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Renal > Renal FA (Physiology and Pathology) > Flashcards

Renal FA (Physiology and Pathology) Flashcards

1
Q

Kidney embryology

A
  1. Pronephros (up till wk4)
  2. Mesonephros (first trimester)
  3. Metanepros (appears in wk 5)
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2
Q

Ureteric bud

A

derived from mesonephric duct

gives rise to ureter, pelvises, calyces, collecting ducts

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3
Q

Metanephric mesenchyme

A

gives rise to glomerulus through to DCT

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4
Q

Ureteropelvic junction

A

Last to canalize

Most common site of obstruction (hydronephrosis)

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5
Q

Potter sequence- POTTER

A 
Pulmonary hypoplasia
Oligohydramnios
Twisted face (low set ears, overbite, flattened nose)
Twisted skin
Extremity defects
Renal failure

Due to failure of ureteric bud formation

Can be cause by ARPKD, bilateral renal agencies, chronic placental insufficiency

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6
Q

Horseshoe kidney

A

Inferior pole of the kidneys fuse
Gets trapped under INFERIOR MESENTERIC ARTERY (IMA)
Kidneys function normally

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7
Q

Associations/ complications with horseshoe kidney

A

hydronephrosis, renal stones, infection, renal cancer

See more commonly in Turner and trisomies

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8
Q

Unilateral renal agenesis

A 
ureter bud (pelvix, calyx, collecting duct ureter) fails to develop
metanephric mesenchyme (glomerulus and DCT) also does not develop
Causes complete absence of kidney and ureter
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9
Q

Multicystic dysplastic kidney

A

Ureteric bud develops
UB fails to induce differentiation of metanephric mesenchyme
Causes non-functional kidney with cysts and connective tissue

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10
Q

Duplex collecting system

A

bifurcation of one ureteric bud (or just two) before entering the metanephric mesenchyme causes Y-shaped bifid ureter
Associated with vesicoureteral reflux/ obstruction
Increase UTI risk

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11
Q

Congenital solitary functioning kidney

A

Born with only one functioning kidney

Generally asymptomatic with compensatory hypertrophy of contralateral kidney (which also may have some anomalies)

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12
Q

Left kidney

A

Longer renal vein- so generally taken for donor transplantation

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13
Q

Renal blood flow

A

Renal artery –> Segmental artery –> Interlobar artery –> arcuate artery –> interlobular artery –> afferent arteriole –> glomerulus –> efferent arteriole –> vasa recta/ peritubular capillaries –> venous outflow

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14
Q

Components of the glomerular filtration barrier

A

Podocytes, basement membrane, and endothelial cells (around the arterioles)

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15
Q

Mesangial cells of the glomerulus

A

Remove trapped residues and aggregated protein from the basement membrane

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16
Q

Afferent vs. Efferent arterioles

A

Afferent: arriving
Efferent: exiting

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17
Q

Ureters

A

Pass Under the uterine artery or under the vas deferent (water under the bridge)
Ligation of the uterine (cardinal ligament) or ovarian vessels (suspensory/ infundibulopelvic ligament) may damage ureter

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18
Q

Fluid compartments (60-40-20)

A

60% total body water (40% ICF + 20% ECF); 40% non water mass

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19
Q

ECF vs. ICF

A

kg –> L (since density of H2O is 1)

For a 70kg person (42kg of TBW; 28kg of non water mass)

1/3 ECF- 14 kg (Interstitial fluid (10.5 kg) and plasma (3.5 kg))
2/3 ICF- 28kg (RBCs (3 kg) and Cells (25 kg))

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20
Q

Plasma volume- measurement

A

Radiolabeling albumin

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21
Q

Extracellular volume- measurement

A

Innulin or Mannitol

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22
Q

Osmolarity

A

285-295 mOsm/kg H2O

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23
Q

Glomerular filtration barrier

A

Filters based on SIZE and net CHARGE

Composed of:
Fenestrated capillaries: size barrier
BM with heparan sulfate: negative charge and size barrier
Epithelial layer consisting of podocyte foot processes: negative charge

Albumin: negatively charged, and therefore repelled by negative charges on BM and epithelium

