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USMLE Step 1 > Renal - First Aid > Flashcards

Renal - First Aid Flashcards

1
Q

Kidney Embryology:

  • week 4
  • then degenerates
A

Pronephros

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2
Q

Kidney Embryology:

  • functions as interim kidney for 1st trimester
  • later contributes to male genital system
A

Mesonephros

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3
Q

Kidney Embryology:

  • permanent
  • first appears in 5th week of gestation
  • nephrogenesis continues through weeks 32–36 of gestation
  • aberrant interaction between ureteric bud and metanephric mesenchyme tissues may result in several congenital malformations of the kidney (eg. renal agenesis, multicystic dysplastic kidney)
A

Metanephros

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4
Q

Kidney Embryology:

  • derived from caudal end of mesonephric duct
  • gives rise to ureter, pelvises, calyces, and collecting ducts
  • fully canalized by 10th week
A

Ureteric Bud

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5
Q

Kidney Embryology:

  • metanephric blastema
  • ureteric bud interacts with this tissue
  • interaction induces differentiation and formation of glomerulus through to distal convoluted tubule (DCT)
A

Metanephric Mesenchyme

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6
Q

Kidney Embryology:

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

A

Ureteropelvic Junction

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7
Q

Renal Congenital Anomalies:

  • oligohydramnios → compression of developing fetus → limb deformities, facial anomalies (eg. low-set ears and retrognathia, flattened nose), compression of chest and lack of amniotic fluid aspiration into fetal lungs → pulmonary hypoplasia (cause of death)
  • causes include ARPKD, obstructive uropathy (eg. posterior urethral valves), bilateral renal agenesis, chronic placental insufficiency
A

Potter Sequence (Syndrome)

POTTER sequence is associated with:

  • Pulmonary hypoplasia
  • Oligohydramnios (trigger)
  • Twisted face
  • Twisted skin
  • Extremity defects
  • Renal failure (in utero)
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8
Q

Renal Congenital Anomalies:

  • inferior poles of both kidneys fuse abnormally
  • as they ascend from pelvis during fetal development, the kidneys get trapped under inferior mesenteric artery and remain low in the abdomen
  • kidneys function normally
  • associated with hydronephrosis (eg. ureteropelvic junction obstruction), renal stones, infection, chromosomal aneuploidy syndromes (eg. Turner syndrome; trisomies 13, 18, 21), and rarely renal cancer
A

Horseshoe Kidney

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9
Q

Renal Congenital Anomalies:

  • condition of being born with only one functioning kidney
  • majority asymptomatic with compensatory hypertrophy of contralateral kidney, but anomalies in contralateral kidney are common
  • often diagnosed prenatally via ultrasound
A

Congenital Solitary Functioning Kidney

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10
Q

Congenital Solitary Functioning Kidney:

ureteric bud fails to develop and induce differentiation of metanephric mesenchyme → complete absence of kidney and ureter

A

Unilateral Renal Agenesis

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11
Q

Congenital Solitary Functioning Kidney:

  • 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
A

Multicystic Dysplastic Kidney

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12
Q

Renal Congenital Anomalies:

  • bifurcation of ureteric bud before it enters the metanephric blastema creates a Y-shaped bifid ureter
  • duplex collecting system can alternatively occur through two ureteric buds reaching and interacting with metanephric blastema
  • strongly associated with vesicoureteral reflux and/or ureteral obstruction
  • ↑ risk for UTIs
A

Duplex Collecting System

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13
Q

Renal Congenital Anomalies:

  • membrane remnant in the posterior urethra in males
  • its persistence can lead to urethral obstruction
  • can be diagnosed prenatally by hydronephrosis and dilated or thick-walled bladder on ultrasound
  • most common cause of bladder outlet obstruction in male infants
A

Posterior Urethral Valves

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14
Q

Kidney Anatomy and Glomerular Structure

A
  • Left kidney is taken during donor transplantation because it has a longer renal vein.
  • Afferent = Arriving
  • Efferent = Exiting
  • Renal Blood Blow: renal artery → segmental artery → interlobar artery → arcuate artery → interlobular artery → afferent arteriole → glomerulus → efferent arteriole → vasa recta/peritubular capillaries → venous outflow
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15
Q

Course of Ureters

A
  • Course of Ureters: arises from renal pelvis, travels under gonadal arteries → over common iliac artery → under uterine artery/vas deferens (retroperitoneal)
  • Gynecologic procedures (eg. ligation of uterine or ovarian vessels) may damage ureter → ureteral obstruction or leak.
  • Muscle fibers within the intramural part of the ureter prevent urine reflux.
  • 3 Constrictions of Ureters:
    • Ureteropelvic Junction
    • Pelvic Inlet
    • Ureterovesical Junction
  • Water (ureters) flows over the iliacs and under the bridge (uterine artery or vas deferens).
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16
Q

Fluid Compartments

A
  • HIKIN’: HIgh K+ INtracellularly
  • 60–40–20 rule (% of body weight for average person):
    • 60% total body water
    • 40% ICF, mainly composed of K+, Mg2+, organic phosphates (eg. ATP)
    • 20% ECF, mainly composed of Na+, Cl–, HCO3–, albumin
  • Plasma volume can be measured by radiolabeling albumin.
  • Extracellular volume can be measured by inulin or mannitol.
  • Osmolality = 285–295 mOsm/kg H2O
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17
Q

Glomerular Filtration Barrier

A
  • Responsible for filtration of plasma according to size and charge selectivity.
  • Composed of:
    • fenestrated capillary endothelium
    • basement membrane with type IV collagen chains and heparan sulfate
    • epithelial layer consisting of podocyte foot processes
  • Charge Barrier
    • all 3 layers contain ⊝ charged glycoproteins that prevent entry of ⊝ charged molecules (eg. albumin)
  • Size Barrier
    • fenestrated capillary endothelium (prevent entry of > 100 nm molecules/blood cells)
    • podocyte foot processes interpose with basement membrane
    • slit diaphragm (prevent entry of molecules > 50–60 nm)
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18
Q

Renal Clearance

A

Cx = (UxV)/Px = volume of plasma from which the substance is completely cleared per unit time

  • If Cx < GFR: net tubular reabsorption of X
  • If Cx > GFR: net tubular secretion of X
  • If Cx = GFR: no net secretion or reabsorption
Cx = clearance of X (mL/min)
Ux = urine concentration of X (eg, mg/mL)
Px = plasma concentration of X (eg, mg/mL)
V = urine flow rate (mL/min)
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19
Q

Glomerular Filtration Rate

A
  • Inulin clearance can be used to calculate GFR because it is freely filtered and is neither reabsorbed nor secreted.
  • GFR = Uinulin × V/Pinulin = Cinulin = Kf [(PGC – PBS) – (πGC – πBS)]
    • GC = glomerular capillary
    • BS = Bowman space
    • πBS normally equals zero
    • Kf = filtration coefficient
  • Normal GFR ≈ 100 mL/min.
  • Creatinine clearance is an approximate measure of GFR. Slightly overestimates GFR because creatinine is moderately secreted by renal tubules.
  • Incremental reductions in GFR define the stages of chronic kidney disease.
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20
Q

