Kidneys

KIDNEY ANATOMY


URINARY TRACT ANATOMY

  • Consists of kidneys, ureters, bladder and urethra

  • The paired kidneys are bean shaped, retroperitoneal organs located in the posterior aspect of the right and left upper quadrants

  • Each consists of two parts:

    • The renal parenchyma (primary function of the organ) includes the renal medulla and the renal cortex, and it includes the renal pyramids

    • The renal sinus includes the renal collecting system, including the calyces and the renal pelvis

  • The kidney can be divided into an upper (superior) pole, mid portion, which includes the renal hilum, and a lower (inferior) pole

  • There are several renal variants that may later the appearance of the kidneys 

  • Upper poles more medial, lower poles more lateral

  • Upper poles more posterior, lower poles more anterior

  • Morrison’s pouch

  • Left perisplenic space

  • Right lower than left

  • Lower poles displaced laterally because of the psoas muscles

  • Normal Size:

    • 9 – 12 cm in length

    • 2.5 – 4 cm AP

    • 4 – 6 cm diameter (width)

From the kidney outward:

  • Renal Capsule

  • Fat (Perinephric)

  • Gerota’s fascia/Zuckerlandl fascia

  • Fat


Gross anatomy

  • PARENCHYMA (The functional tissue)

  • Cortex

  • Medulla – Medullary Pyramids

  • SINUS

    • Renal Papillae

    • Minor calyces

    • Major calyces

    • Renal pelvis

  • CORTEX & Columns of Bertin

    • Renal corpuscle

    • Proximal & Distal Convoluted Tubule

  • MEDULLARY PYRAMIDS

    • Loop of Henle

    • Collecting Ducts

  • SINUS

    • Papillae, Calyces & Renal Pelvis

VASCULAR ANATOMY

  • Renal arteries are branches off the renal aorta

    • Located just below the level of the SMA

MICROSCOPIC ANATOMY - THE NEPHRON

  • Functional unit of the kidneys

  • 1-1.5 million nephrons per kidney

RENAL CORPUSCLE

  • Glomerulus 

  • Bowmans (glomerular) capsule

  • Where filtration takes place

THE NEPHRON

  • Juxtamedullary (15%)

    • Closer to the medullary pyramids

    • Make concentrated urine

  • Cortical (85%)


ANATOMICAL VARIANTS:

  • Compensatory hypertrophy

    • Enlargement of the unaffected contralateral kidney with unilateral renal agenesis or compromised renal function

    • Unilateral renal agenesis with compensatory hypertrophy of the normal right kidney

  • Dromedary hump

    • Bulge on the lateral border of the kidney (often the left)

  • Duplicated collecting system

    • division of the renal sinus - in this variant, there are two separate renal sinuses

  • Ectopic kidney

    • Pelvic kidney

      • One or both kidneys may be located in the pelvis; most common location of ectopic kidney

    • Crossed fused ectopia

      • Both kidneys are fused and on the same side of the body

    • Thoracic kidney

      • Kidney sits partially or completely in the chest

  • Extrarenal pelvis

    • Renal pelvis is located outside of the renal hilum

  • Fetal lobulations

    • Lobulated or bumpy outline to the kidneys seen in adults

  • Horseshoe kidneys

    • Two kidneys that cross the midline and connect at their lower poles by an isthmus

    • The isthmus travels anteriorly to the abdominal aorta and IVC

  • Hypertrophic column of Bertin

    • Enlargement of renal column seen as an indentation of the renal sinus

  • Junctional parenchymal defect

    • Results from incomplete fusion of the two embryologic components of the kidney

    • Appears as a hyperechoic, wedge-shaped structure on the anterior portion of the kidney; located between the upper and middle sections of the kidney 

  • Malrotated kidney

    • The kidney sits in the renal fossa but is positioned off of the normal axis

  • Renal agenesis

    • Congenital absence of the kidney

    • Bilateral agenesis is not compatible with life

    • Unilateral is often an incidental finding

  • Renal hypoplasia

    • The underdevelopment of the kidney in which there are too few nephrons

  • Renal sinus lipomatosis

    • Excessive fat within the renal pelvis

    • Renal pelvis will be large and echogenic

  • Nephroptosis

    • Also known as floating kidney and renal ptosis, is a condition in which the kidney descends more than two vertebral bodies (or >5 cm) during a position change from supine to upright

  • Supernumerary kidney

    • A third smaller kidney

  • Ureterocele 

    • Cystic dilatation of the terminal ureter either entirely within the bladder or extending into the urethra

    • Most often associated with a duplicated collecting system

    • Uni or Bilateral

    • More common in females

    • Give rise to obstruction or recurrent/persistent UTIs.

  • Congenital megacalyces

    • Caused by underdevelopment of the papillae

    • Enlarged clubbed calyces, normal cortical thickness

    • Normal pelvis and ureter!

    • No obstruction

  • Aberrant vessels

    • As kidney ascends, it derives its blood supply from the aorta at successively higher levels

    • Lower vessels regress usually

    • If they don’t, aberrant arteries are present

    • May compress ureter


KIDNEY SCANNING

NORMAL SONOGRAPHIC APPEARANCE OF THE KIDNEYS

  • Bean shaped organs

  • Cortex typically appears homogenous, consisting of medium- to low-level echoes

  • Sinus has more of an echogenic appearance

  • Medulla hypoechoic relative to cortex

  • Kidney cortices should either be isoechoic or more hypoechoic than the normal liver and spleen

  • Corticomedullary junction

  • Ureters are not typically seen. If seen an investigation for urinary obstruction should be conducted

  • Shape and contour smooth

  • Cortex hypoechoic/isoechoic to liver

  • Medulla hypoechoic relative to cortex

  • Corticomedullary junction

  • Sinus echogenic

  • Renal pelvis 

  • Length: 9 – 12cm

  • AP: 2 - 3cm

  • Width: 4 - 5cm

  • Volume: LxWxHx0.523=mL

  • Cortex: >1cm

KIDNEY PHYSIOLOGY

  • The kidneys perform multiple functions in the body

  • We need to be familiar with those functions so that we can recognize changes in the organ and wider body system changes that may point to impairment of various kidney functions

