Wake Renal

Front 1

Name 7 functions of the kidney

Back 1

Regulation of water and electrolyte balance, excretion of metabolic waste, excretion of bioactive substance (drugs), regulation of arterial blood pressure, regulation of RBC production, regulation of vitamin D production, gluconeogenesis

Front 2

What cells make up the juxtaglomerular apparatus?

Back 2

Macula densa (Na+ sensor in the distal tubule), the juxtaglomerular cells (renin releasing granular cells in the afferent arteriole), and the extraglomerular matrix make up the juxtaglomerular apparatus

Front 3

What percentage of the cardiac output do the kidneys receive on average?

Back 3

20% (1.2 L/min out of 6 L/min)

Front 4

What are the layers of the filtration barrier in the kidney from blood to filtrate?

Back 4

Endothelial cells (separated by pores or fenestra), the basement membrane (lamina rara externa, lamina densa, lamina rara interna), and the podocytes (with enzymatic and structural proteins and a filtration slit maintained by a diaphragm)

Front 5

What are two methods of selectivity implemented by the glomerular membrane?

Back 5

Surface charge and pore size. The gel between the blood flow and the basement membrane is negatively charged and the fenestra and filtration slits of the podocytes filter based on size

Front 6

What is hydraulic conductivity and for what characteristic of glomerular capillaries does it account for?

Back 6

Hydraulic conductivity is the intrinsic permeability of a membrane. It is very high in the glomerulus accounting for the high water permeability for those capillaries.

Front 7

How do you calculate the filtration across a single glomerulus?

Back 7

Single nephron GFR=Kf([Pg-Pbs]-π)
π=colloid osmotic pressure

Front 8

What forces contribute to the ultrafiltration pressure gradient and how does it change as you move from the afferent to efferent ends of the glomerulus?

Back 8

The ultrafiltration pressure gradient takes into account the pressures in both the glomerular capillaries and Bowman's capsule, both of which stay constant, and the colloid osmotic pressure which increases as you move across the glomerulus. This change in colloid osmotic pressure results in a decrease in the ultrafiltration pressure gradient as you move from the afferent arteriole to the efferent arteriole

Front 9

What is Brenner's hypothesis?

Back 9

Brenner's hypothesis is that persistently elevated Pg is a major determinant of development and progression of kidney disease (declining GFR)

Front 10

How can persistent elevation of Pgc lead to decline in GFR?

Back 10

Damage to the slit diaphragm, the podocyte, or the glomerular basement membrane can result in:
* decreased # of podocytes: detatchment, apoptosis from increased ATII, glucose, capillary blood pressure, ROS, and p53
* protein leak: size and charge selectivity effacement
* glomerulosclerosis: damaged basement membrane bulges, attaches to the capsule and starts focal segmental glomerulosclerosis
* decreased GFR: decreased filtration slit area of the capillary endothelium

Front 11

How is the GFR measured (not eGFR)?

Back 11

GFR is the amount of blood filtered by the kidney per unit time. It is measured using the clearance of Inulin. GFR is the concentration of Inulin in the urine times the urine flow rate divided by the concentration of Inulin in the plasma

Front 12

How is the clearance of a substance calculated?

Back 12

Clearance is the volume of plasma completely cleared of a substance per unit time. It is equal to the concentration of Z in the urine, times the urine flow rate, divided by the concentration of Z in the plasma

Front 13

How does the plasma clearance of creatinine vary in response to GFR?

Back 13

As GFR increases, plasma creatinine decreases

Front 14

What are two methods of estimating GFR and how do they differ?

Back 14

* Cockcroft-Gault. For females, multiply by 0.85: [(140-age)*leanBW]/(serum creatinine*72)
* MDRD is based on serum creatinine, age, sex, and if the patient is african american or not

Front 15

How is eGFR used to assess stage kidney disease?

Back 15

* Stage I: >90
* Stage II: 60-89
* Stage III: 30-59
* Stage IV: 15-29
* Stage V: <15

Front 16

How does ATII result in the progression of the glomerular and kidney damage?

Back 16

Angiotensin II directly increases the glomerular capillary pressure which, through shear/stretch stress, can lead to glomerular and tubulointerstitial fibrosis. ATII also the release of cytokines that degrade the extracellular matrix of the kidneys, adding to the fibrosis.

Front 17

What class of drugs will slow the progression of CKD?

Back 17

* ACEi and ARBs and the only class of anti-hypertensives that will slow progression of CKD. ACEi and ARBs selectively dilate the efferent arteriole, reducing resistance, decreasing glomerular capillary pressure, and over the long term slowing the progression to fibrosis.
* Other types of anti-hypertensives will decrease systemic blood but not glomerular capillary blood pressure

Front 18

What are three ways used to measure renal blood flow?

Back 18

Using an electromagnetic flowmeter, a doppler ultrasound flowmeter, or a chemical marker

Front 19

How is the Fick Principle used to measure RBF?

Back 19

RPF= (urine blood flow*concentration of PAH in the urine)/(concentration of PAH in the arterial plasma-concentration of PAH in the venous plasma).

PAH (para-aminohippurate) is extracted in one pass through the kidney.

Front 20

How is a filtered load calculated?

Back 20

Filtered load is the plasma concentration of the substance*GFR

Front 21

How is clearance used to determine whether a substance is reabsorbed or secreted?

Back 21

If the clearance of substance Z < clearance of inulin then substance Z is reabsorbed within the kidney (ex. glucose). If the clearance of substance Z > clearance of inulin, then substance Z is secreted by the kidney (ex. PAH, urate, drugs)

Front 22

What are the regulators of renal arteriolar tone and how do they affect tone?

Back 22

* Vasoconstrictors: adenosine, angiotensin II, endothelin, norepinephrine, some prostaglandins
* Vasodilators: bradykinin, nitric oxide, prostaglandins

Front 23

How is filtration fraction calculated?

Back 23

Filtration fraction = GFR/RBF

Front 24

What are the main substances reabsorbed or secreted by the proximal tubule (S1 & S2, and S3)

Back 24

* S1 & S2: Na+, glucose, HCO3-, phosphate, lactate, and amino acids are reabsorbed via 2˚ active transport
* S3: Urate, PAH are secreted

Front 25

Where are aquaporin channels found and what function do they serve?

Back 25

Aquaporin-1 (in the PCT) and aquaporin-2 (in the principal cell of CCT) have high intrinsic water permeability and greatly increase the reabsorption of water

Front 26

How is HCO3- reabsorbed in the proximal convoluted tubule?

Back 26

* H+ is secreted into the lumen when Na+ is reabsorbed via the NHE-3 transporter. That H+ binds HCO3- in the lumen, becoming H2CO3. H2CO3 is broken down into CO2 and H2O by carbonic anhydrase IV and that CO2 and H2O diffuse into the cell.
* In the cell, the CO2 and H2O are converted into H2CO3 by carbonic anhydrase II and that H2CO3 will dissociate into H+ and HCO3- spontaneously.
* The HCO3- is transported to the blood stream along with the absorbed Na+ via the NBCe1 transporter. The H+ is then ready to be secreted again.

Front 27

How do water permeability and the interstitial concentration gradient explain the absorption of water and salt reabsorption in the thin ascending loop of Henle?

Back 27

* The thin descending loop of Henle is highly permeable to water and not permeable to salt or urea. The interstitum at the tip of the loop of Henle has a high osmotic pressure, so water will flow out of the lumen and will be reabsorbed, concentrating the urine.
* The thin ascending loop of Henle is permeable to salt, but not water. Salt will flow down its concentration gradient and into the interstitum

Front 28

How does osmotic pressure compare at the cortex and papilla?

Back 28

Osmotic pressure increases as you move towards the papilla. Osmotic pressure is 300 in the cortex and increases to 1200 at the papilla

Front 29

What electrolytes are reabsorbed at the thick ascending tubule and what mechanisms allow for that reabsorption?

Back 29

* The NKCC-2 transporter is responsible for bringing in Na+, Cl-, and K+ (which cycles back out again via ROMK)
* The transportation by NKCC-2 leaves an increased positive charge in the lumen of the TALH. This positive charge creates a charge gradient that allows Ca2+ and Mg2+ to diffuse into the blood paracellularly.

Front 30

What receptor is responsible for the function of the distal convoluted tubule? What are genetic defects that affect this transporter?

Back 30

* The NCCT co-transporter is responsible for reabsorbing Na+ and Cl-.
* Gordon's syndrome (gain of function) leads to hypertension and volume expansion. Gitelman's syndrome (loss of function) leads to salt wasting, hypotension, and hypokalemia.

Front 31

What is regulated at the collecting duct?

Back 31

* The absorption of water (via aquaporin stimulation by anti-diuretic hormone)
* Na+ reabsorption (via ENaC and is up-regulated by aldosterone)
* K+ excretion (via ROMK and is up-regulated by aldosterone)
* Acid-base balance (via the a-intercalated cells releasing H+ and the ß-intercalated cells secreting HCO3-)

Front 32

What are the roles of the three types of cells in the collecting ducts?

Back 32

* Principal cells: Na+ reabsorption (ENaC) and K+ secretion (ROMK) (both regulated by aldosterone) and H2O absorption (regulated via ADH)
* a-intercalated cells: acid (H+) secretion, bicarbonate reabsorption
* ß-intercalated cells: bicarbonate secretion

Front 33

What factors regulate K+ secretion by the principal cells of the collecting duct?

Back 33

* Aldosterone stimulation
* Na+ delivery to the distal tubule
* Charge differences (negative lumen) across the tubule
* Tubular fluid flow rate

Front 34

What effect does aldosterone have on the a-intercalated cell?

Back 34

Aldosterone binds the mineralcorticoid receptor which up-regulates the 2 ATPase transporters that secrete H+ into the lumen

Front 35

What amino acid is used to make ammonium? And where and why is it secreted?

Back 35

* Ingesting protein will drop the blood pH creating an acidosis. The protein also means more glutamine available to be metabolized to ammonium.
* Each glutamine generates ammonium and a bicarbonate. The ammonium is excreted and the bicarbonate raises the blood pH.
* Ammonium (NH4+) is secreted in the proximal tubule in response to drop in blood pH. It rides in on NHE-3 in the place of hydrogen, is reabsorbed instead of potassium by the NKCC transporter in the TALH and is then secreted into the collecting duct and is excreted.

Front 36

What is the pathophysiology for DRTA?

Back 36

* Distal renal tubule acidosis is a defect in either the AE1 transporter responsible for absorbing HCO3- or the H-ATPase responsible for secreting H+ from the a-intercalated cells in the collecting duct
* With H+ unable to be secreted and HCO3- unable to be absorbed a metabolic acidosis develops

Front 37

What is the pathophysiology of Gitelman's syndrome? What are the resulting processes?

Back 37

* In Gitelman's syndrome there is a loss of function in the NCCT transporter of the distal tubule. This results in an increase in Na+ delivery downstream to the ENaC transporter, which results in increased K+ secretion
* Renal salt wasting, hypokalemia, metabolic alkalosis, volume depletion, relative hypotension.
* Salt craving

Front 38

What is the pathophysiology of Liddle's syndrome? How will the syndrome present and how is it treated?

Back 38

* Liddle's syndrome is a cytoplasmic tail mutation of the ENaC transporter of the principal cell in the collecting duct, preventing ubiquitination and degradation. This mutation leads to a gain of function.
* Volume expansion, hypertension, low aldosterone and plasma renin, metabolic alkalosis, hypokalemia
* Treat with amiloride or triamterene to block ENac

Front 39

What is the pathophysiology of pseudohyperaldosteronism? How do patients present and how is it treated?

Back 39

* A mutation in the membrane spanning region of the ENaC channel or aldosterone receptor preventing proper folding and insertion into the membrane. This results in a loss of ENaC function.
* Volume depletion, hypotension, elevated serum aldosterone and renin, hyperkalemia, metabolic acidosis, salt-wasting
* Treat with Na+ supplementation

Front 40

How much of our body is water and how is it separated intracellularly, extracellularly, plasma, and blood volume?

Back 40

* Our bodies are ~60% water
* 2/3 intracellularly (~24L)
* 1/3 (~3L plasma, ~6L extracellular fluid or blood volume)

Front 41

Is more body water kept in the intracellular or extracellular fluid?

Back 41

For both men and women more body water is kept as intracellular fluid

Front 42

What is the predominant intracellular ion? Extracellular?

Back 42

Intracellular ion is K+ and the extracellular ion is Na+

Front 43

What is the adequate, upper limit, average daily intakes of Na+? What groups have special limits and what is it?

Back 43

* 1.5 g/day is the adequate intake
* 2.3 g/day is the upper limit
* 3.6 g/day is the average
* >51, blacks, hypertensives, diabetics, and kidney disease patient should consume less than 1.5 g/day

Front 44

What are the major factors that regulate excretion of sodium by the kidney?

Back 44

* Glomerular filtration rate: increasing GFR increases Na+ excretion
* Renal perfusion pressure: baroreceptors detect increased stretch and will release prostaglandins and NO and increase sodium excretion
* Sympathetic stimulation: (a1) constricts glomerular afferent arteriole decreasing GFR, stimulation of proximal Na+ reabsorption by NHE-3, (ß1) increases renin release
* Renin-angiotensin-aldosterone system: angiotenisin II increases GFR by constricting the efferent arteriole, increases Na+ reabsorption at the proximal tubule causing volume expansion, vasoconstricts peripheral vessels, and causes local prostaglandin release which increases renal blood flow
* Natriuretic hormones: atrial natriuretic peptide, dopamine, nitric oxide

Front 45

Describe the regional absorption of Na+ within the kidney

Back 45

* ~67% absorbed by the proximal tubule
* ~25% absorbed by the TALH
* ~5% absorbed by the distal tubule
* ~ 3% absorbed by the collecting duct
* <1% is excreted in the urine

Front 46

What is FENa and how is it calculated?

Back 46

* Fraction of excreted sodium is the fraction of Na+ filtered that is excreted.
* FENa is the concentration of sodium in the urine divided by the concentration of sodium in the plasma times the GFR time 100
* FENa% = [(U/P)*GFR]*100

Front 47

Where is renin released from?

Back 47

Renin is stored and released by the granular cells in the juxtaglomerular apparatus

Front 48

How do macula densa cells contribute to tubuloglomerular feedback?

Back 48

* Macula densa cells have an NKCC-2 transporter. In the presence of high luminal Cl, Cl- will be brought into the cell and stimulate the release of NO into the juxtaglomerular matrix. This NO changes the concentration of Ca2+ and cAMP in the granular cells of the afferent arteriole and decreases renin release.
* Low Cl- transport through NKCC stimulates PGE2 release into juxtaglomerular matrix which stimulates renin release

Front 49

What are the factors affecting renin release?

Back 49

* Distal sodium delivery: osmoreceptors in the macula densa
* Renal perfusion pressure: renal baroreceptors in the granular cells
* Sympathetic nervous system: neural baroreceptors communicate with granular cells

Front 50

What are the natriuretic hormones, where are they produced, and what is their goal?

Back 50

Natriuretic hormones increase sodium and water excretion, decreasing blood pressure
* Atrial natriuretic peptide is released by atrial myocytes in response to atrial stretch and plasma volume expansion.
* Dopamine and nitric oxide are both produced intrarenally

Front 51

How does ANP accomplish its goal?

Back 51

Atrial natriuretic peptide increases GFR by dilating the afferent arteriole, decreases Na+ reabsorption, and decreases renin release

Front 52

How does NO accomplish it intrarenal natriuretic goal?

Back 52

Decreases renin and decreases Na+ reabsorption and responds to increased sodium intake (mediates salt-sensitivity)

Front 53

How does dopamine accomplish it intrarenal natriuretic goal?

Back 53

Dopamine decreases Na+ reabsorption by blocking NHE-3 and the Na+/K+-ATPase in the proximal tubule and the principal cell of the collecting duct, diminishing the Na+ gradient necessary for reabsorption. Dopamine also increases renal blood flow.