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24
Q

Charge barrier compromised

A

Lost in nephrotic syndrome

Causes albuminuria, hypoproteinemia, generalized edema, and hyperlipidemia

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25
Q

Renal clearance

A

Clx = Ux * V/ Px where
Px: plasma concentration (mg/mL)
Ux: urine concentration (mg/mL)
V: urine flow rate

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26
Q

Filtration vs. Secretion

A

Filtration: First pass dump into BC
Secretion: Second pass dump (material from interstitium/ capillaries to tubular lumen to be removed)
Reabsorption: Moved from lumen to capillaries/intersititium

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27
Q

Clearance Rate

A

Equal to: Filtration Rate - Reabsorption Rate + Secretion Rate

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28
Q

Clearance vs. GFR

A

If Clx = GFR: indicates no net secretion or absorption of X
If Clx > GFR: indicates net tubular secretion of X
If Clx < GFR: indicates net tubular reabsorption of X

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29
Q

Calculating GFR

A

Use GFR = Cl = UV/P for INNULIN

Innulin is freely filtered and neither reabsorbed nor secreted

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30
Q

Creatinine Cl vs. GFR

A

Creatinine is secreted so CrCl slightly overestimates GFR (assumes all that is cleared is filtered- when in reality some is also secreted)

vs. urea (which is reabsorbed, so Urea clearance slightly underestimates what is filtered (since some of it is reabsorbed))

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31
Q

Normal GFR

A

Around 100 mL/min

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32
Q

Effective renal plasma flow

A

Can be estimated using PAH (because nearly 100% cleared (via filtration and secretion))

eRPF = U(PAH) * V/ P (PAH) = Cl (PAH)

eRPF slightly underestimates true renal plasma flow

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33
Q

Renal Blood Flow

A

RBF = RPF/ (1-Hct)

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34
Q

Plasma

A

1 - hematocrit

Hct (refers to percentage of blood volume comprised of RBCs/ RBC volume in blood)

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35
Q

GFR vs. RPF

A

GFR: Amount that is filtered by the kidney at the glomerulus per unit time
RPF: Amount of plasma that flows into the kidney per unit time

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36
Q

Filtration fraction (FF)

A 
Filtration fraction (FF) = GFR/RPF
Normal is 20%
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37
Q

Filtered load (mg/min)

A

Filtered load = GFR * Plasma concentration

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38
Q

Glomerulus- Afferent arteriole (things that constrict vs. dilate)

A

Afferent:

Constrict: NSAIDs (Decreases GFR and RBF)

Dilate: Prostaglandins (Increases GFR and RBF)

No change in filtration fraction

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39
Q

Glomerulus- Efferent arteriole (things that constrict vs. dilate)

A

Efferent:

Constrict: Angiotensin II (Increases GFR, Decreases RBF); Increases FF

Dilate: ACE-Inhibitors (Decreases GFR- less residence time in pipe due to big exit, Increases RBF); Decreases FF

Memory pearly: ACE-Is are good for diabetic nephropathy, because it opens up the constricted efferent arterioles

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40
Q

Glomerular dynamics- protein concentration, ureter constriction, and dehydration

A

Protein concentration: As protein conc increases, GFR decreases, RPF doesn’t change, so FF decreases

Ureter constriction: As ureter gets constricted, less can be filtered (enter the tubular lumen), so GFR decreases, RBF stays the same, FF decreases

Dehydration: As body gets dehydrated, protein/ solute concentration increases, GFR decreases, RPF decreases (because of RAAS activation), and FF stays the same

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41
Q

Reabsorption calculation

A

Reabsorption = Filtered load - Excretion/Clearance rate (assuming no secretion) = GFRPx - UxV

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42
Q

Secretion calculation

A

Secretion = Excretion/Clearance Rate - Filtered load (assuming no reabsorp) = UxV - GFRPx

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43
Q

Fractional excretion of sodium- FE (Na)

A

Na+ excreted/ Na+ filtered = U (Na) * V/ (GFR * P (Na))

Assuming GFR can be estimated by CrCL = U (Cr) * V/ (P (Cr)):

FE Na = U (Na) * P (Cr)/ (U (Cr) * P (Na))

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44
Q

Glucose clearance

A

Under normal plasma level (60-120 mg/dL), should be completely reabsorbed in PCT via Na+/glucose transport

