- Azotemia – Raised blood urea nitrogen (BUN) and creatinine from reduced glomerular filtration rate (GFR).
- Uremia – Azotemia associated with metabolic and endocrine abnormalities due to renal damage.
- Nephritic syndrome – Glomerular disease causing haematuria, proteinuria and HTN. Rapidly progressive glomerulonephritis is nephritic syndrome with rapid decline in GFR.
- Nephrotic syndrome – Glomerular diseaes causing heavy proteinuria with hypoalbuminaemia, severe oedema, hyperlipidemia, lipiduria.
Acute kidney injury (AKI, acute renal failure) – Oliguria, anuria and recent azotemia. From glomerular, intersitital, vascular or tubular injury.
- Prerenal – Renal hypoperfusion from haemorrhage, shock, hypovolaemia, congestive heart failure.
- Renal – Glomerular, interstitial or tubular disease.
- Postrenal – Urine obstruction.
Chronic renal failure (CRF) – Prolonged uremia. End result of all chronic parenchymal disase. Diminished renal reserve is GFR <50% normal, renal insufficiency 20-50%, CRF <20-25%, end-stage renal disease <5%.
Medical renal (parenchymal) disease causes increased echogenicity ± loss of corticomedullary differentiation. DDx includes:
- Acute/chronic glomerulonephritis
- Hypertensive nephrosclerosis
- Diabetic glomerulosclerosis
- Lupus nephritis
- AIDS-related nephropathy – Focal/segmental glomerulosclerosis with tubular abnormality. AIDS may also cause diffuse infection with calcification (PCP, MAI, TB), nephrotoxicity from drugs, lymphoma, dehydration.
Large kidneys >130mm from deposition of protein, cells or fluid.
- Bilateral implies systemic disease, often requires biopsy.
- Acute glomerulonephritis
- Lupus nephritis
- Diabetic glomerulosclerosis
- Acute tubular necrosis (ATN) – Most common cause of acute kidney injury, usually from renal ischaemia or nephrotoxicity (drugs, contrast agents).
- Acute cortical necrosis
- Acute bilateral pyelonephritis
- Multiple myeloma
- Urate deposition
- Acute infarction – Renal vein or arterial thrombosis.
- Acute obstruction
- Acute pyelonephritis
- Duplicated collecting system
- Compensatory hypertrophy
Small kidneys (<90mm) usually from irreversible end stage disease.
- Bilateral implies systemic disease
- Arterial hypotension
- Generalised arteriosclerosis
- Nephrosclerosis from systemic HTN
- Chronic glomerulonephritis
- Uraemic medullary cystic disease
- Unilateral implies local unilateral process
- Renal artery stenosis – Chronic renal ischaemia, systemic HTN. Small kidney with delayed nephrogram.
- Chronic infarction – Arterial oclusion from embolus, thrombus, trauma.
- Radiation nephritis
- Postobstructive atrophy – After relief of chronic obstruction.
- Postinflammatory atrophy – After chronic infection.
- Congenital hypoplasia
Triple phase renal CT – Includes precontrast (for calculi and calcifications), corticomedullary phase (renal cortex enhancing before medulla), nephrogram phase (~120s and uniform paranchymal enhancement) and pyeologram phase (3-5min, filling of collecting system and ureters). Kidneys actively excrete contrast into collecting tubules, hence renal masses will be hypodense. CT-IVP is 3D reformatting of collecting systems and ureters to mimic an IVP.
Congenital and Developmental
Junctional parenchymal defect – Incomplete fusion of upper and lower poles with wedged defect at junction of upper and middle 1/3s.
Most glomerular diseases are immunologically mediated (immune complexes trapped in glomeruli) cf tubular and interstitial diseases which are mostly toxic or infectious.
Primary glomerulonephritis/glomerulopathy involves only the kidney:
- Acute proliferative glomerulonephritis – Post-infectious (immune complexes 1-4/52 posterior streptococcal infection) or other.