Front 54

How does ADH regulate water excretion?

Back 54

Anti-diuretic hormone binds the vasopressin receptor on the basal side of the principal cells in the collecting duct. Through cAMP, this binding causes aquaporin-2 channels to migrate to the apical membrane, drastically increasing the permeability to water. Water flows basally through the AQP3/AQP4 channels.

Front 55

Which region of the kidney has the highest osmolarity?

Back 55

Osmolarity of the kidney is highest in the medulla (1200 mOsm/kg) and lowest in the cortex (300 mOsm/kg)

Front 56

What are the two factors responsible for water reabsorption?

Back 56

The ADH/AQP2 pathway and the hyperosmolarity of the medulla are the two factors responsible for water reabsorption

Front 57

What is the pathophysiology of diabetes insipidus?

Back 57

Diabetes insipidus is the inability to consume water due to the impermeability of the principal cell of the collecting duct.
* Central: No ADH secreted into the blood
* Nephrogenic: Altered ADH receptor or AQP2 channel

Front 58

Where in the kidney tubule is free water generated and where is it reabsorbed?

Back 58

Free water is generated in the TALH and it is reabsorbed in the collecting duct by aquaporin channels of the principal cels

Front 59

How is ADH secretion regulated?

Back 59

* Plasma osmolarity: osmoreceptors in the hypothalamus will respond to high plasma osmolarity by stimulating ADH release from the posterior pituitary gland. ADH will increase free water reabsorption, decreasing plasma osmolarity, resulting in a negative feedback loop
* Stretch receptors in the aortic arch, carotid arteries, and left atrium: decreased arterial volume creates less arterial stretch, triggering an increase in ADH by the posterior pituitary

Front 60

How does CHF lead to edema?

Back 60

Low cardiac output leads to decreased arterial filling and vascular stretch, which increases the antinatriuretic (RAAS and sympathetic tone) and antidiuretic (ADH) responses and decreases the natriuretic response (arterial natriuretic peptide, NO, and dopamine). This balance leads to Na+ and water retention, or peripheral edema

Front 61

How does hepatic cirrhosis lead to edema?

Back 61

Increased portal pressure causes fluid extravasation from the liver surface, decreasing the arterial filling of the hepatic veins. This decrease in arterial filling up-regulates anti-natriuretic (RAAS and sympathetic tone) and anti-diuretic (ADH) systems and down-regulates natriuretic systems (ANP, NO, dopamine) causing Na+ and water retention, or peripheral edema

Front 62

What are the major pathophysiological types of hyponatremia?

Back 62

High ADH due to decreased arterial volume
* Decreased extracellular fluid volume: hypovolemic hyponatremia, total volume depletion, diarrhea
* Increased extracellular fluid volume: hypervolemic hyponatremia, generalized edema, cirrhosis, CHF
* Inappropriate ADH secretion: increased ADH secretion not due to changes in plasma osmolarity or arterial volume and maintaining normal endocrine and renal funciton (carcinomas, pulmonary disorders, CNS disorders, HIV, drugs)

Front 63

What is the pathophysiology of SIADH

Back 63

Syndrome of inappropriate ADH secretion is increased ADH secretion not due to changes in plasma osmolarity or arterial volume and maintaining normal endocrine and renal funciton. It can be caused by carcinomas, pulmonary disorders, CNS disorders, HIV, or drugs

Front 64

What are the clinical consequences of hyponatremia?

Back 64

Hyponatremia is a bad prognostic factor. It can cause altered mental status (confusion, coma, seizures, and increase risk of falls in the elderly)

Front 65

Why is it important to maintain proper concentrations of potassium?

Back 65

Potassium is the ion responsible for maintaining the action potentials of cardiac cells, neurons, and muscle cells

Front 66

What is the normal value for serum potassium?

Back 66

4.0 mEq/L

Front 67

What are the three methods of controlling potassium homeostasis?

Back 67

Cellular distribution, renal excretion, and GI excretion

Front 68

How does the body regulate cellular potassium distribution?

Back 68

* Insulin: Binds the insulin receptor, facilitating K+ uptake. In hyperkalemia insulin will also activate Na+/K+ ATPase transporting K+ out of the blood.
* Cathecolamines: Activate the production of cAMP, via ß2 stimulation, upregulating the Na+/K+ ATPase
* Acid-base control will respond to an acidosis by stimulating K+ secretion from the cells

Front 69

Where is main site of K+ regulation in the kidney?

Back 69

The principal cells of the cortical collecting duct

Front 70

What is the affect of aldosterone in the principal cell?

Back 70

Aldosterone binds to an intracellular receptor and upregulates ENaC, ROMK, and NA+/K+ ATPase resulting in increased sodium reabsorption and increased potassium excretion

Front 71

What are the 4 determinants of renal potassium secretion?

Back 71

Aldosterone activity, distal Na+ delivery, tubular flow rate, and total body potassium

Front 72

What are some causes of hypokalemia, how does it present, and how do you treat it?

Back 72

* Diet, alkalosis, stress, insulin, diarrhea
* Muscle weakness, cardiac arrhythmias, rhabdomyolysis, ileus, hyperglycemia, polyuria (from impaired concentrating ability). As K+ decreases, T wave decreases in amplitude and U wave increases in amplitude, QRS interval increases
* IV K+ and volume replacement, K+ sparing diuretics

Front 73

What are some causes of hyperkalemia, how does it present, and how do you treat it?

Back 73

* Diet, renal failure, hypoaldosteronism, K-sparing diuretics, diet, acidosis, cell lysis (chemotherapy, blood draw), ß-blockers, digitalis, ACEi and ARBs (decrease GFR)
* Muscle weakness, cardiac arrhythmias (increases T-wave, shortens QT interval, and widens QRS)
* Calcium infusion changes the normal threshold required for depolarization, insulin, NaHCO3 infusion or ß-agonist will shift K+ into the cell, or give kayexelate (oral resin that binds potassium in the GI tract so it can be excreted in the feces), furosemide, or hemodialysis to remove K+ from the body

Front 74

What transporter is mutated in Gordon's syndrome?

Back 74

Gordon's syndrome is a NCCT gain of function resulting in hypertension

Front 75

What transporter is mutated in Gitelman's syndrome?

Back 75

Gitelman's syndrome is a NCCT loss of function resulting in hypotension

Front 76

What transporter is mutated in Liddle's syndrome?

Back 76

Liddle's syndrome is a ENaC gain of function resulting in very severe hypertension

Front 77

What is the mutation of pseudoaldosteronism type I?

Back 77

A hereditary mutation of ENaC subunits. It can cause hypo or hypertension

Front 78

What transporter is mutated in Barter's syndrome?

Back 78

Barter's syndrome is a mutation of the NKCC-2 transporter resulting in loss of function and hypotension

Front 79

What is Guyton's theory of hypertension?

Back 79

Hypertension is a isorder of volume regulation caused by an impairment in renal sodium excretion

Front 80

Explain the concept of pressure natriuresis

Back 80

An increase in renal perfusion pressure will increase Na+ excretion. This process is mediated by prostaglandins and nitric oxide

Front 81

Describe long-term autoregulation of blood flow and how it affects cardiac output

Back 81

When there is an increase in cardiac output there is a compensatory increase in total peripheral resistance, via vasoconstriction, to protect end-organ tissues from over-perfusion. This increase in TPR causes an increase in blood pressure, while generating a negativ feedback on cardiac output, returning it to normal. A steady hypertensive state is high TPR and blood pressure with a normal cardiac output

Front 82

Define autoregulation

Back 82

Autoregulation is the intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure

Front 83

Do neurohumoral or hemodynamic mechanisms have a larger impact on regulating Na+ excretion over a wide range of Na+ intakes?

Back 83

Renal Na+ excretion over a wide range of intakes is regulated mainly by neurohumoral mechanisms

Front 84

How does increasing aldosterone decrease the kidney's ability to maintain a constant blood pressure as Na+ intake and output increases?

Back 84

Increasing aldosterone lessens the kidney's ability to maintain a constant blood pressure as Na+ intake increases. The aldosterone will increase renal tubule sodium reabsorption and cause a right shift in the pressure diuresis curve.

Front 85

Is renal artery stenosis salt-sensitive or not?

Back 85

Renal artery stenosis is not salt-sensitive. It causes low renal perfusion pressure which stimulate renin release in the absence of Na+

Front 86

Is 1˚ hyperaldoseteronism salt sensitive or not?

Back 86

1˚ hyperaldosteronism is salt-sensitive. The increased aldosterone will cause the renal tubules to reabsorb more Na+

Front 87

What is mannitol, how does it function, what are its indications and side effects?

Back 87

* Mannitol is an inert sugar that is filtered but cannot be reabsorbed
* It is an anti-hypertensive that works by increasing the osmotic pressure of the ultrafiltrate, retaining water in the tubule
* Mannitol is indicated in brain edema. Also maintaining urine flow in AKI and diluting renal toxins
* Side effects include volume depletion, hypernatremia, volume overload (if in renal failure), and tubule toxicity

Front 88

Name three examples of osmotic diuresis

Back 88

Mannitol (inert, filtered but not reabsorbed sugar), glucosuria (in DM), and the use of contrast media

Front 89

What is acetazolamide, how does it function, what are its indications and side effects? Name others in the same class of drug

Back 89

* Acetazolamide is a sulfonamide anti-hypertensive that works by inhibiting carbonic anhydrase resulting in an increase in Na+ and HCO3- excretion
* Acetazolamide is indicated in glaucoma, aspirin intoxication (to increase urine pH), mountain sickness, and correction of severe alkalosis in CHF
* It can cause allergic reactions, metabolic acidosis, kidney stones, and patients can develop a tolerance
* Topiramate, zonisamide, indisulam

Front 90

What is the mechanism of action for thiazides, what are its indications and side effects?

Back 90

* Thiazide diuretics block the NCCT transporter in the distal convoluted tubule
* They are the first line drugs for hypertension and are also indicated in the prevention of kidney stones, and hypercaliuria because they cause Ca2+ retention, increasing bone density and decreasing fractures
* Its side effects are volume depletion, electrolyte abnormalities (hypokalemia, metabolic alkalosis, hyperglycemia, hyperuricemia), allergies, and slight renal vasoconstriction when GFR <30 ml/min

Front 91

What is the renal presentation of Gitelman's syndrome?

Back 91

Gitelman's syndrome (a loss of NCCT function) results in volume depletion, renal salt wasting, hypotension, hypokalemia, and metabolic acidosis

Front 92

What is the renal presentation of Gordon's syndrome? How is it treated?

Back 92

Gordon's syndrome (a gain of NCCT function) results in hypertension, hyperkalemia, and metabolic acidosis. It is treated with thiazide diuretics

Front 93

Why do thiazides cause hypokalemia?

Back 93

By blocking NCCT, thiazides deliver more Na+ to the ENaC in the collecting tubule. Increased ENaC function increases K+ secretion by ROMK causing potassium wasting and hypokalemia

Front 94

What is the mechanism of action for furosemide, what are its indications and side effects?

Back 94

* Furosemide blocks the function of the NKCC-2 transporter in the TALH. It is the most potent and effective diuretic.
* It is indicated in CHF and its edema, pulmonary edema, kidney disease with low GFR, hypertension, and hypercalcemia
* It causes significant metabolic alkalosis, volume and electrolyte depletion (Na+, Cl-, K+, Ca2+, Mg2+), as well as hyperglycemia, hyperuricemia, allergy, and ototoxicty

Front 95

Why do thiazide diuretics decrease Ca2+ excretion while loop diuretics increase Ca2+ excretion?

Back 95

* Thiazides, which inhibit NCCT in the distal tubule, decrease the reabsorption of Na+ into the cell. A basally located Na+/Ca2+ transporter will pump Na+ into the cell and Ca2+ into the blood stream to compesate for the decrease intracellular sodium.
* Loop diuretics block NKCC-2 action. Blocking this action eliminates the electical gradient needed to reabsorb Ca2+ (or Mg2+, Na+, and Cl-)

Front 96

What are the two categories of potassium sparing diuretics? What are their indications and side effects?

Back 96

* Na+ channel blockers (amiloride and triamterene) and aldosterone antagonists (spirololactone and eplernone)
* They are indicated in combination with other hypertensives, to prevent K+ loss, for refratory edema, ascites with secondary hyperaldosteronism, and nephrogenic diabetes insipidus
* They all cause hyperkalemia. Spironolactone causes gynecomastia, breast pain, decreased libido, and impotence. Eplerenone causes less breast pain and vaginal bleeding

Front 97

What is the renal presentation of Liddle's syndrome? How is it treated?

Back 97

Liddle's syndrome, a gain of ENaC function results in volume expansion, hypertension, hypokalemia, metabolic alkalosis. It responds to amiloride and triamterene

Front 98

Which classes of diuretics cause hypokalemia and which cause hyperkalemia?

Back 98

Loop and thiazide diuretics cause hypokalemia. Na+ channel blockers and aldosterone antagonists are K+ sparing diuretics and cause hyperkalemia

Front 99

What diuretics cause metabolic alkalosis and which cause metabolic acidosis and why?

Back 99

Loop and thiazide diuretics cause metabolic alkalosis. They both increase Na+ distal delivery and cause Cl-, K+, and H+ loss while decreasing the extracellular volume. Carbonic anhydrase inhibitors and K+ sparing diuretics cause metabolic acidosis.

Front 100

Name some aquaretics and describe their function and indication

Back 100

Aquaretics, such as tolvaptan, satavaptan, lixivaptan, and conivaptan (IV) are vasopressin-2 receptor blockers. Aquaretics block the function of anti-diuretic hormone preventing water from being reabsorbed. They are indicated in hyponatremia from syndrome of inappropriate ADH release (SIADH)

Front 101

What are the differences between cortical and juxtamedullary nephrons?

Back 101

Cortical nephrons are located in the mid to outer cortex, it has a short loop of Henle that only extends a short distance into the outer medulla. Juxtamedullary nephrons are located in the inner cortex near the border with the medulla and has a longer, thinner loop that extends well into the medulla

Front 102

What are the two capillary beds in the kidneys called and where are they located?

Back 102

Peritubular capillaries are in the cortex and the vasa recta is located in the medulla

Front 103

How do you distinguish capillaries from kidney tubules?

Back 103

Kidney tubules have cuboidal epithelium. Capillaries have squamous epithelium

Front 104

What are the functions of the mesangial cells?

Back 104

Physical support for the glomerular capillaries, control of blood flow by contracting in response to angiotensin II, phagocytosis of extracellular debris, especially from the GBM

Front 105

What type of epithelium lines the ureters, bladder, and urethra?

Back 105

Transitional epithelium or urothelium is designed to increase in surface area as the bladder fills with urine. They have a cobblestone appearance

Front 106

What is the function of the prostate?

Back 106

The prostate seccretes fluid that contains a variety of enzymes and other components that facilitate sperm function and contributes approximately 1/4 the volume of semen

Front 107

What is the best way to evaluate renal function?

Back 107

Urinalysis testing

Front 108

When should urinalysis test be done?

Back 108

During a sports physical, at a first complete history and physical, at an initial evaluation of hypertension, if there is systemic disease with renal involvement, with UTIs, and with a fever in a hospitalized patient

Front 109

What does urinalysis test for?

Back 109

Nitrates, glucose, heme pigment, protein, leukocyte esterase, and bilirubin

Front 110

Name 3 scenarios when a urinalysis will come back positive for heme pigment

Back 110

Hemolysis, rhabdomyolysis, and hematuria

Front 111

With what condition do you see waxy casts?

Back 111

Advanced kidney failure

Front 112

With what kidney syndrome do you see oval fat bodies?

Back 112

Nephrotic syndrome

Front 113

What are the three phosphates in triple phosphate crystals, what do the crystals look like and what do they symbolize?

