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Neonatal Pathophysiology > Renal > Flashcards

Renal Flashcards

1
Q

When does nephrogenesis begin?

A

early in the 4th week as 3 sets of kidneys

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2
Q

When does the final set of kidneys develop and become functional?

A

develop in 5th week and functional around 9th week

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3
Q

What is the major component of amniotic fluid after 18-20 weeks?

A

urine; this is when AFI becomes crucial

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4
Q

When is nephrogenesis complete?

A

at 34-36 weeks

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5
Q

What is the effect of prematurity on post-natal nephrogensesis?

A

not accelerated and may be blunted; may be all the nephrons you get (at birth)

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6
Q

What are the primary functions of the renal system?

A

1) maintenance of body homeostasis

2) endocrine regulation

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7
Q

What hormones does the renal system control?

A
  • erythropoietin
  • calcitriol
  • renin
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8
Q

What is erythropoietin?

A

hypoxia-sensing cells that stimulate bone marrow to make more RBCs

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9
Q

What is calcitriol?

A

active form of vitamin D that works together with parathyroid hormone to maintain Ca++ balance

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10
Q

What is renin?

A

controls the volume of blood and therefore BP

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11
Q

How does the renal system maintain systemic homeostasis?

A
  • disposes of nitrogenous wastes

- controls composition of blood

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12
Q

In what way do the kidneys control the composition of blood?

A
  • regulates electrolyte homeostasis

- regulates acid-base balance

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13
Q

What is pyelectasis (or pelviectasis)?

A

mild dilation of the renal pelvis; measures 4-10mm in 2nd trimester; 97% will spontaneously resolve

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14
Q

What is hydronephrosis?

A

an exaggeration of pelviectasis; dilation >10mm; seen in 1-4% of all pregnancies; M>F

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15
Q

Why is it important to f/u a suspected hydronephrosis?

A

etiology is typically an obstruction

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16
Q

The term kidney typically has how many nephrons?

A

~ 1 million (300k- 2million)

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17
Q

A nephron consists of what two portions?

A

glomerulus & renal tubule

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18
Q

What are the two different types of nephrons?

A

cortical nephron & juxtaglomerular nephron

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19
Q

What is a cortical nephron?

A

the glomerulus and tubular system in the outer cortex

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20
Q

What is a juxtaglomerular nephron?

A

the tubular system that penetrates into the medulla

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21
Q

How does blood ENTER the glomerular tuft?

A

A-fferent arteriole

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22
Q

How does blood EXIT the glomerular tuft?

A

E-fferent arteriole

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23
Q

How many capillaries does the glomerular tuft have?

A

~ 50 tiny capillaries

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24
Q

What do the slit-like pores in the arterioles of the glomerulus permit?

A

allow passage of H20 and small solutes and restrict larger molecules, like proteins and red blood cells, from transferring into the bowman’s capsule

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25
Q

Which arteriole is more dilated in the glomerulus?

A

the A-fferent; this allows more blood to enter the capsule than is leaving generating a higher hydrostatic pressure facilitating diffusion

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26
Q

What is GFR?

A

the amount of filtrate that flows out of all renal nephrons of both kidneys in 1 minute

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27
Q

How does the GFR of a FT infant at birth compare to an adult?

A

term GFR 30-50% of adult; nephrogenesis is complete by 32 weeks, but maturity takes awhile

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28
Q

How does the GFR of a PT infant (28 wks) at birth compare to a FT infant?

A

1/2 of term functioning

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29
Q

Describe the progression of GFR maturation in the FT infant postnatally.

A
  • determined by renal vascular resistance (very high in the fetus and falls after birth)
  • doubles in 1st 2 weeks
  • reaches adult value by 2 years of age
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30
Q

What are the physiologic processes that occur in the tubular system?

A

selective reabsorption or secretion of varoius substances in different portions of tubular system (through both active and passive transport mechanisms)

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31
Q

What must be transported with Na or K?

A

Cl-; to maintain electric neutrality

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32
Q

Where is the most Na absorbed in the tubular system?