Kidney function

  • Controlling blood concentration and volume by removing selected amounts of water and solutes

  • Regulating blood pH

  • Removing toxic wastes from the blood

  • Producing enzymes and hormones

Kidney testing

  • Urinalysis

  • Blood urea nitrogen (BUN)

  • Creatinine

ENZYMES AND HORMONES

  • Renin

    • Enzyme released by the juxtaglomerular cells in the afferent arteriole as a result of low blood pressure

  • Erythropoietin

    • Hormone released by the kidneys in response to hypoxia – stimulates RBC production by the red bone marrow

  • Calcitrol

    • Activated form of Vitamin D. Hormone which increases blood calcium (Ca2+) mainly by increasing the uptake of calcium from the intestines, and reabsorption of calcium by the peritubular capillaries in the kidneys

Whats happening in the kidneys:

  • 1200 mL blood entering the kidneys per minute

  • 90% passes through the nephrons

  • 1% of fluid eliminated


Urine formation


REGULATION OF BLOOD VOLUME AND THE KIDNEY

Kidneys need a large volume of blood to:

  • Make urine

  • Nourish the tissues of the kidney itself

GLOMERULAR FILTRATION RATE (GFR)

3 Pressures

  • Glomerular hydrostatic  pressure

  • Capsular hydrostatic pressure

  • Blood colloid osmotic pressure 


Glomerular blood hydrostatic pressure (GBHP):

  • The blood pressure in the glomerular capillaries (≈ 55mmHg)

  • Promotes filtration


Capsular hydrostatic pressure (CHP)

  • hydrostatic pressure exerted against the filtration membrane by fluid already in the capsular space and the renal tubules (≈ 15mmHg)

  • Opposes filtration


Blood colloid osmotic pressure (BCOP)

  • Due to the presence of proteins such as albumin and globulins, and fibrinogen and blood plasmas (≈ 30mmHg)

  • Opposes filtration

Net filtration pressure (NFP):
NFP = GBHP - CHP - BCOP

GLOMERULAR FILTRATION RATE:

  • Needs to be constant

    • As systemic BP rises and falls throughout the day, the GFR has to remain constant

    • Too high – not enough time to reabsorb in the tubules

    • Too low – not enough removal of wastes from the blood

  • Increase systemic BP

    • Increases arteriole hydrostatic pressure

    • Increases GFR

  • Decrease systemic BP

    • Decrease arteriole hydrostatic pressure

    • Decreases GFR

  • Regulation of GFR

    • Autoregulation

    • Neural regulation

    • Hormonal regulation

Autoregulation 

MYOGENIC

  • Muscles in the arterioles

  • Renin – angiotensin system

    • Distal convoluted tubules contacts afferent arteriole

    • Macula densa: dense crowding of cells

    • Granular cells in afferent arteriole: releases renin

    • Mesangial cells: help regulate GFR


INSTANT RESPONSE TO CHANGE IN BP

  • As systemic BP rises

  • GFR rises

  • Blood vessel walls stretched due to increased BP

  • Response: afferent arterioles contracts – GFR falls

  • As systemic BP falls

    • GFR falls

    • Blood vessel walls stretched less due to decreasing BP

    • Response: afferent arterioles dilate – GFR rises



Tubuloglomerular feedback

  • Macula densa

    • A dense crowding of cells in the DCT

    • Special distal tubular epithelial cells which detect chloride

    • Located in the wall of a portion of the distal convoluted tubule which lies between the afferent and efferent arterioles.

    • Sensitive to NaCl concentration.

    • The macula densa cells are in constant communication with the juxtaglomerular granular cells in the afferent arteriole

    • A decrease in sodium chloride concentration initiates a signal from the macula densa that has two effects:  

  1. It decreases resistance to blood flow in the afferent arterioles, which raises glomerular hydrostatic pressure and helps return the glomerular filtration rate (GFR) toward normal

  2. It increases renin release from the juxtaglomerular cells of the afferent and efferent arterioles, which are the major storage sites for renin.

  • Juxtaglomerular cells

    • Granular cells in the walls of the afferent arteriole 

    • Modified smooth muscle cells in afferent and efferent arterioles

    • Granular cells located in the wall of the afferent arteriole

    • Modified smooth muscle cells in afferent & efferent arterioles

    • They secrete the enzyme Renin in response to low systemic blood pressure

  • Mesangial cells

    • Between the DCT and arterioles

    • Located in the space between the distal convoluted tubule and the afferent arteriole

    • Primary function is to remove trapped residues and aggregated protein from the basement membrane thus keeping the filter free of debris

Autoregulation - tubuloglomerular feedback

  • The macula densa provides feedback to the glomerulus via the JGA

  • Elevated BP-Filtrate moves too rapidly along the renal tubules 

  • Less Na+ and Cl- reabsorbed back into the bloodstream (too much in the tubule)

  • Macula densa cells detect increased Na+ and Cl- in the distal convoluted tubule

  • A message is sent to the juxtaglomerular apparatus to cause the afferent arteriole to contract

    • This decreases the GFR to normal

  • The opposite occurs with decrease BP

Hormonal regulation - response to low systemic blood pressure 

  • Renin-angiotensin-aldosterone system

  • Antidiuretic hormone (ADH)

JGA

  • Renin is produced in Juxtaglomerular/Granular cells (Walls of Afferent Arteriole)

  • The release of renin is stimulated by a drop in systemic BP which causes a decrease in the GFR.

  • This starts a chain reaction called the Renin –Angiotensin - Aldosterone Reaction

RENIN-ANGIOTENSIN-ALDOSTERONE REACTION

  • Renin is released by the JGA when blood pressure and blood volume decrease.

  • This triggers a chain reaction:

    • Angiotensin I is produced by the liver.

    • Angiotensin I is an inactive hormone.

  • Angiotensin I travels to the lungs via the bloodstream and is converted to Angiotensin II by angiotensin converting enzyme (ACE).

  • Angiotensin II is the active form of angiotensin. This hormone is a vasoconstrictor which acts on systemic arteries causing them to contract and increase systemic blood pressure.