Back 113

Magnesium, ammonium, and phosphate make up triple phosphate crystals. They look like coffin lids and have a bad prognosis

Front 114

What sedimentation is seen in pre-renal failure?

Back 114

Hyaline casts

Front 115

What sedimentation is seen in glomerular renal failure?

Back 115

RBC casts

Front 116

What sedimentation is seen in tubular renal failure?

Back 116

Granular casts

Front 117

Differentiate HIV nephropathy and rapidly progressive glomerulonephritis by time course, urinalysis, and race predominance

Back 117

HIV nephropathy will have a slow time course, proteinuria without RBCs, and is much more common in african americans. Rapidly progressive glomerulonephropathy is fast, produces RBC casts and can occur in african americans or whites

Front 118

How is calcium distributed in the body?

Back 118

45% bound to protein, 50% ionized, and 5% complexed.

Front 119

How is serum calcium corrected?

Back 119

Corrected calcium = ([4-serum albumin]*0.8)+ serum calcium

Front 120

From where do we get vitamin D?

Back 120

We get vitamin D from the sun, the liver of cold water fish, and fortified milk

Front 121

What is the active form of vitamin D and where is it activated?

Back 121

Vitamin D is converted into calcitriol (1,25-hydroxy vitmain D) in the kidney by 25 hydroxy vitamin D 1-alpha hydrolase

Front 122

What are the functions of calcitriol?

Back 122

Calcitirol increases Ca2+ and phosphate absorption by the intestines and increases calcium and phosphate resorption from bones

Front 123

What are the functions of PTH?

Back 123

Parathyroid hormone stimulates calcium and phosphate resorption from bone and absorption by intestine, but also increases phosphorus excretion. Net result is an increase in serum calcium and a decrease in serum phosphate

Front 124

What are three major problems in renal failure?

Back 124

Decreased urinary phosphorus excretion (starting 30-60, stage III), decrease calcitriol production, and increased PTH production

Front 125

Is ammonium an acid or a base?

Back 125

Ammonium (NH4+) is an acid. Ammonia (NH3) is a base

Front 126

What is the role of buffers?

Back 126

Buffers are weak acids and bases that can resist changes in acidity and alkalinity by partially dissociating and neutralizing the solution

Front 127

Name some non-bicarbonate buffer systems

Back 127

* Proteins like hemoglobin
* Phosphates: inorganic (urinary buffers) or organic (intracellular buffers)
* Ammonium

Front 128

In what form in most of CO2 transported in the blood?

Back 128

Most is HCO3-, then Hgb-CO2, and finally as CO2

Front 129

Name some endogenous sources of acid and alkali

Back 129

* Methionine, cysteine make sulfuric acid
* Phosphoric acid, bicarbonate
* Glucose makes lactic acid and pyruvic acid
* Triglycerides make acetoacetic acid
* Nucleoproteins make uric acid

Front 130

Where in the kidney is majority of the HCO3- reabsorbed and where is new bicarbonate generated?

Back 130

90% of filtered bicarbonate is reabsorbed in the proximal tubule and that is where NH3 is generated and secreted to be used in the distal tubule. In the distal tubule, NH3 accepts and neutralizes secreted H+. NH4+ interacts with a-ketoglutarate to generate glucose and new bicarbonate (which is taken up into the blood)

Front 131

How does the pH, PCO2, HCO3, and PO2 of venous blood compare to arterial blood

Back 131

Venous blood has approximately:
* 0.02-0.04 units lower pH
* 6-8 mmHg higher PCO2
* 1-2 mEg/L higher HCO3
* 60 mmHg lower PO2

Front 132

What are the steps for interpreting acid-base disorders?

Back 132

* Is the pH acidemic or alkalemic?
* Did the pH and HCO3 move in the same direction? Is the abnormal pH due to changes in PCO2 (respiratory) of HCO3 (metabolic)?
* Is appropriate compensation present? (Rule of 7s)
* What is the anion gap? (Na+)-[(Cl-)+(HCO3-)]

Front 133

What is the rule of 7s and what is it used for?

Back 133

The rule of 7s is used to interpret whether appropriate compensation is present for acid-base disorders.
* Metabolic acidosis: pCO2 = 1.5*HCO3+8
* Metabolic alkalosis: ∆10 HCO3 = ∆6 pCO2
* Respiratory acidosis, acute: ∆10 pCO2 = ∆1 HCO3
* Respiratory acidosis, chronic: ∆10 pCO2 = ∆3.5 HCO3
* Respiratory alkalosis, acute: ∆10 pCO2 = ∆2 HCO3
* Respiratory alkalosis, chronic: ∆10 pCO2 = ∆5 HCO3

Front 134

What is the anion gap used for and how is it calculated?

Back 134

The anion gap is used to determine the etiology of a metabolic acidosis. Normal range is 10-12. MUDPILES have high anion gaps, 2-3 times the upper limit of normal.
* anion gap = (Na+) - [(Cl-)+(HCO3-)]

Front 135

What is the differential diagnosis of a patient with an elevated anion gap?

Back 135

Elevated anion gaps (2-3 times the upper limit of normal, 10-12) can only occur with certain metabolic acidoses. MUDPILES.
* Methanol, Uremia, Diabetic ketoacidosis, Paraldehyde, Iron (isoniazid, inhalants, idiopathic), Lactic acidosis, Ethylene glycol, Salicylates

Front 136

What is the differential diagnosis of a metabolic acidosis with a normal anion gap?

Back 136

* GI loss of bicarbonate: diarrhea, ileal loop bladder
* Renal loss of bicarbonate or failure of acid secretion: renal tubular acidosis, adrenal insufficiency, carbonic anhydrase inhibitors
* Addition of hydrochloric acid: Ammonium chloride, arginine-HCl, lysine-HCl

Front 137

What are some systemic effects of metabolic acidosis?

Back 137

* Cardiovascular: hypotension, arrhythmia
* Pulmonary: Hyperventilation, reduced O2 delivery
* Gastrointestinal: Hypomotility, decreased absorption
* Renal: Na+ and K+ wasting, uric acid retention
* Metabolic: Protein catabolism, altered production and response of catecholamine, aldosterone, PTH, and vitamin D

Front 138

What is the goal for correcting a metabolic acidosis and how is it accomplished?

Back 138

The goal of correction is a pH≥7.20 and HCO3-≥12 mEg/L. To correct, calculate the HCO3 deficit (or H+ surplus):
* (HCO3 desired - HCO3 measured) * 0.5 * body weight
*NaHCO3 can be administered via IV up to 150 mEq/L

Front 139

What are some mechanisms causing metabolic alkalosis?

Back 139

* Net loss of H+ via the GI tract or kidneys: vomiting, nasogastric drainage, hyperaldosteronism
* Alkali loading (with renal insufficiency): ≥1000 mEq HCO3-/day for normal individuals
* Disproportionate loss of chloride with increased HCO3- absorption by the kidney: diuretics, mineralcorticoid excess, idiopathic chloride-resistant alkalosis (severe potassium depletion)

Front 140

What is the differential diagnosis of chloride-responsive metabolic alkalosis? Are they renal or non-renal pathologies?

Back 140

Chloride-responsive (urine Cl < 25 mEq/L) metabolic alkaloses are usually non-renal pathologies.
* Gastric fluid loss (vomiting, NG suction), diuretics (post-chronic use), post-hypercarbic state, low chloride intake (rare), stool loss (rare)

Front 141

What is the differential diagnosis of chloride-resistant metabolic alkalosis? Are they renal or non-renal pathologies?

Back 141

Chloride-resistant (urine Cl > 40 mEq/L) metabolic alkalosis are usually renal pathologies.
* Primary hyperaldosteronism, Bartter's syndrome, Gitelman's syndrome, Cushing's syndrome, renal failure (with bicarbonate loading), idiopathic

Front 142

What are the systemic effects of metabolic alkalosis?

Back 142

* Cardiovascular: hypotension, arrhythmia
* Pulmonary: Hypoventilation
* CNS: Obtundation, delirium, decreased seizure threshold
* Neuromuscular: tetany
* Metabolic: hypokalemia, hypophosphatemia, decreased ionized calcium, increased anaerobic glycolysis and lactic acid production, leftward shift of oxyhemoglobin curve

Front 143

What is the goal for correcting a metabolic alkalosis and how is it accomplished?

Back 143

The goal of correction is a pH≤7.60 and HCO3-≤45 mEg/L.
* Chloride-responsive: Prevent with Cl- and K+ supplements, H2 antagonists, or PPIs. Correct by administering NaCl, KCl, or acetazolamide
* Chloride-resistant: treat the underlying defect, restrict Na+, supplement with K+

Front 144

What is the differential diagnosis of acute respiratory acidosis?

Back 144

* Airway obstruction: aspiration, bronchospasm, laryngospasm, obstructive sleep apnea
* Circulatory collapse: caridac arrest, pulmonary embolism
* CNS depression: medications, anesthesia, stroke, central sleep apnea
* Ventilatory restriction: pneumothorax, pneumonia
* Iatrogenic: mechanical ventilation, bronchoscopy

Front 145

What is the differential diagnosis of chronic respiratory acidosis?

Back 145

* Airway obstruction: COPD
* CNS: medications, stroke, central sleep apnea, brain tumor, obesity-hypoventilation syndrome
* Neuromuscular: muscular dystrophy, multiple sclerosis, amyotrophic lateral sclerosis, poliomyelitis
* Ventilatory restriction: kyphoscoliosis, hydrothorax, interstitial fibrosis, morbid obesity

Front 146

What are the systemic effects of respiratory acidosis?

Back 146

* Cardiovascular: hypertension, arrhythmia
* CNS: increased cerebral blood flow and intracranial pressure, obtundation, confusion, seizures
* Metabolic: altered catecholamine production and response, increased renin and aldosterone production, increased renal excretion

Front 147

How do you treat acute respiratory acidosis?

Back 147

Treat underlying cause, treat hypoxemia, HCO3 usually isn't needed

Front 148

How do you treat chronic respiratory acidosis?

Back 148

Treat COPD, look for complicating metabolic alkalosis, don't reduce PCO2 to rapidly (to avoid life-threatening alkalemia)

Front 149

What is the differential diagnosis for respiratory alkalosis?

Back 149

* Hypoxia: altitude sickness, hypotension, severe anemia, pulmonary disease
* CNS: anxiety-hyerventilation syndrome, stroke, CNS trauma or infection, brain tumor
* Medication: Salicyates, nicotine, vasopressors, progesterone
* Other: pregnancy, liver failure, sepsis, iatrogenic (mechanical ventilation)

Front 150

What drug can be responsible for respiratory alkalosis and metabolic acidosis?

Back 150

Salicylates can cause respiratory alkalosis and metabolic acidosis with an elevated anion gap

Front 151

What are clinical manifestation of respiratory alkalosis?

Back 151

* Acute: extremity parasthesias, chest tightness, circumoral numbness, lightheadedness, seizures, cardiovascular (tachycardia, decreased SVR and cerebral blood flow, BP and CO stay the same)
* Chronic: usually asymptomatic, cardiovascular (BP stays the same, cerebral blood flow returns to normal, renal blood flow decreases), extracellular fluid decreases causing hematocrit to increase

Front 152

How to you treat respiratory alkalosis?

Back 152

It is rarely life-threatening so diagnosis, not treatment, is important. Exclude metabolic acidosis and hypoxemia before using paper bag in anxiety-hyperventilation syndrome

Front 153

What acid-base disorder should you consider in a mechanically-ventilated patient with arrhythmias?

Back 153

Respiratory alkalosis

Front 154

What are some causes of elevated BUN and creatinine that can confound BUN/Cr as an indicator of kidney function?

Back 154

* BUN: GI bleeding, catabolic states, high protein diet, amino acid infusions, tetracycline, steroids
* Creatinine: rhabdomyolysis, cimetidine, trimethoprim, probenacid

Front 155

How is AKI defined?

Back 155

Acute kidney injury is defined by either the AKIN criteria or RIFLE classification
* RIFLE: Three graded levels of dysfunction measured by increase in serum creatinine, drop in GFR, and urine output (kidney risk, injury, failure) with two possible outcomes, kidney loss (dialysis for at least 4 weeks) and ESRD (dialysis for at least 3 months)

Front 156

What are the main pathophysiological mechanisms of pre-renal AKI?

Back 156

* True intravascular hypovolemia: extrarenal (diarrhea, vomiting, GI bleed, blood loss, burns) or renal (diuretics, diabetes insipidus
* Decreased effective circulatory volume: CHF, cirrhosis, shock
* Intrarenal vasoconstriction: Hypercalcemia, contrast dye, cyclosporine/tacrolimus
* Renal artery disease, NSAIDs, ACEi/ARB

Front 157

What are the blood chemistry and urinalysis findings in pre-renal AKI?

Back 157

* BUN/Cr > 20:1 (low urinary flow allows for increases urea absorption)
* FENa <1%, FEurea <35% (if on diuretics), UNa <20 (increased Na reabsorption in response to hypovolemia)
* Monitor for ARF complications (hyperkalemia, acidosis)
* Bland urinalysis

Front 158

How do you treat pre-renal AKI?

Back 158

Normalize effective kidney blood flow quickly, to avoid progression to intrinsic injury.
* Give isotonic fluids, blood products, or pressor agents
* Stop drugs that exacerbate the condition
* Treat underlying disease

Front 159

Where are the 4 locations where renal parenchyma can be disrupted in intrinsic AKI?

Back 159

Vascular/microvascular, glomerular, interstitium, tubules

Front 160

What are some causes for the 4 types of intrinsic AKI?

Back 160

* Vascular: Thrombotic microangiopathy, renal atheroembolism, small vessel vasculitis
* Glomerular: Anti-GBM, lupus, post-infectious GN, membranoproliferative GN, IgA, H-S purpura
* Interstitial: drugs, infection, systemic disease
* Tubular: ischemia, nephrotoxin, rhabdomyolysis, radiocontrast agents

Front 161

What is the most common cause of community-acquired ARF and how does it present

Back 161

Acute tubular necrosis. Can be caused by ischemia, nephrotoxins, radiocontrast agents, or rhabdomyolysis.
* Prolonged pre-renal symptoms: infection, fever, diarrhea, diuretics, orthostatic lightheadedness, thirst
* History: hypotension, recent surgeries, contrast administration, neprotoxins
* Physical exam: hypovolemia, orthostatic hypotension, tachycardia, dry mucous membrane, decreased turgor, oliguria

Front 162

What are some mechanistic ways pre-renal AKI can progress to acute tubular necrosis?

Back 162

Pre-renal AKI and ATN are two extremes of the same clinical spectrum. Prolonged pre-renal AKI overwhelms the kidney's compensation mechanisms
* Ischemia: prolonged hypoperfusion, crush injury & trauma, septic shock, pancreatitis
* Endotoxins: hemoglobin, myoglobin, uric acid, immunoglobulin light chains,
* Exotoxins: heavy metals (lead), ethylene glycol, contrast dye, antibiotics (aminoglycosides, amphotericin B)

Front 163

What are the three phases of ATN?

Back 163

* Initiation: inciting damage causes necrosis which blocks the lumen, reducing GFR and causing vasoconstriction, prolonging ischemia and resulting in oliguria
* Maintenance: ongoing renal failure, creatinine increases
* Recovery: tubular epithelium regenerate but are unable to absorb H2O and electrolytes, causing poyluria. BUN/Cr normalizes

Front 164

What are the blood chemistry and urinalysis findings in ATN?

Back 164

* Elevated BUN and Cr. BUN/Cr < 20:1
* FENa >2%, UNa >40, urine osmolarity <350
* Classic "muddy brown casts" in urine

Front 165

How do you treat ATN?

Back 165

* Largely supportively: improve renal perfusion, avoid nephrotoxins
* Medical therapy: correct volume status, electrolyte disturbances, and acidosis

Front 166

What is the pathogenesis and risk factors of contrast induced nephropathy?