A

the proximal convoluted tubule (65%)

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33
Q

Where do phosphate and ammonia buffer systems begin?

A

in the proximal convoluted tubule

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34
Q

What is the function of the phosphate and ammonia buffer system?

A

to help maintain normal acid-base balance

  • bind with H+ ions
  • generate new bicarbonate ions
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35
Q

What electrolyte is actively transported in the Loop of Henle?

A

Cl-

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36
Q

What is passively transported in the Loop of Henle?

A

coupled with the active transport of Cl-, to maintain electrical neutrality, passive transport occurs with : Na, K, Ca and Mg

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37
Q

What is not absorbed in the Loop of Henle?

A

H20

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38
Q

How do loop diuretics work?

A

they block Cl- and therefore, indirectly block the reabsorption of Na, K, Ca and Mg

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39
Q

What hormones function to “fine tune” the solutes reabsorbed in the distal convoluted tubule and collecting duct?

A

aldosterone, antidiuretic and parathyroid hormones

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40
Q

What electrolyte does aldosterone facilitate the reabsorption of?

A

Na in exchange for K and H

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41
Q

What does antidiuretic hormone facilitate the reabsorption of?

A

H20

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42
Q

What electrolyte does parathyroid facilitate the reabsorption of?

A

Ca

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43
Q

Where is the juxtaglomerular apparatus found and what is it’s function?

A

The juxtaglomerular apparatus is a specialized structure formed by the distal convoluted tubule and the glomerular afferent arteriole. It is located near the vascular pole of the glomerulus and its main function is to regulate blood pressure and the filtration rate of the glomerulus.

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44
Q

Where are the macula densa cells found and what are their function?

A

The macula densa is a collection of specialized epithelial cells in the distal convoluted tubule that detect sodium concentration of the fluid in the tubule.

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45
Q

What is the reaction of the macula densa cells to elevated sodium levels?

A

In response to elevated sodium, the macula densa cells trigger contraction of the afferent arteriole, reducing flow of blood to the glomerulus and the glomerular filtration rate. (decreasing hydrostatic pressure to “push” solutes out).

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46
Q

What is the reaction of the juxtaglomerular apparatus to hypotension?

A

The juxtaglomerular cells, derived from smooth muscle cells, of the afferent arteriole secrete renin when blood pressure in the arteriole falls. Renin increases blood pressure via the renin-angiotensin-aldosterone system.

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47
Q

Where is aldosterone manufactured?

A

is synthesized from cholesterol in the adrenal cortex

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48
Q

What triggers the release of aldosterone?

A

1) the presence of angiotensin II

2) elevated K serum levels

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49
Q

Where does aldosterone work in the tubular system?

A

late distal convoluted tubule and the collecting duct

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50
Q

How is the glomerulus affected by prematurity?

A

1) immature autoregulation of afferent arteriolar dilation and efferent arteriolar constriction
2) receptor site on afferent and efferent arteries (underdeveloped and hyporesponsive)

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51
Q

How is the proximal tubule affected by prematurity?

A

1) loss of Na, Ca, HCO3, glucose, protein
2) immature phosphate and ammonia buffer systems
30 delayed drug clearance

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52
Q

How is the distal tubule and collecting duct affected by prematurity?

A

1) hyporesponsiveness to aldosterone (leading to loss of Na, retention of K & H)
2) low circulating lveles of ADH
3) hyporesponsiveness to ADH (limited concentrating ability)

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53
Q

What is the indicated treatment for metabolic acidosis d/t renal immaturity?

A

1) art lines: use 1/2 Na ace instead of 1/4 NS
2) omit cysteine from TPN
3) add Na and K to TPN as acetate

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54
Q

When should cysteine be added to the TPN?

A

once pH balance is achieved

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55
Q

What is the benefit of keeping a preterm infant slightly alkalotic?

A

making a preterm slightly alkalotic will keep pH normal allowing for permissive hypercapnea

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56
Q

How long does it take for the neonatal kidney to renally compensate for respiratory acidosis?

