kidney function is indicated by the
GFR (glomerular filtration rate)
The kidneys of children reach adult GFR at approximately
1 year of age, but measured GFR vary by age book says 2 years
GFR can be estimated (eGFR) with what equation
schwartz equation
eGFR mL/minute/1.73m2 = (k) (height)/serum creatinine
k = constant of 0.413 for all ages/genders
height is measured in cm
serum creatinine is measured in mg/dL
renal blood flow is dependent on
intravascular volume and adequate cardiac output with oxygenated blood
equation used to determine whether kidney dysfunction is only a result of hypoperfusion to kidney
fractional excretion of sodium
normal BUN-to-creatinine ratio
10:1 to 20:1
Elevated BUN-to-creatinine ratios are associated with
shock or dehydration with acute kidney failure
can also be from nephrolithiasis or gastrointestinal or pulmonary hemorrhage
Low BUN-to-creatinine ratios are associated with
rhabdomyolysis, syndrome of inappropriate antidiuretic hormone secretion, lung disease, malignancy, low dietary protein intake or certain medications
an abrupt cessation or significant decline in the kidneys ability to eliminate waste products, regulate acid-base balance and regulate electrolyte balance
Acute renal failure
resorption of electrolytes occurs predominantly where
the proximal convoluted tubule
renal wasting of sodium can be due to
pseudohypoaldosteronism following a chronic tubular injury (bilat hydronephrosis), true hypoaldosteronism (congenital adrenal hyperplasia) or excessive diuretic use.
acidosis increases serum
potassium as hydrogen ion displaces potassium from the intracellular compartment and alkalosis is associated with decreases in serum potassium with reversed cation movement
under hyperkalemic conditions, _____ is secreted and ____ is eliminated by the kidney
aldosterone is secreted
potassium is eliminated
tubular reuptake of potassium occurs in the
proximal tubule and the thick ascending loop of henle
medications associated with magnesium wasting are associated with
natriuresis and/or general tubular epithelial cell damage:
loop and thiazide diuretics, calcineurin inhibitors, cisplatin, ifosfamide, amphotericin B and aminoglycosides
transient wasting of _____ can occur following recover from AKI
magnesium
_____ has been associated with hypokalemia due to kaliuresis
hypomagnesemia
Development of nephrogenic structures begins
3rd-5th week of gestation
Development of nephrogenic structures requires angiotensin II. What maternal medication can cause harm to this process
Ace inhibitors can result in fatal renal dysplasia
Fetal kidneys require only ____ of cardiac output
10%
At birth, cardiac output _____ and renal vascular resistance ______
increases
decreases
increase in GFR and renal blood flow
Renal blood flow is dependent on
intravascular volume and sufficient cardiac output
collection of epithelial cells within the distal convoluted tubule that (in conjunction with arterioles) senses the Na levels
Juxtaglomerular apparatus (JGA)
renal response to Decreased renal blood flow
renin secretion which increases reabsorb of NA which increases intravascular volume
renal response of Sympathetic pathways activated
vasoconstriction of renal arterioles → increased GFR/intraglomerular pressure
what are some medications mentioned that affects renal blood flow d/t inhibition of afferent arterioles dilation
Prostaglandin inhibitor therapy to promote PDA closure can cause AKI
IV acetaminophen (also used to promote PDA closure) has some transient oliguria noted
ACEs/ARbs can affect intraglomerular pressure by decreasing the efferent arteriolar tone. Using prior to delivery or during neonatal period has been associated with acute kidney failure
eGFR is influenced by the
serum creatinine
useful for populations in which creatinine cannot be used (hepatic failure, spina bifida, malnutrition) to detect kidney injury
Cystatin C serum concentration
what is testicular torsion
twisting of the spermatic cord causing compromised blood flow to the testicle
2 types of testicular torsion
intravaginal
extravaginal
spermatic cord twists around the tunica vaginalis
intravaginal testicular torsion
spermatic cord twists proximal to the tunica vaginalis (entire scrotal contents)
extravaginal testicular torsion
which type of testicular torsion is more commonly seen
intravaginal (accounts for 90% of testicular torsion cases)
what happens that allows for a intravaginal testicular torsion to occur
it is a congenital malformation resulting in abnormal fixation allowing the epididymis, spermatic cord and testicle to hang freely in the scrotal sac. This allows the structures to twist within the tunica vaginalis
what is the deformity called seen in intravaginal testicular torsion
usually a bilateral deformity referred to as “Bell Clapper” deformity
which testicular torsion occurs perinatally during the descent of the testes and may even be present at birth
Extravaginal testicular torsion
what are the predisposing factors in testicular torsion
trauma
testicular tumor
testicles lying in horizontal plane
history of cryptorchidism and increasing testicular volume
what ages does testicular torsion most commonly present?
children < 3 years old
after puberty
clinical presentation of testicular torsion
sudden onset of pain in the testis, usually unrelenting
testis is enlarged and tender
absence of cremasteric reflex
affected testicle higher in scrotum
what is gold standard for diagnosis of testicular torsion
ultrasound
what ultrasound finding is diagnostic for testicular torsion
absence of blood flow to the involved testis; twisting of spermatic cord
treatment for testicular torsion
emergent surgical exploration
manual detorsion of testis
affix testis to scrotal wall to prevent recurrence (Orchiopexy)
in most cases, contralateral testis will also be explored and fixed with nonabsorbable sutures to prevent future torsion
if the testicle cannot be salvaged, it is removed. (orchiectomy)
IV fluids, NPO, analgesia when prepping for OR
If loss of testis, support from child life, social/spiritual support may be beneficial
what window do you have before there is irreversible testicular injury in a testicular torsion
4-8 hours generally speaking
if the testicle cannot be salvaged, it is removed.