Back 166

* Vasoconstriction of renal arteries causes direct tubular injury
* Risk factors are underlying renal insufficiency, diabetic nephropathy, heart failure, percutaneous coronary intervention, high dose of contrast agent

Front 167

What is the clinical presentation and diagnosis of contrast induced nephropathy?

Back 167

* Non-oliguric renal failure 12-24 hours after contrast study
* Similar diagnosis to ATN

Front 168

How do you avoid and treat contrast induced nephropathy?

Back 168

* Avoid contrast for high risk individuals, use nonionic, low osmolal agents, use low doses of contrast, avoid repetitive, closely spaced studies, avoid volume depletion and NSAIDs
* Treat by volume expansion with isotonic bicarbonate or isotonic saline

Front 169

What is the clinical presentation of atheroembolic disease, what are its renal manifestations, and how?

Back 169

* Blue toe syndrome, CVA, livedo reticularis, GI manifestations
* Manifests in older patients, causes marked renal impairment, not uncommon
* Urine will be bland. If active, eosinophils will be present. Can have nephrotic range proteinuria. Hypocomplementemia

Front 170

What is acute interstitial nephritis, what are its common cause, what are the results of its urinalysis, and how is it treated?

Back 170

* Renal injury characterized histopathologically by inflamation and edema of the renal interstitium.
* Caused by drugs, infections, or autoimmune disorders.
* White cells, eosinophilia, white and red cell casts
* Remove offending agent, corticosteroids

Front 171

What is the clinical presentation of post-renal AKI and how is it diagnosed?

Back 171

* Flank or colicky pain, changes in urine output, palpable kidney or bladder, bladder symptoms (weak stream, hesitancy, post-void dribbling), hypertension, recurrent UTIs, possible hematuria
* Elevated BUN/Cr, FEna >2-4%, bland urine sediment (hematuria suggests stones or tumors), crystals, use imaging

Front 172

What is post-obstructive diuresis?

Back 172

Post-obstructive diuresis is polyuria commonly seen following sever bilateral obstruction. Can be from osmotic diuresis caused by urea retention, volume overload, or a tubular concentration defect

Front 173

What injury does a BUN/Cr >20:1 suggest? <20:1?

Back 173

* BUN/Cr > 20:1 is a pre-renal injury
* BUN/Cr < 20:1 is an intrinsic injury

Front 174

When do you see epithelial cell and muddy brown casts on urinalysis?

Back 174

ATN

Front 175

When do you see RBC casts?

Back 175

Glomerulonephritis

Front 176

What are the urine sediment findings in pre- and post-renal AKI?

Back 176

Both pre-renal and post-renal AKI produce a bland urinalysis

Front 177

When is renal biopsy indicated? What are its contraindications?

Back 177

* Unexplained acute or sub-acute renal failure
* Small kidneys, severe hypertension, multiple bilateral cysts, hydronephrosis, active infection, uncooperative patient

Front 178

How do you treat AKI?

Back 178

* Prevent it in the first place.
* Identify high risk groups: kidney disease, diabetics, solitary kidney, multiple myeloma
* Avoid nephrotoxins: contrast, aminoglycosides, NSAIDs

Front 179

What are the indications for dialysis?

Back 179

AEIOU.
* Acidosis: persistent metabolic acidosis with pH < 7.2 and bicarbonate therapy
* Electrolyte abnormalities: persistent hyperkalemia ± EKG changes
* Intoxication
* Overload: refractory volume despite diuretics
* Uremia: altered mental status, pericardial rub

Front 180

What is the leading cause of kidney disease and ESRD in the US?

Back 180

Diabetic nephropathy

Front 181

What are the structural and functional changes seen in diabetic nephropathy?

Back 181

* Structural: GBM thickening, mesangial matrix expansion, glomerular sclerosis
* Functional: Persistent albuminemia, worsening hypertension, progressive decline in GFR

Front 182

What are the main processes responsible for diabetic nephropathy?

Back 182

* Glomerular hyperfiltration: afferent dilation and efferent constriction
* Renal hypertrophy: elevated blood sugar stimulates growth factors (TGF-ß) and decreases antiproliferative factors
* Mesangial expansion and nodule formation: increased intracellular glucose glycated matrix proteins (AGEs) which accumulate in mesangium stimulate TGF-ß, and decrease matrix metalloproteinases
* Proteinuria development: accumulation of type IV collagen widening GBM and podocyte effacement disrupts permselectivity.
* Tubulointerstitial fibrosis: regulated by TGF-ß and ischemic hyalinosis

Front 183

What are the 5 stages in the natural history of diabetic nephropathy?

Back 183

* Renal hypertrophy and hyperfiltration causing elevated GFR and urine albumin excretion
* 5-10 years: normoalbuminuria with elevated GFR and increased mesangial matrix
* 5-15 years: microalbuminuria (30-300 mg/d)
* 10-20 years: overt proteinuria (>300 mg/d)
* 15-25 years: decline in GFR (10 mL/min/yr) with ESRD after 5-7 yrs of nephrotic range proteinuria

Front 184

What are risk factors for developing diabetic nephropathy?

Back 184

Race/ethnicity (african americans, mexicans, pima indians), having a genetic sibling or parent with diabetic nephropathy, duration of having diabetes and glycemic control, males, high blood pressure

Front 185

How do you screen for diabetic nephropathy?

Back 185

* Type I DM: screen annually after 5 years
* Type II DM: screen annually from time of diagnosis
* Screen every 6 months if UAER > 30 mg/d
* Check urine albumin levels early in the morning on 2 occasions separated by 3-6 months. Persistent microalbuminuria is 30-300 mg/d

Front 186

Why do we screen for diabetic nephropathy?

Back 186

Microalbuminuria predicts high renal and cardiovascular risk

Front 187

How is diabetic nephropathy diagnosed?

Back 187

Persistent albuminuria (30-300 mg/d) with biopsy being definitive

Front 188

When should you consider a kidney biopsy in a diabetic patient?

Back 188

Accelerated renal failure, an acute nephrotic syndrome, refractory hypertension, macroscopic hematuria, or signs and symptoms of systemic disease

Front 189

What are some biopsy findings in diabetic nephropathy?

Back 189

GBM thickening, mesangial matrix expansion, arteriolar hyalinosis, glomerular sclerosis, andkimmelstein-wilson nodules

Front 190

What is the treatment for diabetic nephropathy?

Back 190

ACEi/ARB to minimize proteinuria and keep BP at goal of 130/80 and schedule regular monitoring every 4-6 months

Front 191

What are risk factors for diabetic nephropathy progression?

Back 191

Worsening proteinuria, poor glycemic control (HgA1C<7), hypertension (≥130/80), male

Front 192

What are modified maintenance goals in the diabetic nephropathy patient

Back 192

* Minimize proteinuria
* HgA1c<7
* Blood pressure <130/80
* LDL<100 (or <70 if other CV risk factors present)

Front 193

What are the reno-protective effects of ACEi?

Back 193

ACE inhibitors confer renal protection by lowering systemic BP, decreasing intra-glomerular pressure, increasing renal blood flow, decreasing proteinuria, inhibiting ATII effects, and inhibiting macrophage activation, proliferation, and migration

Front 194

How is hematuria defined?

Back 194

Microscopic hematuria is greater than 2-3 RBCs per high powered field. Macroscopic hematuria is gross hematuria or red urine

Front 195

What are causes of persistent, isolated hematuria with or without proteinuria?

Back 195

IgA nephropathy, thin basement membrane nephropathy, and Alport's syndrome

Front 196

How is a nephritic syndrome characterized?

Back 196

A nephritic syndrome has active urinary sediments (inflammation, dysmorphic RBC with RBC casts, non-nephrotic range proteinuria), hypertension, edema, and ARF

Front 197

What are the respective differential diagnoses for the age groups <15, 15-40, and >40?

Back 197

* <15: PIGN, IgA nephropathy, Alport's, TBM, H-S pupura, MPGN
* 15-40: IgA nephropathy, TBM, SLE, Alport's, MPGN, RPGN
* >40: RPGN, vasculitis, PIGN

Front 198

What nephritic syndrome is the most common worldwide?

Back 198

IgA nephropathy

Front 199

What is the clinical picture of post-infectious GN?

Back 199

A male, 2-14 years old, 2 weeks after a strep pharyngeal infection or 4 weeks after a skin infection, that presents a a nephritic picture

Front 200

What is the pathology of PIGN?

Back 200

Post-infectious GN is an immune response to a nephritogenic group A ß–hemolytic strep infection. Antibodies are directed at the bacterial antigen or an intrinsic glomerular epitope and activate the local complement cascade.

Front 201

What are the biopsy findings in PIGN?

Back 201

* LM: diffuse mesangial proliferation and an enlarged tuft from neutophils
* IF: C3 and IgM deposits in a mesangial pattern, a garland pattern (capillary loops), or starry-sky pattern (mix of the two)
* EM: subepithelial hump deposits

Front 202

How is PIGN treated?

Back 202

Supportively. Treat HTN, manage volume, treat infection

Front 203

What is the pathophysiology of Berger's disease?

Back 203

Mesangial deposition of underglycosylated IgA produced by the mucosa of the skin and GI tract and defectively handled by Kupfer cells in the liver

Front 204

What is the epidemiology of Berger's disease and what are some of it's secondary causes?

Back 204

IgA nephropathy
* Non-white, males in the 2nd to 3rd decade of life
* 2˚ causes: RA, ankylosing spondylitis, psoriasis, IBD, cirrhosis, dermatitis herpitiformis

Front 205

What are the signs and symptoms of Berger's disease?

Back 205

IgA nephropathy will have persistent microscopic hematuria, proteinuria <1 gm, synpharyngitic hematuria, normal complement

Front 206

What are the biopsy findings in Berger's disease?

Back 206

* LM: diffuse mesangioproliferative changes of mesagnial hypercellularity and matrix expansion
* EM: mesangial deposits

Front 207

What is the prognosis of Berger's disease? What suggests good or bad prognoses?

Back 207

* 20% progress to ESRD in 20 years
* Gross hematuria is a good prognostic factor
* HTN, older age, heavy proteinuria, and renal failure are bad prognostic factors

Front 208

How is Berger's disease treated?

Back 208

* ACEi/ARB to limit proteinuria
* Fish oil to decrease cytokines
* Immunosuppression if the disease is aggressive
* Tonsillectomy will lessen episodes of gross hematuria

Front 209

What is the pathogenesis and clinical picture of Hencoh-shonlein purpura?

Back 209

* Mesangial deposition of underglycosylated IgA produced by the mucosa of the skin and GI tract and defectively handled by Kupfer cells in the liver, causes a systemic vasculitis affecting the GI tract, renal tissue, and skin.
* Children have skin manifestations, adults have renal involvement. More common in the winter.

Front 210

What is hereditary nephritis and what is its main complicating syndrome?

Back 210

* Hereditary nephritis or thin basement membrane nephropathy is an inherited glomerular disease caused by the absence or abnormal distribution of a-3,4,5 chains of type IV collagen. This collagen is present in the basement membrane of the eyes, kidneys, and cochlea
* Alport's is it's progressive complicating syndrome and is associated with hearing loss and ocular abnormalities. X-linked mutation is a-5, autosomal recessive mutations are either a-3 or a-4.

Front 211

What is the presentation and diagnosis of Alport's syndrome?

Back 211

* Young males with persistent microscopic hematuria, deafness, and potentially ocular abnormalities. HTN and proteinuria develop later. >90% reach ESRD by 35
* 2 or more: microscopic hematuria (age<10), deafness, family history of renal failure. Confirm with biopsy showing laminated basement membrane and type IV collagen

Front 212

How do you treat hereditary nephritis?

Back 212

Conservatively. ACEi/ARB for proteinuria and BP control

Front 213

What is thin basement membrane nephropathy?

Back 213

A lifelong non-progressive disorder associated with a family history of hematuria

Front 214

What is the normal age range for membranoproliferative GN?

Back 214

8-30 with no gender predominance

Front 215

What are 2˚ causes for MPGN?

Back 215

Malignancy, HCV, chronic infections (endocarditis), visceral abscess, cryoglobulinemia

Front 216

What is the pathogenesis of thrombotic microangiopathy?

Back 216

Mesangiolysis leads to dissolution of the mesangial matrix anchoring to the GBM disrupting the structural integrity of the glomerular tuft and resulting in the confluence of groups of capillary loops sharing mesangial support. The leads to the formulation of microaneurysms and, when adjacent lobules are present, blood cysts

Front 217

What is the glycocalyx?

Back 217

The glycocalyx, or fuzzy coat, is the negatively charged layer of glycoproteins emanating from the cell membrane of the podocytes and their foot processes

Front 218

Describe the layer organization of the glomerular basement membrane

Back 218

The electron dense lamina densa is surrounded by two thinner electron-lucent layers known as the lamina rara externa and lamina rara interna

Front 219

What is the function of nephrin?

Back 219

Nephrin is a transmembrane protein responsible for the structural integrity of the slit diaphragm

Front 220

What are immunological and non-immunological mechanisms of glomerular injury?

Back 220

* Immunological: endogenous (GBM, M-type phospholipase A2, DNA) or exogenous (HBV, HIV)
* Non-immunological: ischemia, hyperfiltration, podocytopathy, non-enzymatic glycation, intrarenal reflux, deposition of amyloid material or abnormal immunoglobulin chains

Front 221

What is the common pathologic finding in the rapidly progressive GNs and what causes the finding?

Back 221

Crescents are the result of disruption of glomerular capillaries or a proliferative phenotype of injury

Front 222

What are the definitions of non-oliguria, oliguria, and anuria?

Back 222

* Nonoliguria >4000 cc/d
* Oliguria <4000 cc/d
* Anuria is NO urine

Front 223

What is the EM finding characteristic of crescents?

Back 223

Wrinkling of GBM with focal disruptions

Front 224

What are the three main mechanisms of rapidly progressive GNs?

Back 224

All are antibody mediated injuries
* Anti-GBM: renal-limited and Goodpasture's
* Immune complex: associated with systemic disease, often secondary to an illness
* Pauci-immune: Granulomatosis with polyangiitis, Microscopic polyagniitis, Allergic granulomatosis

Front 225

Which rapidly progressive GNs have the highest frequency of crescents?

Back 225

The anti-GBM and pauci-immune glomeruloneprhitises are more likely to have crescents

Front 226

What is the epidemiologic difference between Goodpasture's and renal limited anti-GBM GN?

Back 226

* Goodpasture's presents in males during the 2nd and 3rd decades
* Renal limited presents in females during the 6th and 7th decades

Front 227

What is the pathogenesis of anti-GBM disease?

Back 227

Antibodies against the non-collagenous domain of the a3 chain of type IV collagen which is usually hidden. The autoantigen is exposed by environmental factors (hydrocarbons, tobacco, oxidants). Antibodies can cross react with the pulmonary alveolar basement membrane causing alveolar hemorrhage and Goodpasture's disease

Front 228

What are the biopsy findings in anti-GBM disease?

Back 228

LM: crescents, fibrinoid necrosis, synchronous lesions, glomerulosclerosis, and tubulointerstitial changes
IF: linear staining of GBM with IgG
EM: absence of immune complex deposits

Front 229

How do you diagnose anti-GBM?

Back 229

Detect antibodies (a3 chain of non-collagenous domain of type IV collagen), concurrent ANCA titer

Front 230

What is the treatment for anti-GBM?

Back 230

* Rapid initiation of plasmapheresis
* Steroids, cyclophosphamide

Front 231

What did MPO-ANCA used to be called, what is it an antibody towards, and what disease is it implicated in?

Back 231

MPO-ANCA is an antibody against myeloperoxidase. It used to be called pANCA and it is implicated in microscopic polyangiitis.

Front 232

What did PR3-ANCA used to be called, what is it an antibody towards, and what disease is it implicated in?

