Exam 4 Flashcards
Renal Disease - clinical presentation and labs
o Abnormal growth
o Hypertension (HTN)
o Dehydration
o Edema
UA: blood or protein in urine
acute renal failure - clinical presentation
altered mental status
nausea/vomiting
malaise
Due to electrolyte imbalance
note: this is also for end-stage chronic renal failure
chronic renal failure
hypertension
lab abnormalities (proteinuria, elevated BUN or Cr, anemia, electrolyte abnormalities)
growth failure, rickets
poor feeding
Note: this is when they have not reached end-stage failure yet
- slow process
acute renal failure - pre-renal causes
- including UA and lab findings
dec circulating vol: blood loos, dehydration, shock, hearty failure
blocked blood flow to kidneys: thrombi, masses, trauma
UA: inc. Na and H2O reabsorption, conc. urine (high SG), low urine output
Labs: high BUN and Cr (BUN>Cr), low urine Na, high specific gravity
acute renal failure - renal causes
- including UA and lab findings
damage to tubules (ischemia, toxins), microvascular injury (HUS), glomerular injury (PSGN, HSP, SLE), or interstitial cell injury (drugs)
UA: high urine Na, urine sediment
Labs: high BUN and Cr (Cr>BUN)
acute renal failure - post-renal causes
- including UA and lab findings
anything causing obstruction to urine flow, including anatomical abnormalities or acquire obstructions (renal stones, foreign body, mass, trauma)
- poor urine output
UA: high urine Na, low urine specific gravity
chronic renal failure - causes
intrinsic damage (ischemia, toxins), microvascular injury (HUS), glomerular injury (PSGN, HSP, SLE), interstitial injury (drugs)
DM
renal scarring from missed CAKUT
PKD: polycystic kidney disease
end-stage renal disease
GFR<15%; requires dialysis and medications (to take the place of hormones the kidney would have produced)
Optimal tx = renal transplantation
HUS - clinical presentation
HUS: hemolytic-uremic syndrome
bacterial (E. Coli O:157) cause of ARF (<5y/o) - shiga toxin targets endothelial layer of blood vessels throughout body
- vomit, bloody diarrhea
- petechial rash
- kidney damage and ARF
Triad: microangiopathic hemolytic anemia, thrombocytopenia, renal injury
using creatinine to estimate renal function
As renal fx decreases, serum creatinine level rise proportionally
- for every doubling of serum creatinine, the renal clearance (GFR) has been halved
estimate of urinary protein loss using single UA (instead of 24 hrs)
Urine Protein/Creatinine Ratio (both expressed in mg/dl)
• <0.2 Normal
• >2.0 Nephrotic range (WU for urinary loss of protein)
renal tubular acidosis: what happens and clinical presentation
either insufficient secretion of H+ (type I - permanent) or issue w/ HCO3 reabsorption (type II - kids outgrow by age 4)
- results in metabolic acidosis
Clinical Presentation:
- growth failure
- polyuria, dehydration
- rickets
- renal stones
renal tubular acidosis - evaluation
CMP (included in work-up of a pt w/ growth failure): includes serum bicarbonate, all electrolytes, BUN & Cr
Venous blood gas: lungs should be increasing CO2 excretion in response to the metabolic acidosis
Renal U/S looking for renal stones or hydronephrosis:
• Metabolic acidosis, elevated BUN/Cr, renal stones → refer to nephrology for suspected RTA
• Patients with hydronephrosis → refer to urologist to look for obstructive anomalies
differential diagnosis for red urine
trauma, external (perineal or meatus) irritation)
infants: urate crystals in 1st week of life - normal
Pyridium (urinary tract anestetic): causes red urine
rhabdomyolysis: see myoglobinuria due to severe muscle breakdown
renal stones (renal US/abd x-ray)
upper tract bleeding: dark urine, dysmorphic RBCs and cases (nephron level)
- PSGN, IgA nephropathy, HSP, SLE, MPGN