orchiectomy
affix testis to scrotal wall to prevent recurrence
Orchiopexy
ovarian torsion
twisting of adnexal structures compromising blood flow to the ovary
ovarian torsion is usually associated with a
cyst or mass
the occurrence of ovarian torsion peaks in
adolescence
clinical presentation of ovarian torsion
acute onset of abd pain caused by ischemia (more common on R side)
nausea and vomiting
in ovarian torsion the abd pain is more common on what side
R
what diagnostic is the definitive study for ovarian torsion
Doppler US
what is seen on Doppler US to diagnose ovarian torsion
assess for absence of blood flow in the involved ovary or associated ovarian cyst or mass
false negative results are possible depending on severity of torsion
what additional imaging is reserved for patients with nondefinitive findings on US and intermittent symptoms of ovarian torsion
Abd CT or MRI
Other than imaging what else will you order when you suspect ovarian torsion and why
CBC - evaluate for anemia
Urinalysis to evaluate for UTI
B-hCG to evaluate for pregnancy
Treatment of ovarian torsion
medical emergency
Emergent surgical exploration
Detorsion of involved ovary
cystectomy if indicated
rarely is oophorectomy indicated; ovary can often be salvaged for up to 24 hours after the onset of abd pain
an ovary can often be salvaged in ovarian torsion for up to ___ hours after the onset of abd pain
24
Hemolytic Uremic Syndrome (HUS) is a disease of the
microcirculation
HUS is characterized by
hemolytic anemia, thrombocytopenia, and acute renal failure (ARF).
HUS is most frequently seen in
children < 4 years of age
HUS is the most common cause of
Acute renal failure (ARF)
etiology of HUS
contamination of water, meat, fruits and vegetables with infectious bacteria; peak incidence during summer.
E. coli 0157:H7 is the most common etiology of post-diarrheal (D+) HUS
what season is peak occurrence of HUS
Summer
what pathogen is the most common etiology of post-diarrheal (D+) HUS
E. Coli 0157:H7
what are the 2 types of HUS
D+ HUS and
D- HUS
which type of HUS is Postdiarrheal or typical HUS
D+
which type of HUS is atypical or sporadic HUS
D-
which HUS is more severe
D-
which HUS occurs in previously healthy children
what illness did they have recently?
D+
gastroenteritis
what pathogen and toxins are associated with D+ HUS
Bacterial verotoxins are absorbed through intestinal mucosa (produced by E.coli 0157:H7 infection) - Shiga toxin is the most common cause.
shigella dysenteriae
Citrobacter freundii
other subtypes of E.coli
what toxin is the most common cause of D+ HUS
shiga toxin
which type of HUS carries a higher mortality rate
D- (50%)
as opposed to D+ (3-5%)
which type of HUS is associated with ESRD
D- in 50% of cases
D - is more common in _____ but may also begin in the _____ period
adulthood
neonatal period
which type of HUS may have a familial link
D-
D- HUS occurs primarily in what season and is associated with what prodrome?
Year round
not associated with GI prodrome like D+
causative factors of D- HUS
inherited factor H deficiency
(inhibits complement activation, membrane cofactor protein mutations
streptococcus pneumoniae infection
medications including cyclosporine and Tacrolimus
what pathogen is associated with D- HUS
streptococcus pneumoniae
what medications are associated with D- HUS
Cyclosporine
Tacrolimus
D+HUS occurs as a result of _______, esp ___ ____, absorbed by the intestinal mucosa, which damage _____ cells and ______, producing a prodrome of _____ ________.
verotoxins Shiga toxin endothelial cells erythrocytes Hemorrhagic enterocolitis
endothelial swelling of the glomerular arterioles in the kidneys secondary to HUS results in a decrease in ________, _________, and __________
GFR
Proteinuria
hematuria
In HUS, this characteristic _______ precipitates the release of ____ ____, ___ ___, and ____ ___ in the small vessels of the kidney, gut and CNS, resulting in ___ ____; shearing of RBCs as they pass through narrowed vessels, ______ ______ and ____ and ______.
microangiopathy clotting factors platelet aggregation fibrin deposition hemolytic anemia renal cortical injury ARF thrombocytopenia
triad is
thrombocytopenia
ARF
microangiopathic hemolytic anemia
incubation period of D+ HUS in a healthy child with exposure to contaminated source
3-5 days
symptoms of D+ HUS
abd pain watery, nonbloody diarrhea fever weakness lethargy irritability
In D+ HUS progression to hemorrhagic colitis occurs how long after onset of diarrhea
5-7 days
findings in D+HUS
pallor
petechiae
ecchymoses
hematuria
oliguria (abnormally small amount of urine)
azotemia (elevated levels of urea and other nitrogen compounds in blood)
HTN
progresses to anuria hepatomegaly splenomegaly hematemesis edema
tremors and seizures (20% of cases)
diagnostic for HUS
patient history
presence of microangiopathic hemolytic anemia
ARF
abnormal findings for HUS
reticulocytosis
abnormal RBC morphology
schistocytes, burr and helmet cells on smear
fragmented erythrocytes
anemia - decreased plasma haptoglobin
thrombocytopenia
leukocytosis is common
coagulation profile is often normal
stool cultures often positive for E.coli 0157:H7 or other toxin producing bacteria (not always detected)
elevated BUN, serum creatinine, bilirubin, potassium
Coombs negative
microscopic hematuria, proteinuria and casts on urinalysis
what testing should be done at diagnosis of D+ HUS and repeated 2 weeks later and why?