Glucosuria begins at a P (glucose) of 200 mg/dL and at a filtered load of 375 mg/min all transporter get saturated (and no more glucose is reabsorbed)

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45
Q

Splay: glucose clearance

A

concentration difference between maximal renal absorption and concentration in urine

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46
Q

Nephron physiology- PCT

A

Reabsorbs all glucose and AAs (as well as most ions- bicarb, Na+, Cl-, etc)
Generates and secretes ammonia and H+
PTH- acts here to cause increase phosphate (PO4 3-) excretion
Acetazolamide- acts here to inhibit carbonic anhydrase and increase bicarb excretion
Angiotensin II- Stimulate Na+/H+ exchange in low blood volume states (Na+ and HCO3- reabsorbed, H+ excreted)

60-80% Na+ reabsorbed here

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47
Q

Thin descending loop of Henle

A

Passively reabsorbs H2O

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48
Q

Thick ascending loop of Henle

A

reabsorbs Na+, K+, and Cl-
paracellularly absorbs Ca2+ and Mg2+

Loop diuretics act here (and therefore can cause loss of K+, Ca2+, NOT Mg2+)- LOOps LOSE Ca2+

10-20% of Na+ absorbed here

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49
Q

Early DCT

A

reabsorbs Na+ and Cl-

PTH- acts here to increase Ca2+/Na+ exchange to retain Ca2+ and excrete Na+

Thiazides- act here and inhibit Na+/Cl- cotransproter

5-10% of Na+ reabsorbed here

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50
Q

Collecting tubule

A

Reabsorbs Na+ in exchange for secreting K+ and H+

Aldosterone- Acts on MC receptor –> mRNA –> increases ENaC activity

ADH- acts on V2 receptor; inserts aquaporin H2O channels on apical side

3-5% Na+ absorbed

Therefore- diuretics that act here (amiloride, triamterene, and aldosterone antagonists) will be K+ sparing (as they excrete Na+)

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51
Q

Renal tubular defects (Fanconi first and all others in alphabetical order)

A

Fanconi SYNDROME

Bartter syndrome

Gitelman syndrome

Liddle syndrome

SAME- Syndrome of Apparent Mineralocorticoid Excess

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52
Q

Fanconi SYNDROME

A

Fanconi SYNDROME- PCT defect (caused by biochemical hereditary defects, drugs, lead poisoning, etc.)- can cause metabolic acidosis

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53
Q

Bartter syndrome

A

Bartter syndrome- Ascending LOH defect (AR)- (looks like people who use loop diuretics chronically)

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54
Q

Gitelman syndrome

A

Gitelman syndrome- DCT defect (AR)- (looks like people who use thiazides chronically- less severe than Bartter)

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55
Q

Liddle syndrome

A

Liddle syndrome- Gain of function; increased Na+ reabsorption in CT (AD)- looks like hyperaldosteronism, but does aldosterone is nearly undetectable; tx with Amiloride (inhibits ENaCs)

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56
Q

SAME- Syndrome of Apparent Mineralocorticoid Excess

A

SAME: Cortisol tries to be the SAME as aldosterone

Deficiency of 11-B hydroxysteroid dehydrogenase (can be induced by black licorice)

Normally converts cortisol (active) to cortisone (inactive on MR receptors)

Excess cortisol cross-reacts with MR and causes symptoms of hyperaldo

Tx: corticosteroids (suppress endogenous cortisol prodn)

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57
Q

RAAS System

A

Angiotensinogen converted to Angiotensin I by renin

Angiotensin I converted to Angiotensin II by ACE in pulmonary endothelial cells

Angiotensin II causes systemic effects (Increases aldo production in adrenal cortex (glomerulosa), vasoconstricts- vasculature and efferent arteriole of glomerulus, increases ADH secretion by posterior pituitary, increases PCT Na+/H+ activity, stimulates thirst)

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58
Q

Renin

A

Secreted by JG cells

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59
Q

ATII

A

Maintains blood volume and pressure; affects baroreceptor function

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60
Q

ANP and BNP

A

released from atria (ANP) and ventricles of heart (BNP) when increase volume/ stretch is detected

dilates afferent arteriole and constricts efferent to promote filtration/ natriuresis