lower tract bleeding: red urine, whole RBCs, no casts (below nephron)
- usually UTI in PEDS
main diseases that cause types of nephritis and resulting hematuria
post-streptococcal glomerulonephritis (PSGN)
IgA nephropathy
Henoch-Schonlein purpura
Systemic Lupus Erythematosus
Membranoproliferative glomerulonephritis
post-streptococcal glomerulonephritis (PSGN) - clinical presentation
recent URI, sore throat, impetigo
dark urine, edema, HTN, proteinuria
low C3 (transient)
NOTE: most common cause of acute glomerulonephritis (immune-mediated inflammation)
IgA nephropathy - clinical presentation - clinical presentation
males, recurrent hematuria (gross - red), possible URI
normal C3
NOTE: most common cause of chronic glomerulonephritis (immune-mediated inflammation)
Henoch-Schonlein purpura - clinical presentation
most common form of vasculitis in kids (IgA vasculitis)
palpable purpura
arthritic/jt pain
abdominal pain
renal dz (nephritis = hematuria)
NOTE: if renal involved (hematuria) or HTN –> involved nephrology
Systemic Lupus Erythematosus - clinical presentation
hematuria
recurrent/prolonged fever
malar/butterfly rash
arthritic jt sxs
low C3 (active phase - transient)
membranoproliferative glomerulonephritis (MPGN) - clinical presentation
looks like PSGN, but does not resolve in 4-6 weeks
hematuria
edema
HTN
proteinuria
low C3 (persistent)
proteinuria: definition and cause
abnormal levels of protein in urine (due to glomerular capillary membrane damage by disease)
urine dipstick results and correlation to values for urinary protein loss
Trace or negative is normal • 1+: 30 mg/dl • 2+: 100 mg/dl • 3+: 300 mg/dl • 4+: 1000 mg/dl
main diseases that cause nephrotic syndrome and resulting proteinuria
orthostatic proteinuria
nephrotic syndrome
Nil disease
mesangial nephropathy
focal segmental glomerulosclerosis
orthostatic proteinuria - clinical presentation
adolescent / benign
asymptomatic (no edema, no HTN) - occurs w/ activity
- protein/Cr < 2.0
- found incidentally
Note: get F/U first AM UA to verify negative for protein (and get could times in coming yr)
nephrotic syndrome - clinical presentation
any age (2-5 yrs)
- sudden onset of pitting edema or ascites
- proteinuria (nephrotic range: protein/Cr >2.0)
- low serum protein (albumin)
- inc. lipids, inc. clotting, infections
NOTE: most likely dx for proteinuria
- tx w/ Pred - if does not resolve consider chronic dz
Nil disease (minimal change) - clinical presentation
idiopathic nephrotic syndrome (< 6yrs)
- periorbital/pretibial edema
- proteinuria (nephrotic range: protein/Cr >2.0)
- low serum protein (albumin)
- Cr may be low
- HTN and ascites (+/-)
- possibly hematuria
mesangial nephropathy - clinical presentation
occurs at any age
- proteinuria (nephrotic range: protein/Cr >2.0)
- low serum protein (albumin)
- edema
focal segmental glomerulosclerosis - clinical presentation
idiopathic nephrotic syndrome (> 6yrs)
- proteinuria (nephrotic range: protein/Cr >2.0)
- low serum protein (albumin)
- Cr is HIGH
- significant hematuria
- HTN
Ddx for peri-orbital edema
infection, CHF, renal disorders (nephrotic syndrome - Nil disease)
- MUST get a UA if not clear infection to look at protein or blood
nephrotic syndrome
syndrome comprising signs of nephrosis (proteinuria, hypoalbuminemia, and edema)
- loss of protein through the kidneys (proteinuria) leads to low protein levels in the blood (hypoproteinemia including hypoalbuminemia), which causes water to be drawn into soft tissues (edema)
usually managed in primary care and resolves in 2-3 weeks
referral for obstructive uropathy on U/S
urologist
referral for renal damage (as indicated by proteinuria and possibly hematuria)
nephrologist
blood pressure classification - pediatrics
o Normal: <90%
o High: 90-95%
