high success rate (71%) can be achieved.
N
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Slide Seminar – I : Pathology of Glomerular Diseases - Case 1
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 2
Case 2
H/O
• 71 yrs female presented with anorexia, dysphagia and weight
loss for last 6 months and history of back and shoulder pain.
P/E:
• Epigastric and right upper quadrant pain. BP 143/80. No skin
lesions, no edema.
Laboratory findings:
• U/A Protein 500mg/day, RBCs 10-15/HPF, hyaline and
granular casts
• Creatinine 2.5mg/dL, BUN 30.0 mg/dL, FANA 1:320 to
1:1280, RF 1:10240
• Patient also had tightness of skin, intermittent claudications
and dysphagia.
• She developed hypertension, renal crisis and expired.
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? Diagnosis
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 2
Case 2
Glomeruli:
• Some normal, others show focal fibrinoid
necrosis, crescents extremely rare
• Complete necrosis in areas of infarction
• JG apparatus may be prominent in scleroderma
crisis, but not in chronic lesions
IF:
• Glomeruli and vessels show non-immunologic
trapping of Ig (IgM > others), C3 and fibrin
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 2
Case 2
Final Diagnosis:
Renal involvement in progressive
systemic sclerosis (scleroderma) with
changes of scleroderma crisis.
Scleroderma (Progressive Systemic
Sclerosis)
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 2
Vascular changes:
Case 2
• Mucoid edematous intimal proliferation mainly of interlobular arteries
> small arcuate arteries with external diameter bet 150 to 500 m
• Large arcuate and interlobar arteries usually spared
• Size predilections not absolute - large arteries and arterioles may be
involved
• Moderate to marked luminal narrowing by hypocellular, mucoid,
edematous, concentric intimal proliferation.
• Intimal ground substance:
– clear or basophilic by H&E, stains metachromatically with
toluidine blue, colloidal iron, and Alcian blue indication acid
mucopolysaccharides
– Stains light with PAS and negative with mucicarmine
– Light blue or clear with trichrome stain-indicating minimal or
absent mature collagen
• Whorled or concentric pattern of myointimal cells within the mucoid
material (onion-peel pattern), fibrin may be present
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 2
Case 2
Scleroderma Renal Crisis Defined as:
• Onset or aggravation of HTN (BP > 160/90 mm
Hg), appearance of grade III or IV retinopathy
• Elevation of plasma renin activity > twice normal
• Rapid deterioration of renal function within 1
month
Renal histology:
• Characteristic vascular lesions of scleroderma
often associated with infarcts
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 2
Case 2
References:
1. Denton CP, Black CM. Scleroderma--clinical and pathological
advances. Best Pract Res Clin Rheumatol. 2004 Jun;18(3):271-90
2. Steen VD. Scleroderma renal crisis. Rheum Dis Clin North Am. 2003
May; 29(2):315-33.
3. Zeng X, Chen J, Dong Y. Clinicopathological study of renal
involvement in patients with systemic sclerosis Chin Med J (Engl).
1998 Mar;111(3):224-7.
4. Chung L, Utz PJ. Antibodies in scleroderma: direct pathogenicity and
phenotypic associations. Curr Rheumatol Rep. 2004 Apr;6(2):156-63.
5. Mayes MD. Scleroderma epidemiology. Rheum Dis Clin North Am.
2003 May;29(2):239-54.
6. Mouthon L, Garcia De La Pena-Lefebvre P, Chanseaud Y, Tamby
MC, Boissier MC, Guillevin L. Pathogenesis of systemic scleroderma:
immunological aspects. Ann Med Interne (Paris). 2002
May;153(3):167-78.
7. Hawk A, English JC 3rd. Localized and systemic scleroderma. Semin
Cutan Med Surg. 2001 Mar;20(1):27-37.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 3
Case 3
H/O
• 52 year Caucasian male presented with flank pain and red
urine.
P/E:
• BP 130/80 mm Hg, Lower extremity pitting edema
• No family history or previous history of renal disease or
infection and not on any medications.
Laboratory findings:
• U/A: 3+ protein ( 7.0 Gms/day), Many RBCs/HPF, 2-4
WBC/HPF, no red blood cell cast, rare granular casts and oval
fat bodies.
• Other tests:
• BUN 23mg/dL, creatinine 2.3 mg/dL, Cholesterol 280 mg/dl,
Serologic tests for lupus, and ANCA tests negative. Anti
GBM-antibody neg.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 3
Case 3
Clinical Differential Diagnosis
– Post infectious glomerulonephritis
– Glomerulonephritis (MPGN, LE, etc)
– RPGN
Diagnosis
Membranous glomerulopathy
associated with renal vein
thrombosis (RVT)
Follow up:
– Renal ultrasound confirmed presence of RVT.