- Rapidly progressive glomerulonephritis
- Mebranous glomerulopathy
- Minimal change disease
- Focal segmental glomerulosclerosis
- Membranoproliferative glomerulonephritis
- IgA nephropathy
- Chronic glomerulonephritis
Secondary glomerulonephritis is from systemic immunological, vascular, metabolic or hereditary conditions.
- Diabetes mellitus
- Goodpasture syndrome – Anti-GBM antibodies. May also cross-react with basement membranes of lung alveoli.
- Microscopic polyarteritis/polyangiitis
- Wegener granulomatosis
- Henoch-Schonlein purpura
- Bacterial endocarditis
- Alport sydrnome
- Thin basement membrane disease
- Fabry disease
Chronic glomerulonephritis causes symmetrically atrophic kdineys with diffusely granular surfaces, cortical thining, increased peripelvic fat. Dialysis causes arterial intimal thickening, extensive deposition of calcium oxalate in tubules and interstitium, acquired cystic disease.
Tubular and Interstitial Diseases
Most tubular diseases also involve the interstitium.
Acute Tubular Necrosis (ATN)
Most common cause of acute kidney injury (AKI, acute renal failure), reversible. Tubular cell injury causes reduced vasoconstriction (tubuloglomerular feedback), casts with obstruction, reduced GFR. Intrarenal vasoconstriction also reduces GFR. Initiation phase from the inciting event; maintenance phase with sustained oliguria and uremia; recovery phase with increasing urine volume, which may become polyuric due to damaged tubules. Causes include:
- Ischaemia – Hypovolaemia (shock), malignant HTN, thrombotic microangiopathies (haemolytic uraemic syndrome HUS, thrombotic thrombocytopenic pupura TTP, DIC).
- Nephrotoxic – Direct toxic injury to tubules from drugs (gentamicin, antibiotics), contrast, myoglobin, haemoglobin, radiation, heavy metals (mercury), organic solvents.
- Urinary obstruction – From tumours, prostatic hypertrophy, blood clots.
- Acute tubulointerstitial nephritis – Most from drug hypersensitivity.
Acute nephritis causes intersitial oedema, inflammation, focal tubular necrosis. Chronic disease causes interstitial fibrosis, wide-spread tubular atrophy. Impaired ability to concentrate urine with polyuria, nocturia, electrolyte disorders (metabolic acidosis). Causes include:
- Infection – Acute and chronic pyelonephropathy (including reflux nephropathy and chronic obstruction).
- Acute drug-induced interstitial nephritis – Hypersensitivity to synthetic penicillins/antibiotics, diuretics, NSAIDs, allopurinol, cimetidine.
- Analgesic nephropathy – Chronic tubulointerstitial nephritis and renal papillary necrosis, F>M. Increased risk of papillary TCC of the renal pelvis.
- Haevy metals – Lead, cadmium.
- Metabolic – Urate/gouty nephropathy (precipitation of urate crystals in tubules), nephrocalcinosis, acute phosphate nephropathy, hypokalaemic nephropathy, oxalate nephropathy.
- Light-chain cast nephropathy (myeloma kidney) – Myltiple myeloma from Bence Jones proteinuria, amyloidosis.
- Immunologic – Transplant rejection, Sjrogren syndrome, sarcoidosis.
Inflammation and Infection
Usually ascending UTI from coliform G-neg (esp E.Coli, Proteus, Klebsiella, Enterobacter), Strep.faecalis, staphylococci. In immunocompromised polyomavirus, CMV, adenovirus. There is infection of the bladder, vesicoureteral reflux (commonly congenital or acquired from persistent bladder atony), intrarenal reflux (more common in upper and lower poles where papillae have flattened or concave tips). Haematogenous infection less common, from septicemia or infective endocarditis; increased risk with obstruction, debilitated patients, immunosuppression. Involves tubules, interstitium and renal pelvis with patchy inflammation, tubular necrosis. Uncomplicated infection is often normal on imaging. Image if fails to respond or if patient is severely ill, CT more sensitive. Oedema with diffuse/focal swelling, haemorrhagic inflammation (areas of high precontrast HU), streaks/wedges of poor enhancement extending to capsule, perinephric fascia/septal thickening and stranding. Urothelial enhancement (DDx inflammation from JJ stent, reflux etc). US disruption of corticomedullary junction, usually hypoechoic but may be iso/hyper-echoic. Inflammatory foci are eventually replaced with irregular cortical scars with depressions, fibrosis, deformation of underling calyx and pelvis. Complications include:
- Papillary necrosis – Mostly diabetics and co-existing obstruction, usually bilateral.
