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Nephrology > nelson essential > Flashcards

nelson essential Flashcards

1
Q

What is needed for normal renal function?

A
  1. intact flomerular filtration - regulated by pressure, arterial tone, renin played a part in it
  2. intact tubular function: includes the proximal tubule, loop of hence and distal tubule
    to result in urine formation
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2
Q

What does the proximal tubule do?

A

isosmotic reabsorption

  • reabsorbs 2/3 of filtered volume, sodium and chloride
  • almost completely reabsorbes glucose, amino acids, potassium and phosphate
  • reabsorb 75% of bicarbonate - where it exceeds the threshold, it gets spilled into the urine
  • also secretes organic acids, penicillins, other drugs
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3
Q

which part of the kidney makes calcitriol

A

proximal tubule cells make calcitriol (aka 1,25 OH2) in response to PTH and intracellular Ca/PO4 concentrations

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4
Q

what happens in the loop of Henle

A 
reabsorb NaCl (25%) of what is filtered in the glomerulus 
active chloride transport makes the gradient needed to concentrate urine
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5
Q

What does the distal tubule do

A

includes

  1. distal convoluted tubule : active sodium absorption, helps to dilute urine
  2. collecting ducts -
    - primary site of ADH response
    - aldosterone regulates Na/K and Na/H exchange
    - active H ion secretion to acidify the urine
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6
Q

What is the urinary anion gap?

A

measures the renal ammonia production - the gap between measured anions and cations are largely of NH4
normal urinary gap is 1meq/kg body weight

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7
Q

cause of decreased urinary anion gap

A

problems with renal acid excretion or ammonia production

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8
Q

true or false - preterm newborns are less capable to concentrate urine than term newborns?

A

true
their maximum urinary concentrating capacity is only 400 mosm/L (vs 600-800 mosm/L for full-term newborn) , which is less than in older children and adults

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9
Q

why are infants less capable to excrete a water load than adults

A

because lower GCF (although they can dilute urine similar to adults )

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10
Q

when does GFR reach adult levels

A

age 1-2
GCF in newborn is 40 ml/min/1.73m2
in adult 100-120 ml/min/1.73 m2

neonate can absorb Na efficiently ASAP, but takes 2 years for bicarb

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11
Q

Differential of flank mass in neonate

A
  1. multicystic dysplasia
  2. urinary tract obstruction (hydronephrosis)
  3. polycystic disease
  4. tumor
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12
Q

Differential of hematuria in a neonate

A
  1. acute tubular/cortical necrosis
  2. Urinary tract malformation
  3. trauma
  4. renal vein thrombosis
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13
Q

Differential of anuria/oliguria in a neonate

A
  1. renal agenesis
  2. obstruction
  3. acute tubular necrosis
  4. vascular thrombosis
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14
Q

creatinine affected by which

A

mucle mass, age (plasma creatinine )

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15
Q

BUN affected by which

A

hydration, nutrition, catabolism, tissue breakdown

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16
Q

cause of false positive nitrite test

A 
prolonged contact (ie uncircumsied)
gross hematuria
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17
Q

measure of proteinuria

A

protein/creatinine ratio - very good approximation of 24 hour protein clearance
2.0 in children

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18
Q

nephrotic proteinuria

A

urine protein/creatinine >2.0 or 24 hour protein 40 mg/m2/hour
(normal is <4 mg/m2/hour)

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19
Q

Definition of nephrotic syndrome

A
  1. heavy proteinuria (mainly albumin)
  2. hypoptroteinemia (albumin 250 mg/dL) (- elevated cholesterol/TG
  3. edema

**renal blood flow and GFR not usually diminished, rather get change in oncotic pressure and fluid shifts

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20
Q

Causes of primary nephrotic syndrome

A
  1. Minimal change disease - most common, in >80% of children 35% of these kids progress to renal failure
  2. Membranoproliferative glomerulonephritis - low complement with signs of glomerular renal disease , 5-15%, usually persistent, high likelihood of renal failure
  3. membranous nephropathy - <5%, in teens, with systemic infections/meds
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21
Q

teenager with nephrotic syndrome, has hep B, what type of nephrotic syndrome most likely?