Serum ELISA testing to determine the presence of antibodies to Shiga toxin E.coli serotypes
Typical D+ HUS supportive therapy
no abx (can stimulate the bacteria to release more toxins that can damage platelets, blood vessels and kidneys)
Dialysis (about 50% of patients)
Correct electrolyte imbalances, azotemia
manage fluid overload
maintain adequate nutrition and caloric intake while observing renal protective diet
correct anemia (75% of patients require PRBC transfusion)
control HTN
Oral Calcium channel blocker (ie) nifedipine
IV calcium channel blocker (ie nicardipine) or nitroprusside
what is the prognosis for D+ HUS
90% of pt survive the acute phase
more than 50% recover full renal function
long term follow up for D+ HUS
monitor BP and urinalysis
complications are uncommon, however, proteinuria
decreased GFR
HTN
may recur up to 1 year later
D- HUS treatment
plasmapheresis - consider for pts with factor H deficiency to limit renal involvement temporarily but does not prevent progression to ESRD and has not been shown to prevent recurrence of D-HUS
Kidney transplant (8-30% if recurrence persists)
Long term care for D-HUS
monitoring of BP and urinalysis
Proteinuria, decreased GFR and HTN may recur up to 1 year later
Platelets and HUS
Platelet count is low
elevate the bleeding time
bc it only effects primary hemostasis and not secondary, PT/PTT is normal
thrombocytopenia should have platelet counts less than
150,000
what do you see clinically when the primary hemostasis is effected in HUS
you can be asymptomatic or
mucocutaneous (superficial) bleeding which includes skin bleeding and mucosal bleeding
what type of bleeding occurs when the primary hemostasis is effected in HUS
mucocutaneous (superficial) bleeding
no deep or anatomical bleeding - this occurs when secondary hemostasis is effected (hemarthroses, deep muscle bleeding, cranial bleeding)
skin bleeding includes
petechiae (1-2 mm)
purpura (0.3-1cm)
ecchymoses (>1cm)
mucosal bleeding includes
epistaxis (most common)
bleeding from superficial scratch
easy bruising
gingival bleeding
menorrhagia
GI bleeding
hemoptysis
hematuria
intracranial hemorrhage (severe)
what kind of anemia happens in HUS
normocytic
maybe later if sooooo severe it can become microcytic
In HUS is the normocytic anemia
hemolytic or non-hemolytic
hemolytic
In HUS is the normocytic anemia
intravascular or extravascular
intravascular hemolysis
In HUS is the normocytic anemia
intrinsic or extrinsic (extra-corpuscular)
extrinsic (extra-corpuscular)
In HUS is the normocytic anemia
immune or non-immune
non-immune
coombs test in HUS will be
negative
what is the problem in microangiopathic hemolytic anemia (MAHA) seen in HUS
platelets clump together, causing shearing of RBCs (schistocytes) causes destruction of the RBCs (hemolysis) of the hemoglobin forming heme and globin. Heme has iron and protoporphyrin. the protoporphyrin will become unconjugated bilirubin -> liver to become conjugated bilirubin and there is elevated bili levels sometimes.
LDH will rise when there is hemolysis
also there is hemoglobin floating freely in the blood stream that will end up in the kidney tubule leading to hemoglobinuria and the iron can also end up in the kidney tubule causing hemosiderinuria
triad for HUS
microangiopathic hemolytic anemia (MAHA)
thrombocytopenia
acute renal failure
and dont forget the bloody diarrhea
anemia - what all is low on blood counts
RBC
Hgb
HCT
MCV will be normal, low or high in HUS
normal
LDH will be normal, low or high in HUS
high
Haptoglobin will be normal, low or high in HUS
low
BUN will be normal low or high in HUS
high
Creatinine will be normal low or high in HUS
high
what should not be transfused in HUS
Platelets, will worsen the clotting at the epithelial injury
what common virus can lead to HUS
influenzae
bacterial infection of the Upper urinary tract caused by an ascending infection originated in the lower urinary tract
pyelonephritis
most common pathogens for pyelonephritis
gram positive bacteria: Enterococcus spp. and Staph aureus
Gram negative bacteria: E.coli, Klebsiella spp., Proteus spp. , P. aeruginosa, Serratia spp. and Enterobacter aerogenes
___ to ____% of children with febrile UTI also have ____ _____
60-65%
acute pyelonephritis
patho of pyelonephritis
bacterial invasion into the upper urinary tract with patchy interstitial inflammation and collections of neutrophils, leading ot tubular necrosis
clinical presentation of pyelonephritis
fever lethargy tachycardia tachypnea dehydration pain (abd, suprapubic, flank, and/or costovertebral) odorous urine
diagnostic eval of pyelonephritis
what tests will you order and what will they show
urinalysis - leukocyte esterase and nitrates
Urine culture - critical for determining organism and appropriate abx
BMP - to check kidney function
CBC with diff - evaluation of WBC count and diff
Blood culture - check for bacteremia
CRP - elevated -> indicates inflammatory process
Erythrocyte sedimentation rate (ESR) - elevated indicates an inflammatory process
Renal ultrasound for children 2-24 months
management of pylenonephritis
IV abx
Hydration
renal ultrasound
voiding cystourethrography (VCUG) in some cases - for children with recurrent febrile UTI who have evidence of abnormalities on ultrasound
inflammation within the kidney
nephritis
types of nephritis
primary
secondary
hereditary
which type of nephritis is the most common form and what infection is it most commonly seen with
primary
acute poststreptococcal GN
Pathophysiology for _______
deposits of immunoglobulines, complement and cell-mediated immune reactions lead to inflammation and injury
nephritis
clinical presentation of nephritis
history of recent throat infection
decreased urine output
dark urine
fatigue
headaches
rash on buttocks and posterior legs (specific to secondary gn)
arthralgia (specific to secondary gn)
weight loss (specific to secondary gn)
elevated BP
edema
other signs of fluid overload/CHF
diagnostic evaluation for nephritis
what should you order
electrolyte panel creatinine BUN CBC with diff Urinalysis Urine culture Throat culture
if acute postreptococcal GN is suspected, a serum antistreptolysin-O (ASO) titer should be checked
To assess for systemic disease, autoimmune panels such as serum complement levels (C3, C4), lupus serologies, anti-DNase B, perinuclear antineutrophil antibody (P-ANCA), cellular antineutrophil cytoplasmic antibody (C-ANCA) and IgA are useful.
