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Pediatric Clinical Medicine > Renal Diseases > Flashcards

Renal Diseases Flashcards

1
Q

In primary care, often have reason to be concerned about the possibility of kidney disease in kids who present with ____ or __ in their urine or with __ or ___ problems

A

blood or protein in their urine or with hypertension or growth problems

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2
Q

Functions of the kidney

A
  1. Filtration and Elimination of waste products in the form of blood urea nitrogen (BUN), uric acid and creatinine
  2. Maintain circulatory volume and acid-base balance
  3. Hormonal regulation and Hormonal response
  4. Blood pressure regulation
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3
Q

in dehydration/shock situations, the kidney will maintain circulatory volume at the expense of ____, which, along with the lung, maintains the optimum ____

A

acid-base regulation

pH of our blood.

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4
Q

The kidney is responsible for producing what?

A
  1. renin
  2. erythropoietin
  3. active form of vitamin D
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5
Q

what is Renin?

A

a key component in the renin-angiotensin-aldosterone regulation of blood pressure

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6
Q

What is erythropoietin

A

The hormone which signals the bone marrow to produce red blood cells

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7
Q

How does ADH affect the kidney

A

increase reabsorption of H20

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8
Q

How does PTH affect the kidney

A

Increase reabsorption of Ca2+

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9
Q

How does aldosterone affect the kidney

A

Increase reabsorption of Na+ and excretion of K+

-increases BP

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10
Q

How does ANH,ANP hormone affect the kidney?

A

Decrease reabsorption of Na+

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11
Q

Describe the renin-angiotensin cascade

A

Decreased BP–> renin released from kidney–> cleaves angiotensinogen from liver into angiotensin I–> cleaved by ACE from lung into angiotensin II–> vasoconstricts BV and stimulates adrenal cortex to release aldosterone–> increase Na+ and H20 reabsorption = increase BP

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12
Q

Clinical presentation of renal failure

A
  1. AMS
  2. N/V
  3. malaise
    * caused by significant electrolyte imbalances
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13
Q

Presentation of chronic renal insufficiency

A
  1. HTN
  2. various lab abnormalities: proteinuria or elevated BUN or Cr
  3. growth failure
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14
Q

Causes of pre-renal acute failure

A
  • etiologies which decrease circulating volume:
    1. blood loss,
    2. dehydration,
    3. shock including anaphylaxis, cardiogenic or septic, heart failure)
  • or blocked blood flow to the kidneys:
    4. renal artery thrombi/masses or
    5. trauma
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15
Q

Lab findings with pre-renal failure

A
  1. High BUN and Cr w/ BUN greater than Cr*
  2. Low urine Na+**
  3. High urine specific gravity*
  4. low urine output
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16
Q

Causes of intrinsic renal failure

A
  1. damage to the tubules (shock, toxins)
  2. microvascular injury (HUS)
  3. glomerular injury (PSGN, HSP, SLE)
  4. Interstitial cell injury (Drugs)
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17
Q

Describe the prognosis of intrinsic renal failure

A

While some intrinsic renal failure is recoverable, some of the causes listed here can result in permanent renal damage and some degree of chronic renal insufficiency/failure

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18
Q

Causes of post renal failure

A
  1. anything that causes obstruction to urine flow such as anatomical abnormalities:
  2. UPJ obstruction
  3. posterior urethral valves,
  4. neurogenic bladder
  5. or acquired obstructions:
  6. renal stones
  7. Foreign body,
  8. masses,
  9. trauma
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19
Q

in post renal failure, Because the obstruction needs to be bilateral or at the level of the bladder or lower to cause symptoms of acute renal failure, the consequence of ___ is rarely seen

A

poor urine output

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20
Q

Lab findings associated with intrinsic renal failure

A
  1. High BUN and Cr with Cr greater than BUN*

2. high urine Na+, urine sediment

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21
Q

Lab findings associated with post renal failure

A
  1. high urine Na+

2. low urine specific gravity*

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22
Q

Whatever the cause, as renal function decreases the serum creatinine level will ___.