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61
Q

ADH

A

Regulates osmolarity, responds to low blood volume states

62
Q

Aldosterone

A

Regulates ECF and Na+ content;

63
Q

Juxtaglomerular apparatus

A

SECRETE renin in responses to decreased renal blood pressure and increased sympathetic tone (B1)

Beta-blockers: inhibit renin release (by inhibiting N1 receptors of the JGA)

(as opposed to macula densa- which only sense decreased Na+)

64
Q

Macula densa

A

SENSE decreased NaCl delivery to DCT –> talk to JGA –> increase renin release –> constrict efferent arteriole –> GFR increases, but RPF decreases

65
Q

Kidney endocrine functions

A

Erythropoietin
Calciferol
Prostaglandins
Dopamine

66
Q

Erythropoietin

A

Release by interstitial cells in peritubular capillary bed

Stimulate RBC proliferation in bone marrow

Supplemented in CKD

67
Q

Calciferol

A

PCT- activates Vit D (calcitriol- active form)

converts 25-OH Vit D3 to 1, 25- (OH)2 Vit D3 via 1 alpha hydroxylase

68
Q

Prostaglandins

A

Vasodilate the afferent arterioles to increase RBF

69
Q

NSAIDs

A

Constrict afferent arteriole (may result in acute renal failure)

70
Q

Dopamine

A 
Also secreted by the PCT
Promotes natriuresis (increases RBF)
At high doses- vasoconstrictor
71
Q

Potassium shifts- out of the cell (HYPERkalemia)

DO LABS

A 
Digitalis
hyperOsmolarity
Lysis of cells
Acidosis (H+/K+ "exchanger")
Beta blocker
high blood Sugar (insulin deficiency)
72
Q

Potassium shifts- into the cell (HYPOkalemia)

A

INsulin (shifts K+ INto the cells)

Opposite of the things above (alkalosis, beta agonist, hypo-osmolarity)

73
Q

Presentation of Hyponatremia

A

Nausea and malaise, stupor, coma, seizures

74
Q

Presentation of Hyperkalemia

A

Similar to hypo: stupor, coma, + irritability

75
Q

Presentation of Hypokalemia

A

U wave, flattened T wave

Arrhythmias, muscle cramps, spasm, weakness

76
Q

Presentation of Hyperkalemia

A

Wide QRS, peaked T waves

Arrhythmias, muscle weakness

77
Q

Presentation of Hypocalcemia

A

Tetany, seizures, QT prolongation, twitching (Chvostek sign- lip twitches when tapping facial nerve), Trousseau sign- spasm/ curvature of hand with BP cuff, tingling of lips and mouth

78
Q

Presentation of Hypercalcemia

A

Stones (renal), bones (pain), groans (abdominal pain), thrones (increased urinary frequency), and psychiatric overtones (anxiety, altered mental status)

Do not necessary have increased Ca2+ urinary excretion

79
Q

Presentation of Hypomagnesemia

A

Tetany, torsades de pointes, hypokalemia

80
Q

Presentation of Hypermagnesemia

A

Decreased deep tendon reflexes, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia

81
Q

Presentation of Hypophosphatemia

A

Bone loss, osteomalacia (adults), rickets (kids)

82
Q

Presentation of Hyperphosphatemia

A

Renal stones, metastatic calcifications, and hypocalcemia

83
Q

Henderson-Hasselbach equation

A

pH = 6.1 + log ([HCO3-]/ .03*P (CO2))

84
Q

Metabolic Acidosis- increased anion gap

A

Increased anion gap: MUDPILES

Methanol (formic acid)
Uremia
DKA
Propylene glycol
Isoniazid and iron supplements
Lactic acidosis
Ethylene glycol (oxalic acid)
Salicylates (late)
85
Q

Metabolic Acidosis- normal anion gap

A 
Normal anion gap- HARDASS
Hyperalimentation (IV nutrition overdose)
Acetazolaminde
Renal tubular acidosis
Diarrhea
Addison disease
Spironolactone
Saline infusion
86
Q

Metabolic Alkalosis

A

Loop diuretics
Vomiting
Antacids
Hyperaldosteronism

87
Q

Respiratory Acidosis

A 
Things that keep CO2 in: hypoventilation
Airway obstruction
Acute and chronic lung disease
Opioids, sedatives
Weakening of muscles
88
Q