  • The increase in systemic blood pressure increases the GFR in the glomerulus back to a normal level

ALDOSTERONE

  • It’s release is stimulated by the Renin-Angiotensin system.

  • Released by the Adrenal Cortex

  • Increases sodium reabsorption and potassium secretion in DCT

  • Water follows due to osmosis

  • Decreases urinary output

  • Increases blood volume and blood pressure

ADH

  • Released by the Posterior Pituitary Gland

  • Stimulated by lack of fluid in body:

    • Sweating

    • Diarrhea

    • Hemorrhage

    • Dehydration

  • Increases water reabsorbed in Distal Convoluted Tubule (DCT)

  • Decreases urinary output to increase blood volume


NEURAL REGULATION

  • With hemorrhage or exercise - sympathetic nervous system releases norepinephrine and causes afferent arterioles to constrict significantly

  • GFR decreases

    • Urine output reduced (conservation of blood volume)

    • Greater blood flow to other body tissues

Pathology can affect the GFR

  • If there is an obstruction somewhere in the urinary tract, the glomerular filtration rate will be affected

  • If there is disease of the renal parenchyma, the GFR and ultimately the composition of urine will be affected

BOWMAN'S SPACE 

  • Hydrostatic pressure in the capsule is increased when there is a urinary tract obstruction

  • Decreases GFR

PLASMA ONCOTIC PRESSURE

  • Plasma proteins aid in controlling blood volume (water follows protein)

  • If plasma proteins decrease,

    • Plasma oncotic pressure decreases

    • More fluid leaks into Bowman’s space

    • GFR increases

RENAL FAILURE

  • The Nephrons become damaged

  • They allow proteins and other large molecules to be filtered through the glomerulus and become part of urine


URINE COMPOSITION

  • Substances found: 

    • Water

    • Urea

    • Uric acid

    • Creatinine

    • Amino acids

    • Electrolytes

  • Substances not found:

    • Glucose 

    • ketones 

    • proteins 

    • Hemoglobin

    • Blood cells

Lab tests

  • Blood urea nitrogen (BUN)

  • Creatinine 

  • Urinalysis


UREA: 

  • Urea is a waste product of protein catabolism

  • Formed by liver and transported to kidneys by the blood

  • Should be excreted from the blood into the urine

  • Increases with kidney disease

  • Other causes: shock, dehydration, GI hemorrhage, diabetes, infection


CREATININE:

  • By product of muscle energy production (creatine phosphate)

  • More sensitive blood test than BUN

  • Related to body mass

  • Should be excreted from the blood into the urine

  • Increases with kidney disease


URINALYSIS:

  • pH value (measure of the acidity of the urine. Normal values, depending on diet, range from about 5 to 7, where values under 5 are too acidic, and values over 7 are not acidic enough)

  • Protein (not usually found in urine)

  • Sugar (glucose, not usually found in urine)

  • Nitrite (not usually found in urine)

  • Ketone (a metabolic product, not usually found in urine)

  • Bilirubin (breakdown product of hemoglobin, not usually found in urine)

  • Urobilinogen (breakdown product of bilirubin, not usually found in urine)

  • Red blood cells (erythrocytes, not usually found in urine)

  • White blood cells (leukocytes, not usually found in urine)

  • Creatinine (breakdown product of muscle metabolism, an indicator of kidney function)

  • Bacteria (not usually found in urine)

  • Urinary casts (cylindrical stuck-together structures that form in the renal tubules, not usually found in urine)

  • Crystals (found if there are high concentrations of certain substances in the urine, not usually found in urine)

  • Epithelial cells (cells that line the ureter, bladder and urethra)



URETERS AND BLADDER


Pelvic anatomy


Medial umbilical ligament (urachus):

The urachus is the fibrous vestigial remnant of the embryonic allantois.

The lumen of the urachus usually obliterates following birth and becomes known as the median umbilical ligament which is in turn covered by a midline linear fibrous fold of parietal peritoneum (the median umbilical fold) 3. This fold extends from the apex of the bladder to the umbilicus. It is located in the retropubic space.

If the lumen does not completely involute, a spectrum of urachal remnants may persist, including:

  • patent urachus

  • urachal cyst

  • urachal-umbilical sinus

  • vesicourachal diverticulum

A urachal remnant may transform into an adenocarcinoma


Anatomy of bladder and urethra

  • The urinary bladder, located in the anterior pelvis, is a retroperitoneal temporary storage organ for urine

  • It is located posterior to the symphysis pubis

  • In males it is positioned superior to the prostate gland and anterior to the seminal vesicles

  • In females it is anterior to the the vagina, uterus and rectum

  • The bladder includes an area referred to as the trigone, which is where the two UVJs and the opening for the urethra are located

  • The urethra is the tube that extends from the trigone to the outside of the body

  • Voiding or urination is the process of allowing urine to exit the bladder through the urethra

EMBRYOLOGY-ALLANTOIS

  • Embryonic structure that develops along with the amnion and the chorion.

  • Function – Collect liquid waste from the embryo

  • Remnant of the allantois.

  • Function – Drains the fetal urinary bladder and lies within the umbilical cord.

  • Adults – Dried up remnant of the urachus. Lies in the space of Retzius: Called the Medial Umbilical Ligament

LATERAL UMBILICAL LIGAMENTS: dried up remnants of the fetal umbilical arteries


BLADDER WALL LAYERS:

  • Bladder Wall Layers:

    • Outer layer: 

      • Superior – Visceral peritoneum

      • Walls – Adventitia

    • Muscular layer – Detrusor muscle

    • Submucosa

    • Mucosa – Transitional and squamous cells (continuous with the lining of the ureters and the renal collecting systems.


SONOGRAPHIC ANATOMY

  • Anechoic

  • Thin echogenic walls

  • Reverb anteriorly

  • Measure 

    • L x W x H x 0.523 = mL

    • Volume, pre and post void

    • average adult volume for men is 350-750 ml and in women is 250-550 ml

Bladder volume - post void

  • PVR less than 50 ml is adequate bladder emptying

  • PVR more than 200 ml is inadequate emptying

Normal bladder wall thickness

  • This should be assessed when the bladder is properly distended.