Ex- a child whose normal Cr is 0.5, who now has a Cr of 2.0, how has their GFR changed?

A

rise proportionally

-so that for every doubling of serum creatinine, the renal clearance, expressed as glomerular filtration rate (GFR), has been halved.

For example a child whose normal Cr is 0.5, who now has a Cr of 2.0 (doubled twice 0.5 to1, 1 to 2) has decreased their GFR to 25% (halved twice 100%to50%,50%to 25%).

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23
Q

Obvious renal failure does not result until ___% of nephrons are lost in both kidneys (progressively)

A

75%

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24
Q

End-stage renal disease is defined by

A

as GFR less than 15% and requires dialysis as well as medications to take the place of hormones the kidney would have produced

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25
Q

What kind fistula is commonly used for hemodialysis and peritoneal dialysis

A
  • hemodialysis: forearm AV fistula

- peritoneal dialysis: peritoneal shunt

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26
Q

causes of chronic renal insufficiency

A
  1. intrinsic ones
  2. DM
  3. renal scarring from missed urinary malformation
  4. PKD
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27
Q

What causes HUS (hemolytic-uremic syndrome)?

A

E. Coli O:157 bacteria found in fresh vegetables, undercooked hamburger, unpasteurized fruit and milk, petting zoos

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28
Q

Initial illness of HUS presents as

A

vomiting and bloody diarrhea after ingestion of the bacteria

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29
Q

How does E. Coli O:157 cause HUS?

A
  • This strain of E. Coli carries a Shiga toxin, which targets the endothelial cell layer of blood vessels, which results in cell death and microthrombi. The damaged blood vessels result in shearing forces on the passing RBC’s, resulting in hemolysis.
  • The vessel damage occurs in the nephron of the kidney, resulting in kidney damage and possible acute renal failure
  • There is additional microvascular bleeding in the skin resulting in a petechial rash
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30
Q

how do HUS damaged cells appear?

A

“helmet” cells

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31
Q

Work up and treatment of HUS

A
  1. All patients with bloody diarrhea will have a stool culture, but if you suspect exposure to E. Coli O:157, you must specify that on the lab order
  2. The treatment of the initial diarrheal illness consists of supportive inpatient care, as antibiotic treatment is associated with an increased likelihood of HUS
  3. sometimes requires dialysis and transfusions
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32
Q

Who is most at risk for HUS after E. Coli O:157 diarrhea?

A

young and elderly

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33
Q

describe the prognosis of HUS

A

variable w/ some pts dying and others having a complete recovery and some w/ residual renal insufficiency

*most pediatric patients do recover

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34
Q

Presentation of renal tubular acidosis (RTA) in children

A
  1. usually presents as growth failure
  2. polyuria
  3. episodes of dehydration
  4. rickets
  5. renal stones
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35
Q

What is Rickets

A

a bony deformity of the legs, which involves the femur and tibia resulting in patellas that are rotated laterally

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36
Q

Renal rickets, due to RTA, is caused by:

A

abnormalities of electrolytes including calcium and phosphorous, due to the kidney’s poor ability to control the reabsorption and secretion of electrolytes.

  • Renal rickets is so rarely seen in the US that RTA is an important differential to consider here
  • caused by nutritional deficiencys in developing countries
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37
Q

What is the difference between Type I and II RTA?

A
  • Type I RTA- there is insufficient secretion of H+ into the urine, again resulting in a metabolic acidosis. As the blood pH drops, hypokalemia can result.
  • usually permanent defect
  • Type II RTA- the proximal tubule does not resorb bicarbonate ion, resulting in a metabolic acidosis.
  • typically outgrown by age 4yr
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38
Q

How do you treat RTA type I and II

A
  1. . Both types can be treated with large amounts of buffer (citrate) to overcome how much they are losing in their urine, and treatment of this disorder is managed by a nephrologist.
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39
Q

From a primary care standpoint, the work-up of a pt w/ growth failure includes:

A
  1. CMP- which will include serum bicarbonate, as well as all electrolytes, BUN and Cr
  2. venous blood gas, as the lungs should be increasing CO2 excretion in response to the metabolic acidosis, if the problem is renal in origin.
  3. A renal ULTZ looking for renal stones or hydronephrosis
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40
Q

When should you refer a pediatric patient to nephrology with suspected RTA?