A

as long as 3 days

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57
Q

How should a negative Na and H20 blanace in the 1st few days of life be interpreted in the preterm neonate?

A
  • appropriate adaptation to extrauterine life

we have no established optimal rate or extent of weight loss for preterm infants

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58
Q

What pathologic conditions are a/w excessive fluid administration?

A

1) severe RDS
2) CLD
3) pulmonary edema
4) congestive heart failure
5) PDA
6) IVH
7) NEC
“ a dry lung is a happy lung”

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59
Q

What do PT and FT infants have a limited ability to do as it relates to renal physiology?

A

excrete a large Na or H2O load

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60
Q

What is the renal threshold?

A

the renal threshold is the concentration of a substance dissolved in the blood above which the kidneys begin to remove it into the urine. When the renal threshold of a substance is exceeded, reabsorption of the substance by the proximal convoluted tubule is incomplete; consequently, part of the substance remains in the urine.

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61
Q

What is the renal threshold of bicarbonate in the neonate compared to an adult?

A

lower; FT: 21 MEq/L; PT: 18 MEq/L- may be as low as 14 MEq/L

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62
Q

What is the recommended TF for a VLBW PT infant?

A

90 mL/kg/d; may be better to decrease this to 70-80 if possible

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63
Q

What is the target serum Na for a VLBW PT infant?

A

target Na in transitional period is 140-145; on the higher side
(serum 130-135 is ok if the infant is on diuretics after the transitional period)

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64
Q

When should Na be added to TPN?

A

do not add Na to IVF for 24-72h or until serum Na is <140

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65
Q

How should hyponatremia be interpreted?

A

as excessive fluid intake; heme dilution

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66
Q

How should hypernatremia be interpreted?

A

as inadequate fluid intake or insensiblewater loss; heme concentration

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67
Q

Which state is more common in the preterm infant: hyper or hypo natremia?

A

hypernatremia

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68
Q

Why is it important for PT infants to have a positive Na balance after transitional period?

A

to facilitate optimal growth; don’t overdo it if the baby has lung disease

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69
Q

What is the Na requirement of preterm infants after the transitional period?

A

2-4 MEq/kg/d

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70
Q

What is the Na content of NS?

A

0.154mEq/mL

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71
Q

What is the Na content of 1/2 NS?

A

0.075 mEq/mL

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72
Q

What is the Na content of 1/4 NS?

A

0.037 mEq/mL

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73
Q

Why is a positive K balance important?

A

to facilitate optimal growth

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74
Q

When should K be added to TPN?

A

don’t add K until UOP is well established and K is falling

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75
Q

What are the effects of renal failure?

A

1) decrease in GFR
2) increase in waste products
3) fluid and electrolyte imbalance
4) the endocrine fx will be impaired as well

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76
Q

What is the mechanism of pre-renal failure?

A

essentially due to hypoperfusion of the kidney

  • systemic hypoperfusion
  • regional renal hypoperfusion
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77
Q

What is the prognosis of prerenal failure?

A

reversible if diagnosed early > can prevent intrinsic renal failure and subsequent need for transplant

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78
Q

What can cause pre renal failure?

A

1) maternal medications
2) antepartum hemorrhage
3) cardiogenic shock
4) hypothermia
5) postpartum hemorrhage
6) hypovolemia
7) cardiac
8) obstruction of venous return
9) hypoxia
10) septic shock
11) metabolic problems
12) polycythemia/ hyperviscosity
13) ECMO
14) medications that reduce blood flow

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79
Q

What maternal medications can induce prerenal failure in the neonate?

A

1) ACE inhibitors
2) NSAIDS
3) Cyclooxygenase inhibitors (celebrex)

80
Q

What antepartum hemorrhage conditions can result in prerenal failure in the neonate?

A

1) TTTS
2) Fetomaternal transfusion shortly before birth
3) Abruption
4) cord accidents

81
Q

What cardiogenic conditions can result in prerenal failure in the neonate?