low serum C3 levels with respect to nephritis would be indicative of
secondary GN
treatment of nephritis
ABX - first line is PCN
Treat HTN or acute renal insufficiency
- judicious fluid mgmt
- sodium restricted diet
- diuretics
- calcium channel antagonists, vasodilators or ACE inhibitors
treatment for secondary forms of glomerulonephritis (GN)
corticosteroids
cyclophosphamide
both to counteract the inflammatory process
most common glomerular cause of hematuria
Acute poststreptococcal glomerulonephritis
Acute poststreptococcal glomerulonephritis is caused by a prior infection with
specific nephritogenic strains of a beta-hemolytic streptococcus of the throat or skin
Acute poststreptococcal glomerulonephritis commonly follows what infection during the cold weather months
Group A streptococcal pharyngitis
Acute poststreptococcal glomerulonephritis commonly follows what infection during the warm weather months
streptococcal skin infections or pyoderma
clinical presentation of
Acute poststreptococcal glomerulonephritis
gross hematuria
edema
HTN
renal insufficiency
diagnostics for Acute poststreptococcal glomerulonephritis
urinalysis - RBCs - RBC casts, proteinuria and polymorphonuclear leukocytes
Elevated ASO titer
complement level - C3 initially decreased then returns to normal 6-8 weeks after presentation (sometimes sooner)
Throat culture positive for group A streptococcus can confirm diagnosis
Management for Acute poststreptococcal glomerulonephritis
PCN - 10 day course
if allergic to PCN - cephalosporins or macrolides
Acute renal insufficiency - furosemide
HTN - antihypertensives and sodium restriction
group A B-hemolytic streptococci produces what enzyme that does what to RBCs
streptolysin that lyses (destroys) RBCs
Group A B-hemolytic streptococci produces what type of reaction
Type III hypersensitivity
immune complexes
antibodies (IgG and IgM)
get clogged in the glomerular basement membrane (GBM) (subepithelial) antibodies bind to antigens in the GBM
initiates a inflammatory reaction in the glomerulus - involves C3 complement, cytokines, oxidants and proteases that damages the podocytes (epithelial cells in the glomerular basement membrane)
that damage allows larger molecules to filter through - like RBCs and proteins - causes hematuria and proteinuria. The urine is cola colored. Also oliguria (low urine production)
Acute poststreptococcal glomerulonephritis is a nephrotic syndrome or a nephritic syndrome
nephritic syndrome
in Acute poststreptococcal glomerulonephritis you have oliguria…..so this means you have less fluid excreted from the body so you have
more fluid retained
peripheral edema
periorbital edema
Acute poststreptococcal glomerulonephritis usually affects what age group?
____ weeks after skin infection such as impetigo and
___ weeks after a throat infection such as pharyngitis
children
6 weeks
1-2 weeks after
in Acute poststreptococcal glomerulonephritis
under light microscopy the glomerulus looks
under electron microscopy….
under immunofluorescence …
enlarged and hypercellular
subepithelial deposits referred to as “humps”
“starry sky” with a granular appearance
IgA nephropathy usually accompanies what kind of infection
Resp or GI infections
kidney filtration disorder in which too much protein is filtered out of the blood, leaking into the urine which results in what?