Respiratory Alkalosis

A 
Things that get too much CO2 out: hyperventilation
Hysteria
Hypoxemia
Salicylates (early)
Tumor
Pulmonary embolism
89
Q

Renal Tubular Acidosis

A 
3 types:
Type I (distal): Too little H+ is being secreted, therefore too much K+ being excreted (hypokalemia)- Urine pH > 5.5

Type II: Too little bicarb being absorbed (hypokalemia)- Urine pH < 5.5

Type IV: Hypoaldosteronism –> Na+ wasted and K+ retained (hyperkalemia)- Urine pH < 5.5

90
Q

Casts

A

Indicate that hematuria/pyuria is of glomerular or renal tubular origin

(Casts will not be present in bladder cancer, kidney stones, cystitis, etc.)

91
Q

RBC casts

A

GN, malignant HTN

92
Q

WBC casts

A

Tubulointerstitial inflammation, acute pyelo (bacterial in kidneys), transplant rejection, UTIs (specifically in diabetes)

93
Q

Fatty casts

A

Nephrotic syndrome

Associated with maltese cross sign

94
Q

Granular (muddy brown casts)

A

ATN

95
Q

Waxy casts

A

End stage renal disease, chronic renal failure

96
Q

Hyaline casts

A

Aka Tamm-Horsefall mucoprotein

Non-specific; can be normal

97
Q

Nephritic syndrome

A

Characterized by:

  1. No proteinuria (<3.5 g/day)
  2. Azotemia (high levels of nitrogenous compounds)
  3. HTN
  4. RBC casts in urine (Hematuria)
  5. Oliguria

It is an Inflammatory process

98
Q

Nephrotic syndrome

A

Characterized by:

  1. Proteinuria (> 3.5 g/day)
  2. Edema
  3. Hyperlipidemia
  4. Hypoalbuminemia

Hyper coagulability can be seen due to wasting of antithrombin III

99
Q

Kidney stones

A

Presents with unilateral flank tenderness, colicky pain radiating to groin, and hematuria

100
Q

Stones- calcium

A

Calcium oxalate (envelope) more common than calcium phosphate (wedge shaped)

Radiopaque on X-ray and CT

Causes: Ethylene glycol ingestion, Vit C abuse, hypocalcitraturia, Malabsorption (Crohns)

Tx: thiazides

101
Q

Stones- Ammonium magnesium phosphate (struvite)

A

Most common cause of staghorn calculi
Caused by infection from urease + organisms (e.g. Proteus, Staph saprophyticus, Klebsiella)

Radiopaque on X-ray and CT

Tx: Tx underlying infection, surgery to remove stone

102
Q

Stones- Uric acid

A

About 5% of all stones

Risk factors: decreased urine volume, arid climates, and acidic pH

Rhomboid or rosette shape

Radiolucent on X-ray; visible on ultrasound

Strong association with hyperuricemia (gout), and seen in disease with high cell turnover (leukemia)

Tx: alkalization of urine, allopurinol

103
Q

Stones- Cystine

A

Cystinuria: Hereditary condition causing defects in absorption of COLA (cysteine, ornithine, lysine, and arginine)

Sodium cyanide nitroprusside test +

Urine crystal is hexagonal in shape (SIXteine stones have SIX sides)

Tx: low sodium diet, alkalization agent if needed, chelation if refractory

104
Q

Hydronephrosis

A

Distention/ dilation of renal pelvis and calyces

Caused by obstruction (stones, BPH, cancer, ureter injury); vesicoureteral reflux

Raised Cr only seen if bilateral involvement

Can cause atrophy of renal cortex and medulla

105
Q

Renal cell carcinoma (Hypernephroma)

A

Most common primary tumor of the kidney

RCC associated with VHL (also show hemangioblastoma (brain tumor) and pheochromocytoma)

Originates from PCT cells filled with accumulated lipids and carbs

106
Q

RCC risk factors

A

Men ages 50-70
Smoking
Obesity

107
Q

RCC- S&S

A

hematuria, palpable mass, polycythemia, flak pain, fever weight loss

Mets to lung and bone

Often associated with paraneoplastic syndrome (ectopic EPO, ACTH, PTHrP, renin)