A

birth asphxyia

82
Q

How can hypothermia result in prerenal failure in the neonate?

A

a drop in core body temp greater than 2degrees Celsius can cause a severe decrease in GFR

83
Q

What postpartum hemorrhage conditions can result in prerenal failure in the neonate?

A

1) IVH
2) subgaleal hemorrhage
3) adrenal hemorrhage

84
Q

What conditions can cause a state of hypovolemia in the neonate that can induce prerenal failure?

A

1) dehydration/ poor feeding/ BM jaundice

2) increased GI losses (ex: pyloric stenosis and short gut)

85
Q

How can septic conditions can result in prerenal failure in the neonate?

A

1) endotoxin effects on the heart
2) endotoxin effects on the blood vessels
3) edema with 3rd spacing (NEC)

86
Q

How can metabolic conditions can result in prerenal failure in the neonate?

A

1) hypoglycemia
2) hypocalcemia

both are r/t impaired myocardial fx

87
Q

What medications can induce prerenal failure in the neonate?

A

1) Indocin/ibuprofen
2) ACE inhibitors
3) phenylephrine eye gtts

88
Q

What is the mechanism of post renal failure?

A

kidney damage due to mechanical obstruction of urine flow somewhere in the urinary sytem

89
Q

What is the most common cause of hydronephrosis in male infants?

A

posterior uretheral valves

90
Q

If the cause of post renal failure in the neonate is due to posterior urethral valves, what actions are indicated?

A

urology consult, urinary catheter needs to be placed, renal u/s, VCUG, resection of laser ablation of valves and a PT infant may require a vesicostomy

91
Q

What are other causes of post renal failure in the newborn?

A

1) Ureteropelvic junction obstruction (UPJ)
2) Ureterovesical junction obstruction (UVJ)
3) neurogenic bladder (myelomeningocele)
4) Urethral (strictures of obstructed urinary catheter)
5) teratoma
6) calculi (renal stone)
7) renal candidiasis (fungal bezoars)

92
Q

What is acute kidney injury?

A

acute renal failure; intrinsic renal failure

93
Q

What is the incidence of AKI?

A

affects 6-24% of all NICU admissions; every infant admitted is at risk

94
Q

What is often the first presenting sign of AKI?

A

low UOP

95
Q

What is oliguria?

A

UOP <1mL/kg/h

96
Q

What is the prognosis for AKI?

A

early recognition may revere condition and improve the outcome; non-oliguric AKI/ARF has a better prognosis

97
Q

What is significant in the family history that may indicate AKI?

A

a h/o congenital renal dz

98
Q

What is significant in the perinatal history that may indicate AKI?

A
  • prenatal US
  • history of asphyxia (low APGAR scores)
  • abruption
99
Q

What is significant in the physical exam that may indicate AKI?

A
  • abdominal masses
  • genitals, ears, kidneys
  • 2 vessels cord (not necessarily a problem)
100
Q

What is the final common pathway underlying ARF/AKI regardless of etiology?

A

decreased GFR

101
Q

What is the consequence of any prolongation of any pre renal or post renal failure conditions?

A

will lead to structural damage to the kidneys; necrosis of the nephrons

102
Q

What are causes of renal failure?

A

1) acute tubular necrosis
2) congenital anomalies of renal/ urinary system
3) renal vein thrombosis
4) renal artery thrombosis
5) DIC
6) UAC
7) sepsis
8) nephrotoxins

103
Q

What is the cause of acute tubular necrosis?

A
  • prolonged hypoperfusion

- prolonged ischemia/hypoxia

104
Q

What congenital anomalies of the renal/ urinary system can cause intrinsic renal failure?

A

1) renal agenesis
2) polycystic kidney dz
3) congenital nephrotic syndrome of Finnish type
4) renal hypoplasia/ dysplasia

105
Q

What is the clinical presentation of renal vein thrombosis in the IDM with polycythemia and hyperviscosity?

A
  • hematuria
  • enlarged kidneys
  • thrombocytopenia
  • anemia
106
Q

What is the clinical presentation of renal artery thrombosis?

