Notes #10: Renal Infections / Inflammations / Calcifications / Obstruction
also known as uremia toxic condition associated with renal insufficiency symptoms secondary to retention of nitrogenous waste products
High Blood Pressure Nausea, vomiting GI ulcers, inflammations d/t increase serum ammonia Cardiac arrhythmias d/t potassium, Calcium imbalances Edema and fluid retention Anemia d/t decrease in erythropoietin Urine flow changes Dizziness Coma, convulsions Nephrotic Syndrome (not a single entity but a stage in chronic renal disease marked by proteinuria, decreased plasma protein, rise in serum lipids, edema) Elevated BUN, creatinine, ammonia
Acute renal failure:
sudden impairment symptoms develop within hours or a few days usually secondary to radiation, chemical, or toxin exposure, to sudden decrease in blood volume, or to acute infection
Chronic renal failure:
result of chronic renal disease
develops over many years
Major Classifications of Renal Disease:
Type I Renal Disease:
any of a large group of renal medical diseases that originate with injury or infection of the glomeruli and lead to renal failure.
Initially edema and enlargement of the kidney Progressive increase in echogenicity of the cortex Progressive decrease in size Increased definition of cortico- medullary junction Pyramids may appear enlarged as cortex shrinks
Echogenicity of cortex and size of the kidney correspond to severity of disease, prognosis of kidney
Grade 1: Renal cortex echogenicity = liver Grade 2: Renal cortex echogenicity > liver Grade 3: Renal cortex echogenicity = sinus echoes
Small (length <10cm) echogenic kidneys = poor prognosis Normal sized echogenic kidneys = better prognosis
Type II Renal Disease:
Renal Inflammations and miscellaneous renal diseases that originate in the pelvis or medulla. These diseases have multiple causative agents usually coming from the ureter and leading to pyelonephritis. Type II disease may eventually cause renal failure by generalized progression into the cortex. Type II diseases are, however, more variable in appearance and outcome than are Type I.
Variable in appearance Show disruption of pyramid - medullary echoes Distort normal anatomy and eliminate corticomedullary boundary definition
Type I Renal Diseases:
Prerenal Origin of Renal Failure:
diminished blood flow to kidneys can lead to interstitial damage Congestive Heart Failure Decreased Blood Volume from hemorrhage or surgery Renal Artery Stenosis Metabolic vascular diseases such as Diabetes Renal Vein Thrombosis (may be secondary to renal cellcarcinoma, retroperitoneal tumors, diabetes)
Sonographic Analysis: Echogenic material within RV or RA Normal Venous Pattern in RV may be absent Vascular calcifications - shadowing in pelvic area
Large group of diseases where the initial pathological involvement is the glomeruli located in the cortex of the kidney Leads to proteinuria, hypertension, and other signs of renal failure.
Causative Agents: Infectious agents carried through the blood system Strep, Malaria, Syphilis
Toxins such as snake venom, drugs, metals, fumes Pressure damage due to PKD, severe hydronephrosis Autoimmune Inflammation due to lupus nephritis, Goodpasture's Syndrome - antibodies to lung, kidney Acute cortical necrosis Ischemic necrosis d/t shock, hemorrhage, burns, Intrarenal arterial stenosis of venous thrombosis toxemia of pregnancy, severe dehydration
May be localized or generalized Leads to increased cortical echogenicity in the area due to necrosis, calcific deposits and fibrosis
Deposition of abnormal protein fibers in amounts sufficient to impair renal function Associated with acute and chronic infections, and immunologic disorders such as rheumatoid arthritis, lupus, certain tumors (especially myeloma), and aging Deposits occur in spleen, liver, kidneys, lymph nodes, heart, lungs, GI tract, throughout body Leads to rubbery consistency - renal failure
Type II Renal Disease:
Acute Tubular Necrosis:
Results from tubular epithelial destruction Toxins common cause Sonographically normal kidneys Symptoms of acute renal failure with nl kidneys - likely ATN Particularly a problem with renal transplants from cadaever
Similar to ATN, but secondary to alcohol or drug abuse In some cases the pyramids may be prominent or swollen
Renal Papillary Necrosis:
Associated with diabetes, severe infantile diarrhea, obstructive uropathy, sickle cell anemia, acute or chronic pyelonephritis, chronic alcoholism Presents with small cystic areas or increased echogenicity in the medulla
Inflammatory disease secondary to long-standing obstruction Xanthro = yellow lipid deposits Enlarged kidneys with stones present in majority of cases Staghorn calculi-large stone center Single or multiple renal masses present, usually hypoechoic or anechoic Abscesses filled with yellow lipid usually peripelvic Debris filled dilated calyces May be segmental associated with obstruction of single calyces Distortion of normal anatomy
Bacterial Interstitial Nephritis (Pyelonephritis):
May result from infection, obstruction, urinary stasis Kidney may appear normal initially Decreased echogenicity throughout kidney and enlargement Obliteration of corticomedullary junction - sinus echoes also appear less echogenic, blend into parenchyma Dilated calyces single or multiple
Focal Nephronia, and Abscesses may develop
Symptoms: Fever, chills and flank pain
Localized Infections aka Focal Nephronia, aka Lobal Nephronia, aka Acute Focal Bacterial Nephritis Localized Inflammatory Mass Small ill-defined borders Wedge shaped area of reduced echogenicity without liquidification
Abscess Formation Liquidification, pus formation Better border definition, liquid component Irregular shape Enhancement, Debris, fluid/debris levels Increasing size of mass area
Carbuncle Mature abscess Thick-walled, discrete, complex, round shape, decreasing size
Emphysematous Infection contain gas which cause stong echoes and shadowing
Infection may remain within the kidney of may break throught the renal capsule to the perirenal space where it tends to localize in fat posterior/lateral to the kidney near psoas muscle. May cause elevation of the kidney. Gerota's fascia usually prevents further spread.