Nephrotic syndrome
proteinuria
edema
hyperlipidemia
etiologies of nephrotic syndrome
idiopathic (90%)
believed to have immunopathogenesis
genetic disorders
secondary causes include infection, drugs, immunologic/allergic disorders, associated with malignant disease, glomerular filtration
idiopathic causes of childhood nephrotic sydnrome
IgA nephropathy minimal change disease focal segmental glomerulosclerosis membranoproliferative GN (MPGN) mesangial proliferative membranous nephropathy
secondary causes of childhood nephrotic syndrome
diabetes Henoch-schonlein purpura hepatitis B or C SLE - systemic lupus erythematosus (lupus) malignancy vasculitis streptococcal infection Human immunodeficiency syndrome congenital syphilis, toxoplasmosis, cytomegalovirus, rubella malaria certain meds
what medications can be secondary causes of nephrotic syndrome
penicillamine gold nonsteroidal anti inflammatory medications interferon mercury pamidronate lithium
what are some genetic causes for childhood nephrotic syndrome
Nail-patella syndrome
Pierson syndrome
patho of nephrotic syndrome
injury to podocytes which cause collapse of the podocyte structure -> spacing and fracture of protein barrier -> allows neg charged proteins to move free across the disrupted filtration membrane -> proteinuria, edema, decreased circulating albumin -> increased interstitial edema -> increased synthesis of lipoproteins and decreased lipid catabolism -> hyperlipidemia
clinical presentation of nephrotic syndrome
edema - most notably periorbital edema
frothy or foamy urine
sudden increase in weight with edema
HTN
Hypoalbuminemia
Hyperlipidemia (LDL and triglycerides)
(can also have ascites and pleural effusions)
nephrotic syndrome diagnostics
Urine dipstick to look for proteinuria
24 hour urine collection (ideal) - >3.5g/day (book says > 4g/day for older children and adults and 40mg/m2/hr or 50mg/kg/day in young children)
CBC with diff
complete metabolic panel with serum albumin
Serum C3/C4 complement
antinuclear antibody
hepatitis B and C
HIV testing
Immunologic studies (IgG, IgM, IgE)
kidney biopsy
management of nephrotic syndrome
high dose steroids (prednisone 2mg/kg/day for 6 weeks divided into 3 doses) (book says divided into 2 doses)
treatment is continued until pt is in remission (3 days with zero trace protein via urine dipstick)
once proteinuria is resolved -> maintenance dose of steroids - 2mg/kg every other morning, then tapered off over 6 weeks
if no remission after initial treatment or have frequent relapses -> pt is considered steroid resistant -> begin cytotoxic medications such as cyclosporine A (relapse is high when this med is discontinued), cyclophosphamide or chlorambucil. Other options are levamisole (however not common due to risk of drug induced vasculitis), mycophenolate mofetil, sirolimus, tacrolimus and are usually given with high-dose methylprednisolone to induce remission.
supportive therapy includes ACE inhibitors/ARBS, statins, diuretics and restricting dietary sodium to 1500 to 2,000 mg/day
severe edema can require treatment with 25% albumin and diuretics - monitor for HTN, pulmonary edema and CHF
Furosemide and other diuretics can cause electrolyte imbalances (hypokalemia, hyponatremia, deplete intravascular volume -> puts pt at higher risk for kidney failure)
OTC antacids or H2 blockers to protect gastric mucosa from prolonged steroid use
hallmark of nephrotic syndrome is (labs)
massive proteinuria and decreased circulating albumin levels
nephritis that includes systemic vasculitis of the small vessels
Henoch-Schonlein Purpura nephritis
Henoch-Schonlein Purpura nephritis is seen in what age group
any age from infancy to adulthood but overwhelmingly a childhood disease
Henoch-Schonlein Purpura nephritis is mediated by the formation of what
immune complexes containing IgA within the skin, intestines and glomeruli
Henoch-Schonlein Purpura nephritis symptoms usually present _ to __ weeks after what 2 infections with what pathogens
1-3
URI
Gastrointestinal infection such as
(Epstein-Barr virus, Parvovirus B19, Helicobacter pylori infection, Yersinia infection, Shigella infection, Salmonella infection) or environmental allergen exposure (medications, foods, insect bites)
what kind of rash is associated with Henoch-Schonlein Purpura nephritis
raised, non-blanching, purpuric rash most prominent on buttocks and lower legs
what other symptoms are associated with Henoch-Schonlein Purpura nephritis other than rash
abd pain
arthralgias
glomerulonephritis
(may be acute or insidious)
diagnostics of Henoch-Schonlein Purpura nephritis
clinical presentation
gross hematuria
urinalysis: microscopic or gross hematuria and proteinuria
CBC: Leukocytosis with eosinophilia, thrombocytosis
D-dimer - increased
PT and PTT - decreased
IgA levels -may be increased
stool guaiac - occult blood
kidney biopsy findings are indistinguishable from IgA nephropathy
Henoch-Schonlein Purpura nephritis management
resolves spontaneously in >90% patients
symptomatic management of systemic complications is treatment of choice
prednisone 1-2mg/kg/day for 14 days in some cases (more severe)
Plasmapheresis, high dose IVIG and immunosuppressant therapy may be needed for refractory cases
Recurrence of symptoms in Henoch-Schonlein Purpura nephritis
as many as 1/3 of patients may have recurrence of symptoms
what can cause isolated hematuria
IgA nephropathy (or it can cause nephritic syndrome)
why is 24 hr urine collection optimal
a dipstick can tell you that their is protein in the urine, a 24 hour urine collection can quantify it
what range of proteinuria is associated with nephrotic syndrome
severe proteinuria
>3.5g/day
(book says > 4g/day for older children and adults and 40mg/m2/hr or 50mg/kg/day in young children)
what range of proteinuria is associated with nephritic syndrome or isolated proteinurea
Moderate proteinuria
1-3.5g/day
what is an alternative to 24 hour protein collection (in young children the first urine of the day is often used)
Urine protein/urine creatinine ratio using spot urine samples
normal levels - 0.2mg protein/mg creatinine in children older than 2
less than 0.5 mg protein/mg creatinine in children age 6 months to 2 years
any abnormal numbers needs further eval
macroscopic vs microscopic hematuria
macroscopic can be seen by the eye
microscopic can be seen in dipstick testing or microscopy.