A
  • hematuria
  • enlarged kidneys
  • thrombocytopenia
  • anemia
    AND decreased temp and pulses in lower extremities
107
Q

What is the mechanism of injury for a UAC to induce intrinsic renal failure?

A
  • possible compromised blood flow to kidney

- induced by hyperosmolar solutions

108
Q

What septic states can induce intrinsic renal failure?

A

1) congenital syphillis
2) toxoplasmosis
3) candidiasis
4) pyelonephritis

109
Q

What nephrotoxins can induce intrinsic renal failure?

A

1) aminoglycosides
2) amphotericin B
3) Acyclovir
4) contrast agents
(full recovery is expected over time; may require dialysis)

110
Q

What is the indicated treatment for AKI/ARF?

A

there is no specific therapy; treat the underlying cause

111
Q

What is the indication for a renal US?

A

to assess for structural abnormalities

112
Q

What is the indication for a doppler renal US?

A

to assess for:

1) presence of blood flow
2) direction of blood flow
3) velocity of blood flow

113
Q

What is the indication for a renal resistive index (RRI)?

A

to measure peak systolic and diastolic flow

114
Q

What is the fluid challenge?

A
  • infuse 10-20 mL/kg of NS over 1-2 h

- chase with lasix (1-4 mg/kg/dose IV)

115
Q

When is the fluid challenge indicated?

A

to r/o hypovolemia

116
Q

What do the results of the fluid challenge indicate?

A
  • if UOP increases then it was prerenal failure

- in no change then the pt is in renal failure and there is actual damage to the nephron

117
Q

What is the indication for dopamine in the treatment of renal failure?

A

to increase renal perfusion

118
Q

How much dopamine should be given for renal perfusion?

A

low dose 3-5 mcg/kg/min; in VLBW infants the dose can be as low as 1-2 mcg/kg/min

119
Q

What is the indication for hydrocortisone in the treatment of renal failure?

A

for suspected adrenal insufficiency

120
Q

How much hydrocortisone should be given for adrenal insufficiency?

A

physiologic dosing; start at 3mg/kg/d divided Q6h

* if also hypotensive, can increase to 5mg/kg/d divided Q6h

121
Q

What lab work is indicated for the evaluation of renal failure?

A

1) CBC with diff & plt ( r/o sepsis; r/o thrombocytopenia)
2) blood culture (sepsis is often the cause of ARF/AKI)
3) therapeutic drug monitoring (watch abx levels closely; if creatinine is increased, decreased frequency, NOT dose)
4) UA (evaluate for hematuria)

122
Q

What is the risk with taping an indwelling cath to the thigh of a male infant?

A

may cause damage to posterior urethra; can cause strictures

123
Q

How should hematuria be interpreted?

A
  • blood on urine dipstick may be r/t PRBC tx w/i 3d

- UA will determine if it is true blood or hemoglobin (through microanalysis)

124
Q

What can be interpreted as evidence of tubular damage in a UA?

A
  • presence of casts, tubular cells and protein
125
Q

What are urinary casts?

A

urinary casts are formed in distal convoluted tubule or collecting duct

126
Q

How should the protein result be interpreted from a UA?

A

trace + 1 is acceptable in PT; should not occur with FT

127
Q

What is BUN?

A
  • non specific marker of ARF/AKI
  • reflects accumulation of nitrogenous wastes
  • reflects dietary intake of protein
  • reflects liver’s ability to synthesize urea
    (can be as high as 50 in an otherwise healthy baby)
128
Q

What is creatinine?

A
  • specific marker of ARF/AKI
129
Q

How should creatinine values be interpreted?

A
  • needs serial monitoring
  • in 1st week of life, may reflect maternal creatinine
  • concerning if serum creatinine levels don’t fall within a week after birth
  • if > 1 mg/dL in FT
  • if > 1.5 mg/dL in PT
  • if level rising by 0.2 mg/kg/d
  • if creatinine doubles, it indicates that 50% of renal function has been lost
130
Q

What is the fractional excretion of Na in urine?