- Pyonephrosis – Infection in setting of obstruction with dilated and obstructed collecting system. Echogenic debris with urine-debris level, may have gas. 10% indistinguishable from uncomplicated hydronephrosis. Tx urgent drainage.
- Acute lobar nephronia (ALN, focal bacterial nephritis) – Inflammatory hypodense masses in parenchyma, ?before abscess formation.
- Intrarenal or perirenal abscess/carbuncle – Increased risk with diabetes, obstruction, immunocompromise, drug abuse, chronic disease, incomplete ABs. Focal/diffuse wedge-shaped lesions, focal mass-like lesions, multiple diffuse mass-like lesions. Those >20mm require drainage.
- Emphysematous pyelonephritis – Rapidly progressive and life-threatening infection (mortality >50%) with streaks of gas in renal parenchyma, dirty shadowing on USS. Mixed flora with G-neg. Most patients have diabetes, obstruction or immunocompromise.
(Chronic interstitial nephritis). Chronic tubulointerstitial inflammation and renal scarring with involvement of the calyces and pelvis (cf other tubulointerstitial nephritis). Damage to papilla with calyceal blunting/dilation/deformity and papillary flattening, irregular corticomedullary scarring (cf diffuse symmetrical in glomerulonephritis), usually lobar with normal interposed calyces. Types include:
- Reflux nephropathy (most common) – From childhood VUR of infected urine. Unilateral or bilateral, worse in upper and lower poles. Reflux may cause damage in absence of infection when severe (sterile reflux).
- Chronic obstructive pyelonophritis – Urinary stasis (from calculi, chronic obstruction, neurogenic bladder, ileal conduits) predisposes to recurrent infections.
- Xanthogranulomatous pyleonephritis (XGPN) – Rare, from obstruction (calculus esp staghorn in 75%) and chronic infection (usually Proteus mirabilis). Parenchyma is destroyed, replaced with xanthoma cells (lipid-laden macrophages), but no macroscopic fat (cf AML). Focal or diffuse hydronephrosis, complex heterogeneous mass.
Usually after primary TB up to 10-15y later, only 10% have active TB, only 30% show previous TB on CXR. Asymptomatic haematuria or sterile pyuria. Parenchymal destruction and cavity formation -> scarring, parenchymal masses (granuloma), fibrosis causing collecting system and ureteric strictures, calcification. End-stage hydronephrotic sacs or atrophic calcified masses (TB autonephrectomy).
Infiltrative/segmental lesions with maintained renal contour include lymphoma, leukemia, TCC, SCC.
Renal Cell Carcinoma (RCC)
(Adenocarcinoma of the kidney). 1% of cancers, 85% of renal neoplasms, 50-70yo, M:F 2:1, bilateral in 2%, multicentric in 25%. Increased risk with smoking, obesity, HTN, unopposed oestrogen, asbestos, petroleum products, heavy metals, CRF, acquired cystic disease, TS, vHL (clear cell). Types include:
- Clear cell (75%) – May be familial, vHL.
- Papillary (15%) – Hypovascular, frequently multifocal, may be familial AD, associated with dialysis-associated cystic disease.
