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My step 1 mnemonics > Renal > Flashcards

Renal Flashcards

1
Q

Pronephros

A
  • week 4; then degenerates.
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2
Q

Mesonephros

A

functions as an interim kidney for 1st trimester; later contributes to male genital system.

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3
Q

Metanephros development time frame:

A

permanent; first appears in 5th week of gestation; nephrogenesis continues through weeks 32- 36 of gestation.

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4
Q

Ureteric bud

A

(metanephric diverticulum) derived from the caudal end of the mesonephric duct; gives rise to ureter, pelvises, calyces, collecting ducts;

fully canalized by 10th week (Me-10-nephric diverticulum)

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5
Q

Metanephric mesenchyme

A

(ie, metanephric blastema) - ureteric bud interacts with this tissue;

interaction induces differentiation and formation of glomerulus through to distal convoluted tubule (DCT)

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6
Q

Ureteropelvic junction

A

last to canalize - most common site of obstruction (can be detected on prenatal ultrasound as hydronephrosis).

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7
Q

Horseshoe kidney associated with:

A

C - cancer (renal, rare)
H - hydronephrosis (eg, ureteropelvic junction obstruction)
I - infection
C - chromosomal aneuploidy syndromes (eg, Turner syndrome; trisom ies 13, 18, 21)
S - stones with

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8
Q

Unilateral renal agenesis

A

Ureteric bud fails to develop and induce differentiation of metanephric mesenchyme - complete absence of kidney and ureter.

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9
Q

Multicystic dysplastic kidney

A

Ureteric bud fails to induce differentiation of metanephric mesenchyme - nonfunctional kidney consisting of cysts and connective tissue.
Predominantly nonhereditary and usually unilateral; bilateral leads to Potter sequence.

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10
Q

Duplex collecting system

A

Blastema creates a Y-shaped bifid ureter.

Strongly associated with vesicoureteral reflux and/or ureteral obstruction, inc risk for UTI’s.

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11
Q

Posterior urethral valves

A

Membrane remnant in the posterior urethra in males;

It can be diagnosed prenatally by hydronephrosis and dilated or thick-walled bladder on ultrasound.

The most common cause of bladder outlet obstruction in male infants.

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12
Q

Renal vasculature

A

renal artery - segmental artery - interlobar artery - arcuate artery - interlobular artery - afferent arteriole - glomerulus - efferent arteriole - vasa rectal peritubular capillaries - venous outflow.

SI-AI-A

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13
Q

Course of ureter

_______within the _____ part of the ureter prevents urine reflux.

A

arises from the renal pelvis, travels under gonadal arteries -> over common iliac artery ->under uterine artery/vas deferens

(retroperitoneal).

Muscle fibers within the intramural part of the ureter prevents urine reflux.

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14
Q

Blood supply to ureter:

A

PR MAGIC VID
• Proximal:
P - Proximal
R - renal arteries

• Middle:
M -Middle
A - aorta
G - gonadal artery
I - internal iliac arteries
C - common iliac

• Distal:
V - Vesical arteries (superior)
I - internal Iliac
D - Distal

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15
Q

Glomerular filtration barrier

A

Composed of:

  • Fenestrated capillary endothelium (prevents entry of > 100 nm)
  • Basement membrane with type IV collagen chains and heparan sulfate
  • Visceral epithelial layer consisting of podocyte foot processes (prevents entry of molecules > 50- 60 nm)

Charge barrier- all 3 layers contain (-) charged glycoproteins-prevents (-) molecules entery.

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16
Q

Normal GFR

A

= 100 mL/min.

Creatinine clearance is an approximate measure of GFR. Slightly overestimates GFR because creatinine is moderately secreted by renal tubules.

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17
Q

Plasma volume =

A

Plasma volume = TBV x (I - Hct).

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18
Q

eRPF=?

A

eRPF = uPAH x V/pPAH = cPAH·

eRPF underestimates true renal plasma flow (RPF) slightly.

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19
Q

Renal blood flow (RBF) = ?

% of CO?

A

Renal blood flow (RBF) = RPF/(l - Hct).

Usually 20 - 25% of cardiac output.

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20
Q

Filtration fraction (FF) = ?

A 
Filtration fraction (FF) = GFR/RPF
Normal FF = 20% .
Filtered load (mg/min)= CFR (mL/min)
x plasma concentTation (mg/mL).
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21
Q

Filtered load (mg/min) =?