– Patient received anticoagulation.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 3
Case 3
In RVT and GN:
• Renal biopsy shows glomerular changes by LM,
EM and IF.
• Margination of PMNs in glomerular capillaries.
• Other changes include interstitial edema, and
variable chronic Tubulo-interstitial disease -often
out of proportion to the glomerular lesion.
• Margination of PMNs and tubulo-interstitial
changes out of proportion to the renal lesion are
morphologic clues to the presence of
complicating RVT
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 3
Case 3
• Association between RVT and renal disease first
described in 1840 by Rayer et al.
• RVT can be a superimposed feature in a number of
glomerulopathies (MGN, MPGN, Lupus nephritis,
amyloid etc.)
• Lesser association with MCD, FSGS and diabetes with
nephrotic syndrome.
• Overall incidence in MGN and MPGN ranges from 554% with average of 20-30%
• Risk of RVT increases with low serum albumin below
2g/dL with↑-antiplasmin and ↓antithrombin III levels.
• RVT is associated with hypercoagulable state and
assays for fibrinogen degradation products (FDP),
antithrombin III (AT III), VIIIR:AG, and fibrinogen confirm
a state of hypercoagulation.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 3
Case 3
Several explanations are offered:
• Considered as a secondary complication therefore
associated with any renal disease with nephrotic
syndrome.
• Experimental increases in renal vein pressure by ligature
in dogs do not produce massive proteinuria unless
contralateral nephrectomy is performed and do not
reveal histologic lesions similar to man. Remission of
proteinuria
does
not
occur
after
relief
of
occlusion/pressure on vein
• With all available data RVT is considered as a
complication and not a cause of nephrotic syndrome
and/or renal lesions.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 4
Case 4
• 52 yrs old male presented with a history of fatigue, alcohol
use, and depression for several years
• He had a creatinine of 2.9 mg% about 1 year prior to biopsy.
• He had been drinking a lot of water, and was using topical
antibiotics for chronic eye problems and NSAIDs quite
regularly for headaches.
• He had cervical lymphadenopathy and lymph node biopsy 3
years ago revealed hyperplasia.
• Kidneys are noted to be enlarged on sonography.
• Parotid glands appear enlarged.
• Creatinine at the time of biopsy was 3.1 mg%.
• HIV and hepatitis B and C, and other serologies are negative.
• What do you see? What is your differential diagnosis? What
would you predict as the prognosis?
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Case 4
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 4
Case 4
Diagnosis:
Diffuse interstitial nephritis with
chronic changes in a patient with
Sjogren’s syndrome
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 4
Case 4
• The biopsy reveals interstitial nephritis, with mixed infiltrate,
including eosinophils. Macrophages (CD68 positive) are
numerous. Extensive interstitial fibrosis and tubular atrophy
are noted. One glomerulus has a segmental scar, and there
is moderate arteriosclerosis. Immunofluorescence studies are
negative. EM is deferred. A diagnosis of subacute and
chronic interstitial nephritis with eosinophils, rule out drug
reaction, was made.
• On further analysis of the patient, sicca syndrome was
diagnosed. Pulmonary and rheumatology consults were
obtained, and a diagnosis of Sjogren’s syndrome was made,
though the disease usually occurs in females, and serologies
were negative. The patient was put on steroid therapy. His
energy improved, lympadenopathy and parotid enlargement
regressed, and creatinine improved to 1.5 mg%.
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Slide Seminar- II: Pathology of Renal Transplant - Case 4
• While eosinophils are not typical in the interstitial
infiltrates in Sjogren’s syndrome, they have been
described. However, drug reaction cannot be ruled out.
TINU syndrome was considered, but did not fit the
clinical picture. His recovery of function is impressive, in
view of the extensive fibrosis.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 4
Case 4
References:
1. Goules A, Masouridi S, Tzioufas AG, et al. Clinically
significant and biopsy-documented renal involvement in
primary Sjogren syndrome.
Medicine (Baltimore)
79:241-9, 2000
2. Sessa , Meroni M, Barttini G, et al. Acute renal failure
due to idiopathic tubulo-interstitial nephritis:uveitis:
TINU syndrome. Case report and review of the
literature. J Nephrol 13:377-80, 2000
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 5
Case 5
• A 60 yrs old woman presents within a week of new onset
of atrial fibrillation.
• She had an episode of hypotension, and was noted to
have a rise in creatinine.
• She also had noted red urine episodically for some time,
and was found to have hemolysis. She undergoes renal
biopsy to determine the etiology of her acute renal
failure.