- Chromophobe cell (5%)
- Collecting/Bellini duct (1%)
- Uncommon sarcomatoid change in any of the above, poor prognosis
Hyper/iso/hypo-dense, heterogeneous, enhances less than normal parenchyma, pseudocapsule (high density rim, lucent on CE), altered renal contour (cf TCC). Variable echogenicity, 10% predominantly cystic. Coarse, punctate central calcification in 25%. Haemorrhage and necrosis common. Occasional AV shunts with early venous filling. Usually hypervascular with numerous abnormal feeding vessels (large capsular veins) very specific. Extends into renal veins in 30% (filling defect, enlarged), IVC in 10%, perirenal fat (nodules reflect tumour, stranding may be previous inflammation/oedema), adjacent muscles, metastases in 40% at diagnosis (ipsilateral adrenal, contralateral kidney, brain, lung, bone, liver). Bony metastases are typically expansile, lytic.
- Stage I – Confined to renal capsule. T1 <25mm, T2 >25mm.
- Stage II – T3a perinephric fat but within renal fascia.
- Stage IIIa – T3b renal vein, T3c IVC below diaphragm, T4b IVC above diaphragm.
- Stage IIIb – Local nodes >15mm.
- Stage IIIc – Local nodes and tumour thrombus.
- Stage IVa – T4a direct invasion of adjacent organs.
- Stage IVb – Distant metastases.
Tx nephrectomy with removal of renal fascia, adrenal gland, perinephric fat and hilar LN; smaller <30mm RCCs partial nephrectomy. Preop biopsy only if it may be a metastasis. Biopsy of well-differentiated RCC is difficult to differentiate from normal cells.
5-10% of primary renal tumours, from renal pelvis urothelium. Range from benign papillomas to invasive transitional cell carcinomas. Usually detected early due to haematuria, may cause obstruction. 50% have concomitant bladder urothelial tumour. Increased risk with analgesic nephropathy. Most are localised to the urothelium, but may be infiltrating mass-like. Tends to maintain renal outline until very large (cf RCC).
Uncommon benign mesenchymal tumour of varying abnormal fat (~5% have no fat), smooth muscle and vessels lacking elastic wall. 85% are sporadic solitary, unilateral, most middle-aged women. 15% are associated with tuberous sclerosis (33% of those with TS have AMLs), being multicentric, bilateral. Prone to haemorrhage especially when aneurysms are present (common), bleed may be massive (Wunderlich syndrome). Even small quantities of fat (without calcification) is diagnostic of AML, but occasionally fat may be seen in RCC associated with calcification (ossification with marrow fat) or engulfment of adjacent fat. Very hyperechoic (>/= sinus fat) and uniform (cf echogenic RCC). Slow-growing. Larger tumours (>40mm) Tx with resection or embolisation. DDx renal sinus lipomatosis, retroperitoneal lipoma/liposarcoma.
Rare benign tumour of eosinophilic epithelial cells (oncocytes) containing multiple mitochondria. Well-encapsulated, large with average 50-80mm (may be up to 250mm), most solitary (5% multiple/bilateral esp familial cases). Aspherical, homogeneous. Stellate central scar in 50% of larger tumours is diagnostic, mut may mimic necrosis in RCC. Spoke-wheel radiating vessels on angiography. Most indistinguishable from RCC. Rarely haemorrhage/calcification/necrosis. Tx resection.
Multilocular Cystic Nephroma (MLCN)
Uncommon, benign cluster of noncommunicating cysts of varying size herniating into renal hilum. Thick capsule with thin septations. Most M<4yo, F40-60yo. Tx surgical excision to exclude RCC. May recur after excision.
Renal Papillary Adenoma
In 7-22% at autopsy. Small usually <5mm, from renal tubular epithelium. Invariably in cortex. May metastasize if >30mm.
Primary renal lymphoma is rare, but commonly involved in metastatic or direct invasion. Most NHL. May be diffuse enlargement, multiple bilateral masses, solitary bulky tumour, infiltrative segmental, invasion into renal sinus, perirenal tumour surrounding kidneys infiltrating under the capsule. Homogeneous, hypoechoic with uniform fine low-level echoes, round, poorly enhancing, extensive adenopathy.
