Renal Parenchymal Dieases.pptx

2,156 views 46 slides Nov 24, 2022
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About This Presentation

Imaging of Renal Parenchymal Diseases,
Renal failure


Slide Content

Renal Failure & Renal Parenchymal Disease Dr. Niranjan Patil DEPARTMENT OF RADIODIAGNOSIS DR D Y PATIL HOSPITAL KOLHAPUR

Acute Renal Failure Rapid deterioration in renal function characterized by : - azotemia with - decline in glomerular filtration rate (GFR) - which may or may not be accompanied by Oliguria (urine output <400 ml/d) Chronic Renal Failure • Kidney damage or decreased renal function for ≥ 3months duration resulting in GFR of less than 60 mL/min/1.17m2

Causes of A cute renal failure PRERENAL Cardiogenic shock Anaphylaxis Sepsis Renal ar ter y stenosis Severe dehydration INTRARENAL Acute Tubular necrosis -Hemolysis -Antibiotics -Contrast nephrotoxicty 2. Glomerulopathy -SLE -HSP -Postinfective glomerulonephritis POSTRENAL Renal vein Thrombosis Obstruction due to; -Calculi - Hemorrahge - Tumor Causes of Chronic renal failure PRERENAL Renal artery stenosis chronic dehydration congestive heart failure cirrhosis INTRARENAL 1. common causes -Diabetic n ephropathy -Hypertensive -Glomerulosclerosis 2. Glomerulonephritis 3. congenital ADPKD 4. Renal tubular acidosis 5. Drugs 6. TB 7. Gout 8. AIDS nephropathy POSTRENAL Neurogenic bladder Ureteric/bladder outlet Obstruction Retroperitoneal fibrosis

Enlarged kidneys in the setting of AKI increased renal cortical echogenicity and loss of the normal corticomedullary differentiation Increased cortical thickness Small or atrophic kidneys are often seen with CKD Markedly increased renal cortical echogenicity is seen in CKD Decreased cortical thickness reduced renal cortical thickness <6 mm Ultrasonography Acute RF Chronic RF

P reserved interpapillary line is a useful landmark for evaluating loss of renal parenchyma. Interpapillary line is drawn through the tips of papilla (base of the calyces) the distance from this line to lateral surface of kidney is the renal parenchymal thickness which averages to 2.5–3 cm. Distance s less than 2 cm are suggestive of parenchymal loss while those greater than 3.5 cm indicate mass lesion or infiltration. INTERPAPPILARY LINE

Morphological criteria to categorize renal parenchymal disease

UNILATERA L LARGE SMOOTH KIDNEY Renal vein thrombosis Acute arterial infarction Xanthogranulomatous pyelonephritis Obstructive uropathy Acute pyelonephritis Compensatory hypertrophy

Renal Vein Thrombosis USG E nlargement and unilateral hypoechoic parenchyma Doppler findings include: reversal of arterial diastolic flow absent venous flow visualization of thrombus within the lumen high resistance in the renal artery with elevated RI reversal of arterial diastolic flow

the thrombosis is observed as a filling defect during venous phase imaging following intravenous contrast Long linear filling defect in the left renal vein. CT findings

Renal infarction Renal infarction results from interruption of the normal blood supply to part of, or to the whole kidney.   Causes of renal infarction include Thromboembolism Aortic dissection Renal artery stenosis

Power doppler Colour doppler Ultrasound Hyperechoic Absence of flow in the renal artery Infarcts will appear as wedge-shaped regions of nonperfusion  

contrast-enhanced CT demonstrate hypoattenuation of the posteroinferior part of the kidney with surrounding stranding. There is preservation of the very outer layer of parenchyma ( cortical rim sign ). cortical rim sign

Xanthogranulomatous pyelonephritis bear paw sign  

Without dilated PCS Unilateral smooth enlarged kidney Progressively dense Nephrogram Obstructive uropathy With dilated PCS Absent nephrogram + Echogenic collection in PCS Dilated calyces with contracted pelvis containing calculus s/o xanthogranulomatous pyelonephritis Acute venous thrombosis Renal infarct • Cortical rim enhancement • Angiography Thrombus/ Embolus • Filling defect in renal vein with a/w renal enlargement Acute pyelonephritis Clinical diagnosis • Bacteremia • Pyuria • Flank pain

Acute urinary obstruction causes a large, smooth left kidney with delayed contrast excretion and prolonged nephrogram . Acute pyelonephritis. Generalized enlargement of the left kidney with decreased density of contrast material in the collecting system

PROLIFERATIVE AND NECROTIZING DISORDERS 1. Acute glomerulonephritis. 2. Polyarteritis nodosa . 3. Wegener's granulomatosis. DEPOSITION OF ABNORMAL PROTEINS 1. Amyloid 2. Multiple myeloma. ABNORMAL FLUID ACCUMULATION 1. Acute tubular necrosis. 2. Acute cortical necrosis NEOPLASTIC INFILTRATION 1. Leukaemia and lymphoma. INFLAMMATORY CELL INFILTRATION 1. Acute interstitial nephritis. BILATERAL LARGE SMOOTH KIDNEY

- Renal cause of AKI characterized by tubular epithelial cell damage from toxins or ischemia - Most common Reversible cause of renal failure • Etiology 1. Ischemia: Hypotension (most common cause), hypovolemia, renal vasoconstriction, DIC 2. Toxins – Exogenous: Iodinated contrast media, antibiotics, chemotherapeutic drugs, organic solvents, heavy metals – Endogenous: Hemolysis, rhabdomyolysis, uric acid, oxalate Acute Tubular Necrosis