  • Radiopedia

    • > 3mm when distended

    • > 5mm when not-distended


Urethral sphincters

  • Sit at the neck of the bladder and control urinary output:

  • Internal – Part of the detrusor muscle.

    • Involuntary.

  • External – Part of the pelvic floor muscles.

    • Voluntary


ANATOMY - URETERS

  • The bilateral ureters are small tubes that connect the kidney to the bladder

  • The proximal ureter unites with the renal pelvis at the ureteropelvic junction (UPJ)

  • The ureters enter the bladder posteriorly at the superolateral margin of the trigone

  • The distal ureter unites with the bladder at the ureterovesical junction (UVJ)

  • The ureters provide a means whereby urine can travel from the kidneys to the urinary bladder

  • Transmit urine via peristalsis

  • Composed of 3 layers

    • Fascia

    • Smooth muscle

    • Epithelial cells (Transitional cells) 

  • Lined with transitional cells like the bladder/Renal collecting  system

  • Begin at renal pelvis

  • End at bladder trigone

  • Enter bladder posteriorly

  • Anterior to iliac vessels

  • Tubular and retroperitoneal

  • Begin at the renal pelvis

  • End at the bladder trigone.

  • Anterior to the iliac vessels


JUNCTIONS

  • Ureteropelvic Junction (UPJ)

    • Junction of the renal pelvis and the proximal ureter.

    • Can be a site of obstruction

      • Congenital UPJ Obstruction

      • Kidney stones

  • Ureterovesical junction (UVJ)

    • Junction between the distal ureter and the bladder.

    • Posterolateral portion of the bladder at the Trigone

    • Can be a site of obstruction or reflux


CONGENITAL ANOMALIES OF THE URINARY BLADDER AND URETERS


BLADDER DUPLICATION:

  • Rare anomaly

  • 3 Types:

    • Peritoneal Fold – Complete or Incomplete

    • A Septum dividing the bladder either sagittaly or coronally

    • A Transverse band of muscle dividing the bladder into 2 unequal cavities

  • Complications:

    • Unilateral reflux

    • Obstruction

    • Infection

BLADDER AGENESIS

  • Rare 

  • Most infants are still bornm all surviving infants are female


POSTERIOR URETHRAL VALVES 

  • Most common cause of bladder outlet obstruction in males

  • Obstruction of the prostatic urethra at the level of the verumontanum in the prostate gland.

  • Urethral valves occur when a boy is born with extra flaps of tissue that have grown in his urethra, the tube through which urine exits the urinary tract.

  • Dilated prostatic urethra inferior to the bladder neck

  • “Key hole” sonographic sign


BLADDER EXSTROPHY

  • Midline ventral defect of the abdominal wall below umbilicus

    • Usually diagnosed prenatally!

    • Often associated with other abnormalities (musculoskeletal, gastrointestinal, and genital tract)

  • Bladder protrudes through the defect

  • Rare (1/30,000 births)

  • Male predominance (2:1)

ECTOPIC URETER

  • ​​Ureter terminates at an abnormal location (other than the trigone of the bladder)

  • The most common scenario for ectopic attachment of the distal ureter is from complete duplication of the renal collecting system:

    • Upper pole ureter – ectopic – inferior/medial

    • Lower pole ureter – normal attachment

  • Ureters can attach ectopically to various pelvic structures.

    • Males – urethra, seminal vesicles, vas deferens or ejaculatory duct

    • Females – bladder neck, urethra, vagina or uterus

URETEROCELE

  • Cystic dilatation of the terminal ureter either entirely within the bladder or extending into the urethra

  • Most often associated with a duplicated collecting system

  • Uni or Bilateral

  • More common in females

  • Give rise to obstruction or recurrent/persistent UTI’s.

  • Cyst-like “Ballooning” of mucosal layer of distal ureter at the vesico-ureteral junction.

  • Expand and contract with Bladder filling

  • May be unilateral or bilateral

  • May occur with normal or ectopic ureters (from a complete duplication)

  • Complications:

    • May obstruct ureter (resulting in reflux and hydronephrosis of kidney)

    • May obstruct the bladder outlet (urethra)

URACHAL ABNORMALITIES

Urachus – fibrous remanent of the allantois (the channel the drains the fetal bladder into the umbilical cord) 

  • Urachal abnormalities occur when the allantois fails to close fully or partially

  • Types of urachal abnormalities: 

A. Patent urachus = 50%

B. Urachal Cyst = 30%

C. Urachal Sinus =15%

D. Urachal Diverticulum =5%

PATENT URACHUS

  • persistent channel between bladder and umbilicus 

  • Usually associated with urethral obstruction

  • patient presents with constant umbilical drainage (urine) and periumbilical infection 

URACHAL CYST

  • An encapsulation of fluid within a portion of the urachus

  • Closed at both the cranial and caudal ends

  • Presents as palpable mass with possible fever and dysuria

  • Risk of developing urachal adenocarcinoma

REFLUX

  • Retrograde urine - back up the ureter into the renal collecting system

  • Risk of ascending UTIs


Congenital Abnormalities 


Pathology

Patient Population

Signs & Symptoms

Things to know

Sonographic Appearance

Image

Congenital Megacalyces (megacalycosis)

Rare 

Caused by underdevelopment of the papillae


No obstruction

Enlarged clubbed calyces

Normal renal pelvis and ureter

Congenital Megaureter

May be associated with:

Congenital megacalyces & ipsilateral dysplasia

Not caused by obstruction

Enlarged ureter

Autosomal Dominant Polycystic Kidney DIsease

“Adult”

Usually 40-50yrs

Associated with cysts in other organs:

Hepatic cysts (30-60%)

Pancreatic cysts (10%)

Splenic cysts (5%)

Cerebral aneurysm (18-40%)

May be a palpable mass

Hypertension 

hematuria

50% of patients develop renal failure

People under 30 with family history – minimum of 2 renal cysts (in one or both kidneys) required for diagnosis