• What are the major findings illustrated here?
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Case 5
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 5
Case 5
Diagnosis:
Diffuse acute tubular injury with
hemoglobin casts in a patient with
PNH
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 5
Case 5
• The biopsy reveals extensive acute tubular injury in a small
cortical sample, with pigmented casts diagnosed as
hemoglobin casts.
• Iron stain documents iron deposition in tubular cells.
• There were also focal edema and inflammation, including
eosinophils in outer medulla – R/O drug reaction.
• The patient had been diagnosed with paroxysmal nocturnal
hemolysis.
• Soon after the biopsy, she underwent mitral replacement. A
few months later, she presented with atrial fibrillation and
developed ischemic bowel requiring resection. Her creatinine
peaked at 4.6 mg%, but at discharge was 1.4 mg%.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 5
Case 5
• Pigmented casts can be seen in hemoglobinurias (eg in
hemolytic transfusion reactions and other forms of
hemolysis as in this case) and in myoglobinuria –
immunostaining can be used to differentiate the two.
• Renal involvement in PNH is usually chronic disease due
to iron stores and microvascular thrombosis – diagnosis
can be made using MRI.
• Occasionally, acute renal failure has been reported with
acute hemolytic episodes – hypotension and/or
thrombosis may underlie the injury, as it is not clear that
hemoglobin is toxic to renal tubules.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 5
Case 5
References
1.
2.
Jose MD, Lynn KL. Acute renal failure in a patient with
paroxysmal nocturnal hemoglobinuria. Clin Nephrol
56:172-4, 2001
Rimola J, Martin J, Puig J, et al. The kidney in
paroxysmal nocturnal haemoglobinuria: MRI findings.
Br J Radiol 77:953, 2004
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 6
Case 6
• A 33 yrs old female was diagnosed with HIV infection 12 years
prior to the biopsy.
• She is on anti-retroviral therapy (indinavir and combivir) with
CD4 counts of 350-400.
• She has had sterile pyuria for 12 months, and had been treated
with anti-tuberculous therapy; however, pyuria persisted.
• She has some lymphadenopathy – a lymph node biopsy done
previously was non-specific.
• On urinalysis, there are 3-5 RBC, 25-30 WBC, 1+ protein.
• Hepatitis B and C are negative.
• ESR is 128.
• Hematocrit and creatinine are normal.
• Renal scan is negative, gynecological work-up is negative.
• What are the major findings on this biopsy? What would you
recommend to this patient?
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Case 6
? Diagnosis
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 6
Case 6
Diagnosis:
Indinavir crystal deposits in a
treated HIV+ patient with antiretroviral agents
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 6
Case 6
• The biopsy reveals deposition of refractile crystals,
spicular or rhomboid in shape, consistent with indinavir
crystals. There is medullary and cortical inflammation
with eosinophils. Fibrosis and tubular atrophy are seen
in the medulla.
Mild tubular injury is seen, with
intratubular cell debris.
• IF studies reveal only scattered peripheral mesangial
staining for C3.
• EM of 1 glomerulus reveals only mild focal podocyte foot
process effacement.
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 6
Case 6
• While tubulointerstitial nephritis may be due to drugs, it
has been described with indinavir crystal deposition.
• Crystals were also found in the urine. The patient was
able to transition from indinavir to another anti-retroviral
agent. She was able to become pregnant with in vitro
fertilization and delivered a baby boy about 3 years after
the biopsy.
• Indinavir and sulfadiazine, both used to treat HIVinfected patients, have become the most frequent cause
of drug-containing urinary calculi; nephrotoxicity may be
reduced by administering with food.
• Leukocyturia was associated with crystalluria and
progressive loss of renal function in a prospective study
of indinavir treated patients.
• Fortunately, less toxic anti-retroviral agents can be
End
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Slide Seminar- III: Pathology of Renovascular & TI Diseases - Case 6
Case 6
References:
1. Aarnoutse RE, WAsmuth JC, Fatkenheuer G, et al.
Administration of indinavir and low-dose ritonavir with food
reduces nephrotoxic peak plasma levels of indinavir. Antivir
Ther 8:309-14, 2003
2. Daudon M, Jungers P.
Drug-induced renal calculi:
epidemiology, prevention and management. Drugs 64:245,
2004
3. Dielman JP, van Rossum AM, Stricker BC, et al. Persistent
leukocyturia and loss of renal function in a prospectively
monitored cohort of HIV-infected patients treated with
indinavir. Acquir Immune Defic Syndr 32:135, 2003
4. Perazella MA. Drug-induced renal failure: update on new
medications and unique mechanisms of nephrotoxicity. Am J
Med Sci 325:349, 2003
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