if the blood is coming from the Glomeruli, the RBCs are usually
dysmorphic or RBCs casts
If the hematuria are due to kidney stones the RBCs are
not dysmorphic and there are no RBC casts
isolated hematuria f/u
it can persist so urinalysis is repeated in 1-4 weeks
when is transient isolated hematuria seen
excessive exercise
abdominal trauma
cancer (higher risk if older than 50)
transient isolated proteinuria is _- _ g of protein lost per day
1-2
repeat in a few days
orthostatic proteinuria is seen in
individual below age 30 when pt is in an upright position - most common cause is orthostatic proteinuria and does not require medical attention
clinical signs of nephritic syndrome
peripheral edema
periorbital edema
HTN
Oliguria (80-400mL/day)
Urinalysis shows glomerular hematuria and proteinuria
24 hour protein test shows 1-3g/day
Rapidly progressive glomerulonephritis falls under what category
nephritic syndrome
clinical signs in rapidly progressive glomerulonephritis
rapidly decrease in eGFR over a few days to 3 months
fatigue
peripheral edema
gross hematuria
HTN
decreased urine output
urinalysis - glomerular hematuria
24 hour protein collection shows 1-2g/day
what streptozyme tests are elevated in throat infections (looking at poststreptococcal glomerulonephritis)
which 2 out of those are for the skin
Antistreptolysin-O
Anti-Hyaluronidase (for both)
Anti-nicotinamide adenine dinucleotidase (ANTI-NAD)
Anti-DNAse B Antibodies (for both)
serum C3 and C4 can be high or low in nephritic syndromes
low
symptoms of IgA nephropathy
gross hematuria
flank pain
in someone who has a URI
Henoch-Schonlein Purpura nephritis is AKA
IgA vasculitis
in IgA vasculitis what does the CBC , PT, PTT look like
normal - rules out thrombocytopenia and coagulopathies
isolated hematuria
nephritic syndrome
plus systemic symptoms like symmetrical rashes, palpable purpura, migratory arthritis, GI symptoms (n/v/abd pain)
think
IgA vasculitis (Henoch-schonlein purpura nephritis)
what is diagnostic for IgA vasculitis
skin biopsy showing leukocytoclastic vasculitis and IgA deposition
what is alport sydnrome
isolated persistent hematuria
genetic condition seen in children that can lead to renal failure and hearing loss
eye exam finding seen in alport syndrome
anterior lenticonus
you suspect alport syndrome
C3 and C4 levels are low
ANA antibodies are seen or not seen
what is done to confirm the diagnosis
kidney biopsy
you suspect alport syndrome
C3 and C4 levels are normal
ANA antibodies are negative
what is done to confirm the diagnosis
genetic testing
a kidney biopsy can also be done
symptoms of SLE (lupus)
migratory polyarticular arthritis arthralgias butterfly rash delirium psychosis
edema occurs when the plasma oncotic pressure _____ due to ______________, causing ___________ which ______
drops due to the loss of circulating albumin, causing fluid to shift into the interstitial space
edema occurs when the plasma oncotic pressure _____ due to ______________, causing ___________ which ______
(nephrotic syndrome)
drops due to the loss of circulating albumin, causing fluid to shift into the interstitial space which further depletes the intravascular volume leading to renal hypoperfusion and stimulates the Renin-angiotensin-aldosterone cycle to retain more sodium and thus more water
In nephrotic syndrome, in addition to abnormal water excretion, there is an increased level of _____ that also contributes to water retention
vasopressin
what causes hyperlipidemia in nephrotic syndrome
increased synthesis of lipoproteins in the liver in response to intravascular protein loss
and
decreased lipid catabolism in response to a loss of lipoprotein lipase (enzyme necessary for lipid breakdown)
if nephrotic syndrome presents within the first 3 months of life, it is caused by _________, and requires ______
specific genetic defects
kidney transplantation
nephrotic syndrome that presents within months 4-12 of life is considered
infantile nephrotic syndrome
Nephrotic syndrome that presents after 1 year is considered
childhood nephrotic syndrome
childhood nephrotic syndrome most common between _ and _ years
2-8
what special populations/gender/age are most likely to get nephrotic syndrome
children
males
Asian, arabian, indian and african american have a higher incidence of idiopathic NS than children of european descent
what races have a higher risk of steroid resistant Nephrotic syndrome and FSGS
African American
Hispanic
due to low serum albumin, ascites, impaired immune system, patients with nephrotic syndrome are at higher risk of
what are the symptoms
associated pathogens
spontaneous bacterial peritonitis
fever
severe abd pain
peritoneal signs
possible sepsis
streptococcus pneumoniae
gram negative organisms
in nephrotic syndrome a renal biopsy is recommended for children ages ____ and older because ____
12 and older
they are more likely to have a diagnosis of FSGS rather than MCNS which puts them at higher risk for progressive kidney failure
nephrotic syndrome relapse is defined as
a recurrence of urine Pr/Cr ratio >= 2 or urine protein >= 2 for 3-5 consecutive days after initial remission
frequently relapsing nephrotic syndrome is defined as
2 or more relapses within the first 6 months of initial treatment or 4 or more relapses in a 12 month period.