Age 30-59 – 2 cysts in each kidney required for diagnosis

Age 60+ - 4 cysts in each kidney required for diagnosis

Multiple large bilateral cysts (cortical and medullary)

Bilaterally enlarged kidneys with multiple cysts of varying size

Check liver, spleen and pancreas for cysts 

Autosomal Recessive

Polycystic Kidney DIsease

“Infantile”

4 types: perinatal, neonatal, infantile, juvenile

Dilated collecting tubules, hepatic cysts and periportal fibrosis

Massively enlarged echogenic kidneys

Lack of cortico-medullary differentiation

Occasionally macroscopic cysts will be seen

Aberrant Vessels

May compress ureter

As kidney ascends, it derives its blood supply from the aorta at successively higher levels

Lower vessels regress usually

If they don’t, aberrant arteries are present

Bladder Diverticula

Can be congenital (rare), more often an acquired condition

Increase risk of:

•Stones within the diverticula

•Infection due to stagnant urine

•Bladder rupture (rare)

Herniation of the bladder mucosa through the muscular wall resulting in a pocket or pouch where urine can collect and become stagnant

Round/oval anechoic areas coming off the bladder

May see urine flow in and out with Color doppler

Look for stones, obstruction, pus

Bladder Fistulas

Can be congenital or acquired

Acquired causes: trauma, surgical complication, inflammation, radiation and neoplasm

Abnormal connection between the bladder and another organ

Vesicovaginal – complication of gynecological or urologic surgeries, bladder Ca or cervical Ca

Vesicoenteric – complication of diverticulitis or Crohns disease

Vesicocutaneous – complication of surgery or trauma

Vesicouterine – rare complication of C-section

Vesicoureteral –  rare complication of hysterectomy

Difficult to see sonographically (tracts are often thin and short)

Vesicovaginal

Vesicouterine 

Pt with Crohns

Reflux 

Congenital cause (ectopic ureter, ureterocele) or acquired

Risk of ascending UTI’s

Movement of urine retrograde (back up into the ureter)


INFECTIONS AND INFLAMMATORY PROCESSES


Pathology

Patient Population

Signs&Symptoms

Things to know

Sonographic Appearance

Image

Acute pyelonephritis

Most commonly caused by an ascending infection in the bladder (85%)

May also result from hematogenous seeding (less common = 15%)

Flank pain and fever

Labs:

Bacteriuria

Pyuria 

Leukocytosis 

Inflammation of the parenchyma if the kidney

May be diffuse or focal

Diffuse: affects the entire cortex of the kidney symmetrically

Focal: affects an area of the kidney parenchyma 

Kidney may appear normal or…..

Enlargement of the renal cortex due to edema

May compress renal sinus

Altered echogenicity of cortex: may be hyperechoic or hypoechoic

Loss of corticomedullary differentiation

May see air in parenchyma

Focal: Are may appear poorly marginated

May be hyperechoic (most common), hypoechoic or mixed echogenicity

diffuse↑

focal↑↓

Perinephric / Perirenal effusion

Fluid in the perinephric space is sometimes seen with pyelonephritis

Renal Abscess / Carbuncle

Immunocompromised or diabetic are at higher risk

Untreated pyelonephritis can lead to parenchymal necrosis and the formation of a renal abscess

Antibiotics and/or intervention required to treat

A renal abscess may spread into the perinephric (perirenal) space by direct extension 

Appear as round, thick-walled hypoechoic complex mass

Posterior enhancement

May have “dirty shadow” due to gas formation

Pyonephrosis 

Cause of obstruction:

Stones or UPJ obstruction (younger age group)

Tumor (older age group)

Purulent material in an obstructed collecting system

Hydronephrosis and possibly a hydroureter as well

Hydronephrosis +/- hydroureter

Mobile debris in the collecting system

May see fluid-debris level 

May see air

Emphysematous pyelonephritis

Females are more prone than males

Patients are extremely ill

Extreme fever

Flank pain

Hyperglycemia

Acidosis and electrolyte imbalance

Uncommon but life-threatening condition

Bacterial infection causes gas formation in the parenchyma

emphysematous Pyelitis – gas in the collecting system

Gassy shadowing originating in the parenchyma

Chronic pyelonephritis

(interstitial nephritis)

Cause if often chronic reflux - accounts for 10-30% of end stage renal disease

May be unilateral or bilateral

If unilateral, may see diffuse compensatory hypertrophy in contralateral kidney

If the disease is multicentric, you may see focal compensatory hypertrophy within the normal parenchyma of the kidney (mimics a mass)

Dilated, blunt calyces

Areas of cortex scarred (appearing thinned or atrophied)

Xanthogranulomatous Pyelonephritis

Usually associated with renal stones and obstruction

More common in females(over males)

More common in diabetic patients 

Chronic suppurative renal infection damages the parenchyma

replacement with fat-laden macrophages

Usually unilateral

May be diffuse, segmental or focal

Enlarged kidney with lack of corticomedullary differentiation

Dilated calyces

Highly echogenic central renal sinus with shadowing

Staghorn Calculi

Renal Sinus Lipomatosis

Renal sinus fat gradually increases with age, obesity & anabolic androgynous steroid use

Excessive renal sinus fat

Can resemble xanthogranulomatous pyelonephritis (w/o staghorn calculus)

Papillary Necrosis

May cause obstruction to renal pelvis

Ischemia and necrosis of the papilla

Papilla slough and/or calcify

May or may not shadow


Hydronephrosis 

Calcified papillae are seen as tiny echogenic foci (with or without shadowing)

Renal Tuberculosis

Frequency

Dysuria 

Nocturia

Urgency 

Gross or microscopic hematuria

Bacteria tuberculosis seeded via blood from extraurinary source (usually lung)

May be focal or bilateral

Initially: Small lesions: echogenic or hypoechoic with echogenic rim

Later: Large cavitations which allow direct communication of the cortex with the renal pelvis and calyces; calcification 

Fungal Infection

(candida albicans)