Ultrasonographic Findings Morphology - Enlarged - Smooth outline Echogenicity Ischemic ATN - Normal cortical and medullary echogenicity Drug related ATN - increased cortical echogenicity and maintained corticomedullary differentiation ○ Perirenal hypoechoic rim ("kidney sweat" ) Color Doppler - Resistive index: ↑ (> 0.7) IMAGING "kidney sweat“ sign

CT Findings

C haracterized by ischemic necrosis of renal cortex with sparing of renal medulla and thin rim of subcapsular cortex . • Etiology ○ Obstetrical complication (> 50% of cases) – Abruptio placentae, septic abortion, eclampsia ○ Hemolytic uremic syndrome, disseminated intravascular coagulopathy, shock, sickle cell anemia, renal allograft rejection Renal Cortical Necrosis

Plain Radiography Cortical calcification: Dual linear opacities paralleling corticomedullary line ("tram line" sign), which is usuall y seen after 4 weeks Imaging

Ultrasonographic Findings Diffusely enlarged kidneys Loss of corticomedullary differentiation ↓ cortical echogenicity acoustic shadow due to cortical calcification

CT Findings cortical rim sign Reverse Rim sign

B/L smooth enlarged kidneys Neonatal/Juvenile age group Associated with striated nephrogram Periportal fibrosis Dilated bile ducts F/O PH ARPCKD Dilated PCS Delayed contrast excretion B/L obst Uropathy Increase serum urea level Nephrogram- progressively dense Intense hyperechoic cortex with hypoechoic medulla HUS Elderly pt. Osteopenia vert. body & Mandibular involvement Mult . Myeloma Child with abnormal peripheral smear increase WBC count Changes in bone Leukemia Absent cortical nephrogram with selective enhancement of medulla + Tram line calcification Acute cortical necrosis Renal involvement following History of drug exposure Clinical features- Rash Eosinophila Proteinuria Hematuria Azotemia Acute interstitial nephritis Acute urate nephropathy

UNILATERAL SMALL SMOOTH KIDNEYS 1. Ischemia due to renal artery stenosis 2. Post-obstructive atrophy 3. End result of renal infarction 4. Congenital hypoplasia 5.Reflux atrophy

Renal artery stenosis Renal artery stenosis (RAS) refers to a narrowing of a renal artery with reduction of internal diameter by at least 60% Etiology Atherosclerosis Polyarteritis nodosa Fibromuscular dysplasia Compression of RA by mass

Ultrasound I ncreased   peak systolic velocity (PSV) : some advocate 180 cm/s  4 I ncreased renal-aortic ratio (RAR), i.e. PSV renal / PSV aorta : usually taken as > 3.5 ​ turbulent flow in a post-stenotic area D ecreased (interlobar)  renal arterial resistive index (RI) : <0.55 in severe stenosis   4. Resistive index  difference between kidneys >5% 

Left intrarenal Doppler examination shows a normal arterial curve with sharp systolic peak and resistance index <0.70

Pulsed Doppler sampling reveals elevated peak systolic velocities (PSV) 366 cm/sec at the site of color aliasing. 

 Turbulent flow is seen downstream in the mid renal artery.

CT angiography shows atherosclerotic calcifications of the right renal artery ostium and a moderate to severe stenosis.

CE-MRA shows a high-grade stenosis of the proximal right renal artery. The right kidney was markedly smaller but smoothly marginated. Parenchymal enhancement of the right kidney was delayed.

Small smooth kidneys Unilateral Bilateral With small PC system With<5 calyces With dilated PC system Cong. hypoplasia H/o radiation therapy Radiation nephritis Abnormal renal Vessels (Art) Dense Faint/Nil Acute ischemia Signs of obstruction Post obstructive atrophy Reflux Reflux atrophy Chr. infarction Nephrogram

1. Generalized arteriosclerosis 2.Benign and Malignant nephrosclerosis 3. Chronic glomerulonephritis 4 . Chronic papillary necrosis 5 . Arterial hypotension 6 . Hereditary nephropathie s BILATERAL SMALL SMOOTH KIDNEYS

Definitions : • Necrosis of renal papilla within medulla secondary to interstitial nephritis or ischemia Renal Papillary Necrosis Causes: A nalgesic nephropathy (M/C cause) D iabete s I nfant in shock P yelonephritis O bstruction , S ickle cell disease E thanol ( Pneumonic to remember causes of renal papillary necrosis— ADIPOSE )

IMAGING Ultrasonographic Findings ○ Early stage – Necrotic renal papillae: Seen as echogenic foci ○ Advanced stage – Single or multiple cystic cavities in medullary pyramids continuous with calyces ± calcification

IVP, CT Urography Findings

Small smooth kidneys Bilateral Delayed or non excretion of contrast Hereditary Nephropathies ( Alport syndrome) Systemic hypertension/ Vessel disease Generalised arterial sclerosis Nephrosclerosis Athero -emboli disease Infection Triangular or bulbous cavitation adjacent to calyx on IVP Chr.Papillary necrosis Cystic lesions in medulla Medullary cystic disease

1.Reflux nephropathy 2.Lobar infarction 3.Tuberculosis 4.Renal dysplasia SMALL SCARRED KIDNEYS

Reflux nephropathy Renal scarring and shrinkage secondary to multiple episodes of acute pyelonephritis during early childhood Most cases secondary to vesicoureteral reflux (VUR)

Urinary bladder shows internal echoes. Color Doppler shows vesicoureteric reflux.

Reflux nephropathy Lobar infarction TB Renal dysplasia 1. Laterality Unilateral Unilateral Bilateral Unilateral 2. No of foci Multifocal Unifocal Multifocal Multifocal 3. Involvement of papillae + - + Ab Development 4. Status of calyces Dilated ` Attenuated Dilated Ab Development 5. Parenchymal thickness 6. Nephrogram Diminished Absent Diminished/Absent Absent 7. Calcification - - + - 8. Cysts - - - +

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