imaging in
DESCRIPTION
imaging US in graft kidneys. It may be helpful in many conditions and it is safe and non invasive.TRANSCRIPT
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IMAGING OF Tx. KIDNEY
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• First successful transplant 1954.• 2 years survival rate > 90 %• Eligible patients are those with ESRD &dialysis
dependent.• Common causes:• Glomerulo &pylonephritis.• Diabetic nephropathy.• PCKD.
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Sonography of Normal Graft
• High-resolution colour Doppler imaging (CDI) with pulsed Doppler (PD) capability is required.• Quick & safe.• Non – invasive. • No intravenous contrast. • No ionizing radiation.
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Gray Scale assess :• The normal renal transplant is easily
visualized in Rt. or LIF lying anterior to the external iliac artery and vein.
• Parenchymal echogenicity.• Definition of the cortico/medullary
junction, collecting system, surrounding soft tissues and estimation of graft volume .
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Transverse colour Doppler image of a normal renal allograft showing its normal position anterior to the external iliac vessels .
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• The renal cortex is readily distinguished from the more echo-poor medulla.
• The renal sinus is normally hyperechoic in the absence of hydronephrosis.
• Small amount of fluid is often seen within the renal pelvis in the immediate postoperative period.
• volume is calculated using ellipsoid formula (0.5 x long x transverse x AP dimensions). • Small perigraft fluid collection is common; mostly
hematomas which resolve spontaneously
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Sagittal scan of a normal transplant. Echopoor medullary pyramids , bright renal cortex.
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Doppler Imaging
• CDI has revolutionized the evaluation of the renal transplant, allowing assessment of renal arterial perfusion and venous patency.
• Show RA anterior and posterior divisions, segmental interlobar, and arcuate arteries and corresponding veins within the graft .
• CDI is useful in differentiating prominent renal vessels from mild pelvicaliectasis which may occur as a consequence of edema at the ureteral anastomosis.
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• Tx .has low arterial vascular bed resistance characterized by streamlined systolic flow and continuous forward diastolic flow .
• Normal main RA velocity is 20 - 52 cm/sec with a mean of 32 cm/sec .
• The Resistivity Index (RI) measures the resistance to arterial flow within the renal vascular bed calculated from the PD arterial waveform .
• An RI < 0.7-0.8 is considered normal , RI > 0.9 is a strong indicator of transplant dysfunction, < o.6 indicates hypo perfusion as in RAS
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Causes of Elevated Resistive Index
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inevitable questions in Renal Graft
1. Is there a treatable renal or extrinsic cause?
2. Is immediate medical or surgical therapy required to save the graft?
3. Is a renal biopsy required for diagnosis?
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Renal Transplant Complications
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Parenchymal Complications 1- Acute Tubular Necrosis (ATN)• ATN occurs in 60% of cadaveric grafts ,the most frequent complication in the
first 48 hours P.O.• ATN is due to reversible ischemic damage to the renal tubular cells prior to
engraftment. Risk factors include:1- Cadaveric graft 2- Hypotension in the donor prior to implantation (aggravated by the use of diuretics or vasoconstrictors to maintain urine output or blood pressure) 3- Long warm (over 30 minutes) and cold (over 24 hours)ischemic times. • ATN can cause severe graft dysfunction , it is usually fully reversible with only
supportive therapy. • Short-term dialysis may be required in severe cases.
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U/S in ATN is quite variable . - The Tx. may appear normal.- In severe cases Tx is enlarged, grossly edematous and echo poor with effaced renal
sinus & loss of normal C/M differentiation. - Tx. with severe ATN generally have elevated RIs > 0.8 but can be normal in first 24 hours.
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ATN with preserved C/M differentiation is. RI 0.88.
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Rejection
• Allograft rejection is either of antibody (humoral) or cellular rejection (lymphocytes)
• Antibody-mediated rejection always involves blood vessels (vascular rejection)
• Rejection occurring within the first month PO is either acute rejection (AR) or accelerated acute rejection (AAR).
• Chronic rejection (CR) is an insidious process developing months to years PO.
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Acute Rejection (AR):• Common, in 30% of cadaveric grafts. • It is important event determining the short (1 year)
and long-term (5 year) graft survival.• Is successfully treated in over 80% of cases using
selective pulsed intravenous corticosteroids --Cs-A, and the monoclonal antibody OKT3 reducing the clinical triad of a tender swollen graft, fever and rising creatinine.
• Cs-A made AR indolent process commonly diagnosed by biopsy done for asymptomatic patient with rising creatinine .
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• AR is characterized pathologically by lymphocytic and polymorphonuclear cell infiltrating the interstitium (tubular ) and/or vessel walls (vascular ).
• The more severe forms of vascular AR are associated with a higher incidence of graft loss.
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Sonographic hallmarks of severe AR include:1. Graft enlargement due to edema 2. Decreased cortical echogenicity and swelling
resulting in loss of C/M differentiation & effaced renal sinus.