Immunocompromised

Diabetics 

Patients with indwelling catheters

Focal parenchymal abscesses

hypoechoic lesions in the cortex

May calcify over time

“Fungus balls”

round, echogenic masses in the collecting system

Mobile

May cause obstruction and hydronephrosis


Parasitic Infections


Pathology

Patient Population

Signs&Symptoms

Things to know

Sonographic Appearance

Image

schistosomiasis

Most common renal parasitic infection

Hematuria

Pyuria

Dysuria

Persistent fever

Hepatomegaly

*recent travel abroad
Lab results: eosinophilia(acute), anemia (chronic)

worms enter via the skin in contaminated water

Enter the bladder via the perineum venous plexus

Worms deposit eggs into the venules of the bladder and ureter walls

Increased risk of squamous cell carcinoma of bladder

Thickened bladder and ureter walls

Pseudotubercles (tubercle-like nodules) in bladder and ureters which may calcify overtime

Kidney normal (early)

Hydatid disease (Echinococcal)

Renal involvement seen in 2-5 % of hydatid infections

Develops into a hydatid cyst

Commonly located in poles

May also be located in the ureter or bladder

anechoic cyst

mural nodules (scolices =larvae)

daughter cysts

hydatid sand (low level echos)

detached endocyst layer (floating membranes)

can calcify (can be eggshell or dense reticular pattern)

Bladder infections (cystitis)

Common

Most often in females due to the short urethra

Fever and chills,

dysuria,

frequent urination

Hematuria

E-coli infection most common cause

In males due to outlet obstruction

Thickened bladder wall (> 3-6 mm , depending on bladder distention)

Can be uniform or focal





UROLITHIASIS - Calcifications of the Urinary System



Pathology

Patient Population

Signs&Symptoms

Things to know

Sonographic Appearance

Image

Urinary Obstruction

Causes:

Intrinsic –calculi, tumor

Extrinsic – compression (due to tumor, pregnancy, retroperitoneal fibrosis, etc.)

Results in hydronephrosis and/or hydroureter

Most common sites:

1.Ureteropelvic Junction (UPJ)

2.Mid Ureter –where the ureter crosses over the iliac vessels

3.Ureterovesicular Junction (UVJ) (aka Vesicoureteral Junction

hydronephrosis

Most often due to obstruction

Will eventually cause damage to parenchyma

Dilatation of the urinary collecting system

Grades:

Mild

Moderate

Severe 

Mild

Moderate

Severe

Hydronephrosis due to extrinsic cause

Ureter compression (ex: ovarian ca mets

Nephrolithiasis (renal calculi)

More common with advancing age and in men

Asymptomatic

If calculus is non-obstructing

Smaller ones pass spontaneously (< 5 mm)

Renal colic (flank pain that radiates to lower abdomen and groin)

Hematuria

Gross

Microscopic

60-80% composed of calcium

Uric acid stones will not shadow

Predisposing conditions:

Dehydration

Urinary Stasis

Hyperuricemia ( ↑ levels of uric acid in blood)

Hypercalcemia (↑ levels of calcium in blood

Hyperparathyroidism

Medications (Diuretics) and supplements

Diseases that increase vitamin D levels 

Echogenic focus (foci) with shadowing

To improve visibility of the shadow:

Use harmonics

Put focus at level of stone

Increase frequency

Decrease beam width

Turn off beam averaging techniques (Sono CT, Xres, applipure)

“Twinkle artifact” with Colour

Ureteral calculi

Due to migration from kidney

Hydroureter

Ureter will be distended proximal to obstruction

Look for bilateral ureteral jets at bladder orifices 

Bladder calculi

Commonly caused by urinary stasis: 

Due outlet obstruction

Cystocele (bladder prolapse)

Neurogenic bladder

Suprapubic pain

Fowl smelling urine

With or without hematuria

May result due to migration from kidney

May cause inflammation and wall thickening due to edema

Check for mobility (ie: rule out a mass)

May adhere to inflamed bladder wall (ie: “hanging” stone) 

Cortical nephrocalcinosis

Common causes: 

Acute cortical necrosis

Chronic glomerulonephritis

Chronic hypercalcemic states

Ethylene glycol poisoning

Sickle Cell disease

Renal Transplant rejection

Calcium deposits in the renal cortex

Tends to be bilateral and diffuse

Can either be cortical or medullary nephrocalcinosis (…or both)

Can be dystrophic calcification or metastatic (via lymphatic or hematologic spread)

Echogenic cortex unilaterally or bilaterally

Calcifications within the cortex

Lack of cortico-medullary differentiation.

Medullary Nephrocalcinosis

Common causes:

Hyperparathyroidism

Renal tubular acidosis

Medullary Sponge Kidney

Bone Metastases

Chronic pyelonephritis

Cushing syndrome

Calcifications within the medullary pyramids.

Begins with echogenic rims around the pyramids

Progresses to echogenic pyramids with or without shadowing














Renal Neoplasms 


Pathology

Patient Population

Signs & Symptoms

Things to know

Sonographic Appearance

Image

Renal Cell Carcinoma

Most common renal parenchymal malignancy

Peak age 50-70


NON-SYNDROMIC:

Unknown, obesity, smoking assoc. With acquired cystic disease from long term renal dialysis

Painless hematuria

Mild flank pain

Palpable mass

Weight loss

RCC tumors can produce several hormones and the following conditions may result:

Erythrocytosis – (Erythropoietin)

Hypercalcemia – (Parathormone, Vitamin D metabolites)

Hypokalemia – (ACTH)

Galactorrhea – Prolactin

Hypertension – Renin

Gynecomastia – (Gonadotropins)


Variable:

Solid mass (hyoer, hypo, mixed)

Complex cystic mass

±Characterize the mass

°Location (upper pole, lower pole, mid, etc)

°Echogenicity

°Size (measure in 3 dimensions)

Check for renal vein / IVC involvement

Check for mets – lymph nodes, liver, contralateral kidney, bladder, etc

Transitional Cell Carcinoma

Most common in Older patients

Painless hematuria

Develops in collecting system:

Renal calyces, renal pelvis, ureters and bladder (most common)

Oncocytoma

More common in men with peak incidence in 60-70 age group

Asymptomatic (discovered incidentally)