A

membranous nephropathy

occurs in teens/kids with systemic infection - i.e. hepatitis B, syphilis, malaria, todo or on gold/penicillamine

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22
Q

What is congenital nephrotic syndrome

A

presents in first 2 months of type
2 common type - #1: Finnish type, autosomal recessive, mutation in nephron
#2: heterogeneous group of abnormalities
prenatal onset - elevated levels of maternal alpha-fetoprotein
Treatment of familial congenital nephrotic syndrome: early nephrectomy, dialysis and transplantation

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23
Q

Name some secondary causes of nephrotic syndrome in kids

A 
SLE
HSP/Wegener/other vasculitides
chronic infections 
allergic reactions
diagetes
amyloidosis
malignancies
CHF, pericarditis
renal vein thrombosis
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24
Q

Clinical presentation of nephrotic syndrome

A

sudden onset pitting edema/ascites - most common
can get anorexia, malaise, abdo pain
BP can be elevated in up to 25%
diarrhea (intestinal edema) and resp distress (pulmonary edema/pleural effusion) can occur

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25
Q

Typical minimal change disease - clinical characteristics

A 
no hematuria (can occasionally have microscopic hematuria in MCNS) 
normal BP
normal complement (if low suggests other cause than minimal change, also if low should do renal biopsy)
26
Q

Differential of proteinuria

A
  1. transient proteinuria - after vigrous exercise, fever, dehydration, seizures, adrenergic agonist therapy; usually mil (urine protein/cr <1), glomerular in origin, always resolves in few days.
  2. postural (orthostatic proteinuria) - normal protein exertion when laying down but significant when upright
    (can also have tubular or glomerular proteinuria)
27
Q

Treatment of nephrotic syndrome

A

> 80% of children with nephrotic syndrome who are t work to relieve the edema, cautious admin of 25% albumin with loop diuretic can help
HTN treat with beta blockers/Ca channel blockers, ACEi for persistent

28
Q

Complications of nephrotic syndrome

A
  1. infections - bacteremia and peritonitis - Strep pneumo, E. coli, Klebsiella -since have urinary loss of immunoglobulins and complement
  2. hyper coagulable state - since lose antithrombin/plasminogen - risk of thromboembolism - sometimes may need blood thinner
  3. increased atherosclerotic vascular disease from hyperlipidemia

can also get SEs of steroids, hypovolemia (from diarrhea/diuretic)

29
Q

Prognosis of nephrotic syndrome

A

most go to remission , 80% with MCNS can have relapse (heavy proteinuria >3 days) can have transient proteinuria with infection, not considered relapse
FSGS - can progress to kidney failure

30
Q

Microscopic hematuria -

A

> 3-5 RBC/HPF on fresh urine, often benign
can have isolated asymptomatic microscopic hematuria in 4% of healthy children
usually it is transient

31
Q

Ddx of hematuria

A
  1. factitius - non pathologic: ie urate cystals, ingested foods, medications, dyes (ie will be negative on urinalysis); pathologic (i.e. hemoglobinuria from hemolytic anemia, myoglobin from rhabdo)
  2. glomerular - immunological (ie GN - PSGN, IgA, membranoproliferative GN, systemic disease ), structural (Alport, Bm disease), toxin (ie HUS)
  3. Tubulointerstitial/parenchymal
  4. lower urinary tract (UTI, trauma/kidney stone, hypercalciuria)
32
Q

Features of acute post streptococcal glomerulonephritis

A 
hematuria - gross or microscopic
proteinuria
hypertension
edema
oliguria
renal insufficiency
age: 2-12 year old
more in boys
usually 5-21 days (mean 10 days) after strep pharyngitis infection and 4-6 weeks after impetigo
33
Q

acute post infections GN

A

same as post strep GN but with other infections - can happen regardless of whether the kid gets antibiotics

34
Q

treatment priorities in GN

A

take care of BP! can cause heart failure, seizures, encephalopathy
treatment is supportive, involves sodium restriction, diuretics and BP meds as needed
treating strep doesn’t prevent PSGN - should still treat with antibiics if active strep infection
occasionally use steroids/other immunosuppression
ACEi - might help (but use with caution)

35
Q

Presentation of IgA nephropathy

A

can vary, acute GN, asymptomatic microscopic hematuria, recurrent gross hematuria CONCURRENT with URTI

36
Q

What is rapidly progressive GN?

A

typical feutres of acute GN but renal insufficiency progresses more quickly and severely
renal biopsy shows crescents
can be idiopathic or secondary to knob types of GN

37
Q

What is Alport syndrome

A

X linked
mutation in type IV collagen - leads to abnormal glomerular basement membrane - asymptomatic microscopic or gross hematuria
Males: progressive renal failure and sensorineural hearing loss in teens/young adults
Females: more benign, but have usually at least microscopic hematuria
prognosis: all have end stage renal disease - men in 30s, women later

38
Q

What is benign familial hematuria

A

autosomal dominant
often have hematuria in 1st degree relatives
usually the renal disease is not progressive, have good prognosis

39
Q

Painless gross hematuria

A

sickle cell, Wilms, strenuous exercise

40
Q

What is nutcracker syndrome?

