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Renal tuberculosis

Ultrasound

Sonographic appearance is non-specific and variable. However ultrasound is useful to demonstrate non-excreting kidney on IVP and to reveal extrarenal spread to adnexa in females and testes in males. Also it may detect intra-abdominal lymphadenopathy.
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early : Normal kidney or small focal cortical lesions with poorly defined border +- calcification. progressive: o papillary destruction with echogenic masses near calyces. o distorted renal parenchyma. o irregularhypoechoic masses connecting to collecting system; no renal pelvic dilatation. o mucosal thickening +- ureteric and bladder involvement. o small, fibrotic thick-walled bladder. o echogenic foci or calcification (granulomas) in bladder wall near ureteric orifice. o Localized or generalized pyonephrosis. late: o Small, shrunken kidney, "paper-thin" cortex and dense dystrophic calcification in collecting system. o May resemble chronic renal disease.

Ultrasound is less sensitive than CT in detection of :


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calyceal, pelvic or ureteral abnormalities. isoechoic parenchymal masses. small calcifications. small cavities that communicate with collecting system.

Ultrasound is unable to evaluate renal fuction.


CT

CT is the most sensitive modality for visualising renal calcifications. Other CT features of renal TB include:
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cortical granulomas calyceal dilatation cortical thinning and scarring strictures of the renal infundibula, pelvis or ureters

Renal Cyst
A fluid-filled sac arising from a dilatation in any part of the nephron or collecting ductpart of the nephron or collecting duct

Nongenetic
Acquired disorders 1. Simple renal cysts solitary or multiple 2. Cysts of the renal sinus (lymphangiectasis) 3. Acquired cystic kidney disease (in patients with chronic renal impairment) 4. Multilocular cyst (multilocular cystic nephroma) 5. Hypokalemia-related cysts Developmental disorders 1. Medullary sponge kidney 2. Multicystic dysplastic kidney

Genetic
Autosomal-dominant 1. Autosomal-dominant polycystic kidney disease 2. Tuberous sclerosis complex 3. von Hippel-Lindau disease 4. Medullary cystic disease 5. Glomerulocystic kidney disease Autosomal-recessive 1. Autosomal-recessive polycystic kidney disease 2. Nephronophthisis X-linked :Orofaciodigital syndrome, type I

Paediatric cystic renal diseases


The paediatric cystic renal diseases comprises a group of conditions that are all either autosomal recessive or non-hereditary:
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autosomal recessive polycystic kidney disease (ARPKD) multicystic dysplastic kidney (MCDK) mulitlocular cystic nephroma (MLCN) nephronophthosis - medullary cystic disease complex

Adult cystic renal disease


Adult cystic renal disease comprises several distinct disease processes:
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adult polycystic kidney disease (APCKD) (also known as autosomal dominant polycystic kidney disease (ADPCKD)) acquired renal cysts (extremely common : 50% in those over the age of 50) o e.g. lithium nephropathy renal cell carcinoma : not a renal cystic disease but essential to remember as 10% of cases of renal cell carcinoma are primarily cystic.

Renal oncocytoma
A renal oncocytoma is a type of relatively benign renal tumour. It can account for approximately 5% of resected primary adult epithelial renal neoplasms, and the main clinical importance of this lesion is the difficulty in pre-operatively distinguishing it from renal cell carcinomas.
Epidemiology

Typically presents sporadically in the 6th to 7th decades with a peak incidence at 55 years of age. There is 2 : 1 male predilection 10,13. Unfortunately these demographics are similar to renal cell carcinoma.
Clinical presentation

Up to three quarters of patients with a renal oncocytoma are asymptomatic. In cases where the mass is large, then a flank or abdominal mass may be the presenting complaint. Occasionally hypertension, haematuria or pain may be the presenting complaint 13.
Associations
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Birt-Hogg-Dub syndrome tuberous sclerosis 8