Usually benign 

May occur in parathyroid, thyroid, adrenal glands, salivary glands and kidneys

° 3-7 % of renal tumors

Vary in size

May be multicentric or bilateral

°Bilateral more often with hereditary syndromes (Birt-Hogg-Dubé, tuberous sclerosis,  hereditary oncocytosis)

°Difficult to distinguish from RCC

°Can be homogenous or heterogenous mass

°Central stellate scar may be seen (1/3 of cases)

Angiomyolipoma

Often found in patients with tuberous sclerosis

Usually small and asymptomatic (usually an incidental finding)

Larger ones may hemorrhage and cause symptoms:

°Hematuria

°Flank Pain

°Palpable mass

Benign renal tumor composed of various tissues

Angio – Blood Vessels

Myo – Muscle

Lipo – Fat

Usually seen as a homogenous, well-defined echogenic cortical mass

May be hypoechoic or heterogeneous if it is larger or there has been hemorrhage within it

Lymphoma  

Always metastatic (non-Hodgkin's more common)

May have direct invasion from retroperitoneal lymph nodes/masses and encase ureters and renal vessels

°Focal (homogenous, hypoechoic solid mass)

°Diffuse (enlarged kidney with disruption of kidney architecture)

°Perirenal spread may appear as hypoechoic perirenal mass of as a “rim” around kidney

May be mistaken for a hematoma

Leukemia

Most often bilateral renal enlargement

Renal involvement may be diffuse or focal

Parenchyma has a coarse, hyperechoic echogenicity

Wilms Tumors (Nephroblastoma)

Most common malignant abdominal tumor of childhood 80% between ages 1-5

Presents as a palpable mass

Arises within the cortex and expands

May be bilateral (5-10%)

Large solid mass that displaces and distorts renal sinus, pyramids and cortex

Often hyperechoic and homogenous

Areas of hemorrhage and necrosis will appear hypoechoic or cystic  


Bladder Neoplasms (Tumors)

**any non-mobile mass in the bladder should be considered malignant 


Pathology

Patient Population

Signs & Symptoms

Things to know

Sonographic Appearance

Image

Papilloma

Benign tumor of the bladder wall

Can develop into transitional cell carcinoma

Transitional Cell Carcinoma (urothelial bladder cancer)

Most common bladder malignancy (95%)

Smoking and analgesic abuse increase risk

Papillary (finger-like projections) or Sessile (flat)

Non-invasive –arise from surface epithelium

Invasive - grows into deeper layers

Squamous Cell Carcinoma

Rare form of bladder cancer (5%)

Very Aggressive!

Associated with:

°Chronic inflammatory conditions

°Neurogenic bladder

°Stones

Adenocarcinoma 

Uncommon (1% of bladder cancers) most associated with urachal cysts

°Non-urachal origin

Diffuse bladder wall thickening

Sonographic appearance:

Urachal origin:

Soft tissue mass located in midline infraumbilical region (along course of urachus)

Usually large tumors (5-6 cm)

Mixed solid-cystic appearance

Peripheral calcification common (70%)

Bladder Metastases

Secondary tumors of the bladder that come from primary tumors of adjacent pelvic organs.

Men: most commonly from prostate cancer

Women: most commonly from cervical or uterine cancer

Spread via lymphatic or vascular vessels


Renal Cystic Diseases

Pathology

Patient Population

Signs&Symptoms

Things to know

Sonographic Appearance

Image

Cortical Cysts

Increases with advancing age (>60 yrs = 33%)

Asymptomatic 

Unless cyst is large which may result in flank pain and hematuria

Can hemorrhage or become infected

Originate from the distal convoluted tubule or collecting duct of the nephron

Simple: 

Anechoic, well-defined walls, round or ovoid, acoustic enhancement (thru transmission)

Complex: 

Internal echoes

can result from hemorrhage or infection

Septations

can result from hemorrhage or infection

Thick wall

Mural nodularity

Simple Complex

Cortical cyst -Milk of Calcium

Sedimented calcium salts layered within a cyst

Seen as echogenic foci with ring-down artifact

Mimics cyst wall calcification

Parapelvic / Peripelvic Cysts

Parapelvic Cysts

Grow from the renal parenchyma next to the renal sinus and grow into the sinus.

Peripelvic Cysts

Grow from the epithelial cells of the renal pelvis and calyces

Parapelvic: Look for cyst walls separating the cystic masses as you scan through the renal sinus/pelvis

Hydronephrosis: Dilated renal pelvis and calyces should communicate as you scan through the sinus

Parapelvic 

hydronephrosis

Medullary Cystic Disease

30-40 age group 

Genetic condition: autosomal dominant

Polyuria, salt-wasting, eventually leads to end stage renal disease

Small cysts in the medulla and at the corticomedullary junction

Small echogenic kidneys with medullary cysts

Medullary Sponge kidney

Associated with : hemihypertrophy, Ehlers-Danlos Syndrome, congenital hypertrophic pyloric stenosis, hyperparathyroidism, Caroli disease and ARPKD

Asymptomatic unless there is stone formation

Renal colic, hematuria, dysuria

ectatic(dilated) collecting tubules

May be focal or diffuse

May develop medullary nephrocalcinosis

Hard to see on U/S

Echogenic renal pyramids (+/- shadowing)

Autosomal Dominant Polycystic Kidney Disease

“Adult” 

Usually present at 40-50yrs

Hypertension and hematuria

May present as palpable mass

Multiple bilateral renal cysts

People under 30 with family history – minimum of 2 renal cysts (in one or both kidneys) required for diagnosis

Age 30-59 – 2 cysts in each kidney required for diagnosis

Age 60+ - 4 cysts in each kidney required for diagnosis

Bilaterally enlarged kidneys with multiple cysts of varying size

Check liver, spleen and pancreas for cysts 

Autosomal Recessive Polycystic Kidney Disease

“Infantile”

4 types:

°Perinatal

°Neonatal

°Infantile

°Juvenile

 

Dilated collecting tubules, hepatic cysts and periportal fibrosis

Massively enlarged echogenic kidneys

Lack of cortico-medullary differentiation

Occasionally macroscopic cysts will be seen

Multicystic Dysplastic Kidney (renal dysplasia, renal dysgenesis & multicystic kidney)