o Significant: 95-99%
o Severe: >99%
BP in PEDS - proper approach to dx of HTN
3 BP measurements on 3 separate occasions
- be sure have right cuff size
- check staff measurements
primary HTN (essential) in PEDS
unlikely unless obese and >12 y/o
- metabolic syndrome = obesity
Note: most common cause of HTN in adolescents
causes of secondary HTN in PEDS
Renal causes (70%):
- renal insufficiency
- nephrotic syndrome / glomerulonephritis
- congenital abnormalities
- structural disorders (Wilms tumor, polycysitc kidney dz)
Vascular causes:
- coarctation of aorta
- renal artery embolism or stenosis
- renal vein thrombosis
- vasculitis
Endocrine cases:
- hyperthyroidism
- pheocromocytoma and neuroblastoma
- hyperaldosteronism
- hypercortisolism (Cushings)
Neurologic causes:
- inc. sympathetic activity (stress, anxiety, pain)
- inc. ICP
Other:
- OSA
- medications
- illicit drugs
evaluation of pediatric pt with HTN
thorough history, ROS, physical exam (focus on secondary causes)
Level 1 work-up: : electrolytes, BUN/Cr, Ca++, thyroid, CBC, U/A + micro, renal U/S
- looks for evidence of renal insufficiency, vasculitis/anemia due to renal disease, renal artery stenosis, and thyroid disorders
- if results pt to specific dz process: treat or refer
- if etiology not discovered: contact nephrologist
management of pediatric pt with HTN
Asymptomatic stage I HTN w/o end organ damage or systemic disease:
• Step 1: therapeutic lifestyle changes
• Step 2: medication
Symptomatic stage II HTN
• Step 1: medication
Hypertensive emergency: prompt hospitalization (parenteral antihypertensive tx with nicardipine, labetalol, esmolol, sodium nitroprusside)
HTN medications used in PEDS
calcium channel blockers, ACE inhibitors, angiotensin receptor blockers, B-blockers, diuretics → more than 1 tx may be needed
- used as step 2 of asymptomatic and step 1 for symptomatic HTN in peds
urinalysis: macroscopic v. microscopic
Macroscopic: uses urine dipstick for pH, presence of protein, glucose, ketones, blood and leukocytes
- Nitrite test may detect bacteriuria if bacteria reduce nitrate to nitrite
Microscopic: confirms pyuria (pus = WBCs), hematuria, casts, crystals
UTI - what is the question you ALWAYS want to ask
about un-investigated or un-diagnosed febrile illness
- sign of recurrent UTI
what can chronic NSAID use cause
proteinuria (spill protein)
anasarca
extreme swelling from nephrotic condition (must go to hospital)
- boys can get a lot of swelling in scrotal area
pediatric UTI - risk factors
Age:
- neonatal uncircumcised boys
- caucasian girls < 24 mo
Obstructive urological abnormalities:
o vesicoureteral reflux (VUR) obstruction
o ureteropelvic junction (UPJ) obstruction
o posterior urethral valves
Dysfunctional voiding (risk factor; also a cause of VUR)
pediatric UTI - most common organism
E. Coli (85%)
pediatric UTI: why so important to dx and tx early
Renal scarring: why UTI in children is important to catch early
- Most common in pts with a hx of recurrent febrile UTI, tx delays >72H, dysfunctional elimination, obstructive uropathies
- Results in renal insufficiency, hypertension and end-stage renal disease
ABX used for suspected UTI based on hx, PE, and dipstick results (awaiting culture)
broad spectrum ABX (cephalosporin - cefixime, cephandir)
UTI: clinical presentation in pediatrics (varies with age)
Pre-term, < 3 mo: poor feeding, apnea/bradycardia, lethargy, tachypnea (fever often absent)
Full-term, < 3 mo: fever, poor wt gain, jaundice (conjugated bili – sign of infection), vomiting
<2yr: suprapubic tenderness, fever >102.2 w/o obvious source (>48hrs), fever >104, uncircumcised or w/ hx of UTI
> 2yr: abd pain, enuresis (inability to control urine), back pain, dysuria, frequency, foul smelling urine