RENAL PARENCHYMAL DISEASE IMAGING.pptx

RADIOLOGY RENAL PARENCHYMAL DISEASE IMAGING

1. Renal Parenchymal Disease and Renal Failure BY Dr. PRAMOD NAGURE D.Y. PATIL MEDICAL COLLEGE AND HOSPITAL RADIODIAGNOSIS DEPARTMENT

2. Acute Renal Failure/Acute Kidney Injury Rapid deterioration in renal function characterized by progressive azotemia with decline in glomerular filtration rate (GFR) which may or may not be accompanied by Oliguria

3. Causes of acute renal failure PRERENAL Cardiogenic shock Anaphylaxis Sepsis Renal aretrey stenosis Severe dehydration INTRARENAL Acute Tubular necrosis -Hemolysis -Antibiotics -Contrast nephrotoxicty Glomerulopathy -SLE -HSP -Postinfective glomerulonephritis POSTRENAL Renal vein Thrombosis Obstruction due to; -Calculi -Hemorrahge -Tumor

4. Chronic Renal Failure • Kidney damage or decreased renal function for ≥ 3months duration resulting in GFR of less than 60 mL/min/1.17m2 Staging • Severity stratified by glomerular filtration rate (GFR) ○ Stage 1: GFR ≥ 90 mL/min/1.73 m² ○ Stage 2: GFR 60-89 ml/min/1.73 m² ○ Stage 3: GFR 30-59 mL/min/1.73 m² ○ Stage 4: GFR 15-29 mL/min/1.73 m² ○ Stage 5: GFR < 15 mL/min/1.73 m²

5. Causes of Chronic renal failure PRERENAL Renal artery stenosis chronic dehydration congestive heart failure cirrhosis INTRARENAL common causes -Diabetic ephropathy -Hypertensive -Glomerulosclerosis Glomerulonephritis congenital ADPKD Renal tubular acidosis Drugs TB Gout AIDS nephropathy POSTRENAL Posterior cortical value Neurogenic bladder Ureteric/bladder outlet Obstruction Retroperitoneal fibrosis

6. Goal for radiological studies in renal failure is as follows: Exclusion of correctable causes of acute renal failure (e.g. obstruction, thrombosis) Estimation of renal size to differentiate acute parenchymal disease from chronic parenchymal disease. Once obstruction is excluded, prerenal, and postrenal causes of renal failures can be managed medically

7. Morphological criteria to categorize renal parenchymal disease

8. Distance s less than 2 cm are suggestive of parenchymal loss while those greater than 3.5 cm indicate mass lesion or infiltration. 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. INTERPAPPILARY LINE

9. Acute Renal Parenchymal Disease Radiographic appearance of ‘Bilateral, large, smooth’ kidneys is usually seen in the setting of renal failure of recent onset. When obstruction is ruled out a similar picture of enlarged smooth kidneys with normal or effaced collecting system is seen that indicates parenchymal disease of recent origin, which is possibly reversible

10. Causes of bilateral large smooth kidneys Proliferative/necrotizing disorders Acute glomerulonephritis Polyarteritis nodosa (microscopic form) Systemic lupus erythematosus Wegener’s granulomatosis Diabetic glomerulosclerosis Plasma cell dyscrasias • Multiple myeloma • Waldenstrom’s macroglobulinemia • Amyloidosis Abnormal fluid accumulation • Acute tubular necrosis • Acute cortical necrosis Acute blockage of tubules • Acute urate nephropathy • Tamm–Horsfall protein • Acute myeloma nephropathy Others Autosomal recessive polycystic kidney disease Leukemia Fabry’s disease

11. Acute Tubular Necrosis Renal cause of AKI characterized by tubular epithelial cell damage from toxins or ischemia • Etiology ○ Ischemia: Hypotension (most common cause), hypovolemia, renal vasoconstriction, DIC ○ Toxins – Exogenous: Iodinated contrast media, antibiotics, chemotherapeutic drugs, organic solvents, heavy metals – Endogenous: Hemolysis, rhabdomyolysis, uric acid, oxalate ○ Sustained prerenal azotemia is most common predisposing factor for acute tubular necrosis

