imaging approach of renal diseases in immuno-compromised patients jacques le roux 11/05/2012

Post on 25-Dec-2015

220 Views

Category:

Documents

1 Downloads

Preview:

Click to see full reader

TRANSCRIPT

Imaging approach Imaging approach of renal diseases in of renal diseases in

immuno-immuno-compromised compromised

patientspatients

Jacques le RouxJacques le Roux11/05/201211/05/2012

•The patients

•The diseases

•Approach - clinical- imaging options- imaging approach

THE PATIENTS

1. The prototype – HIV/AIDS

2. Any chronic disease e.g.•Cancer

- multiple myeloma- leukaemia (most common malignant cause of bilateral ↑ kidneys)- lymphoma (usually NHL) – kidney very common extranodal site

•Collagen vasc diseases e.g. SLE (lupus nephritis)•DM

3. Chemoradiotherapy

4. Transplant patients e.g. kidney, bone marrow

THE DISEASES

A. NEPHROPATHY•This is the diff Δ of renal failure – Pre, renal, post renal

Renal: (parenchyme disease)•Imaging can suggest a diagnosis

- the delayed (persistent) nephrogram/↑echos•Diagnosis remains histological e.g.

1. Acute Tubular Necrosis - oedema•Most common cause of acute renal failure•Due to:

- drugs: Haart, antibiotics (AMPH B), contrast (Iodine), chemotherapy- ischemia (renal art stenosis)- renal transplant rejection

2. Glomerulosclerosis – cell proliferation•DM, Lupus Nephritis

3. Nephrocalsinosis - Calcifications•Hypercalcemia

B. RENAL INFECTIONS1. Acute pyelonephritis - DM (E.coli)2. Emphysematous pyelonephritis – gas forming organisms - life threatening,DM3. Chronic pyelonephritis - reflux , obstruction (stones)4. Opportunistic infections – AIDS related

•Pneumocystis jiroveci •TB, MAI (mycobact avium intracellulare)•Fungi (candida, aspergillus)

C. RENAL TUMORSI. Non AIDS-related in imm. compr. patients

•Non Hodgin Lymphoma•Leukemia•M. Myeloma

II. AIDS-related•NHL•Kaposi•RCC ( 8 times more)

D. DRUGS (AIDS RELATED) – HAART

1. Direct (nephrotoxic)- Nephropathy (ATN)- Stones (dark) - Indinavir- FANCONI syndrome (tubular dysfunction)

•Kidney cannot reabsorb – glucose, amino acids, phosphate•Compl. Osteopenia - rickets

- osteomalacia

2. Indirect – insulin resistance•↑Colesterol→ renal art. stenosis→ HT•DM

APPROACH

•Clinical: - history, renal function (↑ creat.)

•Imaging options:

1. ULTRASOUND - choice for screening (size, hydronephrosis)•Size 9-13 cm•Central echo complex (renal sinus) – dominates sonar picture

- Contains: - fat (↑echos), vessels - renal pelvis (colleting system) - surrounded by parenchyma

•Parenchyma1 Cortex – similar or ↓echos compare to liver2 Medullary pyramids - ↓ egos (sonolucent) compare to cortex

- rounded or cone shape as they bulge into complex

•Difference between cortex and medulla echos creates cortex-medulla differentiation•Color doppler – venous involvement of renal tumors

RENAL PARENCHYMA (NORMAL KIDNEY)

ADULT•Parenchyma equal or ↓ echo as liver•Central Echo Complex ↑ echo

NEONATECortex - ↑ echo compared with liver - Pyramids look like hydroneph

2 CT = choice for renal tumours (replaced KUB and IVP)• Precontrast – think gasses, masses, stones, bones• The 3 phases with contrast (CT -IVP)

i Corticomenullary (early arterial 20 – 90 sec)- cortex enhances before medulla- diff between them

ii Nephrogram ( 2 – 3 minutes)- renal parenchyma uniformly enhance- size, symmetry, contour, density, parench loss

iii Pyelogram – excretory (5 - 15 minutes)- opacity collecting system- calyces cupped or clubbed

• 3D for art and venous structures

3 NM (frans en gerrit se speelveld)• DTPA (glom. function)• MAG 3 (tubular function)• DMSA anatomy (stays in cortex) e.g.