A

Pediatric patients with:

  1. metabolic acidosis,
  2. elevated BUN/Cr,
  3. renal stones

should be referred to nephrology for suspected RTA.

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41
Q

Patients w/ ___ should see a urologist to look for ___

A

hydronephrosis

obstructive anomalies

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42
Q

key elements when assessing a patient with red urine

A
  1. history

2. appropriate lab testing

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43
Q

Infants in the first week of life often have ___ in their urine, leading to a brick-red colored urine in their diaper.
-It is concerning to parents, so reassurance is necessary.

A

urate crystals

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44
Q

what medication can cause red urine?

A

Pyridium- urinary tract anesthetic

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45
Q

What causes myoglobinuria?

A
  1. severe muscle trauma
  2. burns
  3. dehydration

**substantial muscle breakdown

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46
Q

____ is toxic to the renal tubules and can result in acute renal failure.

A

myoglobin

**it is important to watch someone w/ a hx of myoglobinuria

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47
Q

How can you differentiate between and upper (nephron) vs lower tract bleeding?

A

Upper:
-dark “cola-colored” urine
+ dip stick
-urine microscopy w/ dysmorphic RBS and RBC casts

Lower:
-Red or pink urine
+ dip stick
-urine microscopy of WHOLE RBCs w/ NO casts

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48
Q

urine RBC’s ____ is considered clinically insignificant and no work-up is necessary.

A

less than 5/hpf

49
Q

When blood is coming from a damaged nephron will have traveled through the glomerulus when it shouldn’t have, it will be ____

A

dysmorphic or broken

50
Q

RBC’s will get squished together in the ____ forming a red cell cast, a gelatinous tubule-shaped stack of RBC’s

A

distal collecting duct

51
Q

gelatinous tubule-shaped stack of RBC’s

A

RBC casts

52
Q

Where can lower tract bleeding come from?

A
  1. renal calycyes
  2. ureters
  3. bladder
  4. urethra

*often caused by UTIs

53
Q

DDX for red urine

A
  1. infants- urate crystals
  2. meds- Pyridium
  3. Rhabdomyolysis due to trauma, severe dehydration- myoglobinuria
  4. Upper tract (nephron)
  5. Lower tract (calcyces, ureters, bladder, urethra)
  6. menstruation
  7. urine obtained via catheterization
  8. hematuria
54
Q

most common causes of hematuria

A
  1. post-streptococcal glomerulonephritis (PSGN)*
  2. IgA nephropathy
  3. Henoch-Schonlein Purpura (HSP)*
  4. SLE
  5. Membranoproliferative Glomerulonephritis (MPGN)

*managed in primary car w/ phone calls to nephrology

55
Q

Patients diagnosed with HSP only need ___ for signs of hematuria indicating renal involvement

A

urine monitoring

56
Q

What renal disease cause hematuria and have a low C3 complement component, and how do they present?

A
  1. PSGN
  2. SLE
  3. MPGN (persistently low)

*present w/ more gross hematuria vs dark urine of most renal diseases w/ hematuria

57
Q

MPGN is often initially diagnosed as ___ these

A

PSGN

58
Q

How can you differentiate MPGN and PSGN

A

MPGN will have a persistently low C3 level

-PSGN will return to normal in 4-6 weeks

59
Q

What should you do in the setting of persistently low C3 levels?