3. Acute rejection may be accompanied by edema of the P/C system wall and focal echo-poor areas (parenchymal infarction )and perigraft fluid due to necrosis and hemorrhage
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Decreased cortical echogenicity and swelling of the medullary pyramids resulting in loss of C/M differentiation.
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Edema within the renal sinus fat which effacing renal sinus echo complex.
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Edema of the collecting system wall.
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Focal echo-poor areas of parenchymal = infarction Perigraft fluid due to necrosis and hemorrhage.
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- In severe cases, PD characteristically shows reduced, absent or reversed diastolic flow with elevation of the RI .- In mild cases US can be normal & biopsy needed.
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Accelerated Acute Rejection (AAR):
• Typically occurs within the first postoperative week.• Is a combined cellular and humoral immune
response; low levels of circulating antibodies or pre sensitized T- lymphocytes thought to be responsible .
• Unusually severe form of rejection, presenting with oliguria and rapidly rising serum creatinine.
• The prognosis is poor with graft loss in 60% . • U/S findings same as AR and ATN.
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Chronic Rejection (CR):
• Develops months to years after post engraftment due to accumulating antibodies following repeated episodes of AR resulting in progressive vascular compromise of the graft & decline in renal function.
• On U/S , graftis small with thin echogenic cortex and relative sparing of the medullary pyramids .
• The RI is typically normal or slightly elevated. • Biopsy is often required to exclude superimposed
and potentially treatable AR.
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Chronic rejection.
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Cyclosporine Toxicity• Direct nephrotoxic effect of high serum levels
of Cs-A. • Can occur at any time, mostly seen in the
second or third month PO when drug doses are titrated against clinical response.
• Diagnosis established with Tx. dysfunction with high Cs-A levels.
• Sonographic findings are nonspecific and frequently normal
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Vascular Complications
• Renal Vein Thrombosis or Occlusion (RVT)
• Infrequent ,< 1 % but a surgical emergency. • Usually due to extrinsic compression or mobility of
graft, kinking of lengthy vein or surgical tech. problems @ anastomosis site.
• Patients present with oliguria or anuria and elevated creatinine in the immediate PO period.
• Early detection of RVT is critical to preserve graft function as the Tx lacks normal venous ,arterial collaterals & innervation found in native kidneys thus prone to venous infarction and rupture.
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• Treatment is immediate surgical exploration, thrombolysis offered to poor operative candidates.
• U/S findings in RVT include enlarged kidney with absent venous flow on CDI or PD imaging .
• Thrombus in renal vein is diagnostic ,absence does not exclude the lesion.
• Prolonged plateau-like reversal arterial flow in diastole is characteristic of RVT , when seen in combination with absent renal venous flow on CDI .
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Prolonged, plateau-like reversal of diastolic flow= RVT
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RVT with reversal of flow in diastole.
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Renal Artery Thrombosis (RAT)
• Due to technical problems at arterial anastomosis• Tx has no collateral arterial supply, irreversible injury
will result if the ischemic time exceeds 1.5 hours. • Patients present with anuria and hypertension.• If Doppler shows no arterial flow within Tx ,
angiography is indicated to confirm the presence of arterial thrombosis.
• Immediate surgery required when diagnosis established and nephrectomy is frequently necessary
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Renal Artery Stenosis (RAS)
• RAS develops in 12% ,occurs within 1 cm of the anastomosis.
• Rising creatinine ,hypertension and a bruit over the graft suggests the diagnosis.
• Percutaneous angioplasty successful in opening the stenosis in > 90% of cases, with normalization of blood pressure in 75%.
• Ultrasound shows normal kidney morphology , CDI and PD shows high velocity jet exceeding peak flow in the iliac artery
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High grade Tx renal artery stenosis. High velocity jet (4.95 m/s) + Aliasing and turbulent flow.
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CD image RA stenosis shows colour aliasing (arrows) at the site of the jet.
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Angiography demonstrated an 85% stenosis .
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• Aliasing and perivascular colour assignment are seen in high-grade stenosis.
• A low RI 0.6 or less may be highly specific for stenosis • Reduction in pulse amplitude, delayed systolic
upstroke within the renal parenchyma (parvus-tardus phenomenon) are usually seen in significant RA stenosis .
• A systolic acceleration time waveform > 0.07 s should be considered strong evidence of a high-grade RAS.
• In spite of U/S findings, angiography must be performed to locate site of RAS .
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Reduction in pulse amplitude & delayed systolic upstroke of renal artery stenosis.
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Urologic Complications
• Urologic complications occur in10% of renal transplants .
• Early urologic complications are generally technical and usually result from inadequate blood supply to the lower pole of the kidney, or from an imperfect anastomosis between ureter and bladder
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Urinary Fistula and Urinoma
• Leaks and fistulae occur in 2-5% of grafts and account for half of the urologic complications.
• Leaks typically present within 3 weeks of surgery at the ureterovesical junction as a consequence of ischemia and necrosis of the distal ureter due to vascular insufficiency.