- scar tissue – pyelonephr.- Massas

4 MRI – if contraindication

IMAGING APPROACH

KIDNEYS

BILAT RENAL DISEASE UNILATERAL (Systemic-medical) (Focal-surgery)

Acute: Bilat. Large >13cm Chronic (end stage): bilat small <9cm e.g. immuno compromised e.g. HT, DM

A. Nephropathy – is parenchyme disease (Edema, renal failure)

US CT - Large kidneys and smooth - ↑kidneys- ↑echo – parenchyma - Precontrast - ↑Att medulla (prot in tubuli) (cortex more than liver) - Delayed nephrogram or striated- Loss of diff. (stripes in cortex is dilated tubuli with contrast - no-↓echo-renal sinus fat uniform enhancem)

NEPHROPATHY•Large kidney (13cm)•↑Echo – parenchyma•↓Echo renal sinus fat•Loss of diff.

RENAL FAILURE

•Both kidneys small (< 9cm)•↑ echo in parync. compared liver

AIDS NEPHROPATHY – MEDULLARY NEPHROCALCINOSIS

•Medulla pyramids ↑ echo•Cortex and columns of Bertin (cortex between pyramids) normal

ACUTE PYELONEPHRITIS - US•Focal area ↑ echo

RENAL ABSCESS - US •Cystic mass with internal heterogeneous ↑echo fluid (debri)

B. RENAL INFECTIONS

ACUTE PYELONEPHRITIS – CT with contrast•Wedges of ↓Att (edema)•Striated nephrogram

PERIRENAL ABSCESS - CT•↓ Att (fluid)•Gas bubbles

EMPHYSEMATOUS PYELONEPHRITIS (GAS)

X-RAYStriations in parenchyma – is gas in collective system

CHRONIC PYELONEPARITIS (REFLUX NEPHROPATHY)

IVPBlunted calyx with overlying scar

END STAGE RENAL TB

R Small and calcifiedL Compensatory hypertrophy

OPPORTUNISTIC INFECTIONS – IMAGING NON SPECIFIC

•Pneumocystis jiroveci (fungus) MAI, CMV- small cortical calcifications- nephrocalcinosis-striated nephrogram

•Fungi (candida, aspergillus)- micro abscesses-hydronephrosis (fungal ball)

•TB (renal second most common) ,from lungs- Acute - abscesses- Chronic - small scared KIDNEY,Ca++ ,strictures (ureters)

CANDIDA ALBICANS

PyonephrosisNephrostomy in left kidney - previous hydronephrosis

RENAL ABSCESS – LEFT KIDNEY

Pyelogram (excretory)Low att. mass with decreased excretion of contrast

TB ABSCESS - CT WITH CONTRAST

Low att. with Ca⁺⁺

RENAL TB - IVP

• R Hydronephrosis• Stricture mid uret

C. RENAL TUMORS IN IMMUNE COMPROMISED PATIENTS-Look for other sites of involvement

I. NON AIDS-RELATED

1. Non Hodgkin lymphoma•Kidney very common site for extra nodal lymphoma•Renal parenchyma contains no lymph. tissue - comes from retroperitoneal nodes, renal capsule (rich lymph vessels) or with blood/hematogeneous

Lesion (75% bilat.)Classic: - large kidneys

•Tumor surrounds kidney without compression of parenchyma•Encase blood vessels but lumen remains open•No thrombosis of IVC or renal vein•Enhance less than parenchyma

2. Leukaemia•Most common cause of bilat. ↑ kidneys•Chloroma – focal mass in cortex

3. M. Myeloma •Nephrocalsinosis - Hypercalcemia•Punched lytic bone lesions

NON AIDS-RELATED LYMPHOMA (NHL)