A

refer to nephrology as these patients will need a renal biopsy to determine if their hematuria is actually MPGN

60
Q

What is the primary care approach to PGSN

A
  1. manage HTN
  2. tx for GAS if ASO/Streptozyme +
  3. supportive care/wait for remission
61
Q

Presentation of PSGN

A
  1. Recent URI
  2. sore throat or impetigo
  3. may have dark urine,
  4. edema
  5. HTN
  6. proteinuria
  7. Age 2-12 y/o
62
Q

PSGN lab findings

A
  1. ASO + if strep throat
  2. Streptozyme + if impetigo
  3. low C3
63
Q

What is the primary care approach to IgA Nephropathy

A

referral to nephrology

64
Q

What is the primary care approach to suspected MPGN

A

referral to nepthrology

65
Q

What is the primary care approach to HSP

A
  1. supportive care
  2. watch for hematuria or abdominal pain
  3. watch for GI vasculitis- risk for intussusception
  4. involve nephrology if hematuria develops in a pt with HSP
66
Q

What is the primary care approach to SLE

A

refer to rheumatology

67
Q

What is the clinical presentation for IgA nephropathy

A
  1. Male
  2. Adolescent
  3. Recurrent episodes of bloody urine
68
Q

What is the clinical presentation for HSP

A
  1. Palpable purpuric rash
  2. joint swelling/pain
  3. renal/GI vasculitis
  4. 3-15 y/o
69
Q

What is the clinical presentation for SLE

A
  1. hematuria in the setting of recurrent/prolonged fever
  2. malar rash
  3. arthritic joint sx
  4. adolescent
70
Q

What is the clinical presentation for MPGN

A
  1. Hematuria sometimes w/ proteinuria
  2. may look like PSGN
  3. child-young adult
71
Q

What are the lab findings for IgA nephropathy

A
  1. C3 normal
72
Q

What are the lab findings for HSP

A
  1. high WBC
  2. high CRP, ESR
  3. normal plt count
  4. may have hematuria
  5. +/- proteinuria if renal involvement
73
Q

What are the lab findings for SLE

A
  1. Low C3
    • ANA
    • Ab to dsDNA
74
Q

What are the lab findings for MPGN

A
  1. Persistently low C3
75
Q

What should you do if want to test for ANA to assess for SLE nephritis?

A

phone consult w/ pediatric rheumatologist bc ANA are very non-specific and weakly positive ANA’s generate a lot of parental anxiety and fill up the schedules of pediatric rheumatologist, and, at the end, often have a neg. work up for SLE

76
Q

Who should be tested for SLE

A

those who meet the diagnostic SLE criteria

77
Q

How should a gross or symptomatic microscopic hematuria guide your work up?

A
  1. hx of trauma–> CT of abdomen and pelvis
  2. sx of UTI–> urine culture, abx ,recheck UA after
  3. sx of perineal or meatus irritation–> reassurance and supportive care
  4. sx of renal/ureteral stones–> imaging (renal u/s, abdominal plain film)
  5. sx of glomerular source (proteinuria, or RBC casts)–> check BUN/Cr, electrolytes, CBC, C3, C4, Albumine and consider ASO, streptozyme, ANA testing –> refer to nephrologist
78
Q

What should you do w/ a pt w/ hematuria with no obvious cause on hx, physical, or urinalysis?

A

Consider:

  1. urine culture
  2. urine calcium/creatinine ratio
  3. test parents for hematuria
  4. hemoglobin electrophoresis
  5. renal u/s
79
Q

When does protein sometimes spill into the urine

A
  1. activity

2. when glomerular capillary membrane is damaged by disease

80
Q

what is often used in lieu of the 24hr urine collection used to determine urinary protein lossses

A

using a single urinalysis and calculating the urine protein/serum creatinine ratio

*In order to use the ratio, both the urine protein and the creatinine must be expressed in mg/dl.

81
Q

When proteinuria is present with hematuria, consider ___

A

glomerulonephritis

82
Q

When proteinuria is present with hypertension, the patient may have ___

A

significant renal insufficiency

83
Q

what proteinuria is presetnt w/ edema consider __

A

nephrotic syndrome or glomerulonephritis

84
Q

when proteinuria is present with polyuria, consider __

A

chronic renal insufficiency or urinary tract anomalies.