Back 232

PR3-ANCA is an antibody against proteinase-3. It used to be call cANCA and it is implicated in Granulomatosis with polyangiitis (wegner's granulomatosis) and allergic granulomatosis (churg-straus)

Front 233

What is the treatment for the pauci-immune GNs?

Back 233

Steroids and cytotoxic therapy. Plasmapheresis is indicated if the patient is on dialysis at presentation or if there is pulmonary hemorrhage or advanced CKD.

Front 234

What is the most common type of acute GN in the elderly?

Back 234

Rapidly progressive GN or Crescentic GN. (Anti-GBM, immune complex, pauci-immune)

Front 235

What proteins are found in the urine in proteinuria?

Back 235

Proteins secreted from the nephron like Tamm-Horsfall, filtered albumin, and filtered globulins like Bence-Jones proteins

Front 236

What is the nephrotic range of proteinuria?

Back 236

150mg - 3g is proteinuria. >3-3.5g/d is nephrotic range proteinuria

Front 237

What are the ranges for albuminuria?

Back 237

* <30 mg/d is normal
* 30-300 mg/d is microalbuminuria
* >300 mg/d is macroalbuminuria

Front 238

What are some transient causes of proteinuria?

Back 238

Fever, vigorous exercise, exposure to extreme cold

Front 239

What are 3 mechanistic causes of persistent proteinuria?

Back 239

Glomerular (increased protein movement across GBM), tubular (decreased protein reabsorption, fanconi syndrome), overflow (increase plasma protein production that overwhelms kidney capabilities)

Front 240

What are the hallmarks of the nephrotic syndrome?

Back 240

Pathological glomerular protein loss. Proteinuria (>3-3.5 mg/d), edema, hypoalbuminemia, hyperlipidemia

Front 241

Does nephrotic or nephritic syndrome generate a hypercoagulable state and why?

Back 241

The spilling of antithrombin III and other fibrinolytic factors in nephrotic syndrome causes a hypercoagulable state

Front 242

What is the urine sediment finding in nephrotic syndrome?

Back 242

Oval fat bodies from the hypderlipidemia found in nephrotic syndrome

Front 243

What are the biopsy findings of minimal change disease?

Back 243

LM, IF: unremarkable
EM: foot process effacement
Proximal tubules will be laden with lipids

Front 244

What is the hallmark finding of minimal change disease?

Back 244

Visceral epithelial cell damage (foot process effacement). Immunologic dysfunction elaborates cytokine production causing visceral epithelial cell damage

Front 245

What are some secondary causes of minimal change disease?

Back 245

NSAIDs and lymphoma

Front 246

What is the epidemiology, presentation, and treatment of minimal change disease?

Back 246

Minimal change disease is the most common cause of nephrotic syndrome in children. It presents as a sudden onset of massive proteinuria and nephrotic syndrome. MCD is treated with corticosteroids and cytotoxic agents (cyclosporine or cyclophosphamide)

Front 247

What are the biopsy findings in focal segmental glomerulosclerosis?

Back 247

LM: focal and segmental sclerosis and hyalinosis
IF: focal IgM, C3 in sclerotic areas/mesangium
EM: foot process effacement

Front 248

What is the hallmark of FSGS?

Back 248

The hallmark of focal segmental glomerulosclerosis is degeneration and disruption of visceral epithelial cells (foot processes). Hyalinosis and sclerosis result from hyperpermeable areas of GBM

Front 249

What are the primary, hereditary, and secondary etiologies of FSGS?

Back 249

* 1˚: soluble urokinase receptor
* Hereditary: APOL1 variant is a common kidney disease culprit in african americans
* 2˚: HIV, pamidronate, hyperfiltration, heroin, reflux nephropathy

Front 250

What is the epidemiology, presentation, and treatment of FSGS?

Back 250

FSGS is more common in adults and has an indolent presentation. Full nephrotic syndrome is rare with secondary etiologies (HIV, pamidronate). Treatment is ACEi/ARB and if nephrotic syndrome persists the give corticosteroids, cyclosporine, or mycophenolate mofetil. FSGS can recu with days to weeks of transplant

Front 251

How does the biopsy look different between FSGS and HIV-nephropathy?

Back 251

HIV causes a collapsing variant of FSGS, the sclerotic tuft is retracted with proliferation of podocyte foot processes, tubule segments cystically dilate, and tubuloreticular inclusions are found in endothelial cells

Front 252

What is the epidemiology, presentaiton, and treatment of HIV-associated nephropathy?

Back 252

HIV-associated nephropathy is more common in black than whites, is associated with APOL1 variants. It presents as nephrotic syndrome and is usually seen in uncontrolled HIV, but can precede AIDS. Treatment for HIVAN is highly active anti-retroviral therapy (HAART)

Front 253

What are the biopsy findings seen in membranous glomerulopathy?

Back 253

LM: diffuse capillary wall and GBM thickening, with spikes and holes seen on silver stain
IF: granular staining in GBM with IgG and C3
EM: foot process effacement and sub-epithelial immune deposits

Front 254

What is the pathogenesis of membranous glomerulopathy?

Back 254

In situ immune complexes form against various antigens activating complement and forming MAC which attacks glomerular epithelial and mesangial cells causing capillary wall injury and protein leakage

Front 255

What is the likely cause of primary membranous glomerulopathy and what are some secondary causes?

Back 255

M-type phospholipase A2 is the probable cause of primary membranous glomerulopathy. Secondary causes include solid tumor malignancies, infections (HBV, syphilis), lupus, or drugs (NSAIDs, captopril, penicillamine, gold)

Front 256

What is the epidemiology, presentation, and treatment for membranous glomerulopathy?

Back 256

Middle-aged white males present variably, either sudden onset proteinuria with nephrotic syndrome or a more subtle onset if it is a secondary cause. Age appropriate cancer screens should be done and conticosteroids given

Front 257

What are the biopsy findings in membranoproliferative GN type I?

Back 257

LM: endocapillary proliferation, "tram-track" appearance due to GBM splitting from mesangial infiltration, mesangial expansion/hypercellularity
* IF: granular staining in GBM and mesangium of IgG, C3, C1q, C4
EM: subendothelial immune complexes

Front 258

What is the pathogenesis of MPGN type I?

Back 258

Immune complex deposition in the subendothelial and mesangial compartments results in GBM alterations, endocapillary and mesangial proliferation, and leukocyte infiltration

Front 259

What are common secondary causes of MPGN type I?

Back 259

Infections (HCV, endocarditis), a1 antitrypsin deficiency, lupus, blood malignancies (CLL, lymphoma)

Front 260

What is the epidemiology, presentation, and treatment of MPGN type I?

Back 260

MPGN type I is rare and occurs equally in children and adults. It can present as nephritic or nephrotic. Treat the underlying cause and use corticosteroids and immunosuppressive agents. >50% will progress to ESRD

Front 261

What are the biopsy findings in MPGN type II?

Back 261

Dense deposit disease.
LM: endocapillary proliferation, "tram-track" appearance due to GBM splitting from mesangial infiltration, mesangial expansion/hypercellularity
* IF: granular or linear staining of C3 in GBM (but not deposits)
EM: irregular, ribbon-like, electron dense deposited material in the GBM

Front 262

What is the pathogenesis of dense deposit disease?

Back 262

MPGN type II is glomerular damage caused by an alternate complement pathway being constantly activated due to pathologic stabilization of C3 convertase. C3 nephritic factor (C3NeF) is a circulating antibody that binds and stabilizes C3 convertase. A genetic defect in factor H lessens the degradation of C3 convertase.

Front 263

What is the epidemiology, presentation, and treatment of dense deposit disease?

Back 263

Dense deposit disease is rare but occurs in young adults. It has a variable presentation either nephrotic syndrome with hematuria or insidious proteinuria. DDD is treated with eculizimab, plasmapheresis, and immunosuppression. >50% of MPGN type II will progress to ESRD

Front 264

What are the biopsy findings in diabetic nephropathy?

Back 264

* LM: afferent & efferent arteriolar hyalinosis, mesangial expansion, GBM thickening, and nodular glomerulosclerosis (Kimmelstein-Wilson nodules)
* IF: non-specific focal IgG
* EM: foot process effacement, GBM thickening

Front 265

What is the most common cause of ESRD in the US?

Back 265

Diabetic nephropathy

Front 266

What are the biopsy findings in amyloidosis?

Back 266

* LM: fluffy "coton candy" deposition in mesangium, apple-green appearance with Congo Red staining
* IF: usually negative
* EM: randomly arranged fibrils

Front 267

What is the pathogenesis of amyloidosis?

Back 267

Extracellular tissue deposition of protein fibrils in ß-pleated sheets.
* AL: plasma cell dyscrasias cause the deposition of light chain fragments
* AA: inflammation causes the deposition of serum amyloid A

Front 268

What quantifies as pre-hypertension?

Back 268

120-139/80-89

Front 269

What is a normal blood pressure?

Back 269

<120/80

Front 270

What is stage I hypertension?

Back 270

140-159/90-99

Front 271

What is stage II hyper tension?

Back 271

≥160/100

Front 272

What are some risk factors for benign hypertension?

Back 272

Obesity, alcohol (>2 drinks/day), african american, high salt intake (2.3 g/d), high fructose intake, type A personality

Front 273

What is the gross appearance of a kidney with Arterionephrosclerosis?

Back 273

Symmetrical, small, atrophic kidneys with diffuse, fine granularity on the surface. Cortical scarring and shrinking of renal tissue

Front 274

What are the vascular, glomerular, and interstitial changes seen in arterionephrosclerosis?

Back 274

* Chronic hypertension leads to medial hypertrophy and intimal thickening with vessel lumen narrowing. The walls of arterioles and small arteries thicken with the deposition of hyaline material. Vascular disease can cause secondary lesions by enhancing ischemic nephron loss
* Ischemic glomeruli exhibit global of focal segmental sclerosis, possibly mediated by low birth weight, reduced nephrhon number, and APOL1 variant in african americans
* Ischemic induced immune responses cause tubular atrophy with interstitial fibrosis

Front 275

What is the definition of a hypertensive emergency?

Back 275

Hypertensive emergencies are acute, life-threatening episodes of severe hypertension (>180/120 mmHg) with the presence of end organ damage.
* Cerebrovascular: encephalopathy, atherothrombotic infarction, hemorrhage
* Cardiac: dissection, LV failure, MI
* Renal: acute glomerulonephritis, renovascular hypertension, renal crisis from a collagen vascular disease
* Eclampsia

Front 276

What are two clinical syndromes that can result from severe HTN?

Back 276

* Accelerated malignant HTN: severe HTN with papilledema, retinal hemorrhage or exudates, and malignant renal nephrosclerosis
* Hypertensive encephalopathy: severe headache and altered mental status with signs of cerebral edema from hyperperfusion. Reversible with BP correction

Front 277

What is the definition of a hypertensive urgency?

Back 277

A hypertensive emergency is an asymptomatic episode of severe hypertension with a DBP >120 but no clinical evidence of end organ damage

Front 278

What is the mechanism of malignant hypertension?

Back 278

Malignant hypertension is a failure of autoregulation. It is a self-perpetuating cycle with increased ATII causing intrarenal vasoconstriction and renal ischemia, which in turn increases renin secretion. Small vessels become more permeable to fibrinogen and other plasma proteins resulting in endothelial damage, fibrinoid necrosis, and intimal smooth muscle hyperplasia

Front 279

What is the clinical picture for malignant hypertension within the main organ systems?

Back 279

* Cardiac: acute left ventricular failure, aortic dissection, or MI
* Cerebrovascular: hypertensive encephalopathy, intracerebral hemorrhage, subarachnoid hemorrhage, papilledema
* Renal: acute renal failure accompanied by rising creatinine, hematuria, and proteinuria
* Pulmonary: acute pulmonary edema

Front 280

What is the gross and microscopic appearance of a kidney with malignant hypertension?

Back 280

Kidneys with malignant hypertension will be normal sized with a "flea-bitten" appearance from pin point hemorrhagic spots. Under microscope, there will be fibrinoid necrosis, hyperplastic arterioles and glomerular sclerosis.

Front 281

What are lifestyle modifications recommended for BP management?

Back 281

Maintain a healthy body weight (BMI 20-25), limit salt intake (<2 g/d), exercise for 30 min 5 times a week, limit alcohol to 2 drinks/day for men and 1 drink/day for women

Front 282

What are BP recommendations for patients with CKD with and without diabetes?

Back 282

* ≤140/≤90 if urine albumin is <30 mg/d
* ≤130/≤80 if urine albumin is >30 mg/d and treat with ACEi/ARB

Front 283

What is the BP recommendation for a patient with a kidney transplant?

Back 283

≤130/80

Front 284

What is the BP recommendation for children with CKD?

Back 284

Start treatment if BP is above the 90th percentile for age, sex, height and lower to the 50th percentile using an ACEi/ARB

Front 285

How does renal denervation work?

Back 285

Renal denervation reduces the pathologic central sympathetic drive to the kidney and the renal contribution to central sympathetic hyperactivity by delivering low-power radiofrequency energy to deactivate the renal nerves

Front 286

How does renal denervation improve the management of BP?

Back 286

Renal denervation reduces norepinephrine spillover, causes natriuresis, increases renal blood flow lowering plasma renin activity, and decreasing renal afferent signaling ance central sympathetic activation

Front 287

What are the microscopy findings in minimal change disease?

Back 287

LM: normal
IF: no deposits
EM: foot process effacement with microvillous transformation of podocytes

Front 288

What type of material makes up the deposition in FSGS?

Back 288

Hyaline material deposits

Front 289

What are the main findings in membranous glomerulonephropathy?

Back 289

Diffuse capillary wall thickening without inflammation. Spikes and holes seen with silver stain. Subepithelial deposits

Front 290

What are primary and secondary causes of membranous GN?

Back 290

* Primary lesions are from auto-antibodies to M-type Phospholipase A2 receptors
* Secondary causes include HBV, solid malignancies, penicillamine, gold salts, syphilis, sjogren's

Front 291

What glomerulonephropathy exhibits a "tram-track appearance under LM and what is it from?

Back 291

Circumferential mesangial interposition is responsible for the tram-track appearance of MPGN type I. It also has subendothelial and mesangial deposits

Front 292

What glomerulonephropathy exhibits a ribbon-like appearance under LM?

Back 292

MPGN type II

Front 293

Are subendothelial or subepithelial deposits more dangerous and why?

Back 293

Subendothelial deposits are more dangerous because they have closer contact with inflammatory cascade components un blood and are more likely to initiate inflammation

Front 294

What is the most common form of GN in the US?

Back 294

IgA nephropathy (Berger's disease)

Front 295

What is the systemic form of Berger's disease?

Back 295

Henoch-Schönlein purpura. Associated with gut, skin, joint, and renal manifestations

Front 296

What is the clinical picture of IgA nephropathy?

Back 296

Synpharyngitic gross hematuria in adolescent boys and young men with baseline microscopic hematuria

Front 297

What genes are responsible for the different inheritance patterns of hereditary nephritis?

Back 297

X-linked Alport's syndrome is from a-5 subunit of type IV collagen. Autosomal recessive Alport's is from either a-3 or a-4 subunits.

Front 298

What is the EM appearance of hereditary nephritis?

Back 298

Alport's syndrome has a frayed and lamellated glomerular basement membrane with a "basket-weave" appearance.

Front 299

What is the clinical presentation of Goodpasture's syndrome?

Back 299

Respiratory insufficiency, hemoptysis, and acute renal failure

Front 300

How are crescents formed?

Back 300

Severe glomerular injury disrupts the GBM allowing the spillage of fibrin degradation products which are mitogenic for parietal epithelial cells and chemotactic for leukocytes leading to crescent formation

Front 301

What is the hallmark of pauci-immune GNs?

Back 301

Necrotizing glomerulonephritis is the hallmark of ANCA-associated GNs

Front 302

What is the new name for pANCA and what does it target?