Pathology

Macroscopically oncocytomas are tan in colour, similar to the renal cortex, or darker brown (mahogany brown). A rim of compressed normal renal parenchyma is sometimes seen, forming a pseudocapsule 12-13. Marcoscopichaemorrhage is seen in a minority of patients (~20%) 13. Oncocytomas are believed to originate from intercalated tubular cells of the collecting tubules and are composed of large, swollen eosinophilic cells of protuberant mitochondrial components 2,12-13 . Biopsy is usually unhelpful in distinguishing an oncocytoma from a renal cell carcinoma, as the latter may also have oncocytic elements 9. Necrosis is usually absent 12.
Radiographic features

Unfortunately the imaging appearance of oncocytomas is difficult to distinguish from renal cell carcinoma, and as such they are usually resected 9. They appear as sharply demarcated lesions of variable size, but often large at presentation. A potentially helpful sign is the presence of a sharp central stellate scar, which although characteristic of oncocytomas, is only seen in a third of cases 4. Additionally renal cell carcinomas may also demonstrate a central scar 9. The only reliable feature is evidence of metastasis or aggressive infiltration into adjacent structures, in which case the diagnosis of renal cell carcinoma can be safely made.

It is important to carefully evaluate both kidneys, as up to 13% of patients have multiple oncocytomas (renal oncocytosis), and up to 32% have concurrent renal cell carcinomas 13.
Intravenous pyelogram

Oncocytomas appear as sharply demarcated, often large exophytic masses with enhancement during the nephrographic phase.
Ultrasound

Ultrasound demonstrates a well circumscribed mass with echogenicity similar to the rest of the kidney. Occasionally a central scar may be visible 9.
CT

Generally tend be large well demarcated tumours at presentation.


Non contrast
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if less than 3 cm : homogenous attenuation if more than 3 cm : heterogenous attenuation perinephric fat-stranding may be present due to oedema calcification may be present

Post contrast
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small tumours may enhance homogeneously, but usually enhancement is heterogenous and the mass is larger central stellate non-enhancing scar is seen in approximately a third of cases 4 renal vein thrombosis may be present, but tumour thrombus is absent

MRI
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T1 :hypointense compared to renal cortex 14 T2 o hyperintense compared to renal cortex o may demonstrate hypointense central stellate scar T1 C+ : homogeneous enhancement

Angiography

May demonstrate a spoke wheel pattern, of peripheral circumferential vessels penetrating towards the center of the lesion, which again, although characteristic of oncocytomas, may also be seen in renal cell carcinomas.

During the capillary phase the tumour demonstrates a homogenous blush, similar to normal renal parenchyma, lacking the 'bizarre' vascularity typically seen in RCCs 7,9,12. A lucent avascular rim may be seen due to the compressed pseudocapsule12. Microaneuryms have occasionally been reported 12.
Treatment and prognosis

Although renal oncocytomas are benign lesions and metastases are extremely uncommon 6,13, as they cannot be confidently pre-operatively distinguished from renal cell carcinomas, they are surgically resected. If the diagnosis is suspected pre-operatively then renal sparing surgery can be performed.
Differential diagnoses
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renal cell carcinoma (RCC) o the imaging appearances of RCCs and oncocytomas overlap to such a degree that confident pre-operative distinction is not possible metanephric neoplasms o metanephric adenoma o metanephricadenofibroma renal leiomyoma
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TNM Staging of Renal cell carcinoma.

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Primary tumor (T):T0: No evidence of primary tumor T1: Tumor 7 cm or less in the largest dimension, Tumor is confined to the kidney (i.e no penetration through the capsule).

T2: Tumor greater than 7 cm in the largest dimension, Tumor is confined to the kidney (i.e no penetration through the capsule).

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T3a: Tumor penetrates through the kidney capsule into the surrounding fat or the adrenal gland, but not through Gerota's fascia.

T3b: Tumor extends into renal vein(s) or vena cava below diaphragm.

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T3c: Tumor extends into vena cava above diaphragm.

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T4: Tumor invades beyond Gerota's fascia.