A

a measurement of tubular function

- not helpful in PT (nephrogenesis is not complete or if patient was recently given lasix)

131
Q

How should the results of fractional excretion of Na in urine be interpreted?

A

excessive loss of Na indicates tubular damage; differentiates between prerenal and intrinsic renal failure in infants > 32-34 weeks GA

  • prerenal: < 2.5%
  • intrinsic: > 2.5-3%
132
Q

What is the calculation for fractional excretion of Na in urine?

A

(urine Na x serum Cr) / (urine Cr x Serum Na)

133
Q

What is the metabolic presentation of the neonate in renal failure?

A

1) hyponatremia
2) hyperkalemia
3) hypocalcemia
4) hyperphosphatemia
5) metabolic acidosis

134
Q

Why is the neonate in renal failure hyponatremic?

A

d/t decreased UOP and fluid retention; hypoNa is dilutional

135
Q

What treatment is indicated for the neonate with dilutional hyponatremia in renal failure?

A

decreased IVF to insensible H2O (about 30mL in FT/ 50-100 in PT) + UOP

136
Q

What can occur with high output renal failure?

A

hypoNa

  • occurs with both oliguric and nonoliguric ARF/AKI
  • starts when BUN and Cr begin to decrease
  • lasts 24-48h
  • can be a good sign
137
Q

What treatment is indicated for serum Na close to 120 and adequate UOP?

A
  • give 10mL/kg infusion of NS over 30-60 min
138
Q

What treatment is indicated for serum Na <120?

A
  • dangerous level, may result in sz

- in an emergency, consider “hot salts” (3% Na, osmolarity 1.025 mOsm/L); can cause intracranial fluid shifts

139
Q

What is the course of treatment for an infant that is not seizing and Na is > 120?

A

it is best to correct slowly over 24-48 hours

  • add Na to IVF (1-3 mEq/kg)
  • do NOT increase serum Na more than 8 mEq/L in 24h
140
Q

What is the spot Na urine calculation?

A

to determine Na losses in urine
(urine Na x mL UOP in 24h) / wt in g
* then give half of the value for 24h

141
Q

What is the formula to correct serum Na?

A

wt in kg x 0.6 x (CD-CA)= dose in mEq of Na
Concentration desired- concentration actual

  • usually only half of this amount is given over 12-24 hours
142
Q

What actions are indicated for hyperkalemic patient?

A

1) remove all K from IVF
2) give 10% CaGlu to protect heart if EKG ∆ are noted
100-200mg/kg/d over 10-30min
(never through UA)

143
Q

What are immediate treatments to drive K from the intravascular serum?

A

1) 1/2 strength NaHCO3
2) albulterol
3) insulin/glucose gtt

144
Q

How should 1/2 NaHCO3 be administered?

A

1-2 mEq over 10-30min (rapid infusion may increase risk of IVH)
- onset of action is 5-10min

145
Q

How does albuterol affect serum K?

A
  • adrenergic agonist increases plasma insulin concentration (helping to shift K intracellularly)
  • lowers K by 0.5-1.5 mEq/L
  • Onset of action is minimum of 15 min
  • duration of action is 2-3hours
146
Q

How does insulin affect serum K?

A
  • co transports K into cells temporarily
  • continuous gtt 0.1- 0.2 U/kg/h
  • glucose infusion 0.5/kg/h
  • follow blood glucoses Q 15-30 min
147
Q

What measures can rid serum of excess K?

A

1) lasix

2) kayexalate OG/NG/rectally

148
Q

What are the indications for lasix administration?

A

renal fx must be adequate

- give 1mg/kg IV Q12h; onset of action is 5-10min

149
Q

What are the contraindications for kayexalate?

A
  • not to be used in <29 week preterm

- infant with GI problems or poor GI perfusion

150
Q

What is the mechanism of action for kayexalate?

A

exchanges Na for K; rectally works best

151
Q

How is Ca distributed in the body?