Effective Renal Plasma Flow

A
  • Effective renal plasma flow (eRPF) can be estimated using para-aminohippuric acid (PAH) clearance.
  • Between filtration and secretion, there is nearly 100% excretion of all PAH that enters the kidney.
  • eRPF = UPAH × V/PPAH = CPAH
  • Renal Blood Flow (RBF) = RPF/(1 − Hct)—usually 20–25% of cardiac output
  • Plasma Volume = TBV × (1 – Hct)
  • eRPF underestimates true renal plasma flow (RPF) slightly.
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21
Q

Filtration

A
  • Filtration Fraction (FF) = GFR/RPF
    • Normal FF = 20%
  • Filtered Load (mg/min) = GFR (mL/min) × plasma concentration (mg/mL)
  • GFR can be estimated with creatinine clearance.
  • RPF is best estimated with PAH clearance.
  • Prostaglandins Dilate Afferent arteriole (PDA)
  • Angiotensin II Constricts Efferent arteriole (ACE)
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22
Q

Changes in Glomerular Dynamics

A
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23
Q

Calculation of Reabsorption and Secretion Rate

A
  • Filtered Load = GFR × Px
  • Excretion Rate = V × Ux
  • Reabsorption Rate = filtered – excreted
  • Secretion Rate = excreted – filtered
  • FeNa = fractional excretion of sodium
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24
Q

Glucose Clearance

A
  • Glucose at a normal plasma level (range 60–120 mg/dL) is completely reabsorbed in proximal convoluted tubule (PCT) by Na+/glucose cotransport.
  • In adults, at plasma glucose of ∼ 200 mg/dL, glucosuria begins (threshold).
  • At rate of ∼ 375 mg/min, all transporters are fully saturated (Tm).
  • Normal pregnancy is associated with ↑ GFR.
  • With ↑ filtration of all substances, including glucose, the glucose threshold occurs at lower plasma glucose concentrations → glucosuria at normal plasma glucose levels.
  • Sodium-glucose cotransporter 2 (SGLT2) inhibitors (eg. -flozin drugs) result in glucosuria at plasma concentrations < 200 mg/dL.
  • Glucosuria is an important clinical clue to diabetes mellitus.
  • Splay Phenomenon
    • Tm for glucose is reached gradually rather than sharply due to the heterogeneity of nephrons (ie. different Tm points)
    • represented by the portion of the titration curve between threshold and Tm
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25
Q

Nephron Physiology:

Proximal Convoluted Tubule

A
  • contains brush border
  • reabsorbs all glucose and amino acids and most HCO3–, Na+, Cl–, PO43–, K+, H2O, and uric acid
  • isotonic absorption
  • generates and secretes NH3, which enables the kidney to secrete more H+
  • PTH—inhibits Na+/PO43– cotransport → PO43– excretion
  • AT II—stimulates Na+/H+ exchange → ↑ Na+, H2O, and HCO3− reabsorption (permitting contraction alkalosis)
  • 65–80% Na+ reabsorbed
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26
Q

Nephron Physiology:

Loop of Henle

A

Thin Descending Loop of Henle

  • passively reabsorbs H2O
  • via medullary hypertonicity (impermeable to Na+)
  • concentrating segment
  • makes urine hypertonic

Thick Ascending Loop of Henle

  • reabsorbs Na+, K+, and Cl−
  • indirectly induces paracellular reabsorption of Mg2+ and Ca2+ through ⊕ lumen potential generated by K+ backleak
  • impermeable to H2O
  • makes urine less concentrated as it ascends
  • 10–20% Na+ reabsorbed
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27
Q

Nephron Physiology:

Distal Convoluted Tubule

A
  • reabsorbs Na+ and Cl−
  • impermeable to H2O
  • makes urine fully dilute (hypotonic)
  • PTH— ↑ Ca2+/Na+ exchange → Ca2+ reabsorption
  • 5–10% Na+ reabsorbed
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28
Q

Nephron Physiology:

Collecting Tubule

A
  • reabsorbs Na+ in exchange for secreting K+ and H+ (regulated by aldosterone)
  • Aldosterone
    • acts on mineralocorticoid receptor → mRNA → protein synthesis
    • In principal cells: ↑ apical K+ conductance, ↑ Na+/K+ pump, ↑ epithelial Na+ channel (ENaC) activity → lumen negativity → K+ secretion
    • In α-intercalated cells: lumen negativity → ↑ H+ ATPase activity → ↑ H+ secretion → ↑ HCO3−/Cl− exchanger activity
  • ADH
    • acts at V2 receptor → insertion of aquaporin H2O channels on apical side
  • 3–5% Na+ reabsorbed
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29
Q

Renal Tubular Defects

A

The kidneys put out FaBulous Glittering LiquidS (from front to end of tube).

  • Fanconi Syndrome
  • Bartter Syndrome
  • Gitelman Syndrome
  • Liddle Syndrome
  • Syndrome of Apparent Mineralocorticoid Excess
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30
Q

Renal Tubular Defects:

  • generalized reabsorption defect in PCT → ↑ excretion of amino acids, glucose, HCO3–, and PO43–, and all substances reabsorbed by the PCT
  • may lead to metabolic acidosis (proximal RTA), hypophosphatemia, and osteopenia
  • caused by hereditary defects (eg, Wilson disease, tyrosinemia, glycogen storage disease), ischemia, multiple myeloma, nephrotoxins/drugs (eg. ifosfamide, cisplatin, expired tetracyclines), and lead poisoning
A

Fanconi Syndrome

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31
Q

Renal Tubular Defects:

  • resorptive defect in thick ascending loop of Henle (affects Na+/K+/2Cl– cotransporter)
  • metabolic alkalosis, hypokalemia, and hypercalciuria
  • autosomal recessive
  • presents similarly to chronic loop diuretic use
A

Bartter Syndrome

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32
Q

Renal Tubular Defects:

  • reabsorption defect of NaCl in DCT
  • metabolic alkalosis, hypomagnesemia, hypokalemia, and hypocalciuria
  • autosomal recessive
  • presents similarly to lifelong thiazide diuretic use
  • less severe than Bartter syndrome
A

Gitelman Syndrome

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33
Q

Renal Tubular Defects:

  • gain of function mutation → ↑ activity of Na+ channel → ↑ Na+ reabsorption in collecting tubules
  • metabolic alkalosis, hypokalemia, hypertension, and ↓ aldosterone
  • autosomal dominant
  • presents similarly to hyperaldosteronism, but aldosterone is nearly undetectable
  • treated with Amiloride
A

Liddle Syndrome

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34
Q

Renal Tubular Defects:

  • in cells containing mineralocorticoid receptors, 11β-hydroxysteroiddehydrogenase converts cortisol (can activate these receptors) to cortisone (inactive on these receptors)
  • hereditary deficiency of 11β-hydroxysteroid dehydrogenase → excess cortisol → ↑ mineralocorticoid receptor activity
  • metabolic alkalosis, hypokalemia, hypertension
  • ↓ serum aldosterone level
  • autosomal recessive
  • can be acquired from glycyrrhetinic acid (present in licorice), which blocks activity of 11β-hydroxysteroid dehydrogenase
  • treated with K+-sparing diuretics (↓ mineralocorticoid effects) or corticosteroids (exogenous corticosteroid ↓ endogenous cortisol production → ↓ mineralocorticoid receptor activation)
A

Syndrome of Apparent Mineralocorticoid Excess

Cortisol tries to be the SAME as Aldosterone.