A

Filtered load (mg/min) = GFR (mL/min) x plasma concentration (mg/mL).

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22
Q

Filtered load =?

A

Filtered load = GFR x Px

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23
Q

Reabsorption rate = ?

A

Reabsorption rate = filtered - excreted.

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24
Q

Secretion rate = ?

A

Secretion rate = excreted - filtered.

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25
Q

FeNa = ?

A

fractional excretion of sodium.

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26
Q

Excretion rate = ?

A

Excretion rate = V x U

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27
Q

FeNa = equsions

A

= Na+ excreted/Na+ filtered

= V x U / GFR x PNa

= Pcr x UNa/ Ucr x PNa

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28
Q

Glucose clearance

A

In adults, at plasma glucose of - 200 mg/dL, glucosuria begins (threshold). At a rate of about 375 mg/min, all transporters are fully saturated (Tm).

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29
Q

Early PCT - % Na+ reabsorbed?

Other notes

A

65- 80% Na+ reabsorbed.

contains a brush border. Reabsorbs all glucose and amino acids and most HC03-, Na+, Cl-, P04l-, K+, H20, and uric acid. Isotonic absorption.

Generates and secretes NH3, which enables the kidney to secrete more H+

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30
Q

Thin descending loop of Henle - % Na+ reabsorbed?

A

impermeable to Na+

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31
Q

Thick ascending loop of Henle - % Na+ reabsorbed?

Other notes

A

10- 20% Na+ reabsorbed.

lumen potential generated by K+ backleak ->paracellular reabsorption of Mg2+ and Ca2+.

Impermeable to H20.

Makes urine less concentrated as it ascends.

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32
Q

Early DCT % Na+ reabsorbed?

A

Impermeable to H20 - Makes urine fully dilute (hypotonic).

5- 10% Na+ reabsorbed.

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33
Q

Collecting tubule - cells

A

Principle cells - ENac, K+ channel, Na/K+ ATPase activity -> reabsorbs Na+ in exchange for secreting K+

Alfa intercalated cells - Makes urine Acidic -> H+ secretion

Beta intercalated cells - Makes urine Basic -> HCO3- secretion (HCO3-/CI- exchanger on the apical side), reabsorbs H+.

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34
Q

Collecting tubule - % Na+ reabsorbed?

A

3- 5% Na+ reabsorbed.

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35
Q

Aldosterone activity in DCT

A

Aldosterone - mineralocorticoid receptor (mRNA ->protein synthesis)

In Principle cells: inc ENac, K+ channel, Na/K+ ATPase activity.

In Alfa intercalated cells: in H+ATPase -> inc HCO3- /Cl- exchanger.

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36
Q

ADH activity in DCT

A

acts at V2 receptor - insertion of aquaporin H2O channels on the apical side.

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37
Q

Fanconi syndrome CAUSES

A

Wilsons MIG has Lead/Platinum Toxin Tyers!

Wilson disease

M - multiple myeloma
I - ischemia
G - glycogen storage disease

Lead/Cisplatin

Nephrotoxins/drugs (eg, ifosfamide)

Tyrosinemia

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38
Q

Liddle syndrome

A

A gain of function mutation -> inc activity of Na+ channel -> inc Na+ reabsorption in collecting tubules.

Autosomal dominant - Presents similarly to hyperaldosteronism, but aldosterone is nearly undetectable.

Treat with amiloride

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39
Q

Syndrome of
Apparent
Mineralocorticoid
Excess

A

Hereditary 11 beta -HSD deficiency (converts cortisol to cortisone) -> inc cortisol -> Inc mineralocorticoid receptor activity (cortisone inactive in these receptors.

Autosomal recessive or acquired from glycyrrhetinic acid (present in Licorice)

Treat with K+-sparing diuretics (dec mineralocorticoid effects) or corticosteroids (dec endogenous cortisol production)

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40
Q

Renin secreted by ____ in response to:

A

Secreted by JG cells in response to:

Dec renal perfusion pressure (detected by renal baroreceptors in afferent arteriole).

Dec NaCl delivery to macula densa cells.

inc renal sympathetic discharge (beta 1 effect).

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41
Q

AT II

A

Helps maintain blood volume and blood pressure.