12. IMAGING Ultrasonographic Findings • Grayscale ultrasound ○ Morphology – Renal length: Normal or ↑ – Cortical thickness: Normal or ↑ ○ Echogenicity – Normal or ↑ – Usually normal in ischemic ATN, and ↑ in toxic ATN ○ Perirenal hypoechoic rim ("kidney sweat" ) • Color Doppler ○ Resistive index: Normal or ↑ (> 0.7)

13. CT Findings ○ Bilateral renomegaly with patchy nephrogram is seen on CT scan MR Findings • Functional renal imaging ○ Blood oxygen level dependent (BOLD) MR for renal oxygenation ○ Arterial spin labeling (ASL) MR for renal perfusion

14. DIFFERENTIAL DIAGNOSES • Acute glomerulonephritis • HIV nephropathy • Acute interstitial nephritis TREATMENT ○ Correction of volume depletion or overload, electrolyte imbalance, metabolic acidosis ○ Dialysis

15. Renal Cortical Necrosis • Rare form of acute renal injury characterized by ischemic necrosis of renal 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

16. Imaging Plain Radiography and Urography U rographic findings are nonspecific Cortical calcification: Dual linear opacities paralleling corticomedullary line ("tram line" sign), which is usuall y seen after 4 weeks Ultrasonographic Findings • Acute cortical necrosis: ↓ renal cortical echogenicity • In later stages, diffuse ↑ cortical echogenicity and acoustic shadow due to cortical calcification

17. CT Findings • NECT ○ Calcifications in renal cortex and columns of Bertin may indicate prior cortical necrosis • CECT ○ Acute necrosis: ↓ enhancement of renal cortex ○ Preserved enhancement of thin rim of subcapsular cortical tissue due to separate capsular blood supply - CORTICAL RIM SIGN ○ Preserved medullary enhancement ○ ↓ excretion of contrast media into collecting system

18. MR Findings • T1WI ○ ↓ signal intensity inner cortex and columns of Bertin • T2WI ○ ↓ signal intensity inner cortex and columns of Bertin ○ ↑ signal intensity subcapsular rim

19. DIFFERENTIAL DIAGNOSES • Acute tubular necrosis • Renal infarction • Renal vein thrombosis T REATMENT • Treatment of underlying cause • Dialysis; transplantation

20. Leukemia M ost common malignant cause of bilateral renal enlargement in children. Renal enlargement occurs due to infiltration of kidneys by leukemic cells. Imaging Features In leukemic infiltration of kidney, the nephrogram is faint and the collecting system is attenuated. Pelvicalyceal system is often filled with blood clots or uric acid stones which appear as filling defects

21. Acute Interstitial Nephritis (AIN) is an immunologically induced hypersensitivity reaction to an antigen associated with a drug or infection. • Etiology Drugs: antimicrobial agents nonsteroidal anti-inflammatory

22. Imaging Ultrasonography • Normal or increased renal size (due to interstitial edema) • Often increased cortical echogenicity • Decreased renal perfusion on color and power Doppler ultrasound • Increased resistive index values in intrarenal arterial branches Computed Tomography • Kidneys are enlarged in the acute phase. • Delayed postcontrast CT reveals corticomedullary contrast enhancement due to vascular and tubular stasis. Nuclear Scintigraphy • Increased uptake of gallium (nonspecific; increased also in pyelonephritis, glomerular diseases, and malignancy)

23. Renal Amyloidosis Amyloidosis is characterized by the deposits of fibrillar proteinaceous material. As a result of plasma filtering function, kidneys are continuously exposed to abnormal forms of plasma proteins which are deposited in the capillaries of the organ. Primary (AL) and secondary (AA) amyloidosis account for the majority of cases of renal amyloidosis. 30 % of primary amyloidosis patients will eventually develop multiple myeloma. Secondary amyloidosis is a result of chronic inflammatory disease.