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35
Q

Relative Concentrations along Proximal Convoluted Tubules

A
  • Tubular inulin ↑ in concentration (but not amount) along the PCT as a result of water reabsorption.
  • Cl− reabsorption occurs at a slower rate than Na+ in early PCT and then matches the rate of Na+ reabsorption more distally. Thus, its relative concentration ↑ before it plateaus.
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36
Q

Renin-Angiotensin-Aldosterone System

A
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37
Q

Renin-Angiotensin-Aldosterone System:

  • secreted by JG cells in response to ↓ renal perfusion pressure (detected by renal baroreceptors in afferent arteriole)
  • ↑ renal sympathetic discharge (β1 effect)
  • ↓ NaCl delivery to macula densa cells
A

Renin

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38
Q

Renin-Angiotensin-Aldosterone System:

  • helps maintain blood volume and blood pressure
  • affects baroreceptor function
  • limits reflex bradycardia, which would normally accompany its pressor effects
A

Angiotensin II

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39
Q

Renin-Angiotensin-Aldosterone System:

  • released from atria and ventricles in response to ↑ volume
  • may act as a “check” on renin-angiotensin-aldosterone system
  • relaxes vascular smooth muscle via cGMP → ↑ GFR, ↓ renin
  • dilates afferent arteriole, constricts efferent arteriole, and promotes natriuresis
A
  • ANP—atria
  • BNP—ventricles
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40
Q

Renin-Angiotensin-Aldosterone System:

  • primarily regulates serum osmolality
  • also responds to low blood volume states
  • stimulates reabsorption of water in collecting ducts
  • also stimulates reabsorption of urea in collecting ducts to maintain corticopapillary osmotic gradient
A

ADH

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41
Q

Renin-Angiotensin-Aldosterone System:

  • primarily regulates ECF volume and Na+ content
  • responds to low blood volume states
  • responds to hyperkalemia by ↑ K+ excretion
A

Aldosterone

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42
Q

Renal Physiology:

  • consists of mesangial cells, JG cells (modified smooth muscle of afferent arteriole) and the macula densa (NaCl sensor, located at distal end of loop of Henle)
  • JG cells secrete renin in response to ↓ renal blood pressure and ↑ sympathetic tone (β1)
  • macula densa cells sense ↓ NaCl delivery to DCT → ↑ renin release → efferent arteriole vasoconstriction → ↑ GFR
  • maintains GFR via renin-angiotensin-aldosterone system
  • in addition to vasodilatory properties, β-blockers can decrease BP by inhibiting β1‑receptors of the JGA → ↓ renin release
A

Juxtaglomerular Apparatus

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43
Q

Kidney Endocrine Functions:

  • released by interstitial cells in peritubular capillary bed in response to hypoxia
  • stimulates RBC proliferation in bone marrow
  • often supplemented in chronic kidney disease
A

Erythropoietin

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44
Q

Kidney Endocrine Functions:

PCT cells convert 25-OH Vitamin D3 to 1,25-(OH)2 Vitamin D3 (Calcitriol, active form)

A

Calciferol (Vitamin D)

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45
Q

Kidney Endocrine Functions:

  • paracrine secretion vasodilates the afferent arterioles to ↑ RBF
  • NSAIDs block renal-protective _____ synthesis → constriction of afferent arteriole and ↓ GFR; this may result in acute renal failure in low renal blood flow states
A

Prostaglandins

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46
Q

Kidney Endocrine Functions:

  • secreted by PCT cells
  • promotes natriuresis
  • at low doses, dilates interlobular arteries, afferent arterioles, efferent arterioles → ↑ RBF, little or no change in GFR
  • at higher doses, acts as a vasoconstrictor
A

Dopamine

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47
Q

Hormones Acting on the Kidneys

A
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48
Q

Potassium Shifts:

shifts K+ into cell → hypokalemia

A
  • Hypo-osmolarity
  • Alkalosis
  • β-Adrenergic Agonist (↑ Na+/K+ ATPase)
  • Insulin (↑ Na+/K+ ATPase)—insulin shifts K+ into cells
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49
Q

Potassium Shifts:

shifts K+ out of cell → hyperkalemia

A

Hyperkalemia? DO LAβSS:

  • Digitalis (blocks Na+/K+ ATPase)
  • HyperOsmolarity
  • Lysis of Cells (eg. crush injury, rhabdomyolysis,
    tumor lysis syndrome)
  • Acidosis
  • β-blocker
  • High Blood Sugar (insulin deficiency)
  • Succinylcholine (↑ risk in burns/muscle trauma)
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50
Q

Electrolyte Disturbances:

  • nausea
  • malaise
  • stupor
  • coma
  • seizures
A

↓ Na+

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51
Q

Electrolyte Disturbances:

  • irritability
  • stupor
  • coma
A

↑ Na+

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52
Q

Electrolyte Disturbances:

  • U waves and flattened T waves on ECG
  • arrhythmias
  • muscle cramps
  • spasm
  • weakness
A

↓ K+

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53
Q

Electrolyte Disturbances:

  • wide QRS and peaked T waves on ECG
  • arrhythmias
  • muscle weakness
A

↑ K+

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54
Q

Electrolyte Disturbances:

  • tetany
  • seizures
  • QT prolongation
  • twitching (Chvostek sign)
  • spasm (Trousseau sign)
A

↓ Ca2+

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55
Q

Electrolyte Disturbances:

  • stones (renal)
  • bones (pain)
  • groans (abdominal pain)
  • thrones (↑ urinary frequency)
  • psychiatric overtones (anxiety, altered mental status)
A

↑ Ca2+

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56
Q

Electrolyte Disturbances:

  • tetany
  • torsades de pointes
  • hypokalemia
  • hypocalcemia (when < 1.2 mg/dL)
A

↓ Mg2+

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57
Q

Electrolyte Disturbances:

  • ↓ DTRs
  • lethargy
  • bradycardia
  • hypotension
  • cardiac arrest
  • hypocalcemia
A

↑ Mg2+

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58
Q

Electrolyte Disturbances:

  • bone loss
  • osteomalacia (adults)
  • rickets (children)
A

↓ PO43−

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59
Q

Electrolyte Disturbances:

  • renal stones
  • metastatic calcifications
  • hypocalcemia
A

↑ PO43−

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60
Q

Features of Renal Disorders

A
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61
Q

Acid-Base Physiology

A
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62
Q

Acidosis and Alkalosis

63
Q

Renal Pathology:

disorder of the renal tubules that causes normal anion gap (hyperchloremic) metabolic acidosis

A

Renal Tubular Acidosis

64
Q

Renal Tubular Acidosis:

  • inability of α-intercalated cells to secrete H+ → no new HCO3– is generated → metabolic acidosis
  • urine pH > 5.5
  • ↓ serum K+
  • caused by Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract, and autoimmune diseases (eg. SLE)
  • associated with ↑ risk for calcium phosphate kidney stones (due to ↑ urine pH and ↑ bone turnover)
A

Distal Renal Tubular Acidosis (Type 1)

65
Q

Renal Tubular Acidosis:

  • defect in PCT HCO3– reabsorption → ↑ excretion of HCO3– in urine → metabolic acidosis
  • urine can be acidified by α-intercalated cells in collecting duct, but not enough to overcome the increased excretion of HCO3– → metabolic acidosis
  • urine pH < 5.5
  • ↓ serum K+
  • caused by Fanconi syndrome, multiple myeloma, and carbonic anhydrase inhibitors
  • associated with ↑ risk for hypophosphatemic rickets (in Fanconi syndrome)
A

Proximal Renal Tubular Acidosis (Type 2)

66
Q

Renal Tubular Acidosis:

  • hypoaldosteronism or aldosterone resistance
  • hyperkalemia → ↓ NH3 synthesis in PCT → ↓ NH4+ excretion
  • urine pH < 5.5 (or variable)
  • ↑ serum K+
  • caused by ↓ aldosterone production (eg. diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency) or aldosterone resistance (eg. K+-sparing diuretics, nephropathy due to obstruction, TMP-SMX)
A

Hyperkalemic Tubular Acidosis (Type 4)

67
Q

Casts in Urine

A
  • presence of casts indicates that hematuria/pyuria is of glomerular or renal tubular origin
  • bladder cancer, kidney stones → hematuria, no casts
  • acute cystitis → pyuria, no casts
68
Q

Casts in Urine:

  • glomerulonephritis
  • hypertensive emergency
69
Q

Casts in Urine:

  • tubulointerstitial inflammation
  • acute pyelonephritis
  • transplant rejection
70
Q

Casts in Urine:

  • “oval fat bodies”
  • nephrotic syndrome
  • associated with “Maltese cross” sign
A

Fatty casts

71
Q

Casts in Urine:

  • “muddy brown”
  • acute tubular necrosis (ATN)
A

Granular casts

72
Q

Casts in Urine:

end-stage renal disease/chronic renal failure

A

Waxy casts

73
Q

Casts in Urine:

  • nonspecific
  • can be a normal finding
  • often seen in concentrated urine samples
A

Hyaline casts

74
Q

Nomenclature of Glomerular Disorders:

< 50% of glomeruli are involved

75
Q

Nomenclature of Glomerular Disorders:

> 50% of glomeruli are involved

76
Q

Nomenclature of Glomerular Disorders:

hypercellular glomeruli

A

Proliferative

77
Q

Nomenclature of Glomerular Disorders:

thickening of glomerular basement membrane (GBM)

A

Membranous

78
Q

Nomenclature of Glomerular Disorders:

  • 1° disease of the kidney specifically impacting the glomeruli
  • Minimal Change Disease
A

Primary Glomerular Disease

79
Q

Nomenclature of Glomerular Disorders:

  • systemic disease or disease of another organ system that also impacts the glomeruli
  • SLE Nephritis
  • Diabetic Nephropathy
A

Secondary Glomerular Disease

80
Q

Glomerular Diseases

81
Q

Renal Pathology:

  • massive proteinuria (> 3.5 g/day) with hypoalbuminemia, resulting edema, hyperlipidemia
  • frothy urine with fatty casts
  • disruption of glomerular filtration charge barrier may be 1° (eg. direct sclerosis of podocytes) or 2° (systemic process [eg. diabetes] secondarily damages podocytes)
  • severe nephritic syndrome may present with _____ features if damage to GBM is severe enough to damage the charge barrier
  • associated with hypercoagulable state due to antithrombin (AT) III loss in urine and ↑ risk of infection (loss of immunoglobulins in urine and soft tissue compromise by edema)
A

Nephrotic Syndrome

NephrOtic = prOteinuria

82
Q

Causes of Nephrotic Syndrome

A
  • Minimal Change Disease (Lipoid Nephrosis)
  • Focal Segmental Glomerulosclerosis
  • Membranou Nephropathy
  • Amyloidosis
  • Diabetic Glomerulonephropathy
83
Q

Nephrotic Syndrome:

  • most common cause of nephrotic syndrome in children
  • often 1° (idiopathic) and may be triggered by recent infection, immunization, immune stimulus
  • rarely, may be 2° to lymphoma (eg. cytokine-mediated damage)
  • 1° disease has excellent response to corticosteroids
  • Imaging:
    • LM—normal glomeruli (lipid may be seen in PCT cells)
    • IF—⊝
    • EM—effacement of podocyte foot processes
A

Minimal Change Disease (Lipoid Nephrosis)

84
Q

Nephrotic Syndrome:

  • most common cause of nephrotic syndrome in African-Americans and Hispanics
  • can be 1° (idiopathic) or 2° to other conditions (eg. HIV infection, sickle cell disease, heroin abuse, massive obesity, interferon treatment, or congenital malformations)
  • 1° disease has inconsistent response to steroids
  • may progress to CKD
  • Imaging:
    • LM—segmental sclerosis and hyalinosis
    • IF—often ⊝ but may be ⊕ for nonspecific focal deposits of IgM, C3, and C1
    • EM—effacement of foot processes similar to minimal change disease
A

Focal Segmental Glomerulosclerosis

85
Q

Nephrotic Syndrome:

  • also known as Membranous Glomerulonephritis
  • can be 1° (eg. antibodies to phospholipase A2 receptor) or 2° to drugs (eg. NSAIDs, penicillamine, gold), infections (eg. HBV, HCV, syphilis), SLE, or solid tumors
  • 1° disease has poor response to steroids
  • may progress to CKD
  • Imaging:
    • LM—diffuse capillary and GBM thickening
    • IF—granular due to IC deposition
    • EM—“spike and dome” appearance of subepithelial deposits
A

Membranous Nephropathy

86
Q

Nephrotic Syndrome:

  • kidney is the most commonly involved organ
  • associated with chronic conditions that predispose to amyloid deposition (eg. AL amyloid, AA amyloid)
  • Imaging:
    • LM—Congo red stain shows apple-green birefringence under polarized light due to amyloid deposition in the mesangium
A

Amyloidosis

87
Q

Nephrotic Syndrome:

  • most common cause of ESRD in the United States
  • hyperglycemia → nonenzymatic glycation of tissue proteins → mesangial expansion
  • GBM thickening and ↑ permeability
  • hyperfiltration (glomerular HTN and ↑ GFR) → glomerular hypertrophy and glomerular scarring (glomerulosclerosis) leading to further progression of nephropathy
  • LM—Mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)
A

Diabetic Glomerulonephropathy

88
Q

Renal Pathology:

  • inflammatory process
  • when glomeruli are involved, leads to hematuria and RBC casts in urine
  • associated with azotemia, oliguria, hypertension (due to salt retention), proteinuria, and hypercellular/inflamed glomeruli on biopsy
A