Common site of metastases, but most occur late. Most multiple, bilateral, small, irregular. Occasional large and solitary similar to RCC. Primaries include lung, breast, colon, melanoma.
Renal Cystic Disease
Simple cysts in 50% >50yo, rare <30yo. Large >40mm cysts may cause obstruction, pain, haematuria, HTN. Must be round/oval, homogeneous, anechoic with through transmission, -10 to +10HU, low T1 high T2, sharply marginated, thin/imperceptible wall, absent enhancement with lucent defect on nephrostogram/IVU. May cause beak/claw sign with displaced renal parenchyma. Complicated cysts include:
- Haemorrhagic (5%) – Flip-flop phenomenon (hyperdense NECT, hypodense CECT), homogenous (acute) or heterogeneous (clot/debris, calcification), unenhancing, T1 highest in subacute (<72h).
- Infected – Pyelonephritis complicated by liquefactive necrosis. Thick wall, septa, heterogenous enhancing, debri, gas, calcification (chronic), high T1, perinephric inflammatory change.
- Ruptured – Spontaneous.
- Neoplastic wall – Focal thickening or enhancing nodule.
- Calcified (1-3%) – From haemorrhage, infection or ischaemia. Milk of calcium cyst – dependent fluid layer of calcific granules.
- I Benign – Simple cysts with definition as above.
- II Minimally complicated, benign – Thin <2mm septation, thin calcification in wall/septum, hyperdense (high concentration of protein, must be unenhancing, > normal parenchymal density but <90HU, <30mm). No follow-up needed.
- IIF Follow-up (3, 6, 12 month), thought to be benign – Slightly more complicated, more calcification in wall.
- III Biopsy or excision, indeterminate (~50% malignant) – Irregular/thickened/enhancing septa, thick/irregular calcification, irregular margins, uniform thick wall, nonenhancing nodularity, multilocular. Includes haemorrhagic/infected cysts, multilocluar cystic nephroma, multiloculated cysts, cystic RCC.
- IV Malignant – Irregular thick wall or enhancing mass.
Other syndromes associated with renal cysts:
- Von Hippel-Lindau (vHL) – Multiple renal and pancreatic cysts, pheochromocytomas, multiple and bilateral RCCs (in 25-50%), retinal angiomas, cerebellar haemangioblastomas. Autosomal dominant with variable penetrance.
- Tuberous Sclerosis (TS) – Normal renal size, associated with renal AMLs.
Autosomal Dominant Polycystic Kidney disease (ADPKD)
(Adult PKD). Common, AD with high penetrance, mutated PKD1 gene (encodes polycystin 1) on chromosome 16 (85%) or PKD2 gene (polycystin 2) on chromosome 4. May present as early as neonatal period, but most present 30-50yo. Bilateral, several cysts of varying sizes with normal intervening parenchyma, asymmetric. Kidneys enlarged. Cysts commonly complicated by haemorrhage. Gradually increase in size and number with compression and destruction of parenchyma -> HTN, haematuria, chronic renal failure with early death. Cysts also seen in liver (60%), pancreas (10%) and other organs (ovaries, testes, seminal vesicles), seldom causing problems. Associated with intracranial berry aneurysms in 20%, mitral valve prolapse, bicuspid aortic valve, aortic aneurysm, aortic dissection.
Autosomal Recessive Polycystic Kidney Disease (ARPKD)
(Childhood PKD). Range of rare diseases with renal cysts and hepatic fibrosis. Most mutation in PKHD1 gene (encoding fibrocystin) on chromosome 6. Bilateral, relatively symmetric, marked renal enlargement, occasional hepatomegaly. Diffuse dilatation of collecting tubules.
- Perinatal and neonatal PKD (most common) – Severe disease with rapid renal failure and death in infancy.
- Infantile PKD – Predominantly renal disease, presenting in-utero or in infancy. Numerous small 1-2mm ‘cysts’ throughout cortex and medulla with diffuse increased echogenicity, separate cysts may not be appreciated due to small size. Rim of thinned lucent cortex.