24. Imaging Plain Film Radiography • Normal, increased or diminished renal size • Renal artery calcifications Intravenous Pyelography (IVP) • Homogenous nephrogram, with loss of definition of the corticomedullary junction • Usually smooth, rarely minimal to moderately irregular cortical margins • Impaired renal excretion of contrast medium in kidneys, with reduced renal size

25. Ultrasonography • Renal size is usually normal on ultrasonography. • Renal cortical hyperechogenicity, with preserved or diminished corticomedullary distinction. • Amorphous renal calcifications. • Focal renal parenchymal or pelvic masses due to amyloid deposition. • Perirenal soft-tissue mass with calcifications. • Normal or increased interlobar arterial RI and PI values.

26. Computed Tomography • Enlarged kidneys with smooth contours in the early stage, and small kidneys with cortical thinning in chronic stage • Focal parenchymal masses • Amorphous calci fi cations • Pelvic filling defects due to focal amyloid or blood clots of spontaneous hemorrhage • Perirenal soft-tissue masses with calcifi c ations Angiography • Irregular narrowing and tortuosity of interlobar arteries

27. Chronic Renal Parenchymal Disease R enal injury of more prolonged nature often leads to progressive and irreversible loss of nephrons. Such reduction in renal mass subsequently results in bilaterally small kidneys. Renal contour may be smooth or irregular

28. Causes of small kidney

29. 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 ) Definitions : • Necrosis of renal papilla within medulla secondary to interstitial nephritis or ischemia

30. IMAGING IVP, CT Urography Findings • Subtle streak of contrast extending from fornix parallel to long axis of papilla • Triangular or bulbous cavitation of papilla • Widened fornix (necrotic shrinkage of papilla) • Calyx: Club-shaped or saccular (sloughed papilla) • Sloughed papilla: Triangular filling defect within calyx known as LOBSTER CLAW APP ○ Sloughed papilla may have ring calcification

31. CT Findings • Normal, enlarged, or small contracted kidneys • Ring-shaped medullary calcification • Hematoma, lobar infarct, scarring (sickle cell) • Contrast-filled clefts in renal parenchyma • Filling defects: Renal pelvis/ureter (sloughed papillae) Ultrasonographic Findings • Grayscale ultrasound ○ Early stage – Necrotic renal papillae: Seen as echogenic foci ○ Advanced stage – Single or multiple cystic cavities in medullary pyramids continuous with calyces ± calcification

32. DIFFERENTIAL DIAGNOSIS Hydronephrosis Medullary Sponge Kidney Congenital Megacalyces and Megaureter Treatment • Early stage: Symptomatic treatment • Advanced stage (obstruction, infection, failure) ○ Ureteral stent, surgical treatmen t

33. HIV Nephropathy HIV-associated nephropathy (HIVAN) Progressive chronic renal disease in patients with HIV infection histologically characterized by focal and segmental glomerulosclerosis (collapsing glomerulopathy) • Etiology ○ HIV-1 infection

34. IMAGING • Best imaging tool : Ultrasound Ultrasonographic Findings ○ Increased renal echogenicity ○ Decreased corticomedullary differentiation ○ Urothelial thickening ○ Decreased renal sinus fat ○ No hydronephrosis CT Findings • NECT ○ Loss of corticomedullary differentiation • CECT ○ Striated nephrogram

35. DIFFERENTIAL DIAGNOSIS Glomerulonephritis (GN) Acute Tubular Necrosis (ATN) Opportunistic Renal Infections Treatment • Antiretroviral therapy • Angiotensin-converting enzyme (ACE) inhibitors, corticosteroids • Transplantation

36. Benign and Malignant Nephrosclerosis Nephrosclerosis affects the renal arterioles. Malignant nephrosclerosi s progresses very rapidly and damages the arteries. These damaged arteries are unable to provide enough oxygen to the kidney tissues, resulting in kidney failure. The incidence of hypertensive nephrosclerosis increases with advancing age.

37. Imaging Features Kidneys are small and smooth in benign nephrosclerosis; occasionally show shallow infarcts. Normal nephrographic opacification, and excretion into pelvicalyceal system is seen on urography. On ultrasonography, increased central sinus echogenicity due to fat deposition may be seen. Subcapsular and perirenal hemorrhages may be detected as hypoechoic or anechoic m fluid collections. High density fluid (blood) can be better detected on non-contrast CT scan. Blood degradation product may also be identified on MR imaging.

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