Back 302

pANCA is now called MPO-ANCA and it targets myeloperoxidase

Front 303

What is the new name for cANCA and what does it target?

Back 303

cANCA is now called PR3-ANCA and it targets proteinase 3

Front 304

What are the six stages of lupus nephritis?

Back 304

Minimal mesangial, mesangial proliferative, focal, diffuse, membranous, and advanced sclerosing

Front 305

What are the four key changes seen in stages III and IV of lupus nephritis?

Back 305

Tuft necrosis (focal or global), subendothelial deposits, crescents, hyaline thrombi

Front 306

What causes hyaline thrombi?

Back 306

Hyaline thrombi are bright, eosinophilic, homogenous bodies in the capillary lumen that are formed by the presence of cryoglobulin aggregates

Front 307

When do you see a full house profile?

Back 307

In stages III and IV of lupus nephritis

Front 308

What is meant by a wire loop lesion?

Back 308

Wire loop lesions refer to localized thickening of the capillary wall due to massive subendothelial immune complex deposits

Front 309

What are tubuloreticular inclusions and what disease are they associated with?

Back 309

Tubuloreticular inclusions are modifications in the endoplasmic reticulum from elevations in circulating interferon levels. They can be seen in all stages of lupus nephritis and HIVAN

Front 310

Kimmelstein-Wilson nodules are found in what GN?

Back 310

Diabetic nephropathy

Front 311

What are four changes seen under LM in HIVAN?

Back 311

HIV-associated nephropathy is a variant of FSGS characterized by:
* Global collapse of glomerular tufts with architecture preservation
* Podocyte hypertrophy/hyperplasia with large vacuoles containing protein reabsorption droplets
* Endothelial tubuloreticular inclusions
* Patchy clusters of cystically dilated tubules

Front 312

Deposits of what GN are stained by Congo Red stain?

Back 312

Amyloid material deposits in amyloidosis stain positive with Congo Red stain

Front 313

How does the LM biopsy look different in myeloma cast nephropathy and HIVAN?

Back 313

In myeloma cast nephropathy the casts in the dilated tubules appear fractured, like they are in the process of breaking apart

Front 314

Who is at highest risk for developing kidney stones?

Back 314

Middle aged, sedentary, white males that eat an american (high protein) diet and live in the stone belt

Front 315

How does water influence kidney stone production?

Back 315

Increasing water consumption increases urine volume which osmotically increases the excretion of stone constituents

Front 316

What are some common inhibitors and how do they stop kidney stone production?

Back 316

Citrate, magnesium, glycosaminoglycans, and chondroitin sulfate are common inhibitors that complex with stone constituents, increasing their solubility, and covering sites of future crystal growth

Front 317

What are some factors that increase urine calcium?

Back 317

Idiopathic, hyperparathyroidism, antacids, vitamin A or D intoxication, distal RTA, or sarcoidosis

Front 318

How does a low calcium diet affect stone formation risk?

Back 318

A low calcium diet increases the risk of stone formation. The higher the dietary calcium, the more oxalate is bound and excreted via the GI tract. If there isn't enough calcium to bind oxalate in the GI tract, oxalate is absorbed into the blood stream and is excreted into the urine where it is a strong promoter of kidney formation

Front 319

What are the factors that predict calcium calculi formation?

Back 319

* Urine volume and concentration of calcium and oxalate
* pH: acidic urine promotes calcium calculi, basic urine promotes calcium phosphate excretion
* Uric acid is a promoter
* Citrate and magnesium are inhibitors

Front 320

What are 2 factors that affect citrate concentrations in the urine?

Back 320

Acidic environments (increased protein consumption) and hypokalemia favor citrate reabsorption

Front 321

What are the results of a high protein diet?

Back 321

Increases urine acid, sodium, and uric acid excretion, decreases citrate excretion, and increases cholesterol content, and decreases potassium content

Front 322

Is a low calcium or low protein diet more associated with stone formation?

Back 322

A low calcium diet is associated with a higher rate of stone formation than a low protein diet

Front 323

Name three risk factors of uric acid stone production and explain which one is most important.

Back 323

Decreased urine volume, increased uric acid production, and low urinary pH are the main risk factors of uric acid stone production and low urine pH is the most important. As pH decreases, sodium urate dissociates and uric acid is much much less soluble than sodium urate.

Front 324

How does fructose promote stone formation?

Back 324

Fructose increases urinary oxalate excretion and plasma and uric acid levels, all of which increase the rate of stone production. Also important in obesity and gout.

Front 325

What compound can be given to combat cysteine stone formation?

Back 325

Thiola is a compound that binds cysteine allowing it to be excreted, limiting cystine stone formation

Front 326

What are some treatment options to remove kidney stones?

Back 326

Endoscopic or open procedures, stent placements, lithotripsy (an externally applied, focused, high-intensity pulse of ultrasonic energy to cause stone fragmentation

Front 327

What are indications for stone removal?

Back 327

Stones should be removed if they are infected, causing an obstruction, or are painful

Front 328

What is the best way to diagnose a kidney stone?

Back 328

High resolution CT without contrast. Ultrasound will identify most stones in the renal pelvis. Abdominal xray will identify 80% of stones

Front 329

What are some recommendations for preventing stone formation?

Back 329

INCREASE FLUID INTAKE. Encourage a healthier diet of low sodium and protein

Front 330

What medical therapy is used to treat stones?

Back 330

* Thiazide diuretics increase proximal tubule calcium reabsorption
* Allopurinol decreases urinary uric acid

Front 331

What is the most common infection encountered in the outpatient setting?

Back 331

UTIs

Front 332

What makes for a complicated UTI?

Back 332

Complicated UTIs are when there are anatomic, functional, or pharmacologic factors that predispose the patient to persistent infection, recurrent infection, or treatment failure

Front 333

What are some bacterial factors that contribute to the pathogenesis of UTIs?

Back 333

* Increased bacterial adherence to uroepithelial cells by type 1 (mannose-sensitive) or P fimbriae (mannose-resistant)
* Resistance to serum -cidal activity
* Hemolysin production (an important cell toxin in pyelonephritis)
* The ability to synthesize essential amino acids not present in their environment
* Urease production (used by proteus mirabilis in pyelonephritis and urolithiasis)
* Bacterial motility to ascend against urine flow
* Endotoxin production to decrease ureteral peristalsis

Front 334

What types of fimbriae does E-coli have?

Back 334

* Type I fimbriae is mannose-sensitive. Type I fimbriae bind to mannosylated proteins on uroepithelial cell but can be detached by exposure to mannose. They give E. coli a tropism for the bladder (cystitis)
* P fimbriae is mannose-resistant. P fimbriae adhere to glycophospholipids in the outer plasma membrane of uroepithelial cells. They give E. coli a tropism for the upper urinary tract (pyelonephritis)
* TMP-SMX reduces fimbriae synthesis and expression

Front 335

What are two factors that would pre-dispose an E. coli strain to colonize the upper urinary tract causing pyelonephritis?

Back 335

P fimbriae and hemolysin production make E. coli more likely to cause pyelonephritis

Front 336

What are some host factors that prevent UTIs?

Back 336

Urine flow flushes out the urinary tract, urine urea and low pH inhibit bacterial growth, and the length of the urethra limits bacterial availability to areas of infection

Front 337

What are some host factors that could contribute to UTIs?

Back 337

* Obstruction or reflux: urethral stenosis, kidney stones, polycystic kidney disease, spinal cord injury causing incomplete bladder emptying, BPH, pregnancy
* For women, the short urethra and bacterial colonization of the vagina
* Sexual intercourse: facilitates bacterial movement to the bladder, can traumatize the urethra, and spermicides can limit healthy bacterial colonization
* Bladder catheterization bypasses the urethra altogether
* Renal medulla susceptibility: high ammonia concentrations inactivate complement and the high osmolarity inhibits PMN migration

Front 338

What are the common pathogens implicated in community-acquired vs. nosocomial UTIs?

Back 338

* Community-acquired: E. coli, Klebsiella, Proteus
* Nosocomial: E. coli, Proteus (pseudomonas and candida possible)

Front 339

What species of Staph are important to consider in UTIs?

Back 339

Staph saprophyticus is common in young, sexually active females. Staph epidermidis can be considered nosocomially

Front 340

How do cystitis and pyelonephritis manifest differently?

Back 340

* Cystitis: dysuria, frequency, urgency, suprapubic pain
* Pyelonephritis: fever, chills, flank pain (costovertebral angle tenderness), nausea, vomiting, hypotension, tachycardia, ± cystitis symptoms

Front 341

What is asymptomatic bacteriuria and when would you treat it?

Back 341

Asymptomatic bacteriuria is bacteria in the urine (≥10^5 cfu/mL) with NO symptoms. It should only be treated if the patient is pregnant or if they are undergoing a urologic procedure in which bleeding is anticipated

Front 342

How does urethritis present and what are some common causes of it?

Back 342

Urethritis presents as burning on urination without frequency or urgency. Colony counts will be lower. Chlamydia trachomatous and Neisseria gonorrhoeae will produce purulent discharge. Ureaplasma urealyticum or noninfectious (trauma, allergy, chemical)

Front 343

How does prostatitis present and how is it treated?

Back 343

* Prostatitis will present with fever, chills, dysuria, and urinary frequency. Moderate tenderness of suprapubic region and a rectal exam will show an exquisitely tender and diffusely enlarged prostate. Bladder outlet obstruction can develop.
* Needs prolonged antibiotic therapy (4-6 weeks) due to lack of antibiotic penetration. Prostatic massage is contraindicated

Front 344

How are UTIs diagnosed?

Back 344

UTI diagnoses require symptoms plus pyuria (>10 WBC/hpf) detected by dipstick or urinalysis. Sometimes WBC casts are seen in pyelonephritis

Front 345

When should a gram stain be performed with a patient with a UTI?

Back 345

Urine gram stains should be performed if a pyelonephritis UTI is suspected

Front 346

When should a urine culture be performed for a patient with a UTI?

Back 346

Urine cultures should be performed in all UTI cases except young, sexually active women with suspected cystitis. Perform in cases of reccurent UTI, pyelonephritis, and catheter-associated urinary tract infection

Front 347

When should anatomical investigations be performed in a patient with a UTI?

Back 347

* All upper tract diseases
* Relapse or failure to improve after appropriate antibiotic therapy
* Preschool girls after their second UTI
* UTIs in males of any age

Front 348

What is the treatment of uncomplicated cystitis?

Back 348

* Short course therapy (3-5 days) of nitrofuratoin, trimethroprim-sulfamethoxazole (TMP-SMX), and ciprofloxacin
* ß-lactams are an alternative (3-7 days) of amoxicillin-clavulanate, cefdinir, and cefaclor

Front 349

When are short course antibiotic therapies inappropriate for UTIs?

Back 349

In males, pyelonephritis, recurrent or relapsing symptoms, and if the symptoms last more than 7 days

Front 350

What is the treatment for pyelonephritis?

Back 350

Get urine culture and tested for susceptibility and adjust antibiotics based on the results.
* 7-14 days of IV ceftriaxone
* If patient can handle PO, ciprofloxacin, or TMP-SMX

Front 351

What are some ways to prevent UTIs?

Back 351

* Sexually active women should void immediately after intercourse
* Post-coital prophylaxis (TMP-SMX or nitrofurantoin) can be considered in recurrent UTIs
* Cranberry juice or concentrated tablets can prevent cystitis
* In elderly women with atrophic vaginitis intravaginal estrogen can prevent cystitis

Front 352

What is the differential diagnosis for urinary tract obstruction?

Back 352

Congenital (ureteropelvic junction obstruction, posterior urethral valves), ureteral strictures, stones, retroperitoneal fibrosis, extrinsic compression, BPH, urethral strictures, bladder dysfuntion

Front 353

What is the key ultrasound or CT finding that suggests upper urinary tract obstruction?

Back 353

Hydronephrosis

Front 354

What physical exam finding suggests a lower urinary tract obstruction?

Back 354

A distended bladder

Front 355

What are some of the signs and symptoms seen in urinary tract obstruction?

Back 355

Flank or suprapubic pain, UTI, urinary incontinence, anuria. Can present nonspecifically and be found incidentally

Front 356

What is the calculation for GFR using the different pressures involved?

Back 356

GFR = Kf (Pgc-Pt-πgc)

Front 357

Describe the three phases of change in unilateral ureteral obstruction

Back 357

When there is an obstruction, you want to first increase blood flow to try and flush it out. Once the kidney sees that isn't working it stops giving that area blood flow and eventually tubular pressure decreases
* First phase (hrs 1-2): Tubular pressure rises from the backflow from the obstruction. Renal blood flow increases as fluid is not able to be filtered to the glomerulus
* Second phase (hrs 3-4): The renal blood flow starts to decrease and is shifted to the inner cortex where there is the highest metabolic demand
* Third phase (after 5 hrs): renal blood flow continues to fall and tubular pressure starts to decrease

Front 358

What are the two differing mechanisms causing GFR decline in unilateral ureteral obstruction?

Back 358

* In the first phase, GFR decreases because tubular pressure is high, but this is offset somewhat by PGE2 and NO causing afferent vasodilation in an attempt to flush out the obstruction
* In later phases, the kidneys attempt to reduce glomerular pressure by vasoconstricting the afferent arteriole, decreasing renal blood flow and lowering GFR

Front 359

What direction does blood flow in unilateral and bilateral ureteral obstruction?

Back 359

In unilateral, blood flows from the outer cortex to the inner cortex. In bilateral obstruction, blood flows from the inner cortex to the outer cortex. (To stay BUOyant, water must go from IN the boat to OUT of the boat)

Front 360

How does the kidney's response differ in bilateral ureteral obstruction from UUO?

Back 360

* In BUO, the ureteral pressures are much higher than in UUO (when the other kidney can excrete the extra fluid) and no escape route means these increased ureteral pressure persist longer, generating a larger fluid backup.
* This fluid backup stimulates ANP to afferently vasodilate and efferently vasoconstrict in an attempt to flush out the obstruction.
* This results in very little renal blood flow rise and a much more profound collapse of RBF.

Front 361

How does the timing of vasoconstriction and vasodilation differ between UUO and BUO?

Back 361

* In unilateral ureteral obstruction there is early dilation via PG and NO (resulting in increased RBF), followed by prolonged vasocontriction and normalized tubular pressure (Once the kidney realized perfusing that area is futile.
* In bilateral ureteral obstruction there is very little early dilation and more profound vasoconstriction (in an attempt to increase GFR). Due to fluid backup, there is profound post-obstructive diuresis.

Front 362

Explain the mechanism and treatment of post-obstructive diuresis

Back 362

* During bilateral ureteral obstruction there is marked volume expansion and urea buildup. When the obstruction is removed, increased ANP production downregulates Na+ transporters and aquaporin channels resulting in profound fluid loss (200mL/hr or greater).
* Assess risk pre-removal (edema, HTN, CHF, >1L in bladder), follow vitals and urine output, and replace fluid and electrolytes as necessary

Front 363

What are some negatives about IV urogram?

Back 363

Require radiation and contrast media which can be nephrotoxic, is slow, and has limited resolution compared to newer techniques like CT, ultrasound, MR

Front 364

What is renal ultrasound good for?

Back 364

Good for an acute renal insufficiency work-up and for differentiating solid and cystic masses. It is less accurate than CT for detecting masses and stones.

Front 365

What is the best imaging test for renal masses?

Back 365

CT is the best imaging tool for renal masses and cancer staging

Front 366

What imaging test is best to diagnose kidney stones?

Back 366

CT is the best test for diagnosing kidney stones

Front 367

What imaging test is best for evaluating hematuria?

Back 367

CT is best for evaluating hematuria

Front 368

When is a renal MRI indicated?

Back 368

For evaluating renal tumors or imaging renal blood vessels in patients who can't get CT contrast media

Front 369

What is the general description and natural history of ADPKD?