teaching that goes with nephrotic syndrome
monitoring proteinuria at home with urine dipsticks
common childhood illnesses and infections can trigger a relapse such as otitis media and sinusitis
immunizations esp yearly flu and pneumococcal vaccines are very important to prevent bacterial peritonitis
No live viral vaccines while on steroid therapy
side effects of long term steroid use - appetite stimulation, bone demineralization, cushingoid appearance, mood changes, decreased immune function, growth retardation, night sweats, HTN, cataracts
rare side effects - pseudotumor cerebri, depression, steroid psychosis, steroid-induced diabetes
importance of tapering steroid use after extended therapy
maintain physical activity and avoid bed rest to prevent blood clot formation (risk of DVT, renal vein thrombosis, pulmonary embolism)
risks associated with nephrotic syndrome (complications)
obesity
delayed bone growth
dyslipidemia ->increased risk of cardiovascular disease
higher risk of infections
thromboembolism ( loss of antithrombin III factor in the urine, increased fibrinogen, platelet hyperaggregability from volume depletion)
osteoporosis
HTN
decreased visual acuity from cataracts and myopia
males treated with immunosuppressive therapy are at risk for decreased sperm count and motility
what forms of nephrotic syndrome are the most severe
SRNS (steroid resistant nephrotic syndrome)
FSGS (focal segmental glomerulosclerosis)
children with biopsy proven ___ nephrotic syndrome have a 25% chance of relapse after puberty
MCNS (minimal change nephrotic syndrome)
what is the most common form of acute glomerulonephritis (GN)
poststreptococcal glomerulonephritis (PSGN)
what is the most common form of chronic glomerulonephritis (GN)
immunoglobulin (Ig)A nephropathy
most common identifiable lower urinary tract causes of hematuria include
UTI
kidney stones
hypercalciuria
which type of GN occurs most frequently in children 2-12 years of age and is more common in boys. manifestations are typical of acute GN and develop 5-21 days (average 10 days) after ______ infection or 4-6 weeks after _____
poststreptococcal glomerulonephritis (PSGN)
streptococcal pharyngitis (GAS)
impetigo
In PSGN, pay close attention to ______ because it can become severe enough to cause _____ ____, ____
blood pressure
heart failure
seizures
encephalopathy
asymptomatic microscopic hematuria or recurrent gross hematuria
concurrent with a URI
IgA nephropathy
typical features of acute GN where renal insufficiency progresses more quickly and severely.
renal biopsy shows glomerular epithelial cell proliferation with crescents
rapidly progressive glomerulonephritis (RPGN)
early recognition of RPGN is crucial to prevent
progression to ESRD that occurs without prompt treatment
typically caused by x linked chromosome mutations but also has been associated with mutations of genes for type IV collagen, both leading to abnormal glomerular basement membrane (GBM).
may present with microscopic or gross hematuria
males typically develop progressive renal failure and sensorineural hearing loss during adolescence and young adulthood
females typically have a more benign course but usually have at least microscopic hematuria
alport syndrome
caused by mutations leading to isolated glomerular basement membrane thinning
these mutations are often autosomal dominant with hematuria frequently noted in first degree relatives
typically not progressive and usually has an excellent prognosis
thin basement membrane disease
painless gross hematuria may be seen in
strenuous exercise
sickle cell trait/disease
Wilms tumor
hematuria may be associated with pain when due to bleeding from ____ or ____
renal cysts
nutcracker syndrome (renal vein compression)
Gross hematuria following trauma may signify more
severe renal or lower urinary tract injury
associated with dysuria and urinary frequency
UTI
may be associated with asymptomatic hematuria or with flank or abd pain
urolithiasis
can cause both gross and microscopic hematuria and may be associated with urinary tract symptoms such as dysuria and urinary frequency or may be asymptomatic
Hyperalciuria
all patients with hematuria should have
careful history
physical including BP
urinalysis including microscopic evaluation to identify RBCs
glomerular hematuria is suggested by
brownish (tea or cola colored) urine and presence of RBC casts and/or dysmorphic RBCs on urine microsopy
a urine color that is more bright red without RBC casts or dysmorphic RBCs is more suggestive of
lower urinary tract source
presence of low C3 complement narrows the differential diagnosis to
PSGN
membranoproliferative GN
lupus nephritis
children with isolated, asymptomatic microscopic hematuria may be observed with
repeat urinalyses - if persistent, additional evaluation may be appropriate
microscopic hematuria may persist for ____ after resolution of PSGN
for months or even years
children with IgA nephropathy and other forms of chronic Gn have greater risk of progression to
ESRD
the presence of persistent, heavy proteinuria, HTN, decreased kidney function and severe glomerular lesions on biopsy is associated with
poor outcomes
long term follow up for idiopathic isolated asymptomatic microscopic hematuria or suspected thin basement membrane disease
yearly urinalysis to r/o proteinuria and blood measurement to exclude progressive forms of renal disease
excellent prognosis
Lupus Nephritis has ___ stages determined by a _____
6
kidney biopsy
if pt presents with red urine/hematuria
cause not apparent on H&P
urinalysis negative for blood
urate crystals in infants
from medications, foods, dyes
if pt presents with red urine/hematuria
cause not apparent on H&P
urinalysis positive for blood
what should be ordered next
order urine microscopy
if pt presents with red urine/hematuria
cause not apparent on H&P
urinalysis positive for blood
urine microscopy
RBCs confirmed
they are asymptomatic
what is it?
what is the follow up?