Coronal – CT with contrast•Bilat ↑•No enhancement - homogenous

II. AIDS RELATED

1 NHL•Usually multiple nodules•Solitary lesions

2 KAPOSI•Rare in kidney – skin lesions•↓Att

3 RCC (8 times more)•Hypervascular•Trombosis – IVC, renal vein

RCC

Solid ↑ echo mass (upper pole)

AIDS – RELATED LYMPHOMA

Solitary mass – poor enhancement

DRUGS ---- HAART (INDINAVIR) - CALCULI ARE DARK - NO IMAGING SUPERIOR

•SONAR - CALCIFIC FOCI - If you see calculi – calcium, uric-acid, in this case was not related to indinavir

•Indirect signs- Hydronephrosis in the absence of calculi

FANCONI SYNDROME WITH RENAL FAILURE

•Bone scan – T99-MDP•Diffuse bone uptake•Kidney no uptake – kidney failure (no function)

L RAS - MRA

RAS - DOPPLER

Intrarenal art – Tardus parvus waveform•Parvus ↓ systolic peak •Tardus delayed before systolic peak

Main renal art - systolic peak ↑

RENAL TRANSPLANTANATOMY

Kidney•R Iliac fossa – extraperit•Vessels – iliac (ext or common)•Ureter – trigone

ImagingChoice - US - grayscale, doppler - NM - MAG 3Additional - CT – anatomy,VASC, 3 phases - MRI – contra indications

COMPLICATIONS

A. ↓ Kidney function (parenchyme disease)

1. ATN – ischaemia, first week 2. Rejection

• Hyperacute – minutes• Acute – after 1 week• Chronic – after months

3. Drugs (nephrotoxic) – Pat. Becomes ↓ immune• Cyclosporine – after 1 month• Post transplant lymphoproliferate diseases

(a) Lymphoma(b) RCC(c) Kaposi

IMAGING ↓ Kidney Function• US – grayscale (as before), egos,diff• NM - ATN – normal perfusion, ↓ excretion

- Rejection and cyclosporin - ↓ perfusion and excretion• To diff between ATN, rejection, cyclosporin

- Do biopsy (US or CT guidance)

B. Fluid collections - HAUL 1. Hematoma – first day 2. Abscess (fever) – first week 3. Urinoma – first month 4. Lymphocele – after one month

** NM - Urinoma – takes up tracer – is in urine - Lymphocele - no uptake (cold)

- usually – ureter-bladder junction

C. Vascular 1. Prerenal – RAS, RA thrombosis 2. Post renal – RVS, RV thrombosis 3. Complications due to biopsy:

- AVF- Pseudo aneurysm

If you suspect above named – do convent. angiography for stents (RAS)- Thrombectomy (RV thrombosis)- Embolization (AVF)

URINOMAUptake of tracer

LYMPHOCELENo tracer uptake

ATN•Normal perfusion•↓ excretion

PULSE DOPPLER (SPECTRAL WAVE FORM)

•Normal graft - low resistance waveform - flow in sist and diast.

•Acute rejection – end-diastolic flow absent - high RI >.8

•Art. flow reversed in diast.

?Severe rejection / ?ATN / ?renal vein thromb

- ΔΔ from renal vein thrombosis•Color Doppler – vein patent

•Biopsy showed rejection

RENAL VEIN THROMBOSIS•Art. flow reversed in diast. (plateau)•No venous signal in vein

PSEUDOANEURYSMMid ren art– forward and reverse flowDo conv. angio

AVF•Turbulent flow•CT showed early filling of veinDo conv. angio

References

1. Symeonidou C, Imaging And Histopathology Features Of HIV Related Renal Disease, Radiographics 2008; 28: 1339 – 1354.

2. Daneman A, Renal Pyramids Focused Sonography Of Normal And Pathologic Processes, Radiographics 2010; 30: 1287 – 1307.

3. Brandt WE, Fundamentals Of Diagnostic Radiology 3rd ed. 874 – 908.

4. Brown E, Complications Of Renal Transplantation: Evaluation With US And NM, Radiographics 2000; 20: 607 – 622.

top related