Nephritic Syndrome

NephrItic = Inflammatory

89
Q

Causes of Nephritic Syndrome

A
  • Acute Poststreptococcal Glomerulonephritis
  • Rapidly Progressive (Crescentic) Glomerulonephritis
  • Diffuse Proliferative Glomerulonephritis
  • IgA Nephropathy (Berger Disease)
  • Alport Syndrome
  • Membranoproliferative Glomerulonephritis
90
Q

Nephritic Syndrome:

  • most frequently seen in children
  • ~ 2–4 weeks after group A streptococcal infection of pharynx or skin
  • resolves spontaneously in most children
  • may progress to renal insufficiency in adults
  • type III hypersensitivity reaction
  • presents with peripheral and periorbital edema, cola-colored urine, and HTN
  • ⊕ strep titers/serologies and ↓ complement levels (C3) due to consumption
  • Imaging:
    • LM—glomeruli enlarged and hypercellular
    • IF—(“starry sky”) granular appearance (“lumpy-bumpy”) due to IgG, IgM, and C3 deposition along GBM and mesangium
    • EM—subepithelial immune complex (IC) humps
A

Acute Poststreptococcal Glomerulonephritis

91
Q

Nephritic Syndrome:

  • poor prognosis, rapidly deteriorating renal function (days to weeks)
  • Imaging:
    • LM
      • crescent moon shape
      • crescents consist of fibrin and plasma proteins (eg. C3b) with glomerular parietal cells, monocytes, macrophages
  • several disease processes may result in this pattern which may be delineated via IF pattern
    • Linear IF due to antibodies to GBM and alveolar basement membrane:
      • Goodpasture Syndrome—hematuria/hemoptysis, type II hypersensitivity reaction, treated with plasmapheresis
    • Negative IF/Pauci-immune (no Ig/C3 deposition):
      • Granulomatosis with Polyangiitis (Wegener)—PR3-ANCA/c-ANCA
      • Microscopic Polyangiitis—MPO-ANCA/p-ANCA
    • Granular IF
      • PSGN
      • DPGN
A

Rapidly Progressive (Crescentic) Glomerulonephritis

92
Q

Nephritic Syndrome:

  • often due to SLE (“wire lupus”)
  • often present as nephrotic syndrome and nephritic syndrome concurrently
  • Imaging:
    • LM—“wire looping” of capillaries
    • IF—granular
    • EM—subendothelial and sometimes intramembranous IgG-based ICs often with C3 deposition
A

Diffuse Proliferative Glomerulonephritis

93
Q

Nephritic Syndrome:

  • episodic hematuria that occurs concurrently with respiratory or GI tract infections (IgA is secreted by mucosal linings)
  • renal pathology of IgA vasculitis (HSP)
  • Imaging:
    • LM—mesangial proliferation
    • IF—IgA-based IC deposits in mesangium
    • EM—mesangial IC deposition
A

IgA Nephropathy (Berger Disease)

94
Q

Nephritic Syndrome:

  • mutation in type IV collagen → thinning and splitting of glomerular basement membrane
  • most commonly X-linked dominant
  • eye problems (eg. retinopathy, lens dislocation), glomerulonephritis, sensorineural deafness
  • Imaging:
    • EM—“basket-weave”
A

Alport Syndrome

“Can’t see, can’t pee, can’t hear a bee.”

95
Q

Nephritic Syndrome:

  • often co-presents with nephrotic syndrome
  • Ttype I
    • may be 2° to hepatitis B or C infection
    • may also be idiopathic
    • subendothelial IC deposits with granular IF
  • Type II
    • associated with C3 nephritic factor (IgG antibody that stabilizes C3 convertase → persistent complement activation → ↓ C3 levels)
    • intramembranous deposits, also called dense deposit disease
  • in both types, mesangial ingrowth → GBM splitting → “tram-track” appearance on H&E and PAS stains
A

Membranoproliferative Glomerulonephritis

96
Q

Renaal Pathology:

  • can lead to severe complications such as hydronephrosis and pyelonephritis
  • obstructed _____ presents with unilateral flank tenderness, colicky pain radiating to groin, and hematuria
  • treat and prevent by encouraging fluid intake
  • most common presentation:
    • calcium oxalate _____ in patient with hypercalciuria and normocalcemia
A

Kidney Stones

97
Q

Kidney Stones:

  • Precipitates with: hypocitraturia
  • X-Ray: radiopaque
  • CT Scan: radiopaque
  • Urine Crystal: envelope or dumbbell shape
  • most common (80%)
  • more common than calcium phosphate stones
  • hypocitraturia often associated with ↓ urine pH
  • can result from ethylene glycol (antifreeze) ingestion, vitamin C abuse, hypocitraturia, malabsorption (eg. Crohn disease)
  • Treatment:
    • thiazides
    • citrate
    • low-sodium diet
A

Calcium Oxalate

98
Q

Kidney Stones:

  • Precipitates with: ↑ pH
  • X-Ray: radiopaque
  • CT-Scan: radiopaque
  • Urine Crystal: wedge-shaped prism
  • Treatment:
    • low-sodium diet
    • thiazides
A

​Calcium Phosphate

99
Q

Kidney Stones:

  • Precipitates with: ↑ pH
  • X-Ray: Radiopaque
  • CT-Scan: Radiopaque
  • Urine Crystal: coffin lid
  • also known as struvite
  • account for 15% of stones
  • caused by infection with urease ⊕ bugs (eg. Proteus mirabilis, Staphylococcus saprophyticus, Klebsiella) that hydrolyze
  • urea to ammonia → urine alkalinization
  • commonly form staghorn calculi
  • Treatment:
    • eradication of underlying infection
    • surgical removal of stone
A

Ammonium Magnesium Phosphate

100
Q

Kidney Stones:

  • Precipitates with: ↓ pH
  • X-Ray: radiolucent
  • CT-Scan: minimally visible
  • Urine Crystal: rhomboid or rosettes
  • about 5% of all stones
  • Risk Factors:
    • ↓ urine volume
    • arid climates
    • acidic pH
  • strong association with hyperuricemia (eg. gout)
  • often seen in diseases with ↑ cell turnover (eg. leukemia)
  • Treatment:
    • alkalinization of urine
    • allopurinol
A

Uric Acid

radiolUcent

101
Q

Kidney Stones:

  • Precipitates with: ↓ pH
  • X-Ray: faintly radiopaque
  • CT-Scan: moderately radiopaque
  • Urine Crystal: hexagonal
  • hereditary (autosomal recessive) condition in which Cystine-reabsorbing PCT transporter loses function, causing cystinuria
  • transporter defect also results in poor reabsorption of Ornithine, Lysine, and Arginine
  • Cystine is poorly soluble, thus stones form in urine
  • usually begins in childhood
  • can form staghorn calculi
  • sodium cyanide nitroprusside test ⊕
  • Treatment:
    • low sodium diet
    • alkalinization of urine
    • chelating agents if refractory
A

Cystine

“SIXtine” stones have SIX sides.