Back 369

Autosomal dominant polycystic kidney disease is characterized by expanding cysts that ultimately destroy the renal parenchyma and cause renal failure. Serum creatinine levels generally rise after the 4th decade of life and 50% of patients develop ESRD

Front 370

What are the two genes implicated in ADPKD?

Back 370

Autosomal dominant polycystic kidney disease is caused by variants of the PKD gene on chromosome 16 or 4.
* ADPKD type 1 is caused by PKD1 on chromosome 16 creating polycystin-1. This variation accounts for majority of ADPKD in whites and is severe disease due to the development of more cysts at an early age. ESRD by 54.
* ADPKD type 2 is caused by PKD2 on chromosome 4 creating polycystin-2. ESRD by 74

Front 371

How do PKD1/PKD2 cause ADPKD?

Back 371

PKD1 and PKD2 code for the proteins PC1 and PC2 which are flow sensors on the primary cilium of tubules. Normally these proteins sense tubular urine flow and trigger Ca2+ release from the ER, which inhibits the production of cAMP. PC1 and PC2 do not function properly, resulting in decreased Ca2+ and an increase in cAMP production. Increased cAMP activates cell proliferation (via mTOR), Cl- excretion (via CFTR), and intraluminal fluid (via AQP-2)

Front 372

What are potential renal complications of ADPKD?

Back 372

Hypertension, gross hematuria, cystic rupture or bleed, UTI or cyst infection, nephrolithiasis. Renal failure by 60 in 50% of PKD1 (15-20 years earlier than PDK2)

Front 373

What are some extra-renal manifestations of ADPKD?

Back 373

Autosomal dominant polycystic kidney disease can cause cysts in other organs as well.
* Liver: polycystic liver disease, pancreatic cysts
* Intestines: umbilical or inguinal hernias, colonic diverticula
* Heart: mitral valve prolapse, valvular regurgitation, thoracic or coronary aneurysm
* Cerebral: berry or intracranial aneurysm

Front 374

How is ADPKD diagnosed?

Back 374

Autosomal dominant polycystic kidney disease is diagnosed with imaging.
* <40: ≥3 cysts total
* 40-60: ≥4 cysts
* >60: ≥4 cysts in each kidney
If no cysts by 40, no ADPKD. If 30-39 with no cysts, 2% false negative. If younger than 30 with no cysts, no exclusion possible

Front 375

When is cerebral aneurysm screening indicated in patients with ADPKD?

Back 375

Cerebral aneurysm screening is indicated in autosomal dominant polycystic kidney disease patients with positive family history of ICH or cerebral aneurysm, if the patient exhibits warning symptoms, is in a high risk occupation, is planning an upcoming surgery (especially if they are hemodynamically unstable or have HTN), or if the patient needs to be started on anticoagulation

Front 376

What is the management of ADPKD?

Back 376

* Octreotide (somatostatin agonist inhibiting cAMP production), mTOR inhibitors (Sirolimus or Everolimus limit cell proliferation), and Tolvaptan (V2 receptor antagonist block intracellular fluid intake)
* Educate the patient on complications and ESRD progression risks
* Encourage high fluid intake to minimize ADH and decrease cAMP levels
* Control BP with ACEi/ARB
* Treat UTIs early
* Manage cysts and nephrolithiases
* Screen for cerebral aneurysm

Front 377

What kidney disease is octreotide used to treat and what is its mechanism of action?

Back 377

Octreotide is used to treat autosomal dominant polycystic kidney disease and it works as a somatostatin receptor agonist, inhibiting cAMP production

Front 378

What kidney disease are sirolimus and everolimus used to treat and what is their mechanism of action?

Back 378

Sirolimus and everolimus are mTOR antagonists used to treat autosomal dominant polycystic kidney disease. They block cell proliferation

Front 379

What kidney disease is tolvaptan used to treat and what is its mechanism of action?

Back 379

Tolvaptan is a vasopressin-2 receptor blocker used to treat autosomal dominant polycystic kidney disease by limiting the intracellular movement of water

Front 380

What gene/protein is implicated in ARPKD and what gross change does it cause?

Back 380

Autosomal recessive polycystic kidney disease is characterized by dilated collecting ducts that extend through the cortex. These dilatations are caused by a mutation in PKHD1 which codes for fibrocystin

Front 381

How is ARPKD diagnosed and managed?

Back 381

* Autosomal recessive polycystic kidney disease is found at the fetal ultrasound to evaluate kidneys and amniotic fluid in the 16 or 20th week. Potter's phenotype results in neonatal death (30-50%) but milder phenotypes manifest in the first few years of life. Genetic testing identifies 85%
* Manage BP, portal hypertension, and prepare for dialysis/transplant

Front 382

How is tuberous sclerosis characterized? What is the inheritance pattern and genes implicated?

Back 382

Tuberous sclerosis is an autosomal dominant progressive disorder characterized by the development of benign tumors in multiple organs (brain, heart, skin, eyes, kidney, lung, and liver) and an increased risk of malignancy. It is caused by a mutation in TSC1 (hamartin protein) or TSC2 (tuberin protein)

Front 383

What are the clinical manifestations of tuberous sclerosis?

Back 383

Development of benign tumors in multiple organs.
* CNS: seizures in infancy. Mental retardations, cognitive deficits and learning disabilities, or autism. Glioneuronal hamartomas.
* Skin lesions: hypopigmented macules, facial angiofibroma
* Cardiac: rhabdomyoma
* Hamartomas in kidneys, brain, retina, heart, lungs, and skin
* Renal cysts and angiomyolipomas are highly suggestive

Front 384

How is tuberous sclerosis managed?

Back 384

Lots of monitoring. Fundoscopic, ECG, MRIs. Brain and abdominal imaging every 1-3 years, periodic dermatologic evaluation. Genetic counseling.
* Sirolimus, an mTOR inhibitor is approved

Front 385

What is Von Hippel-Lindau? What is its inheritance pattern, and how is it diagnosed and managed?

Back 385

Von Hippel-Lindau is an autosomal dominant loss of function of the VHL tumor suppressor gene resulting in vascular-rich tumors of the eyes, cerebellum, spinal cord, adrenal glands, pancreas, epididymis as well as renal and pancreatic cysts.
* Common tumors are retinal angiomas, hemangioblastomas of the brain and spine, renal cell carcinomas, pheochromocytomas
* Presence of VHL-associated tumor in at risk patient is enough for diagnosis. Patients should be monitored yearly

Front 386

What is medullary cystic kidney disease, what genes are implicated and what is seen on imaging and biopsy?

Back 386

* Medullary cystic kidney disease is an autosomal dominant disease that presents as gout at an early age, polyuria, and a bland urine sediment. It can progress to ESRD between 30-60.
* It is caused by mutations in UMOD (coding for Tamm-Horsfall protein; aka uromodulin), REN, or an unidentified gene in chromosome 1q21
* Imaging of patients with 1q21 mutation will have cysts (40%), no cysts with UMOD or REN mutation. Biopsy will show tubulointerstitial fibrosis

Front 387

What is the definition of chronic kidney disease?

Back 387

Chronic kidney disease is kidney disease for longer than 3 months.
* GFR <60 mL/min
* Structural or functional abnormalities of the kidney with or without decreased GFR (pathological abnormalities or markers of kidney damage, such as abnormalities in blood or urine or imaging)

Front 388

How is CKD staged?

Back 388

* Stage I: GFR≥90
* Stage II: 60≤GFR<90
* Stage III: 30≤GFR<60
* Stage IV: 15≤GFR<30
* Stage V: GFR<15

Front 389

The rate of decline in renal function best correlates with the progression of what pathologic process and what is the mechanism of the pathology?

Back 389

Renal function decline best correlates with the degree of tubulointerstitial fibrosis. Tubulointerstitial fibrosis is caused by ischemia of tubules (from being downstream of sclerosed glomeruli) causing acute and chronic inflammation of the tubular interstitium, which leads to damage or loss of the peritubular capillaries. Proteinuria causes direct tubule epithelium damage

Front 390

What are ways to slow the progression of CKD?

Back 390

Treat the underlying cause, keep blood pressure <130/80 (ACEi/ARB), initiate a statin therapy, smoking cessation

Front 391

What are some complications associated with CKD?

Back 391

Hypertension, proteinuria, hyperkalemia, metabolic acidosis, cardiovascular, mineral bone disease, anemia of CKD, endocrine, uremia

Front 392

What is the preferred hypertension pharmacologies for CKD patients?

Back 392

Goal is <130/80
* 1st line: ACEi/ARB
* 2nd line: thiazide if GFR >40 mL/min, loop is GFR<40 mL/min
* 3rd line: look for compelling indications, calcium channel blocker

Front 393

What is the pharmacological treatment for proteinuria in CKD patients?

Back 393

ACEi/ARB, direct renin inhibitors, aldosterone blockade, NDHP CCBs

Front 394

What is the treatment for anemia of CKD patients?

Back 394

Erythropoiesis stimulating agents (Hg 10-12), iron supplementation

Front 395

What are some endocrine complications of CKD?

Back 395

Hypogonadism, increased gonadotropin and prolactin, erectile dysfunction, decreased libido, menstrual irregularity, anovulation and amenorrhea

Front 396

What causes uremia and what are its signs and symptoms?

Back 396

Uremia is caused by azotemia, or an accumulation of uremic, nitrogen-based toxins.
* Fatigue, pruritus, dysgeusia, anorexia, nausea, vomiting, restless legs, irritability, sleep disturbances
* Serositis, pericarditis, asterixis, sallow skin tone, weight loss, platelet dysfunction, peripheral neuropathy

Front 397

How does the kidney change as we age?

Back 397

* Anatomically: bladder size decreases, vaginal and urethral tissue atrophy, BPH, urinary incontinence
* Physiology: normal GFR loss, muscle mass declines maintaining serum creatinine, kidney mass and blood flow both decrease
* Sodium is conserved and excreted at night, nocturia
* Urine concentrating and diluting capacities are diminished

Front 398

What are some indications for starting a CKD patient on dialysis?

Back 398

Symptoms of uremia (nausea, vomiting, weight loss), hyperkalemia, volume overload, uremic pericarditis, bleeding from platlet dysfunction

Front 399

Who gets kidney failure?

Back 399

The elderly, african americans, diabetics, patients with a family history for ESRD, with multiple comorbidities, or with a failed transplant

Front 400

What are the 4 treatment options for patients with ESRD?

Back 400

* Conservative therapy: death from uremia
* Transplantation: living, related, or deceased
* Hemodialysis: at home or in a center
* Peritoneal dialysis

Front 401

What are some contraindications for hemodialysis?

Back 401

Lack of access, fresh intracranial bleed, hemodynamic instability, GI bleed

Front 402

What is the typical treatment to hemodialysis?

Back 402

3-4 hours 3 times a week

Front 403

What are some contraindications for peritoneal dialysis?

Back 403

If patients won't learn or the home, partner, or abdomen is unusable. If they have a large body weight, a fresh intraabdmonial graft, or an ostomy

Front 404

What is the blood supply and membrane used in peritoneal dialysis?

Back 404

The membrane used is the peritoneum and the mesothelial cells capillaries. The blood supply comes from the mesenteric vessels

Front 405

What are the Wake Forest goals for dialysis modality selection?

Back 405

Have patients get involved and attend learning sessions. Let them try home therapy if they want and limit MD decisions unless medically indicated

Front 406

What are the two mechanisms by which solutes are removed from the blood and added to the dialysate?

Back 406

Solutes move from the blood to the dialysate via diffusion or convection

Front 407

How does the dialysis removal of small molecules differ from medium sized molecules?

Back 407

Small solutes are readily removed by diffusion, so their removal can be enhanced by increasing time per treatment, dialysate flow, blood flow, or a different dialyzer. Larger molecules rely on ultrafiltration transmembrane pressure difference for removal.

Front 408

Does increasing ultrafiltration rates improve the removal of small or middle molecular weight molecules more?

Back 408

Increasing ultrafiltration rates has a bigger impact on the removal of middle molecular weight molecules which rely on transmembrane pressures

Front 409

What are some dialysis associated morbidities?

Back 409

* Hemodialysis: thrombosis, clot, infection, acquired amyloidosis
* Peritoneal: infections, membrane failure
* Both: cardiovascular problems, bone disease

Front 410

What are some contraindications for kidney transplant?

Back 410

Severe CVD, recent malignancy, active infection, obesity, poor functional status, uncontrolled psychiatric disease, active substance abuse, non-adherence to medical regimen, lack of social support or financial resources

Front 411

When should a patient be placed on the kidney transplant list?

Back 411

When their eGFR<20

Front 412

What are the four categories of deceased kidney donors?

Back 412

* SCD: standard criteria donor, >18 and <65, healthy and willing. No proteinuria, reduced kidney function, diabetes, or hypertension
* ECD: expanded criteria donor, >60 or 50-60 with 2+ (CVA as cause of death, terminal creatinine >1.5, history of hypertension)
* DCD: death after cardiac death
* CDC high risk:

Front 413

How are HLAs inherited?

Back 413

Everyone has 6 HLAs, 3 from each parent which are inherited as a haplotype. This means siblings have a 25% chance of being no match or perfect match and 50% chance of being a partial match

Front 414

In what circumstances are HLA antibodies generated?

Back 414

HLA antibodies are made in response to blood transfusions, pregnancy, and tissue transplants

Front 415

What is the mechanistic difference between the direct and indirect pathways of allorecognition?

Back 415

* Direct pathway: donor APCs present peptides to recipient T-cells eliciting a cytotoxic and B-cell antibody response
* Indirect pathway: recipient APCs present donor peptides to recipient T-cells eliciting cytokine and delayed hypersensitivity responses

Front 416

What is the main target site of cytotoxic T cells in cellular rejection of kidney transplants?

Back 416

The proximal tubule causing tubulitis

Front 417

What are the 3 signals used to elicit a T-cell immune response?

Back 417

* Signal 1: APC recognizing the peptide and T-cell receptor
* Signal 2: CD80 binding CD28 and CD40 binding CD154, holding the 2 cells together and up-regulating the response
* Signal 3: IL-2 generated during the response binding its receptor on the T-cell and perpetuating the immune response

Front 418

What are the induction pharmacotherapy options for transplants?

Back 418

* Lymphocyte depleting: very potent. polyclonal (thymoglobulin) or monoclonal (alemtuzumab or muromonab)
* Non-lymphocyte depleting: well tolerated. IL-2 receptor antagonists (basiliximab or daclizumab)

Front 419

What is the mechanism and indications of thymoglobulin? What are is possible side effects?

Back 419

* Thymoglobulin is a depletes T-cells by complement-dependent lysis, apoptosis, and/or antibody-dependent cell-mediated cytotoxicity.
* It is indicated in transplant induction and anti-rejection therapy
* Thymoglobulin can cause infusion-related reactions. Fever, chills, anaphylaxis including hypotension and respiratory distress. Prevent by pre-medicating with corticosteroids, acetaminophen, and diphenhydramine, or slowing the reaction rate
* It can also cause thrombocytopenia, neutropenia, and increases risk of infection in the following months

Front 420

What is the mechanism, indication, and side effect of alemtuzumab?

Back 420

Alemtuzumab is a monoclonal antibody targeting CD52 antigen present on all lymphocytes (B and T-cells). It can cause an infusion reaction (fever, chills, hypotension, bronchospasm), bone marrow suppression, lymphoma, and increased risk of infection

Front 421

What is the mechanism of basilixumab and dalizumab, what is their indication and what are their side effects?

Back 421

Basilixumab and daclizumab are CD25 (IL-2) receptor antagonists. They block signal 3 of the antigen-t-cell immune response. They are indicated as prophylaxis for acute rejection in lower immunologic risk patients. They are well-tolerated and don't require pre-medication

Front 422

What is the maintenance pharmalogical therapy for kidney transplants?