- Juvenile PKD – Liver disease predominates, presents later in childhood. Hepatosplenomegaly and portal HTN, increased liver echogenicity from severe periportal fibrosis (congenital hepatic fibrosis). Kidneys may be enlarged with varying sized cysts or be normal.
Acquired Cystic Kidney Disease of Uraemia
(Dialysis-associated cystic disease). Multiple cysts in patients on long-term haemodialysis, predominantly cortical, rarely >20mm. Often contain calcium oxalate. Occurs in >90% of patients afer 10yrs of ESRF/dialysis. Probably from obstruction of tubules by interstitial fibrosis. Kidneys usually atrophic from chronic renal disease. Associated with RCC at a rate of 7% after 10yrs of dialysis, hence should be screened.
Medullary Sponge Kidney
Unkown aetiology. Dysplastic cylindric/saccular 1-7.5 mm dilatations of collecting tubules in papillae with splayed calyceal cups -> urinary stasis in papilla -> stone formation, infection. Most asymptomatic, usually incidental. Bilateral in 75%, usually symmetric but can be single pyramid/segment. “Paint brush” 3-4 linear densities (contrast) in papillae, “bouquet of flowers” ectatic ducts filled with calcification. Good prognosis, no risk of renal failure, only treat complications (infection, stones).
Progressive variable cysts in the medulla at the corticomedullary junction, from chronic progressive tubular atrophy (cortical tubulointerstitial damage). May be sporadic or familial (AR), mutations in genes NPH1-NPH6 (nephrocystins). Onset in childhood with polyuria, sodium wasting. May be associated with ocular motor abnormalities, retinal dystrophy, liver fibrosis, cerebellar abnormalities. Progresses to terminal renal failure in 5-10yrs.
Adult Medullary Cystic Kidney Disease
Similar to nephronopthisis, inherited AD from mutated MCKD1/MCKD2 genes, adult onset. Progressive tubular atrophy with glomerular sclerosis, medullary cysts (usually too small to see). Renal failure, anaemia, salt wasting. Kidneys normal or small, echogenic parenchyma.
Benign nephrosclerosis is hyaline arteriosclerosis of renal arterioles causing ischaemia with glomerulosclerosis, chronic tubulointerstitial injury with renal atrophy. Increased risk with HTN, diabetes, age, blacks. Fine granular leathery cortical surface from scarring and shrinking. Unusual to cause renal insufficiency, may cause mild proteinuria.
Malignant/accelerated nephrosclerosis is associated with malignant/accelerated hypertension, occuring on a background of chronic renal disease and preexisting hypertension. Vascular damage causes arteriole fibrinoid necrosis with luminal narrowing, renal ischaemia. Cycle of increased renin/angiotensin raising blood pressure with widespread systemic malignant arteriosclerosis.
Most infarcts are due to emboli eg LA mural thrombus, vegetative endocarditis, aortic aneurysm, aortic atherosclerosis. Most are clinically silent, occasionally causes pain. End-artery supply with infarct causing sharply demarkated pallor with peripheral hyperaemia. Wedge-shaped, may have thin rim of preserved subcapsular tissue (collateral capsular circulation). Later V-shaped depressed scar.
Renal Artery Stenosis
Degree of constriction of one renal artery is proportional to the magnitude of hypertension via the stimulation of renin secretion by the juxtaglomerular apparatus. Increased peak systolic velocity with renal:aortic ratio >3.5. Distal tardus-parvus waveform with reduced peak systolic velocity (parvus) and delayed time to peak (tardus, acceleration of <300cm/s2). The ischaemic kidney is usually atrophic, contralateral kidney may have arteriolosclerosis due to hypertension. Causes include:
- Atherosclerotic stenosis (70%) – M>F, increased risk with age, diabetes. Usually at the renal artery origin.
- [[General_Vascular#Fibromuscular Dysplasia (FMD)|Fibromuscular dysplasia]] – Usually middle or distal portions or segmental branches of the renal artery. Unilateral or bilateral.