Often diagnosed prenatally (seen in utero)

Kidney function significantly reduced (may result in renal failure)

Small, malformed kidney composed of multiple cysts, developmental abnormality, possibly due to urinary obstruction during embryonic stage

Usually unilateral (bilateral incompatible with life)

Multiple non-communicating cysts of varying size

Little to no renal parenchyma seen

Normal renal sinus

May see focal echogenic areas (represent tiny cysts)

Multilocular Cystic 

(cystic nephroma)

Rare 

Found in males under 4yrs and in females 4-20 or 40-60

Children present with palpable mass

Adults may be asymptomatic or present with:

Abdominal pain

Hematuria

Hypertension (HTN)

Urinary tract infections (UTI)

Usually benign, has malignant potential

May be unilateral or bilateral 

Mass containing multiple cysts of varying size with a well-defined capsule


Neoplasm - Associated Renal Disease

  • Acquired Cystic Kidney Disease

    • Pts undergoing dialysis for renal failure (40-90%)

    • Can develop both cysts and/or solid tumors (RCC 4-10%)

  • Von Hippel-Lindau Disease

    • Genetic disorder (autosomal dominant)

    • Can develop renal cysts (76%) and/or solid tumors (RCC usually multifocal and bilateral))

  • Tuberous Sclerosis

    • Genetic disorder (autosomal dominant)

    • Can develop renal cysts and/or solid tumors (AML, RCC)









Renal Medical Disease


Pathology

Patient Population

Signs&Symptoms

Things to know

Sonographic Appearance

Image

Acute Tubular Necrosis

Most common cause of acute reversible renal failure

Causes:

Hypotension

Dehydration

Drugs

Solvents

Heavy Metals

Deposition of cellular debris in the renal collecting tubules results in ischemic necrosis

If caused by hypotension is the cause, the kidney may appear normal

If caused by heavy metal, solvents or drugs, the kidneys appear enlarged and hyperechoic kidneys with decreased parenchymal medullary distinction

Acute Cortical Necrosis

Rare cause of acute renal failure

Causes: 

Traumatic blood loss, sepsis, burns, severe dehydration, venom toxicity, pregnancy complications (placental abruption, postpartum hemorrhage, septic abortion)

Ischemic necrosis of the cortex with sparing of the renal pyramids

Hypoechoic cortex initially

With time, atrophy and cortical calcification occur

Glomerulonephritis

Systemic diseases: polyarteritis nodosa, systemic lupus erythematosus, Wegener granulomatosis, Goodpasture syndrome, thrombocytopenic purpura, hemolytic uremic syndrome

Hypertension, hematuria, azotemia (increased nitrogen in the blood)


LUPUS 

Necrosis of the glomerulus 

Can be acute of chronic

Acute: may appear normal or enlarged (common)

Cortex may appear hyperechoic or hypoechoic but medulla is sparred

Acute Interstitial Nephritis (ATN)

Common culprits;

Antibiotics (penicillin, methicillin, rifampin)

Sulfa drugs

Non-steroidal anti-inflammatories

Diuretics (Furosemide, Thiazides)

Acid reducers (Cimetidine) 

Kidney suffers hypersensitive reaction to drug therapy

Enlarged, echogenic kidneys

Chronic Renal Failure

Diabetes (most common)

Hypertension

glomerulonephritis

Long standing assault to the kidneys resulting in gradual progressive loss of function

Non-reversible

Often leads to renal transplant

small, echogenic kidneys with loss of parenchyma



Trauma of the Urinary System


Pathology

Patient Population

Signs&Symptoms

Things to know

Sonographic Appearance

Image

Laceration 

Penetrating trauma

Tear of the tissue

Minor (75-85%) - parenchymal lacerations

Major (10%) - lacerations that extend into the collecting system

Linear defect in cortex (may or may not extend into collecting system)

Hematoma

Perirenal: fluid collection outside of the renal capsule, normal renal contour

Subscapular: fluid beneath the renal capsule, will flatten or indent the renal contour

Retroperitoneal: Fluid collection within the retroperitoneum (in the pararenal space)

Depending on size and location it may push into and deviate surrounding organs   

subscapular:perirenal:retroperitoneal:

AVM/AVF - (arteriovenous malformation / Fistula)

May be congenital (25%) but more often acquired (75%)

Acquired from trauma

Abnormal connection between artery and vein

Mosaic appearance with color Doppler location it may push into and deviate surrounding organs

Bladder trauma

Bladder can rupture or bruise due to pelvic trauma.

Rupture - Free fluid in peritoneal cavity(Urine Ascites).

Urinoma – Focal collection of urine adjacent to the bladder

Bruise - Blood clots in bladder

Bladder Flap Hematoma

Post C-section surgery

Fever, mass in pelvis

Incision through peritoneum

See complex mass between bladder and lower uterine segment

Results in hematoma in vesicouterine space

Ureter Trauma

Complication of gynecologic or urologic surgery

Difficult to see damaged ureter itself, may see a urinoma






Other (Bladder Diverticula & Neurogenic Bladder)


Pathology

Patient Population

Associated with / risk of

Things to know

Sonographic Appearance

Image

Bladder Diverticula

Increase risk of:

Stones within the diverticula

Infection due to stagnant urine

Bladder rupture (rare)

Herniation of the bladder mucosa through the muscular wall resulting in a pocket or pouch where urine can collect and become stagnant

Round/oval anechoic outpouching from the bladder wall

May see urine flowing in and out of diverticula (with use of Color doppler)

Any change in size (from previous)

Check for stones, obstruction, or internal echoes 

hematomas

Usually resolve spontaneously

Variable in size

changes with time

Acute –echogenic heterogeneous mass

With age - Begins to liquify becoming a complex fluid collection

Urinoma 

Most commonly occur from trauma or post operative  procedures (ex: renal transplant = 6% within first 2 weeks)

May be associated with hydronephrosis

Encapsulated collection of extravasated urine

Rarely from high grade collecting system obstruction

Large leaks can result in intraperitoneal urinary ascites

Well-defined anechoic fluid collection