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N - Regional lymph nodes N0: No regional lymph node metastasis N1: Metastasis in a single regional lymph node N2: Metastasis in more than one regional lymph node M - Distant metastasis M0: No distant metastasis M1: Distant metastasis

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Pericallosallipoma
A pericallosallipoma is a fat containing lesion occurring in the interhemispheric fissure closely related to the corpus callosum which is often abnormal. It is the most common location for an intracranial lipoma.
Epidemiology

Pericallosallipomas are rare, found in only 1 in 2,500 to 1 in 25,000 autopsies 6.


Clinical presentation

Approximately 50% of pateints present with seizures 6. The tubulonodular variety (see below) is usually associated with more severe and extensive abnormalities and thus is more frequently symptomatic. With the increasing use of antenatal sonography more and more cases are being detected incidentally in utero.
Pathology

The pathogenesis of a pericallosallipoma is considered to be the result of an abnormal persistence and differentiation of the meninx primitiva into lipomatous tissue 6. Normally resorption occurs between the 8th and the 10th week of gestation.
Associations

They can be associated with


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other anomalies of the corpus callosum : e.gdysgenesis of corpus callosum4 encephalocoeles

Radiographic features

Pericallosallipomas can be grouped into two distinct types based on imaging:


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tubulonodular curvilinear

Tubulonodularlipoma

Tubulonodularpericallosallipomas are the more common variety. They are rounded or lobular and usually measure > 2cm in thickness. They are anteriorly situated and are associated with extensive callosal and often fronto-facial anomalies. The tubulonodular variety can extend into the choroid plexus / lateral ventricles 2-3,6.

Curvilinear lipoma

Curvilinear pericallosallipomas are usually thin, elongated and curvilinear along the corpus callosal margin. They usually measure <1 cm in thickness and are more posteriorly situated. The corpus callosum is only mildly hypoplastic2-3,6. In a small minority of pericallosallipomas, a connection with extracranial subcutaneous lipomas is seen. This may be through a skull defect (cranium bifidum) in which case the masses are continunous with each other, or via a thin fibrous-lipomatous stalk with an apparently intact skull vault 8.
Ultrasound

Ultrasound demonstrates the characteristic appearance of fat : a hyperechoic midline mass in the region of the corpus callosum 5.
CT

CT is diagnostic, demonstrating fat density mass (-80 to -110HU) 7. Additionally the tubulonodular variety may demonstrate peripheral curvilinear calcification sometimes refered to as the bracket sign on coronal reformatted images. The anterior cerebral vessels can be seen coursing though or above the mass, and may have associated vascular malformations or aneurysm formation 6,8. CTA may thus be indicated.
MRI

MRI is the modality of choice to fully characterise no on the extent of the lipoma, but also the frequently associated agenesis / dysgenesis of the corpus callosum. Not surprisingly these masses follow signal intensity of fat on all sequences 2-3,6-7:
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T1
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markedly hyperintense demonstrates signal attenuation on fat suppression sequences

T2 high signal, but marginally lower than CSF demonstrates signal attenuation on fat suppression sequences but not on FLAIR T1 C+ (GAD) : no enhancement GE / EPI / SWI : presence of peripheral calcification leads to blooming
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Additionally peripheral chemical shift artifact may be prominent on some sequences. Again, as vascular abnormalities are associated with these lesions, careful examination of the vessels is essential (best seen on T2 FSE sequences).

Treatment and prognosis

No specific treatment is usually required 9, although seizures if present need medical management. In the rare cases where a cranium bifidum is present then surgical repair may be necessary. Prognosis is generally good but degree of disability is variable, ranging from severe neurological dysfunction and debilitating seizures to completely asymptomatic.
Differential diagnosis

In general there is little differential as few intracranial masses have significant fatty components. The differential includes :
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intracranial dermoid cyst intracranial teratoma fatty falxcerebri : especially to be considered in curvilinear type rare lipomatous transformation of neoplasm : PNET, ependymoma, glioma