Affects baroreceptor function; limits reflex bradycardia, which would normally accompany its pressor effects.

A -Aldosterone

C - constriction (Vasoconstriction)
A - ADH
N - Na+/K+ activity
E - Efferent arteriole

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42
Q

ANP, BNP

A

Released from atria (ANP) and ventricles (BNP) in response to inc volume;

inhibits renin-angiotensin aldosterone system;

relaxes vascular smooth muscle via cGMP -> inc GFR, dec renin.

Dilates afferent arteriole, promotes natriuresis.

43
Q

ADH

A

Primarily regulates serum osmolality;

Responds to low blood volume states.

Reabsorption of water in collecting ducts.

Reabsorption of urea in collecting ducts - maintain corticopapillary osmotic gradient.

44
Q

Aldosterone

A

Primarily regulates ECF volume and Na+ content;

Response to low blood volume states.

Responds to hyperkalemia by inc K+ excretion.

45
Q

Erythropoietin

A

Released by interstitial cells in peritubular capillary bed in response to hypoxia.

kidney disease. Supplementation can cause HTN.

46
Q

Calciferol (vitamin D) made from:

A

PCT cells convert 25 -OH vitamin D3 to 1,25-(OH)2 vitamin D3 (calcitriol, active form).

47
Q

Prostaglandins

A

Paracrine secretion vasodilates the afferent arterioles to inc RBF.

NSAIDs block renal-protective prostaglandin synthesis -> constriction of the afferent arteriole and dec GFR;

this may result in acute kidney injury in low renal blood flow states.

48
Q

Dopamine

A

Secreted by PCT cells, promotes natriuresis.

At low doses - dilates interlobular arteries, afferent arterioles, efferent arterioles -> inc RBF, little or no change in GFR.

At higher doses - it acts as a vasoconstrictor.

49
Q

SHIFTS K+ OUT Of CELL (CAUSING HYPERKALEMIA)

A

D - Digitalis (blocks Na+/K+ ATPase)
O - Osmolarity (Hyper)

L - Lysis of cells (eg, crush injury, rhabdomyolysis, tumor lysis syndrome)
A - Acidosis
B - Beta-blocker
S - Sugar (insulin deficiency)
S - Succinylcholine (risk in burns/muscle trauma)

50
Q

Sodium - Electrolyte disturbances

A

Low presentation- Nausea, malaise, seizures
High presentation- Irritability
Both presentation- stupor, coma

51
Q

Potassium - Electrolyte disturbances

A

High presentation- Wide QRS and peaked T waves on ECG

Both presentation- arrhythmias, muscle weakness

Low presentation - CUTS

C - cramps
U - U waves
T - T wave flattened
S - spasm

52
Q

Calcium - Electrolyte disturbances

A

Low presentation- Tetany, seizures, QT prolongation, twitching, spasms (“seizers” in CNS, heart, muscles)

High presentation:

Stones (renal)
bones (pain)
groans (abdominal pain)
thrones (inc urinary frequency)
psychiatric overtones (anxiety, altered mental status)
53
Q

Magnesium - Electrolyte disturbances

A

Low presentation- Tetany, torsades de pointes, hypokalemia, hypocalcemia (<1.0 mEq/L)

High presentation- DTRs, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia (depressed neurons, cardiovascular system)

Both presentation- hypocalcemia

54
Q

Phosphate - Electrolyte disturbances

A

Low presentation- Bone loss, osteomalacia (adults), rickets (children)

High presentation- Renal stones, metastatic calcifications, hypocalcemia

55
Q

Winters formula:

A

If measured Pco2 > predicted Pco2 -> concomitant respiratory acidosis;

If measured Pco2 < predicted Pco2 -> concomitant respiratory alkalosis;

1.5 x [HCO3-] + 8 +/- 2

56
Q

Respiratory acidosis causes:

A 
M - muscle weakness
O - Opioids
O - obstruction
D - diseases of the lung (acute/chronic)
S - sedatives
57
Q

High anion gap Metabolic acidosis causes:

A

M - Methanol (formic acid)
U - Uremia
D - Diabetic ketoacidosis

P - Propylene glycol
I - Iron tablets or INH
L - Lactic acidosis
E - Ethylene glycol (oxalic acid)
S - Salicylates (late)
58
Q