Renal Vein Thrombosis
From nephrotic syndrome, dehydration, trauma, malignancy, coagulopathy or thrombosis of IVC. Acute thrombosis causes an enlarged hypoechoic oedematous kidney. Incomplete thrombosis doesn’t usually cause enlargement. Reduced renal artery velocities with high resistance waveform. Enlarged venous collaterals.
Usually bilateral, from systemic disorder. Echogenic cortex or medullary pyramids.
- Cortical nephrocalcinosis – Uncommon. From acute cortical necrosis (severe ischaemia), chronic glomerulonephritis or primary hyperoxaluria.
- Medullary nephrocalcinosis – Usually from hypercalcaemic or hypercalciuric states. Most from (‘HAM’) Hyperparathyroidism, renal tubular Acidosis (failure of acidification of the urine resulting in serum metabolic acidosis), Medullary sponge kidney; others include renal TB, renal papillary necrosis, hyperoxaluria, milk-alkali syndrome, hypervitaminosis D, sarcoidosis.
Renal Papillary Necrosis (RPN)
Ischaemic necrosis of the papilla. Causes include:
- Bilateral – Analgesics (middle aged women), diabetes, sickle cell nephropathy (sickling intensified by hypertonic hypoxic medulla causing patchy papillary necrosis and occasionally cortical scarring), acute tubular necrosis, alcohol, severe infantile diarrhoea.
- Unilateral – Obstruction, infection (present in most cases), TB, venous thrombosis, transplanted kidneys.
Reduced tip of papilla enhancement -> necrotising papillitis (coagulative necrosis with inflammation, associated with infection, may extend to cortex causing scars) -> complete or partial necrosis. On ultrasound early echogenic papillae with lucent rims (fluid), advanced cystic cavitie(s) in pyramids.
- Medullary form – Triangular or bulbous cavitation of papilla, ball-on-tee/egg-in-cup (central cavitation into papilla).
- Papillary form – Detachment starting in fornices with streak of contrast extending from fornix, lobster claw, signet ring (detached papilla in contrast-filled cavity with a ‘stone’ of calcium).
- In situ form.
- Sloughed papilla – May be absorbed, be passed, obstruct or calcify (while attached, common in analgesic nephropathy) – ring shadow, triangular filling defect (sloughed papilla in calyx, pelvis, ureter; may have ring-shaped peripheral calcification).
- Healing phase – Atrophy of involved nephrons, loss of renal cortex, hypertrophy of Bertin columns, clubbed/saccular calyx.
DDx of cystic medullae: hydronephrosis, congenital megacalices, parapelvic cysts, caliceal diverticula.
Uroepithelium-lined cavities in renal parenchyma communicating via narrow channel with nearby fornix. Congenital (from ureteral bud remnant) or acquired from infection, reflux, ruptured cyst.
- Perirenal collections – Common, from haematoma, seroma, urinoma, lymphocoele or abscess.
- Renal obstruction – Distended collecting system are common and normal, serial US or radionuclide scans needed to confirm obstruction.
- Diminished renal function – High resistance arterial waveforms (RI >0.8), renal enlargement with thickened cortices, reduced corticomedullary differentiation. Causes include acute tubular necrosis, rejection, drug nephrotoxicity. Biopsy may be required to differentiate the causes.
- Renal artery stenosis – Usually at the anastomosis. Velocity >2m/s, velocity gradient stenotic:poststenotic of >2:1, marked spectral broadening, distal tardus parvus.
- Renal vein thrombosis – High resistance arterial waveform with diastolic flow, absent venous flow.
Diffuse Cortical Necrosis
(Acute cortical necrosis). Uncommon, after obstetric emergency (eg placental abruption), septic shock or extensive surgery. Glomerular and arteriolar microthrombi similar to thrombotic microangiopathy and DIC. Massive ischaemic necrosis sharply limited to the cortex causing pallor. Sudden anuria with rapid uremic death. May be patchy or unilateral with better prognosis.