• This complication is skill dependent ,can be minimized by keeping the transplant ureter short, avoid excessive dissection & stenting.
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• Urine leaks ( urinary ascites or urinomas) manifest as cystic fluid collections in the pelvis separate from the bladder.
• Can enlarge rapidly, but generally do not have septations unless infected.
• Diagnosis can be established by ultrasound-guided needle aspiration revealing high creatinine level in the fluid.
• This distinguishes a urinoma from PO hematoma or lymphocele, the latter having a creatinine level comparable to serum.
• The exact site of leak is best delineated by antegrade pyelography .
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. Urinoma : a technetium-99m mercaptoacetyltriglycine (MAG3) study show abnormal radionuclide activity around the transplant (arrows).
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• Contrast leak at the distal ureteral anastomosis
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Urinoma .
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Ureteral Obstruction and Hydronephrosis
• Ureteral obstruction occurs in 6% of grafts. • Approximately 90% of obstructions occur at the
ureterovesical junction due to fibrosis induced by ischemia or rejection of the ureter.
• PO ureteral edema or blood clots and peritransplant fluid collections (lymphoceles, urinomas, hematomas, and abscesses) may obstruct the ureter.
• Renal calculi are rare in the transplant kidney, < 2% .• Only half of the 18% of patients developing
hydronephrosis are truly obstructed .
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Dilatation confined to the renal pelvis in the early post operative period. NO OBSTRUCTION
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Obstruction
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Hydronephrosis secondary to a ureteral stone .
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Hydronephrosis and a lower pole stone in Tx.
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• The nephrostogram shows a second stone in the distal ureter above a tight stricture causing obstruction
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• Antegrade pyelogram depicting distal ureteric stricture.
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Tx. main renal vein mistaken for hydronephrosis.
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CDI readily confirms that this is a vessel.
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• The immediate treatment of choice for obstructive hydronephrosis is decompression by percutaneous nephrostomy.
• Ureteral strictures can be managed by percutaneous balloon dilatation and stenting, long-term stenting alone, or open repair .
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Lymphocele
• Very common in Tx. population, occurring in 15% of patients, mostly associated with ureteral obstruction
• Most develop within one year of transplantation. • Risk factors include incomplete ligation of the pelvic
lymphatics or a prior episode of severe rejection.• Palpable mass, leg pain and edema and impaired graft
function due to compression of the ureter are the Pt. presentations.
• Diagnosis is confirmed by needle aspiration which shows a creatinine level equivalent to serum.
• Collections are heavily septated , large but usually grow slowly
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Large septated lymphocele
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• The majority of lymphoceles are asymptomatic, requiring no therapy.
• Treatment options for symptomatic non infected lymphoceles include open surgical drainage, percutaneous aspiration with or without injection of a sclerosing agent and laparoscopic marsupialization .
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Aspiration
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Procedure Related ComplicationsHemorrhage
• The complication rate for percutaneous biopsy of the renal graft is approximately 5-8%.
• Perinephric hematomas account for 25-30% of all complications.
• Most are small and do not require additional therapy, hematomas may occasionally compress the ureter and produce hydronephrosis & impaired renal function.
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Sub capsular hematoma following percutaneous biopsy (*).
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Arteriovenous Fistula (AVF)
• Occurs as a consequence of simultaneous laceration of a renal artery branch and an adjacent vein during biopsy.
• Occur in 18% of biopsied kidneys but are almost always small and asymptomatic.
• Observation is the rule ,most thrombose spontaneously
• Embolization is reserved for fistulae associated with hemodynamically significant AV shunting or recurrent hematuria.
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AV fistulae features include:
• Focal colour aliasing within the nidus • Perivascular colour assignment at low flow
velocity settings due to tissue vibration artifact.
• The hallmarks of AV fistulae on PD include low resistance, high velocity arterial flow within the feeding artery and high velocity arterialized venous flow in the associated draining vein
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Mosaic colour assignment due to Arteriovenous fistula (AVF).
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Feeding artery (a) and vein (v) seen entering/leaving the nidus of an AVF (arrow).
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High velocity, low resistance flow due to AVF
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Pulsatile venous flow due to AVF
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Pseudo aneurysm
• Rare and may occur as a consequence of renal biopsy, infection within the graft or dehiscence of the arterial anastomosis.
• Any cystic area developing in or adjacent to the graft on serial ultrasound studies should be interrogated with Doppler to exclude the presence of pseudo aneurysm.
• CDI shows a high velocity jet from the feeding artery with eddying of blood referred to as the Yin-Yang sign within the aneurysm cavity .
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Colour Doppler of pseudo aneurysm. A high velocity jet from the feeding artery enters the aneurysm sac during systole.
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CDI shows the eddying of blood within the sac during diastole ("Yin-Yang" sign).
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• PD shows the jet, turbulent flow within the cavity and the classic biphasic flow pattern at the pseudo aneurysm neck .
• While most regress spontaneously treatment of symptomatic lesions is by embolization or surgical repair .
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Biphasic flow at the neck of a pseudo aneurysm.
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