COLA:

  • Cystine
  • Ornithine
  • Lysine
  • Arginine
102
Q

Renal Pathology:

  • distention/dilation of renal pelvis and calyces
  • usually caused by urinary tract obstruction (eg. renal stones, severe BPH, congenital obstructions, cervical cancer, injury to ureter)
  • other causes include retroperitoneal fibrosis and vesicoureteral reflux
  • dilation occurs proximal to site of pathology
  • serum creatinine becomes elevated if obstruction is bilateral or if patient has an obstructed solitary kidney
  • leads to compression and possible atrophy of renal cortex and medulla
A

Hydronephrosis

103
Q

Renal Pathology:

  • polygonal clear cells filled with accumulated lipids and carbohydrate
  • often golden-yellow due to ↑ 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, and weight loss
  • most common 1° renal malignancy
  • most common in men 50–70 years old
  • ↑ incidence with smoking and obesity
  • associated with paraneoplastic syndromes
  • associated with gene deletion on chromosome 3 (sporadic, or inherited as von Hippel-Lindau syndrome)
  • Treatment:
    • surgery/ablation for localized disease
    • immunotherapy (eg. Aldesleukin) or targeted therapy for metastatic disease, rarely curative
  • resistant to chemotherapy and radiation therapy
A

Renal Cell Carcinoma

“PEAR”-aneoplastic Syndromes

  • PTHrP
  • Ectopic EPO
  • ACTH
  • Renin

RCC = 3 letters = chromosome 3

104
Q

Renal Pathology:

  • benign epithelial cell tumor arising from collecting ducts
  • large eosinophilic cells with abundant
  • mitochondria without perinuclear clearing (vs. chromophobe renal cell carcinoma)
  • presents with painless hematuria, flank pain, and abdominal mass
  • often resected to exclude malignancy (eg. renal cell carcinoma)
A

Renal Oncocytoma

105
Q

Renal Pathology:

  • most common renal malignancy of early childhood (ages 2–4)
  • contains embryonic glomerular structures
  • presents with large, palpable, unilateral flank mass and/or hematuria
  • “loss of function” mutations of tumor suppressor genes WT1 or WT2 on chromosome 11
  • May be a part of several syndromes:
    • WAGR complex
    • Denys-Drash syndrome
    • Beckwith-Wiedemann syndrome
A

Nephroblastoma (Wilms Tumor)

106
Q

Nephroblastoma (Wilms Tumor):

  • Wilms tumor
  • aniridia (absence of iris)
  • genitourinary malformations
  • mental retardation/intellectual disability (WT1 deletion)
A

WAGR Complex

  • Wilms tumor
  • Aniridia (absence of iris)
  • Genitourinary malformations
  • mental Retardation/intellectual disability (WT1 deletion)
107
Q

Nephroblastoma (Wilms Tumor):

  • Wilms tumor
  • diffuse mesangial sclerosis (early-onset nephrotic syndrome)
  • dysgenesis of gonads (male pseudohermaphroditism)
  • WT1 mutation
A

Denys-Drash Syndrome

  • Diffuse mesangial sclerosis
  • Dysgenesis of gonads
108
Q

Nephroblastoma (Wilms Tumor):

  • Wilms tumor
  • macroglossia
  • organomegaly
  • hemihyperplasia (WT2 mutation)
A

Beckwith-Wiedemann Syndrome

109
Q

Renal Pathology:

  • also known as Urothelial Carcinoma
  • most common tumor of urinary tract system (can occur in renal calyces, renal pelvis, ureters, and bladder)
  • can be suggested by painless hematuria (no casts)
  • Associated with:
    • Phenacetin
    • smoking
    • aniline dyes
    • Cyclophosphamide
A

Transitional Cell Carcinoma

Pee SAC:

  • Phenacetin
  • Smoking
  • Aniline dyes
  • Cyclophosphamide
110
Q

Renal Pathology:

  • chronic irritation of urinary bladder → squamous metaplasia → dysplasia and squamous cell carcinoma
  • Risk Factors:
    • Schistosoma haematobium infection (Middle East)
    • chronic cystitis
    • smoking
    • chronic nephrolithiasis
  • presents with painless hematuria
A

Squamous Cell Carcinoma of the Bladder

111
Q

Urinary Incontinence:

  • outlet incompetence (urethral hypermobility or intrinsic sphincteric deficiency) → leak with ↑ intra-abdominal pressure (eg. sneezing, lifting)
  • ↑ risk with obesity, vaginal delivery, and prostate surgery
  • ⊕ bladder stress test (directly observed leakage from urethra upon coughing or Valsalva maneuver)
  • Treatment:
    • pelvic floor muscle strengthening (Kegel) exercises
    • weight loss
    • pessaries
A

Stress Incontinence

112
Q

Urinary Incontinence:

  • overactive bladder (detrusor instability) → leak with urge to void immediately
  • associated with UTI
  • Treatment:
    • Kegel exercises
    • bladder training (timed voiding distraction or relaxation techniques)
    • Antimuscarinics (eg. Oxybutynin)
A

Urgency Incontinence

113
Q

Urinary Incontinence:

features of both stress and urgency incontinence

A

Mixed Incontinence

114
Q

Urinary Incontinence:

  • incomplete emptying (detrusor underactivity or outlet obstruction) → leak with overfilling
  • associated with polyuria (eg. diabetes), bladder outlet obstruction (eg. BPH), neurogenic bladder (eg. MS)
  • ↑ post-void residual (urinary retention) on catheterization or ultrasound
  • Treatment:
    • catheterization
    • relieve obstruction (eg. α-blockers for BPH)
A

Overflow Incontinence

115
Q

Renal Pathology:

  • inflammation of urinary bladder
  • presents as suprapubic pain, dysuria, urinary frequency, and urgency
  • systemic signs (eg. high fever, chills) are usually absent
  • Risk Factors
    • female gender (short urethra)
    • sexual intercourse (“honeymoon cystitis”)
    • indwelling catheter
    • diabetes mellitus
    • impaired bladder emptying
  • 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
  • Lab Findings:
    • ⊕ leukocyte esterase
    • ⊕ nitrites (indicate gram ⊝ organisms)
  • sterile pyuria and ⊝ urine cultures suggest urethritis by Neisseria gonorrhoeae or Chlamydia trachomatis
A

Urinary Tract Infection

(Acute Bacterial Cystitis)

116
Q

Renal Pathology:

  • neutrophils infiltrate renal interstitium
  • affects cortex with relative sparing of glomeruli/vessels
  • presents with fever, flank pain (costovertebral angle tenderness), nausea/vomiting, and chills
  • causes include ascending UTI (E. coli is most common)
  • hematogenous spread to kidney
  • presents with WBCs in urine +/− WBC casts
  • CT would show striated parenchymal enhancement
  • Risk Factors:
    • indwelling urinary catheter
      urinary tract obstruction
    • vesicoureteral reflux
    • diabetes mellitus
    • pregnancy
  • Complications:
    • chronic pyelonephritis
    • renal papillary necrosis
    • perinephric abscess
    • urosepsis
  • Treatment: antibiotics
A

Acute Pyelonephritis

117
Q

Renal Pathology:

  • the result of recurrent 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)
A

Chronic Pyelonephritis

118
Q

Renal Pathology:

  • 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
A

Xanthogranulomatous Pyelonephritis

119
Q

Renal Pathology:

  • formerly known as acute renal failure
  • defined as an abrupt decline in renal function as measured by ↑ creatinine and ↑ BUN or by oliguria/anuria
A

Acute Kidney Injury

120
Q

Acute Kidney Injury:

  • due to ↓ RBF (eg. hypotension) → ↓ GFR
  • Na+/H2O and urea retained by kidney in an attempt to conserve volume → ↑ BUN/creatinine ratio (urea is reabsorbed, creatinine is not) and ↓ FENa
A

Prerenal Azotemia

121
Q

Acute Kidney Injury:

  • most commonly due to acute tubular necrosis (from ischemia or toxins)
  • less commonly due to acute glomerulonephritis (eg. RPGN, hemolytic uremic syndrome) or acute interstitial nephritis
  • in ATN, patchy necrosis → debris obstructing tubule and fluid backflow across necrotic tubule → ↓ GFR
  • urine has epithelial/granular casts
  • urea reabsorption is impaired → ↓ BUN/creatinine ratio and ↑ FENa
A

Intrinsic Renal Failure

122
Q

Acute Kidney Injury:

  • due to outflow obstruction (stones, BPH, neoplasia, congenital anomalies)
  • develops only with bilateral obstruction or in a solitary kidney
A

Postrenal Azotemia

123
Q

Consequences of Renal Failure

A
  • Decline in renal filtration can lead to excess retained nitrogenous waste products and electrolyte disturbances.
  • MAD HUNGER:
    • Metabolic Acidosis
    • Dyslipidemia (especially ↑ triglycerides)
    • Hyperkalemia
    • Uremia—clinical syndrome marked by:
      • nausea and anorexia
      • pericarditis
      • asterixis
      • encephalopathy
      • platelet dysfunction
    • Na+/H2O retention (HF, pulmonary edema, hypertension)
    • Growth retardation and developmental delay
    • Erythropoietin failure (anemia)
    • Renal osteodystrophy
  • 2 Forms of Renal Failure:
    • Acute (eg. ATN)
    • Chronic (eg. hypertension, diabetes mellitus, congenital anomalies)
124
Q

Renal Pathology:

  • hypocalcemia, hyperphosphatemia, and failure of vitamin D hydroxylation associated with chronic renal disease → 2° hyperparathyroidism
  • high serum phosphate can bind with Ca2+ → tissue deposits → ↓ serum Ca2+
  • ↓ 1,25-(OH)2D3 → ↓ intestinal Ca2+ absorption
  • causes subperiosteal thinning of bones
A

Renal Osteodystrophy

125
Q

Renal Pathology:

  • acute interstitial renal inflammation
  • pyuria (classically eosinophils) and azotemia occurring after administration of drugs that act as haptens, inducing hypersensitivity (eg. diuretics, penicillin derivatives, proton pump inhibitors, sulfonamides, rifampin, NSAIDs)
  • less commonly may be 2° to other processes such as systemic infections (eg. Mycoplasma) or autoimmune diseases (eg. Sjögren syndrome, SLE, sarcoidosis)
  • associated with fever, rash, hematuria, pyuria, and costovertebral angle tenderness, but can be asymptomatic
A

Acute Interstitial Nephritis
(Tubulointerstitial Nephritis)

Remember these P’s:

  • Pee (diuretics)
  • Pain-free (NSAIDs)
  • Penicillins and cephalosporins
  • Proton pump inhibitors
  • RifamPin
126
Q

Renal Pathology:

  • most common cause of acute kidney injury in hospitalized patients
  • spontaneously resolves in many cases
  • can be fatal, especially during initial oliguric phase
  • ↑ FENa
A

Acute Tubular Necrosis

127
Q

Stages of Acute Tubular Necrosis

A
  1. Inciting Event
  2. Maintenance Phase—oliguric; lasts 1–3 weeks; risk of hyperkalemia, metabolic acidosis, and uremia
  3. Recovery Phase—polyuric; BUN and serum creatinine fall; risk of hypokalemia and renal wasting of other electrolytes and minerals
128
Q

Acute Tubular Necrosis:

  • 2° to ↓ 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 highly susceptible to injury)
129
Q

Acute Tubular Necrosis:

  • 2° to injury resulting from toxic substances (eg. aminoglycosides, radiocontrast agents, lead, cisplatin, ethylene glycol), crush injury (myoglobinuria), and hemoglobinuria
  • proximal tubules are particularly susceptible to injury
A

Nephrotoxic

130
Q

Renal Pathology:

  • acute generalized cortical infarction of both kidneys
  • likely due to a combination of vasospasm and DIC
  • associated with obstetric catastrophes (eg. abruptio placentae) and septic shock
A

Diffuse Cortical Necrosis

131
Q

Renal Pathology:

  • sloughing of necrotic renal papillae → gross hematuria and proteinuria
  • may be triggered by recent infection or immune stimulus
  • associated with sickle cell disease or trait, acute pyelonephritis, NSAIDs, diabetes mellitus
A

Renal Papillary Necrosis

SAAD papa with papillary necrosis:

  • Sickle cell disease or trait
  • Acute pyelonephritis
  • Analgesics (NSAIDs)
  • Diabetes mellitus
132
Q

Renal Cyst Disorders:

  • numerous cysts in cortex and medulla causing bilateral enlarged kidneys ultimately destroy kidney parenchyma
  • presents with flank pain, hematuria, hypertension, urinary infection, and progressive renal failure in ~ 50% of individuals
  • mutation in PKD1 (85% of cases, chromosome 16) or PKD2 (15% of cases, chromosome 4)
  • death from complications of chronic kidney disease or hypertension (caused by ↑ renin production)
  • associated with berry aneurysms, mitral valve prolapse, benign hepatic cysts, and diverticulosis
  • Treatment:
    • if hypertension or proteinuria develops, treat with ACE inhibitors or ARBs
A

Autosomal Dominant Polycystic Kidney Disease

133
Q

Renal Cyst Disorders:

  • 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
  • concerns beyond neonatal period include systemic hypertension, progressive renal insufficiency, and portal hypertension from congenital hepatic fibrosis
A

Autosomal Recessive Polycystic Kidney Disease

134
Q

Renal Cyst Disorders:

  • also known as Medullary Cystic Kidney Disease
  • inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine
  • medullary cysts usually not visualized
  • smaller kidneys on ultrasound
  • poor prognosis
A

Autosomal Dominant Tubulointerstitial Kidney Disease

135
Q

Renal Cyst Disorders:

  • filled with ultrafiltrate (anechoic on ultrasound)
  • very common and account for majority of all renal masses
  • found incidentally and typically asymptomatic
A

Simple Cysts

136
Q

Renal Cyst Disorders:

those that are septated, enhanced, or have solid components on imaging require follow-up or removal due to risk of renal cell carcinoma

A

Complex Cysts

137
Q

Diuretics Site of Action

138
Q

Diuretics:

  • osmotic diuretic
  • ↑ tubular fluid osmolarity → ↑ urine flow, ↓ intracranial/intraocular pressure
  • used for drug overdose and elevated intracranial/intraocular pressure
  • causes pulmonary edema, dehydration, and hypo- or hypernatremia
  • contraindicated in anuria and HF
139
Q

Diuretics:

  • carbonic anhydrase inhibitor
  • causes self-limited NaHCO3 diuresis and ↓ total body HCO3− stores
  • used for glaucoma, metabolic alkalosis, altitude sickness, and pseudotumor cerebri
  • alkalinizes urine
  • causes proximal renal tubular acidosis, paresthesias, NH3 toxicity, sulfa allergy, and hypokalemia
  • promotes calcium phosphate stone formation (insoluble at high pH)
A

Acetazolamide

“ACID”azolamide causes ACIDosis.