A
  • 50% biologically active as iCa
  • 40% bound to albumin
  • 10% complexed or chelated with citrate, lactate, bicarbonate, phosphate & sulfate
152
Q

What is the threshold for determining hypocalcemia?

A

total Ca < 8 (FT)
total Ca < 7 (PT)
iCa < 4 (FT & PT)

153
Q

What is the indicated acute treatment for hypocalcemia?

A

calcium gluconate 100-200mg/kg via PIV over 10-30 minutes with constant cardiac monitoring

154
Q

What is the primary route of phosphorus elimination in the body?

A

via the kidney

155
Q

What is the effect of hyperphosphatemia?

A

excessive phosphate binds with Ca > decreases Ca level

156
Q

What is the indicated treatment of hyperphosphatemia?

A
  • treat with dietary Ca to bind to PO4 (calcium carbonate)

- treat with phosphate binders (aluminum hydroxide)

157
Q

As acidosis is corrected in the neonate, what electrolyte should be monitored closely?

A

treatment of acidosis increases iCa binding to albumin, resulting in decreased circulating levels of iCa

158
Q

What is the effect of HTN on the nephrons?

A

the force of high blood flow over time damages renal blood vessels that can eventually cause sclerosis and scarring of the nephrons

159
Q

What is the proper way to assess BP?

A
  • 1.5h after a feed or medical intervention
  • infant lying prone or supine
  • appropriately sized BP cuff
  • R upper arm
  • after cuff placement, the infant is left undisturbed for 15 min
  • infant should be asleep or quiet awake state
  • 3 successive BP reading at 2 min intervals
  • record the middle BP
160
Q

What is the recommended kcal range for an infant with renal failure?

A

100-120 kcal/kg/day of glucose and fat

161
Q

What is the recommended protein range for an infant with renal failure?

A

~ 2g/kg/d

* too much protein and too little protein adds to the kidney’s work load

162
Q

How does PM 60/40 formula help renally impaired infants?

A

less phosphate

163
Q

What are the different forms of dialysis?

A

1) hemodialysis

2) peritoneal dialysis

164
Q

What is the dialysis method of choice for infants?

A

peritoneal dialysis

165
Q

What are the contraindications for dialysis in the neonate?

A

1) bowel problems
2) coagulopathies
3) hemodynamic instability
4) extreme prematurity

166
Q

What is the mechanism of action for peritoneal dialysis?

A
  • fairly simple and can be done at home
  • peritoneum acts as semipermeable membrane
  • exchange of solutes and H2O between blood and dialysate
167
Q

What are the benefits of a kidney transplant?

A

BETTER THAN LONG TERM DIALYSIS

  • improved survival
  • improved growth and development
  • improved quality of life
  • complications of dialysis and avoided
168
Q

What factors do NOT affect the prognosis of renal failure in neonates?

A
  • birth weight
  • APGAR scores
  • FeNa
  • peak Cr and BUN
169
Q

What is the cycle of renal failure?

A

nephron loss > hypertrophy of remaining nephrons that have excess flow (hyperfiltration) > sclerosis and cause cellular death

170
Q

What are the recommendations for renal f/u in neonates?

A 
at 1 mo after recovery and annually:
1) hypertension
2) proteinuria
3) elevated BUN and elevated Cr
at 5yrs, good prognosis if normal kidney growth
171
Q

Why is the incidence of mortality decreasing in infants with a h/o renal failure?

A
  • improved transplantation

- improved immunosuppressive medications

172
Q

What are the considerations for urine culture collection?

A

1) no need for a UCX in 1st 3 dol

2) ALWAYS consider UTI in septic patient after that time (liability in HR, SpO2, poor feeding)

173
Q

What is indicative of a UTI in a UCX?

A

> 10^3 mL of a single organism
nitrites
leukocyte esterase
cast cells

174
Q

Why are nitrites indicative of a UTI in a UCX?

A

because bacteria convert urinary nitrates into nitrites (think G neg)

175
Q

Why is leukocyte esterase indicative of a UTI in a UCX?