85
Q

what is 1+ , 2+, 3+, 4+ urine dipstick mean

A 
trace or neg is normal
1+ = 30mg/dl
2+ = 100mg/dl
3+ = 300 mg/dl
4+ = 1000mg/dl
86
Q

what is a normal and a nephrotic range of urine protein/creatinine ratio

A

Normal: less than 0.2

Nephrotic range: over 2.0

87
Q

These patients do not spill protein until they are more active during the day, so this represents an exaggeration of normal physiology

A

orthostatic proteinuria

88
Q

Clinical presentation of orthostatic proteinuria

A
  1. adolescent age
  2. Asymptomtatic
  3. isolated finding
  4. no hematuria
  5. normal BP
  6. normal anatomy
  7. Urine protein/Cr ratio on AM urine slightly higher PM but not nephrotic
89
Q

Clinical presentation of nephrotic syndrome

A
  1. any age, but more common 2-5y/o
  2. edema
  3. proteinuria w/ urine protein/Cr ratio in nephrotic range
  4. low serum albumin
  5. increased lipids
  6. increased risk of clotting, infections, and severe edema
90
Q

Clinical presentation of Minimal change (Nil) Disease

A
  1. less than 6y/o
  2. significant periorbital/pretibial edema
  3. +/- HTN or ascites
  4. proteinuria
  5. low serum albumin
  6. Cr may be low
  7. possible minimal hematuria less than 20-30 RBCs’s/hpf
91
Q

Clinical presentation of Mesangial nephropathy

A
  1. any age
  2. proteinuria
  3. low serum albumin
  4. edema
92
Q

Clinical presentation of Focal Segmental Glomerulosclerosis (FSGS)

A
  1. less than 6y/o
  2. proteinuria
  3. low serum albumin
  4. high serum creatinine
  5. significant hematuria
  6. elevated B/P
93
Q

nephrotic syndrome has an increased risk of what?

A

clotting, infections, and severe edema

94
Q

tx of nephrotic syndrome

A
  1. prednisone 2mg/kg/d (max 80) x 6 weeks, then QOD then taper
  2. follow pt clinicaly for complications and HTN

*managed in primary care unless the edema is severe, there are complications or an alternative dx is considered, or not improving as expected

95
Q

tx of minimal change (Nil) disease

A

prednisone and nephrologist

96
Q

tx of mesangial nephropathy

A

prednisone and nephrologist

97
Q

tx of FSGS

A

nephrologist

  • less responsive to prednisone
  • may progress to renal failure
98
Q

tx of orthostatic proteinuria

A
  1. get f/u first AM urinalysis to verify protienuria
    * . It is sometimes prudent to follow the urinalysis a couple of times in the next year, as their initial small proteinuria may progress into proteinuria that needs further workup
99
Q

What lab should you always get with periorbital swelling

A

urinalysis

100
Q

All proteinuria which falls within nephrotic range will also have an associated ____. It may or may not have ___ or __

A

low serum albumin.

an elevated creatinine or elevated b/p.

101
Q

Most nephrotic syndrome remits in ___

A

2-3 weeks

102
Q

What diseases should be suspected if what was thought to be a nephrotic patient also has or develops hematuria, elevated Cr, or HTN.

A
  1. Minimal change (Nil) disease
  2. mesangial nephropathy
  3. focal segmental glomerulosclerosis (FSGS)

*involve an nephrologist if these occur

103
Q

What should you do if you find 1+ or greater proteinuria in a child incidentally?

A
  1. obtain 1st AM void for urine total protein/creatinine ratio and UA w/ microscopic exam
  2. if 0.2mg or less of protein per mg creatinie and normal UA –> repeat dipstipstick on first AM void in 1 yr
  3. if over 0.2mg protein per me creatinine or abnormal UA–> evaluate fhx, hx of drugs, PE/BP, labs, and other tests–> if normal repeat urine dipstick on at least 2 additional samples
    - -> if abnormal refer to nephrology
104
Q

What should you do if renal utlz reveals obstructive uropathy?

A

referral to urologist NOT nephrologist

*They need to have their obstruction corrected and then if they still have proteinuria, may need to see a nephrologist for management of their possible renal damage.