108
Q

RCC- Tx

A

Resection, if localized
Immunotherapy (aldesleukin) or targeted therapy

Often resistant to chemo and radiation

109
Q

Renal oncocytoma

A

Benign

Tumor of the epithelial cells- arising from collecting ducts

110
Q

Renal oncocytoma histology

A

Abundant eosinophils

No perinuclear clearing (as opposed to RCC)

111
Q

Renal oncocytoma- S&S

A

Painless hematuria, flank pain, and abdominal mass

112
Q

Renal oncocytoma- Tx

A

Often resected to exclude malignancy

113
Q

Wilms tumor

A

Most common renal malignancy of early childhood (2-4yr)

114
Q

Wilms tumor- S&S

A

Presents with large, palpable, unilateral flank mass and/ or hematuria

115
Q

Wilms tumor- genetics

A

Associated with mutations of tumor suppressor genes: WT1 and WT2 on chromosome 11

116
Q

Wilms tumor- associated syndrome

A
  1. WAGR: Wilms tumor, Aniridia, Genitourinary malformations, and mental Retardation (WT1 deletion)
  2. Denys-Drash: nephrotic syndrome, male pseudohermaphroditism (WT1 mutation)
  3. Beckwith-Wiedemann: Wilms tumor, macroglossia, organomegaly, hemihypertrophy (WT2 mutation)
117
Q

Transitional cell carcinoma- S&S

A

Generally affects urinary tract system (but can also affect calyces, pelvis, ureter, and bladder)

Painless hematuria with NO CASTS

118
Q

Transitional cell carcinoma- risk factors (Pee SAC)

A

Pee SAC

```
Phenacetin
Smoking
Aniline dyes
Cyclophosphamide
and Diabetes
~~~

119
Q

Squamous cell carcinoma of the bladder pathogenesis

A

Chronic irritation –> Squamous metaplasia –> dysplasia –> carcinoma

Presents with painless hematuria

120
Q

SCC of the bladder- risk factors

A

Schistosoma hematobium infection
Chronic cystitis or nephrolithiasis
Smoking

121
Q

Stress incontinence

A

Weak outlet (urethral hyper mobility or intrinsic sphincter deficiency)- leak with increased abdominal P (STRESS)

Tx: Kegels, weight loss, pessaries

122
Q

Urgency incontinence

A

Overactive bladder (Detrusor instability)- leak with urge to void immediately

Tx: Kegels, anti-muscarinics (oxybutynin), bladder training (distraction or relaxation techniques)

123
Q

Mixed incontinence

A

Features of stress and urgency incontinence

124
Q

Overflow incontinence

A

Incomplete emptying (due to detrusor under activity or outlet obstruction)

Leak with overfilling

Dx: via increased post-void residual urine volume

Tx: catheterization, relieve obstruction (e.g. via alpha blockers for BPH)

125
Q

Urinary tract infection- S&S

A

Inflammation of bladder
Suprapubic pain, dysuria, urinary frequency, urgency
Systemic sign (fever, chills) generally not present

126
Q

UTI- Risk factors

A 
female (short urethra)
sexual intercourse
indwelling catheter
diabetes mellitus
impaired emptying
127
Q

UTI- common causes

A

E.coli (most common)
Staph saprophyticus
Klebsiella
Proteus mirabilis (urine has ammonia scent)

128
Q

UTI- lab findings

A

+ leukocyte esterase

+ nitrites (indicates gram - infection- specifically E.coli)

129
Q

N. gonorrhea and Chlamydia urethritis presentation

A

Sterile pyuria and - urine cultures

130
Q

Pyelonephritis

A

Acute pyelo- neutrophils (affects CORTEX ONLY); presents with fevers, flank pain (CVA tenderness), n/v, chills; WBCs seen in urine

Chronic pyelo- recurrent pyelo (often due to vesicoureteral reflux, neurogenic bladder, or chronically obstructing kidney stones), affects CORTEX and MEDULLA, blunted calyx; tubules can contain eosinophilic casts (resemble thyroid)

131
Q

Xanthogranulomatous pyelonephritis

A

Characterized by widespread kidney damage due to granulomatous tissue containing foamy macrophages