A

WBCs produce this enzyme when they are sent to the site to “clean it up”

176
Q

What is the major site of action for lasix?

A

the loop of Henle

177
Q

What is the mechanism of action for lasix?

A

blocks ACTIVE Cl reabsorption

  • blocks passive Na reabsorption
  • blocks passive Ca reabsorption
178
Q

What is hypochloremic metabolic alkalosis?

A

Na is decreased d/t cellular depletion of K

  • cellular K exits cells to maintain serum levels
  • serum Na moves into cells to take the place of K
179
Q

What is the indicated treatment for hypochloremic metabolic alkalosis?

A

provide PO or IV KCL

  • repletes cellular K allowing Na to move back into the serum
  • corrects hypocholremia
  • corrects acid base balance
180
Q

What should be considered in the treatment for hypochloremic metabolic alkalosis in an infant <34 weeks?

A

you may need to give a small amount of Na Cl (0.5-1); only if renal fx is still immature and you suspect Na losses are still occuring

181
Q

What are the side effects of lasix therapy?

A

1) ototoxicity

2) nephrocalcinosis

182
Q

What considerations for ototoxicity need to be considered when giving lasix therapy?

A
  • limit high peak doses

- do not administer with concurrent use with other ototoxic drugs (ex: aminoglycosides)

183
Q

What considerations for nephrocalcinosis need to be considered when giving lasix therapy?

A

1) renal calcifications occur in babies after a cumulative dose of 20mg/kg
2) nephrocalcinosis usually resolves in ~ 6 months after d/c lasix use (some ELBW infants will have nephrocalcinosis without a h/o lasix)

184
Q

What is the major site of action for thiazides?

A

distal tubule; since only a small amount of Na is absorbed there, diuretic effect is not as effect as with lasix

185
Q

What is the effect of thiazide therapy on electrolytes?

A
  • preserves Ca (potentiates parathyroid hormone)
  • K is lost due to increased urine flow
  • Cl is lost following Na and K
186
Q

What is the effect of thiazide on serum Ca?

A
  • thiazides stimulate PTH secretion and/or potentiate the effect of PTH
  • thiazides enhance reabsorption of Ca in the proximal tubule, ascending loop of Henle, distal tubule and collecting ducts
  • presence of PTH determines whether or not Ca will be reabsorbed
187
Q

What is the major site of action for spironolactone?

A

distal tubule and collecting tubules

188
Q

What is the mechanism of action for spironolactone?

A
  • inhibits Na reabsorption and therefore inhibits secretion of K
  • diuretic effect is not as great as lasix
189
Q

How is spironolactone used in adjunct with other diuretics to spare K?

A
  • aldactazide (combination of hydrochlorothiazide + spironolactone)
190
Q

Why is GA a consideration for spironolactone administration?

A

K losses may not be spared in PT whose distal tubule is hyporesponsive to the effects of aldosterone

191
Q

What is the effect of ADH in the presence of H2O?

A

ADH acts on the distal tubule and collecting duct to reabsorb H2O ( allows for the excretion of concentrated urine)

192
Q

Where is ADH manufactured and stored?

A

produced by the hypothalamus and stored in the posterior pituitary

193
Q

What effects do prematurity have on ADH?

A

PT (and even some FT) are not very sensitive to ADH and will have diuresis; difficulty concentrating urine

194
Q

What is the cumulative effect of decreased sensitivity to ADH in infants?

A

at increased risk for hypovolemia and dehydration

195
Q

What is SIADH?

A

inappropriate secretion of ADH resulting in dilutional hyponatremia and H2O retention

196
Q

What can cause SIADH?

A

1) perinatal asphyxia
2) RDS
3) IVH
4) MAS
5) pneumothorax

197
Q

What is the function of PTH?

A

1) along with calcitrol, PTH controls reabsorption of Ca in renal tubules
2) reabsorption of Ca is similar to Na reabsorption
* Ca absorbed in the presence of PTH; excreted in the absence of PTH

Neonatal Pathophysiology (17 decks)

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