Normal anion gap Metabolic acidosis causes:

A 
C - chloremia(hyper)
H - hyperalimentation
A - Addison disease
R - Renal tubular acidosis
D - Diarrhea

A - Acetazolamide
S - Spironolactone
S - Saline infusion

59
Q

Respiratory alkalosis causes:

A

Hyperventilation:

P - Pulmonary embolism
A - Anxiety
T - Tumor
H - Hypoxemia 
S - Salicylates (early)
60
Q

Metabolic alkalosis

A

H+ loss (loss of gastric acid):
Vomiting
Antacid use

HCO3- excess (Kidneys):
Loop diuretics
Hyperaldosteronism

61
Q

Renal tubular acidosis -

Urine pH/Serum K+

A

Proximal <5.5 pH< Distal

Both have low K+

Type 4 has high K+ and variable pH

62
Q

Distal renal tubular acidosis (type 1)

DEFECT

A

Inability of alfa-intercalated cells to secrete H+ - no new HCO3- is generated -> metabolic acidosis

63
Q

Proximal renal tubular acidosis (type 2)

DEFECT

A

PCT defect HCO3- reabsorption -> inc excretion of HCO3- in urine -> metabolic acidosis

Urine can be acidified by alfa-intercalated cells in collecting duct, but not enough to overcome the increased excretion of HCO3- -> metabolic acidosis

64
Q

Hyperkalemic tubular acidosis (type 4)

DEFECT

A

Hypoaldosteronism or aldosterone resistance;

hyperkalemia -> dec NH3 synthesis in PCT -> dec NH4+ excretion

65
Q

Distal renal tubular acidosis (type 1) - CAUSES

A

A - analgesic nephropathy / autoimmune diseases (eg, SLE)
B - Amphotericin B toxicity
C - congenital anomalies (obstruction) of urinary tract

66
Q

Proximal renal tubular acidosis (type 2) - CAUSES

A

Mother FuCker: Multiple myeloma, Fanconi syndrome, carbonic anhydrase inhibitors

67
Q

Hyperkalemic tubular acidosis (type 4) - CAUSES

A

Dec aldosterone production:

R - Renin (diabetic hyporeninsm)
A - adrenal insufficiency
N - NSAIDs

T - TMP-SMX
O - obstruction

C - cyclosporine
H - heparin
A - ACE inhibitors, ARBs
D - diuretics (K+-sparing)

68
Q

RBC casts imply

A

Glomerulonephritis, hypertensive emergency.

69
Q

WBC casts imply

A

Tubulointerstitial inflammation, acute pyelonephritis, transplant rejection.

70
Q

Fatty casts (“oval fat bodies”) imply

A

Nephrotic syndrome. Associated with “Maltese cross” sign.

71
Q

Granular casts imply

A

Acute tubular necrosis (ATN). Often “muddy brown” in appearance.

72
Q

Waxy casts imply

A

End-stage renal disease/chronic kidney disease.

73
Q

Hyaline casts imply

A

Nonspecific, can be a normal finding. Form via solidification of Tamm- Horsfall mucoprotein (secreted by renal tubular cells).

74
Q

Renal cell carcinoma - associated with paraneoplastic syndromes and Tx

A

P - PTHrP
E - Ectopic EPO
A - ACTH
R - Renin

Treatment: surgery/ablation for localized disease. immunotherapy (eg, aldesleukin) or targeted therapy for metastatic disease rarely curative.
Resistant to chemotherapy and radiation therapy.

Cut the PEAR!

75
Q

Renal cell carcinoma - Pathology

A

Polygonal dear cells filled with accumulated lipids and carbohydrates. Often golden-yellow a due to inc lipid content.

Originates from PCT -> invades renal vein (may develop varicocele if left-sided) - IVC -> hematogenous spread -> metastasis to lung and bone.

Manifests with hematuria, palpable masses, 2° polycythemia, flank pain, fever, weight loss.

76
Q

Renal oncocytoma

A

Benign epithelial cell tumor arising from collecting ducts.

Large eosinophilic cells with abundant mitochondria without perinuclear clearing a (vs chromophobe renal cell carcinoma).

Presents with painless hematuria, flank pain, abdominal mass.

Often resected to exclude malignancy (eg, renal cell carcinoma).