Important to visualize renal capsule to determine if intrarenal or perirenal abscess.
Treatment: Drainage of abscess under ultrasound or fluoroscopic guidance Surgical removal of mature abscess Nephrectomy in severe cases
Multiple abscesses with debris common Associated with pulmonary Tb and AIDS Strictures in calyces often lead to hydronephrosis Ascites may develop
Echogenic non-shadowing mass in the collecting system often associated with fever, chills, flank pain. Occurs most usually in patients with lowered resistance, from diabetes, malignancy, chronic illness, or medication.
Differential diagnosis: blood clot, tumor, debris
Renal Sinus Lipomatosis:
Replacement lipomatosis in sinus Kidney may be normal in size or enlarged with increased width of central echoes, thin renal parenchyma Common in older patients Sequelae to chronic stone or inflammation Also a normal variant with obesity, aging
Renal Calcification and Obstruction:
Only 5% of renal failure is due to obstruction, but this is the easiest cause to treat. It is essential to screen all patients with symptoms of renal failure for obstruction so quick surgical intervention can be undertaken.
Obstructive Causes of Hydronephrosis:
1.Congenital atresia of urethra, kinking of ureter, mal-position of ureter
2.Foreign bodies, calculi (urate stones most common), sloughed papillae or blood clot.
10. Corrected obstruction
11. Neurogenic bladder post operative or due to chronic disease
Hydronephrosis generally unilateral and asymptomatic
Pyonephrosis is hydronephrosis with coexisting infection, debris/purulent material in fluid
Symptoms if present vary:
Oliguria if bilateral complete obstruction Polyuria may develop in incomplete obstruction due to inability of tubules to concentrate Change in size or force of urine stream Severe colicky pain to vague flank pain
Amount of Fluid dependent on duration of obstruction and renal output - amount of residual cortex more important than amount of fluid.
Slight separation of pelvis or cystic appearance of calyces, infundibulum connection to pelvis separates from renal cyst.
All calyces enlarged, cauliflower shape
Shape of calyces no longer discernible. Kidney can reach up to 20 times normal size. Thinning of cortex usually apparent.
Sites of Obstruction:
UPJ - ureteral pelvic junction
Most common site for obstruction congenital strictures calculi or foreign body obstruction retroperitoneal tumor impingement
UVJ - ureteral vesicle junction Obstruction most commonly due to extrinsic compression, ex. pelvic lymphoma, pelvic abscess, ovarian mass, or large abdominal mass Right sided obstruction most common in women Dilated ureters seen as tubular anechoic structures running from kidney to bladder or as circular anechoic areas posterior to the bladder on transverse view Color flow of ureteral jets can confirm unilateral UVJ obstruction Ultrasound may not locate site of obstruction in ureter
Bilateral Obstruction: Least common site for obstruction
may be due to bladder outlet or urethral obstruction associated with bladder or prostate tumor or cervical carcinoma spinal cord damage, paralysis of bladder, urethral motility problems, other non-obstructive causes
Lesions confused with Hydronephrosis "False Positives"
Central renal cysts Multicystic Kidney Sinus Lipomatosis Peripelvic cysts Sonolucent renal pyramids Lumbar meningomyelocele Pancreatic Pseudocysts Sonolucent Masses (Lymphoma, Leukemia, other mets) Aneurysm/Varices of Renal Vasculature in renal hilum
Associated with failure to recognize obstruction or hydronephrosis "False Negatives"
Staghorn calculi - shadowing obscures visualization Numerous cysts with superimposed hydronephrosis Acute renal disease - no output of urine so minimal dilation
Urinoma "renal pseudocyst"
escape of urine, encapsulated by body
appears as an anechoic mass usually posterior to kidney between the renal capsule and Gerota's fascia.
Can lead to retroperitoneal fibrosis, perinephric abscess
Nephrolithiasis or renal calculi
Results from calcium salts in renal system More frequent in males than females Overall incidence 0.1% - 6% of the population Can arise anywhere in urinary system, but most common in kidney Causes: Hypercalcuria or hypercalcemia due to geographic location (water source), hyperparathyroidism, Vit D intoxication, malignancy, bone disease, dehydration, or Cushing's disease Large single stones may be located in center of kidney with shadowing apparent (Staghorn calculi). These are named by their appearance on radiography. Multiple smaller stones can be visualized by ultrasound in the pelvis or near the corticomedullary border
Classic - small stones or deposits along the corticomedullary borders
Deposits in parenchyma of the kidney
in severe form the entire cortex is strongly echogenic, may appear similar to severe Type I renal disease May not shadow CT can differentiate from renal disease
Medullary pyramids become echogenic while the cortex retains normal echogenicity May not shadow - microscopic aggregates cause scattering of beam, but no shadows
Rare, metabolic disease - hereditary Leads to death before adulthood Presents with renal stones in childhood Calcium oxalate deposits in cortex lead to renal failure Hyperechoic cortex with pelvic stones
Cystic extension of calyces