140
Q

Diuretics:

  • sulfonamide loop diuretics
  • inhibit cotransport system (Na+/K+/2Cl−) of thick ascending limb of loop of Henle
  • abolish hypertonicity of medulla, preventing concentration of urine
  • stimulate PGE release (vasodilatory effect on afferent arteriole); inhibited by NSAIDs
  • ↑ Ca2+ excretion
  • used for edematous states (HF, cirrhosis, nephrotic syndrome, pulmonary edema), hypertension, and hypercalcemia
  • causes ototoxicity, hypokalemia, hypomagnesemia, dehydration, allergy (sulfa), metabolic alkalosis, nephritis (interstitial), and gout
A
  • Furosemide
  • Bumetanide
  • Torsemide

Loops Lose Ca2+.

OHH DAANG!

  • Ototoxicity
  • Hypokalemia
  • Hypomagnesemia
  • Dehydration
  • Allergy (sulfa)
  • Metabolic Alkalosis
  • Nephritis (Interstitial)
  • Gout
141
Q

Diuretics:

  • loop diuretic
  • nonsulfonamide inhibitor of cotransport system (Na+/K+/2Cl−) of thick ascending limb of loop of Henle
  • used for diuresis in patients allergic to sulfa drugs
  • causes similar to Furosemide, but more ototoxic
A

Ethacrynic Acid

Loop earrings hurt your ears.

142
Q

Diuretics:

  • inhibit NaCl reabsorption in early DCT → ↓ diluting capacity of nephron
  • ↓ Ca2+ excretion
  • used for hypertension, HF, idiopathic hypercalciuria, nephrogenic diabetes insipidus, and osteoporosis
  • causes hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia and sulfa allergy
A

Thiazide Diuretics

  • Hydrochlorothiazide
  • Chlorthalidone
  • Metolazone

HyperGLUC:

  • hyperGlycemia
  • hyperLipidemia
  • hyperUricemia
  • hyperCalcemia
143
Q

Diuretics:

  • Spironolactone and Eplerenone are competitive aldosterone receptor antagonists in cortical collecting tubule
  • Triamterene and Amiloride act at the same part of the tubule by blocking Na+ channels in the cortical collecting tubule
  • used for hyperaldosteronism, K+ depletion, HF, hepatic ascites (Spironolactone), nephrogenic DI (Amiloride), and antiandrogen
  • causes hyperkalemia (can lead to arrhythmias)
  • causes endocrine effects with Spironolactone (eg. gynecomastia, antiandrogen effects)
A

Potassium-Sparing Diuretics

TaKe a SEAT.

  • Spironolactone
  • Eplerenone
  • Amiloride
  • Triamterene
144
Q

Diuretics: Electrolyte Changes

Urine NaCl

A
  • ↑ with all diuretics (strength varies based on potency of diuretic effect)
  • serum NaCl may decrease as a result
145
Q

Diuretics: Electrolyte Changes

Urine K+​

A
  • ↑ especially with loop and thiazide diuretics
  • serum K+ may decrease as a result
146
Q

Diuretics: Electrolyte Changes

↓ Blood pH (Acidemia)

A
  • Carbonic Anhydrase Inhibitors: ↓ HCO3− reabsorption
  • K+ Sparing: aldosterone blockade prevents K+ secretion and H+ secretion, hyperkalemia leads to K+ entering all cells (via H+/K+ exchanger) in exchange for H+ exiting cells
147
Q

Diuretics: Electrolyte Changes

↑ Blood pH (Alkalemia)

A
  • Loop Diuretics and Thiazides
  • volume contraction → ↑ AT II → ↑ Na+/H+ exchange in PCT → ↑ HCO3− reabsorption (“contraction alkalosis”)
  • K+ loss leads to K+ exiting all cells (via H+/K+ exchanger) in exchange for H+ entering cells
  • in low K+ state, H+ (rather than K+) is exchanged for Na+ in cortical collecting tubule → alkalosis and “paradoxical aciduria”
148
Q

Diuretics: Electrolyte Changes

Urine Ca2+

A
  • ↑ with loop diuretics: ↓ paracellular Ca2+ reabsorption → hypocalcemia
  • ↓ with thiazides: enhanced Ca2+ reabsorption
149
Q

Angiotensin-Converting Enzyme Inhibitors

A
  • Captopril
  • Enalapril
  • Lisinopril
  • Ramipril
150
Q

Renal Drugs:

  • inhibit ACE → ↓ AT II → ↓ GFR by preventing constriction of efferent arterioles
  • ↑ renin due to loss of negative feedback. Inhibition of ACE also prevents inactivation of bradykinin, a potent vasodilator
  • used for hypertension, HF (↓ mortality), proteinuria, and diabetic nephropathy
  • prevent unfavorable heart remodeling as a result of chronic hypertension
  • in chronic kidney disease (eg. diabetic nephropathy), ↓ intraglomerular pressure, slowing GBM thickening
  • causes cough and angioedema (both due to ↑ bradykinin
  • contraindicated in C1 esterase inhibitor deficiency)
  • teratogen (fetal renal malformations)
  • ↑ Creatinine (↓ GFR)
  • causes hyperkalemia and hypotension
  • used with caution in bilateral renal artery stenosis because ACE inhibitors will further ↓ GFR → renal failure
    *
A

Angiotensin-Converting Enzyme Inhibitors

Captopril’s CATCHH:

  • Cough
  • Angioedema
  • Teratogen
  • ↑ Creatinine
  • Hyperkalemia
  • Hypotension
151
Q

Angiotensin II Receptor Blockers

A
  • Losartan
  • Candesartan
  • Valsartan
152
Q

Renal Drugs:

  • selectively block binding of angiotensin II to AT1 receptor
  • effects similar to ACE inhibitors, but do not increase bradykinin
  • used for hypertension, HF, proteinuria, or chronic kidney disease (eg. diabetic nephropathy) with intolerance to ACE inhibitors (eg. cough, angioedema)
  • causes hyperkalemia, ↓ GFR, and hypotension
  • teratogen
A

Angiotensin II Receptor Blockers

153
Q

Renal Drugs:

  • direct renin inhibitor
  • blocks conversion of angiotensinogen to angiotensin I
  • used for hypertension
  • causes hyperkalemia, ↓ GFR, hypotension, and angioedema
  • relatively contraindicated in patients already taking ACE inhibitors or ARBs and contraindicated in pregnancy

USMLE Step 1 (18 decks)

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