77
Q

WAGR complex-

A

Wilms tumor
Aniridia (absence of the iris)
Genitourinary malformations,
Retardation/intellectual disability

(WT1 deletion)

78
Q

Denys-Drash syndrome-

A

Wilms tumor
Diffuse mesangial sclerosis (early-onset nephrotic syndrome),
Dysgenesis of gonads (male pseudohermaphroditism)

WT1 mutation

G1MS

79
Q

Beckwith-Wiedemann syndrome-

A

(WT2 mutation)

H - Hemihyperplasia
O - Organomegaly
W - Wilms tumor

Much? - Macroglossia

80
Q

Transitional cell carcinoma associated with?

A

can occur in renal calyces, renal pelvis, ureters, and bladder

Causes - problems in your Pee SAC:

P - Phenacetin

S - Smoking
A - Aniline dyes
C - Cyclophosphamide.

81
Q

Squamous cell carcinoma of the bladder

A

Chronic irritation of urinary bladder -> squamous metaplasia -> dysplasia and squamous cell carcinoma.

Risk factors include Schistosoma haematobium infection (Middle East), chronic cystitis, smoking, chronic nephrolithiasis.

Presents with painless hematuria.

82
Q

Stress incontinence - Tx

A

Treatment: pelvic floor muscle strengthening (Kegel) exercises, weight loss, pessaries.

83
Q

Urgency incontinence - Tx

A

Treatment: Kegel exercises, bladder training (timed voiding, distraction or relaxation
techniques}, antimuscarinics (eg, Oxybutynin for Overactive bladder).

84
Q

Overflow incontinence - Tx

A

catheterization, relieve obstruction (eg, alfa-blockers for BPH).

85
Q

Stress incontinence - associations

A

Inc risk with obesity, vaginal delivery, prostate surgery. Positive bladder stress test (directly observed leakage from urethra upon coughing or Valsalva maneuver).

86
Q

Urgency incontinence - associations

A

Overactive bladder (detrusor overactivity) - leak with an urge to void immediately. Associated with UTI.

87
Q

Overflow incontinence - associations

A

Associated with polyuria (eg, diabetes), bladder outlet obstruction (eg, BPH), neurogenic bladder (eg, MS). Inc post-void residual (urinary retention) on catheterization or ultrasound.

88
Q

Acute cystitis - Causes:

A

Causes:
• E coli (most common).
• Staphylococcus saprophyticus- seen in sexually active young women (E coli is still more common in this group).
• Klebsiella.
• Proteus mirabilis-urine has ammonia scent.

Systemic signs (eg, high fever, chills) are usually absent!

89
Q

Acute pyelonephritis - Pathology

A

Neutrophils infiltrate renal interstitium.

Affects cortex with relative sparing of glomeruli/vessels.

Presents with WBCs in urine +/- WBC casts. CT would show striated parenchymal enhancement.

Presents with fevers, flank pain (costovertebral angle tenderness), nausea/vomiting, chills.

Complications include: SCAN
S - sepsis (urosepsis)
C - chronic pyelonephritis
A - abscess (perinephric)
N - necrosis (papillary)

Treatment: antibiotics.

90
Q

Chronic pyelonephritis

A

The result of recurrent or inadequately treated episodes of acute pyelonephritis.

Typically requires predisposition to infection such as vesicoureteral reflux or chronically obstructing kidney stones.

Coarse, asymmetric corticomedullary scarring, blunted calyx.

Tubules can contain eosinophilic casts resembling thyroid tissue (thyroidization of kidney).

91
Q

Xanthogranulomatous pyelonephritis

A

rare;

grossly orange nodules that can mimic tumor nodules;

characterized by widespread kidney damage due to granulomatous tissue containing foamy macrophages.

Associated with Proteus infection.

92
Q

Consequences of renal failure

A

M - Metabolic Acidosis
U - Uremia
P - Potassium (high)

A - Anemia (Erythropoietin failure)
L - Lipidemia (especially high triglycerides)
O - osteodystrophy
N - Na+/H2O retention (HF, pulmonary edema, hypertension)
G - Growth retardation and developmental delay

Uremia- a clinical syndrome marked by: PP + CNS trouble
• Nausea and anorexia
• Pericarditis
• Asterixis
• Encephalopathy
• Platelet dysfunction
93
Q

Acute interstitial nephritis

A

Also called tubulointerstitial nephritis. Acute interstitial renal inflammation. Pyuria (classically eosinophils) and azotemia occurring after the administration of drugs that act as haptens.