132
Q

Diffuse cortical necrosis

A

Cortical infarction of BOTH kidneys

Due to vasospasm and DIC; associated with obstetric catastrophes, septic shock

133
Q

Renal osteodystrophy

A

Hypocalcemia, hyperphos, and failure of Vit D hydroxylation associated with chronic renal disease

Causes secondary hyperparathyroidism

Low calcium causes subperiosteal thinning of bones

134
Q

Acute kidney injury

A

Abrupt decline in renal function (increased creatinine and BUN)

135
Q

Prerenal azotemia

A

Increased BUN/Cr, decreased FENa

Due to decreased RBF; BUN retained to conserve volume but Cr is excreted

Urine osmolality >500
Urine Na+ <20
FENa <1%
Serum BUN/Cr >20

136
Q

Intrinsic renal azotemia

A

Decreased BUN/Cr, increased FENa

Due to acute tubular necrosis or ischemia/toxins

Urine osmolality <350
Urine Na+ >40
FENa >2%
Serum BUN/Cr <15

137
Q

Postrenal azotemia

A

Variable BUN/Cr and FENa (more severe if value is higher)

Urine osmolality <350
Urine Na+ >40
FENa >1% (mild); >2% (severe)
Serum BUN/Cr varies

138
Q

Consequence of renal failure- MAD HUNGER

A

Inability to get rid of nitrogenous wastes can cause:

Metabolic Acidosis
Dyslipidemia (especially higher triglycerides)
Hyperkalemia
Uremia (increased BUN causes cause, pericarditis, asterixis, encephalopathy, platelet dysfunction)
Na+/H2O retention
Growth retardation and developmental delay
Erythropoietin failure (anemia)
Rrenal osteodystrophy

139
Q

Acute interstitial nephritis- the 5 P’s

A

Pyuria (pus in urine) and azotemia after administration of drugs

Penicillins and cephalosporins
Pain-free (NSAIDs)
Pee (diuretics) &amp; sulfonamides
Proton pump inhibitors (-prazoles)
RifamPin
140
Q

Acute tubular necrosis (ATN)- presentation

A

Most common cause of AKI in hospitalized patients
Spontaneously resolves
Can see increased FENa (makes sense because this is a intrinsic renal prob)
Can also see muddy brown casts in urine

141
Q

ATN- stages

A
  1. Inciting event
  2. Maintenance phase (oliguric): 1-3 wks
  3. Recovery phase (polyuric)
142
Q

ATN causes (ischemic and nephrotoxic)

A

Ischemic vs. Nephrotoxic

Ischemic: secondary to decreased RBF; tubular cells may slough off into tubular lumen; PCT highly susceptible to injury

Nephrotoxic: secondary to toxic substances, crush injury, etc.

143
Q

Renal papillary necrosis- SAAD papa with papillary necrosis

A

Gross hematuria and proteinuria (sloughing of necrotic renal papillae)

SAAD
Sickle cell disease or trait
Acute pyelonephritis
Analgesics (NSAIDs)
Diabetes mellitus
144
Q

Renal cyst disorder

A
  1. ADPKD
  2. ARPKD
  3. Medullary cystic disease
  4. Simple vs. complex renal cysts
145
Q

ADPKD- autosomal dominant polycystic kidney disease

A

Cysts in cortex and medulla
Mutation in PKD1 (more common) or PKD2
Associated with berry aneurysms, mitral valve prolapse, and hepatic cysts

146
Q

ADPKD- tx

A

ACE inhibitors (for hypertension)

147
Q

ARPKD

A

Cystic dilation of collecting ducts
Presents in INFANCY
Associated with congenital hepatic fibrosis
Renal failure in utero can lead to Potter sequence

148
Q

ARPKD complications

A

HTN, progressive renal insufficiency, portal HTN (due to hepatic fibrosis)

149
Q

Medullary cystic disease

A

Causes tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine

Medullary cysts are not visualized, but shrunken kidneys are see on US

150
Q

Simple vs. Complex cysts

A

Simple: filled with ultra filtrate (anechoic)- generally asymptomatic and very common

Complex: separated or have solid components- require removal due to increased risk of RCC

Renal (3 decks)

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