Back 422

* Calcineurin inhibitors (tacrolimus, cyclosporine), mTOR inhibitors (sirolimus, everolimus), anti-proliferative agents (azathioprine, mycophenolic acid), corticosteroids, belatacept (blocks T-cell co-stimulation signals)

Front 423

What is the mechanism of action for tacrolimus and cyclosporine, what is their indication, and what are their adverse reactions?

Back 423

* Tacrolimus and cyclosporine are calcineurin inhibitors indicated in kidney transplant maintenance. They block part of the intracellular transduction of signal 1, limiting IL-2 production
* They both are nephrotoxic, cause hypertension, dyslipidemia, hyperglycemia, headaches, and tremors. Cyclosporine also causes gingival hyperplasia and hirsutism. Tacrolimus causes alopecia.
* They are metabolized via cytochrome p450 and have a number of drug interactions that lower and raise the effectiveness

Front 424

What is the mechanism of action for azathioprine and mycophenolic acid, what is their indication, and what are their adverse reactions?

Back 424

Azathioprine and MMF are anti-proliferative agents that inhibit de novo purine synthesis, blocking B and T-cell proliferation. They are indicated in kidney transplant maintenance. MMF causes diarrhea, leukopenia, and anemia. Azathioprine causes bone marrow suppression and pancreatitis

Front 425

What is a major drug interaction with azathioprine?

Back 425

Allopurinol and azathioprine should not be co-administered. Azathioprine is metabolized to an active 6-MP and then inactivated by xanthine oxidase. Allopurinol inhibits xanthine oxidase so co-administration results in increased levels of 6-MP

Front 426

What is the mechanism of action for sirolimus and what are its adverse reactions?

Back 426

Sirolimus is an mTOR receptor antagonist, blocking the propogation IL-2 responses. Its adverse reactions are anemia, leukopenia, thrombocytopenia, delayed wound healing, lyphocele formation, increased cholesteol and triglycerides, proteinuria, edema, and pneumonitis

Front 427

What is the mechanism of action for corticosteroids and what are some side effects?

Back 427

* Corticosteroids block cytokine and cytokine receptor expression from T-cells and APC blocking cytokine generation
* Acne, CNS effects, GI ulcers, HTN, increased appetite, hyperlipidemia, impaired wound healing, impaired growth, myopathy, hyperglycemia, sodium and water retention, cataracts, osteoporosis, increased infection risk

Front 428

What are benefits and risks of steroid withdrawl?

Back 428

* Benefits: decreased long-term intoxicity via cardiovascular risk, HTN, hyperlipidemia, glucose intolerance, weight gain, growth retardation, bone loss

Front 429

What findings are suggestive and confirmatory for acute interstitial nephritis?

Back 429

Eosinophils suggest acute drug-induced tubulointerstitial nephritis, but granulomas are confirmatory evidence

Front 430

What is the clinical context of acute interstitial nephritis?

Back 430

Acute drug-induced tubulointerstitial nephritis has the clinical picture of acute renal dysfunction in temporal proximity with exposure to a particular medicine

Front 431

What are some predisposing factors and implicated organisms for UTIs?

Back 431

* Female gender, obstructions, vesicoureteral reflux, instrumentation, diabetes mellitus
* E. coli, proteus, klebsiella. Nosocomial UTIs can also be caused by pseudomonas, enterobacter, or candida

Front 432

Explain the pathophysiology of vesicoureteral reflux?

Back 432

Vesicoureteral reflux is when pressure in the bladder rises causing urine to back up into the ureters and eventually, up into the renal pelvis and the renal parenchyma. Urine will back up into the polar, compound papillae since are more flat, while the simple papillae are compressed closed

Front 433

What is the important imaging finding for diagnosing a urinary tract obstruction?

Back 433

Hydronephrosis

Front 434

What is a life-threatening variation of acute pyelonephritis and what are its predisposing factors?

Back 434

Emphysematous pyelonephritis is a severe necrotizing infection of the renal parenchyma causing gas formation in the renal calculi and flank crepitus on physical exam. E. coli is often the culprit and diabetes and obstruction are two predisposing factors

Front 435

What is the hallmark biopsy finding of chronic pyelonephritis?

Back 435

Chronic pyelonephritis biopsy will show thyroidization-type tubular atrophy

Front 436

How do tubular changes differ on biopsy of HIVAN and chronic pyelonephritis?

Back 436

In HIVAN, the cystically dilated tubules appear fractured and broken apart, as if they are unfolding. Chronic pyelonephritis presents with thyroidization-type tubular atrophy, where the tubules take on the colloid follicle appearance

Front 437

What are the biopsy findings for xanthogranulomatous pyelonephritis?

Back 437

Zonation is often present with central suppurative inflammation and a peripheral zone containing lipid-laden macrophages and fibroblastic tissue with chronic inflammatory cells and giant cells

Front 438

What area of the kidney will necrose first in atheroembolic renal disease?

Back 438

Atheroembolic renal disease will result in cortical necrosis. Available blood will shunt from the cortex to the medulla since the medullary blood supply is always teetering on hypoxia. This, unfortunately, shunts blood away from the most metabolically active and blood demanding part of the kidney

Front 439

Name 2 nephropathies where mitotic figures can be seen on biopsy

Back 439

In acute tubular necrosis, mitotic figures are a sign of regenerating activity of the tubular epithelium. In HIVAN, the collapsing variant of FSGS, mitotic figures represent the podocytes regressing to a more primitive phenotype, capable of dividing and sometimes producing a pseudocrescentic appearance on trichrome stain

Front 440

What microscopic findings are found in benign hypertension?

Back 440

Arteriolar hyalinosis with medial hyperplasia and fibroelastic intimal thickening

Front 441

What are the microscopic findings of malignant hypertension?

Back 441

Arteriolar fibrinoid necrosis with myxoid intimal thickening and mesangiolysis. Nectrotizing arteriolysis.

Front 442

Describe thrombotic microangiopathy. What conditions is it associated with?

Back 442

Thrombotic microangiopathy is defined by the loss of mesangial anchoring to the basement membrane, an expanded subendothelial space, and marked mesangiolysis. TMA is seen in hemolytic uremic syndrome, thrombotic thrombocytopenia purpura, progressive systemic sclerosis, malignant HTN, radiation nephropathy, calcineurin inhibitor toxicity, antibody mediated rejection, and toxemia of pregnancy

Front 443

What are two situations post-kidney transplant when tubulitis is seen?

Back 443

BK nephropathy and cellular rejection

Front 444

The levels of what class of drugs must be monitored following a kidney transplant?

Back 444

Tacrolimus (CNI) and sirolimus (mTOR inhibitor) levels must be monitored to anticipate dose-related side effects

Front 445

How does thrombotic microangiopathy present?

Back 445

Thrombocytopenia, hemolysis

Front 446

What is a classic finding in acute calcineurin inhibitor toxicity?

Back 446

Vacuolization from tubular toxicity

Front 447

What does PRA stand for, when will it be elevated, and what does it represent?

Back 447

PRA stands for panel reactive antibodies. It represents the percentage of other patients that your patient will react to and lyse. The higher the PRA, the more likely you are to have a rejection. PRA will be higher in patients who have been pregnant, received a blood transfusion, or if you have received a prior transplant.

Front 448

What is the treatment for an early antibody mediated rejection?

Back 448

Early antibody mediated rejections should be treated with plasmapheresis, steroids, and increase immunosuppression

Front 449

What cell is responsible for initiating a cellular rejection following kidney transplant?

Back 449

CD4 T-cells activating cytotoxic T-cells

Front 450

What do you look for when attempting to diagnose a antibody mediated rejection?

Back 450

C4D deposition

Front 451

What do you look for when attempting to diagnose a cellular mediated rejection?

Back 451

Tubulitis

Front 452

What do you look for when attempting to diagnose a BK virus nephropathy?

Back 452

SV40 positive staining

Front 453

What types of infections are kidney transplant patients at risk for 1 month post transplant?

Back 453

Similar infections to non-immunosuppressed surgical patients. Wound infections, UTI, line-related infections

Front 454

What types of infections are kidney transplant patients at risk for 1-6 months post transplant?

Back 454

Immunomodulating viruses like CMV. BK virus, UTIs

Front 455

What types of infections are kidney transplant patients at risk greater than 6 month post transplant?

Back 455

UTIs, community acquired pneumonia, BK virus, opportunistic infections (listeria, nocardia, mycobacteria)

Front 456

What are the two malignancy concerns for post-transplant patients and why are they at an increased risk?

Back 456

Post-transplant patients are at a higher risk for non-melanoma skin cancers and lymphoproliferative disorders due to their immunosuppressive medication regimen

Front 457

What are some common causes of early (<3 months) kidney transplant dysfunction?

Back 457

Vascular issues, extrinsic compression, acute tubular necrosis, acute pyelonephritis, drug toxicity (CNI), acute rejection (antibody or cellular), urinary obstruction

Front 458

What are some common causes of late (>3 months) kidney transplant dysfunction?

Back 458

* Intrinsic: chronic rejection or drug toxicity, late acute rejection, recurrent or de novo renal disease, pyelonephritis, BK virus nephropathy
* Mechanical: ureteral obstruction or stricture

Front 459

What is the presentation, risk factors, diagnosis, and treatment of CMV in a kidney transplant patient?

Back 459

* CMV presents as an actue viral syndrome with leukopenia and possibly tissue invasive disease (hepatitis, pneumonitis, pancreatitis, colitis). Risk of infection is 1-6 months post-transplant
* Risk factor include being sero-negative and having a recent treatment with lymphocyte depleting agents
* It is diagnosed with PCR, showing CMV viremia
* Treat with IV ganciclovir or PO valganciclovir

Front 460

What is the presentation, risk factors, diagnosis, and treatment of BK nephropathy in a kidney transplant patient?

Back 460

* BK nephropathy presents asymptomatically with gradually rising creatinine. Serum PCR levels>100,000 will cause renal insufficiency
* The greater the immunosuppression to higher likelihood of infection
* A viral load PCR is diagnostic. Tubulitis with SV40 positive stain will be present
* Treat by reducing immunosuppression, fluoroquinolone, and cidofovir

Front 461

Where are possible sites of urine leak and what symptoms does it cause?

Back 461

Urine can leak from the pelvis, ureter, or bladder and the body's reaction to urine is peritonitis with pain and ileus

Front 462

What are the features of acute calcineurin inhibitor toxicity?

Back 462

Tacrolimus and cyclosporine toxicity can cause reduced renal blood flow (vasoconstriction) and vacuolization from tubular toxicity

Front 463

What are the features of chronic calcineurin inhibitor toxicity?

Back 463

Tacrolimus and cyclosporine can cause a stripe like interstitial fibrosis and secondary FSGS type glomerular lesions

Front 464

What are potential vascular complications following a kidney transplant

Back 464

Transplant renal artery stenosis or thrombosis, iliac artery dissection, renal vein stenosis or thrombosis

Front 465

What are the main antibody types implicated in antibody mediated kidney transplant rejection

Back 465

Antibody mediated kidney transplant rejection can by propagated by HLA antibodies and/or ABO antibodies

Front 466

What value the predictor for risk of early acute antibody mediated kidney transplant rejection?

Back 466

Panel reactive antibodies, which are 0% if the patient has had no prior sensitizing event, but increases with pregnancy, blood transfusion, or prior kidney transplant

Front 467

What is the pathogenesis of late acute antibody mediated kidney transplant rejection?

Back 467

Late acute antibody mediated kidney transplant rejection is when the patient develops donor specific antibodies despite the immunosuppression regimen. It carries a worse prognosis than early acute antibody mediated kidney transplant rejection

Front 468

How are cellular mediated kidney transplant rejections treated?

Back 468

Depends of the severity of the rejection, the interstitial disease, and prior compliance. Some combination of thymoglobulin and steroids

Front 469

Which nephropathies exhibit a toxic syndrome and which exhibit a functional toxic disorder?

Back 469

* Toxic syndrome: acute renal failure, chronic renal failure, nephrotic syndromes
* Functional toxic disorder: renal tubular acidosis, SIADH, nephrogenic diabetes insipidus

Front 470

What are the characteristics of renal tubular acidosis?

Back 470

The loss of ability to reabsorb bicarbonate or to generate new bicarbonate at the distal tubule

Front 471

What are the renal effects of toluene on the kidney?

Back 471

Toluene is a hydrocarbon that can be abused as an inhalant. It causes a type I RTA where the distal nephron is unable to lower the urine pH creating a hyperchloremic metabolic acidosis, with hypokalemia and a urine ph>5.5

Front 472

How does MDMA affect the kidneys?

Back 472

MDMA, or ecstasy, causes increased release of vasopressin (ADH) and an SIADH picture. Users will be profoundly hyponatremic from a large intake of water and sodium loss

Front 473

How does lithium affect the kidney?

Back 473

Lithium is similar to sodium and cases when there is an increase in the proximal reabsorption of sodium, lithium will be absorbed as well. Lithium has a narrow therapeutic range and so volume depletion or salt restriction will increase lithium reabsorption and the patient will be over treated with lithium
* Lithium downregulates aquaporin-2
* GI symptoms (nausea, vomiting, diarrhea), CNS (tremor, hyperreflexia, chorea, clonus, dysarthria, nystagmus, ataxia), nephrogenic diabetes insipidus cause=ing hypernatremia

Front 474

What type of toxic alcohol is found in antifreeze, windshield washer fluid, solvents

Back 474

* Antifreeze: ethylene glycol
* Windshield washer fluid: methanol
* Solvent: diethylene glycol

Front 475

How does ethylene glycol affect the kidney?

Back 475

* Ethylene glycol is metabolized into a number of different acids that create a metabolic acidosis.
* Oxalic acid binds calcium and create stones.
* Some intermediates are directly toxic to the renal tubules.

Front 476

What are the risk factors for contrast-induced nephropathy?

Back 476

Baseline diminished renal function, diabetes, volume depletion, nephrotoxic drugs, hemodynamic instability, comorbidities

Front 477

What drug can be indicated in hemorrhagic cystitis?

Back 477

Cyclophosphamide therapy

Front 478

What is a hypoplastic kidney?

Back 478

A hypoplastic kidney is a small kidney, free of scars, and containing 6 or fewer lobes and pyramids

Front 479

What is the most common cystic disease of the newborn?

Back 479

Multicystic dysplasia

Front 480

What are the histological hallmarks of renal dysplaisa?

Back 480

Primitive ducts surrounded by cuffs of mesenchymal tissue and islands of primitive cartilage

Front 481

What is the most common variant of renal cell carcinoma?

Back 481

The most common variant of RCC is clear cell. Large nucelar size and nuceoli prominence correlates to higher nuclear grade

Front 482

Which type of papillary renal cell carcinoma has a worse prognosis?

Back 482

Type II

Front 483

Which variant of renal cell carcinoma has the best prognosis?

Back 483

Chromophobe renal cell carcinoma

Front 484

What is the gender predominance for acquired cystic kidney disease?

Back 484

Men are 3 times more likely than women

Front 485

What is the clinical presentation for renal cell carcinoma?

Back 485

Flank pain, hematuria, renal colic, fever, erythrocytosis

Front 486

What is the most common kidney neoplasm is adults?

Back 486

Renal cell carcinoma (clear cell variant)

Front 487

What is the most common kidney neoplasm in children?

Back 487

Wilm's tumor

Front 488

What is a good prognostic sign for Wilm's tumor?

Back 488

Anaplastic features (multipolar mitoses, nuclear enlargement, hyperchromasia) are associated with responsiveness to therapy

Front 489

What is the histopathologic picture of Wilm's tumor?

Back 489

An undifferentiated blastema, an epithelial, and a mesenchymal component

Front 490

What is a angiomyolipoma and what kindey disease is it associated with?

Back 490

An angiomyolipoma is a mixture of prominent blood vessels, spindle-shaped epitheliod smooth muscle cells, and adipose tissue. These sporadic tumors are associated with tuberous sclerosis (hamartin and tuberin)