A

can be a cause of hematuria (with or without pain) - from the compression of the renal vein between other “stuff”

41
Q

hematuria with low complement C3

A

PSGN
membranoproliferative GN
lupus nephritis

42
Q

true or false - all gross hematuria should be investigated

A

true

43
Q

prognosis of post streptococcal GN

A

usually resolves - within 5-10 days
can have microscopic hematuria for months/years- most recover
IgA nephropathy more likely to progress

44
Q

findings associated with poor prognosis in glomerulonephritis

A
  1. persistent/heavy proteinuria
  2. hypertension
  3. decreased kidney function
  4. severe glomerula lesions
45
Q

management plan for isolated asymptomatic microscopic hematuria/familial hematuria

A

usually good prognosis
do yearly urinalysis to rule out proteinuria
and also do BP yearly (rule out progressive forms of renal disease)

46
Q

What are the findings in hemolytic anemic syndrome?

A
  1. microangiopathic hemolytic anemia
  2. thrombocytopenia
  3. renal injury
47
Q

age group of most patients with HUS?

A

usually <5 year old, can happen in older kids

48
Q

What are the prodromal infections most common in HUS?

A
  1. Typical HUS (with diarrhea prodrome): hemorrhagic enterocolitis from verotoxin and then leads to HUS in 5-15% of kids - most common is E. Coli (most commonly E. coli O156: H7, although other strains can also cause ) which can contaminate meat, fruit, veggies or water with verotoxin; Shigella can also cause verotoxin
  2. Atypical HUS:
    - without a diarrhea prodrome
    - can occur at any age , usually MORE SEVERE than with diarrheal illness prodrome
    - infection: Strep pneumo, HIV, genetic and acquired defects in complement regulation, meds, malignancy, SLE and pregnancy
49
Q

Causes of atypical HUS (i.e. not with diarrhea)

A 
infection - strep pneumo, HIV
complement defects (genetic and acquired)
medications
malignancy
SLE
pregnancy
50
Q

How does HUS present

A
  1. initially have bloody diarrhea
  2. 7-10 days later have weakness, lethargy and oliguria/anuria
  3. irritable, pallor petechiae
  4. dehydration often present, but can have volume overload
  5. Hypertension from volume overload or kidney injury
  6. CNS involvement - in 25% of cases ; including seizures
  7. Other organs: pancreatitis, cardiac dysfunction, colonic perforation
51
Q

Lab findings in HUS

A
  1. Evidence of microangiopathic hemolytic anemia: anemia, thrombocytopenia, shistocytes, helmet cells, burr cells on peripheral blood smear, increased LDH, decreased haptoglobin, increased indirect bill, increased AST, elevated reticulocyte count
  2. evidence of renal injury : elevated creatinine; presence of hematuria, proteinuria, pyuria, casts on urinalysis
  3. Other - leukocytosis, positive stool culture for E. coli O157: H7; positive stool test for shiga-toxin; elevated amylase/lipase
52
Q

What is TTP?

A

rare combination of Fever, microangiopathic hemolytic anemia, thrombocytopenia, abnormal renal function and CNS changes - clinically similar to HUS, but usually in older teens/adults
get more CNS manifestations (from microvascular thrombi) in the CNS, can also have significant renal disease; can have recurrent episodes

53
Q

What is the mutation in TTP?

A

most cases are caused by ADAMTS-13 deficiency - responsible for cleaving high molecular weight mol timers of VWF (vs these will be normal in HUS)

54
Q

Coombs test in HUS?

A

negative

55
Q

stool is negative but you think a kid has HUS?

A

totally possible, E coli might be gone by the time HUS is diagnosed

56
Q

Treatment of HUS

A
  1. volume repletion
  2. control hypertension
  3. manage complications of renal insufficiency - including dialysis
57
Q

Should you transfuse platelets in HUS?

A

no, because they may only add to the thrombotic microangiopathy
should only do if active hemorrhage or in anticipation of a procedure

58
Q

Antibiotics for diarrheal illness and antidiarrheal agents- what do they do to the risk of HUS?

A

they might increase the risk of HUS

59
Q

what intervention in the diarrheal phase of HUS might reduce the severity of renal insufficiency?

A

early hydration

most kids survive the acute phase and recover normal renal function

60
Q

Proteinuria

A 
Proteinuria :
- protein/creatinine ratio >0.2
-  24 hour protein excretion :
4 mg/m2/hour
Nephrotic range: 
- protein/creatnine ratio: >2
- 40 mg/m2/hour

Nephrology (5 decks)

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