QRS PPP SSS DM -

D - Diuretics
M -Mycoplasma

Q - Quinolones
R - Rifampin
S - Sulfonamides

P - Pain-free (NSAIDs)
P - Penicillins and cephalosporins
P - Proton pump inhibitors

S - Sjogren syndrome
S - SLE
S - Sarcoidosis

94
Q

Acute tubular necrosis - stages:

A

3 stages:

  1. Inciting event
  2. Maintenance phase - oliguric, fatal (lasts 1- 3 weeks; risk of hyperKalemia, Metabolic acidosis, Uremia -> “full of KUM”)
  3. Recovery phase - polyuric; BUN and serum creatinine fall;
    risk of hypokalemia and renal wasting of other electrolytes and minerals
95
Q

Diffuse cortical necrosis

A

Acute generalized cortical infarction of both kidneys. Likely due to a combination of vasospasm and DIC.
Associated with obstetric catastrophes (eg, abruptio placentae), septic shock.

96
Q

Renal papillary

necrosis

A

Sloughing of necrotic renal papillae -> gross hematuria and proteinuria.

May be triggered by recent infection or immune stimulus.

Associated with:

(SAAD papa with
papillary necrosis)
S -  Sickle cell disease or trait
A -Analgesics (NSAIDs)
D - Diabetes mellitus

Pyelonephritis (Acute)

97
Q

Acute tubular necrosis - causes

A

Can be caused by ischemic or nephrotoxic injury:
• ischemic - 2° to l renal blood flow (eg, hypotension, shock, sepsis, hemorrhage, HF). Results in death of tubular cells that may slough into tubular lumen (PCT and thick ascending limb are high ly susceptible to injury).

• Nephrotoxic - 2° to injury resulting from toxic substances. Proximal tubules are particularly susceptible to injury.
L - lead
A - aminoglycosides
M - myoglobinuria (crush injury)/ hemoglobinuria
P - Platinum drugs (cisplatin)
E - ethylene glycol
R - radiocontrast agents

98
Q

Acute tubular necrosis - causes

A

Can be caused by ischemic or nephrotoxic injury:

• ischemic - 2° to l renal blood flow (eg, hypotension, shock, sepsis, hemorrhage, HF). Results in death of tubular cells that may slough into tubular lumen (PCT and thick ascending limb are high ly susceptible to injury).

• Nephrotoxic - 2° to injury resulting from toxic substances. Proximal tubules are particularly susceptible to injury.
L - lead
A - aminoglycosides
M - myoglobinuria (crush injury)/ hemoglobinuria
P - Platinum drugs (cisplatin)
E - ethylene glycol
R - radiocontrast agents

99
Q

Main causes of renal artery stenosis:

A
  • Atherosclerotic plaques- proximal I/3rd of renal artery, usually in older males, smokers.
  • Fibromuscular dysplasia - distal 2/3rd of renal artery or segmental branches, usually young or middle-aged females.
100
Q

Autosomal dominant
polycystic kidney
disease - Associated with

A

Associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts, diverticulosis.

Presents with flank pain, hematuria, hypertension, urinary infection, progressive renal failure in 50% of individuals.

Treatment: If hypertension or proteinuria develops, treat with ACE inhibitors or ARBs.

101
Q

Autosomal recessive
polycystic kidney
disease

A

Cystic dilation of collecting ducts

Often presents in infancy. Associated with congenital hepatic fibrosis. Significant oliguric renal failure in utero can lead to Potter sequence.

Other - systemic hypertension, progressive renal insufficiency, and portal hypertension from congenital hepatic fibrosis.

102
Q

Autosomal dominant
tubulointerstitial
kidney disease

A

Medullary cystic kidney disease. Causes tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine.

Smaller kidneys on ultrasound. Poor prognosis.

103
Q

Simple vs complex

renal cysts

A

Simple cysts are filled with ultrafiltrate (anechoic on ultrasound).
Very common and account for the majority of all renal masses. Found incidentally and typically asymptomatic.

Complex cysts, including those that are:
septated
enhanced
have solid components on imaging.

Require follow-up or removal due to the risk of renal cell carcinoma.

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