105
Q

What is the work up symptomatic proteinuria

A

if nephrotic syndrome–> tx w/ prednisone and assess respone–> refer to nephrology

if +hematuria glomerulophritic–> see hematuria/GN algorithm

106
Q

What labs should you obtain if you find 1+ or greater proteinuria in a child incidentally with over 0.2mg protein per me creatinine or abnormal UA

A
  1. creatinine
  2. BUN
  3. electrolytes
  4. cholesterol
  5. albumin
107
Q

for BP

  • lower than 90th percentile is: __
  • 90-95th percentile is: __
  • 95-99th percentile is: __
  • Over 99th is: __
A
  • lower than 90th percentile is: normal
  • 90-95th percentile is: high
  • 95-99th percentile is: significant
  • Over 99th is: severe
108
Q

It is important to have __ BP readings on __ separate occasions prior to determining the child is hypertensive, although primary care providers should move forward with an evaluation/management on a child with severe HTN, or evidence of hypertensive emergency with H/A, visual disturbance, seizures, focal neurologic findings, altered mental status or chest pain

A

3

3

109
Q

Children rarely have essential or primary hypertension unless they are __ and __

A

obese and over 12y

*always make sure it is the right cuff size and always recheck staff BP

110
Q

DDX of secondary HTN

A
  1. coarctation of the aorta
  2. renal disease (70%)
    -Post-streptococcal glomerulonephritis (PSGN)
    -renal insufficiency
    -+/- minimal change (Nil) disease
    -Focal Segmental Glomerulosclerosis
    (FSGS)
  3. hyperthyroidism (rare)
  4. pheocromocytoma (rare)
111
Q

When evaluating pediatric HTN, what hx info is important?

A
  1. PMH for UTIs, prematurity w/ umbilical cath or bronchopulmonary displasia
  2. Meds
  3. FHx for DM, HTN, cardiac/renal dz, dyslipidemia
112
Q

When evaluating pediatric HTN, what PE is important?

A
  1. growth: wt and ht failure
  2. VS: BP and HR
  3. HEENT: papilledema
  4. thryoid
  5. cardiac/pulses: murmur, edema, brachiofemoral lag
  6. abdomen: masses, renal bruit
  7. GU: ambiguous genitalia (CAH)
  8. skin: dry or sweating
  9. Neuro: focal deficits
113
Q

When evaluating pediatric HTN, what ROS info is important?

A
  1. HEENT: symptoms of OSA
  2. renal: gross hematuria, edema, enuresis,
  3. cardiac: chest pain, dyspnea, palpitations, claudication,
  4. endocrine: sweating, weight loss, diarrhea(hyperthyroid and pheo), weight gain, constipation (hypothyroid),
  5. rheumatologic: rash, joint symptoms, persistent/recurrent fever,
  6. CNS: H/A, visual changes, gait disturbances
114
Q

What is the level 1 work up for pediatric HTN

A
  1. electrolytes
  2. BUN/Cr
  3. Ca+
  4. thyroid
  5. CBC
  6. UA + micro
  7. renal u/s
  • done in primary care
115
Q

The Level 1 work-up for HTN is done in primary care, looking for evidence of:

A
  1. renal insufficiency,
  2. vasculitis/anemia due to renal disease,
  3. thyroid disorders
  4. renal artery stenosis.

*If the history, PE or labs point toward a disease process listed here, treat or refer as appropriate.

116
Q

What is the level 2 workup for pediatric HTN?

A

*sometimes necessary to do in primary care– but contact a nephrologist for further guidance

  1. fasting glucose
  2. lipid panel
  3. plasma renin activity
  4. serum aldosterone and cortisol
  5. echo
117
Q

When do you refer a kid to cardiology for HTN?

A
  1. evidence of aortic coarctation
  2. evidence of CHF

**never refer pt to cardiology for HTN of uncertain etiology

118
Q

What renal disease can cause HTN

A
  1. Post-streptococcal glomerulonephritis (PSGN)
  2. renal insufficiency
  3. +/- minimal change (Nil) disease
  4. Focal Segmental Glomerulosclerosis
  5. ESRD

Pediatric Clinical Medicine (18 decks)

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