what should be done if hematuria persists
isolated microscopic hematuria
repeat urinalysis x 2 at least one week apart
if symptoms persist…consider
urine calcium to creatinine ratios
test first degree relatives for hematuria
Hgb electrophoresis to r/o sickle cell
serum chemistries
renal us
if pt presents with red urine/hematuria
cause not apparent on H&P
urinalysis positive for blood
urine microscopy
RBCs confirmed
they are symptomatic (symptomatic microscopic hematuria or gross hematuria)
what orders should come next?
urine culture
urine calcium to creatinine ratio
urine protein to creatinine ratio
serum chemistries
serum albumin
C3 and C4 complement
CBC
renal US
Renal biopsy in selected cases
HTN is a red flag in the presence of hematuria that the etiology might be ____ in origin
renal
Growth retardation or recent rapid weight gain in the presence of hematuria can be signs of
kidney disease
If urine is positive for RBCs , RBC casts and proteinuria and there is a history of edema and hypertension, then what labs would you order to further evaluate kidney function
electrolytes bicarbonate BUN Creatinine glucose total and ionized calcium albumin phosphorous eGFR CBC and diff protein-creatinine ratio complement C3 &C4 Antistreptolysin O titer
hypocalcemia is usually r/t ________ and amenable with _____ and ______
hyperphosphatemia
Vit D
phosphate binders
an abrupt cessation or significant decline in the kidney’s ability to eliminate waste products, regulate acid - base balance, and regulate electrolyte balance
acute renal failure
sudden sustained decrease in the GFR occuring over a period of hours to days
AKI
acute renal failure and AKI
term used changed from acute renal failure to AKI
what criterion was the first step towards defining AKI
Rifle Criteria
KDIGO AKI defininition
increase in SCr by >0.3 mg/dl within 48 hours
or
increase in SCr to x 1.5 times baseline within the prior 7 days
or
urine volume <0.5ml/kg/h for 6 hours
Evaluation of AKI
medication history looking for nephrotoxic agents
vital signs
Fluid balance - urine output
serum electrolytes and CBC
consider hepatic panel if concern for hepatorenal syndrome
chest x ray if resp symptoms
KDIGO-AKI staging
Stage 1
Serum creatinine
1.5-1.9 times baseline
>0.3 mg/dl (>26.5mmol/l) increase
and/or
urine output
<0.5ml/hg/h for 6-12 hours
KDIGO - AKI staging
stage 2
Serum creatinine 2.0-2.9 times baseline
and/or
urine output <0.5ml/kg/h for 12 hours
KDIGO AKI staging
stage 3
SCr 3 times baseline
increase in Serum creatinine to >4.0mg/dl
initiation of renal replacement therapy
<18 yrs - decrease in eGFR to <35ml/min per 1.73m2
and/or
urine output
<0.3ml/kg/h x 24 hours
anuria for x 12 hours
management of AKI
judicious fluid mgmt to restore intravascular volume or diuresis depending on clinical status (urine output replacement and calculated insensible losses may be warranted)
treat electrolyte imbalances
treat HTN
renal support if indicated
adjust meds that are excreted renally
what calculation can you use to guide fluid management
calculation of fractional excretion of sodium
prerenal kidney disease causes of acute renal failure in children
dehydration/depleted intravascular volume
distributive volume issues/decreased effective intravascular volume
intrinsic kidney disease causes of acute renal failure in children
acute tubular necrosis
ischemia/hypoxia in kidneys
medication/drug-induced
infection (HUS, PSGN)
INterstitial nephritis
GN
renal artery or venous thrombosis
endogenous toxins (myoglobin)
exogenous toxins (methanol, ethylene glycol)
idiopathic
obstructive uropathy causes of acute renal failure in children
bilat ureteral obstruction
kidney obstruction
specific genetic conditions associated with acute renal failure
polycystic kidney disease
alport syndrome
nephrotic syndrome (focal segmental glomerulosclerosis, membranoproliferative GN)
SLE
Diabetes
presenting symptoms of acute renal failure
oliguria/anuria
edema
electrolyte abnormalities
decreased appetite
nausea
fatigue
SOB
HTN
confusion
Hyponatremia is common in acute renal failure, what are you at risk for at what level
how do you treat?
risk for seizure activity if serum sodium is <125mEq/L. Treat with hypertonic saline (ie) 3% saline)
Hyperkalemia EKG findings
peaked T waves
prolongation of PR interval
widening of QRS complex
flattening of P waves
what can be used to shift potassium into cells to avoid ventricular tachycardia/fibrillation
glucose
sodium bicarbonate
insulin
albuterol
what med can stabilize the cardiac cell membrane in the presence of hyperkalemia setting of acute renal failure
calcium chloride
what med can exchange potassium and sodium in the colon in the presence of hyperkalemia setting of acute renal failure
sodium polystyrene
emergent dialysis is often indicated for serum potassium levels
> 7mEq/L
HTN therapy in acute renal failure
avoid ACE inhibitors. Goal is normal blood pressure for gender and height
name some nephrotoxic medications
aminoglycosides Vancomycin Bactrim Zosyn anticholinergics amphotericin immunosuppressive agents chemo NSAIDS RAAS blockers (ACE ARB) IV contrast Diuretics
PMH r/t AKI focusted history
Heart disease liver disease oncologic disease BMT spinal cord injury recent surgery CKD Previous AKI episodes Previous kidney stones
HPI specific to kidney
change in urination pattern-frequency
urgency
stream
drippling
feeling incomplete emptying
dysuria
flank pain
HPI specific to AKI
recent illnesses n/v/d oral intake fever UOP rashes hemodynamic changes weight gain edema
AKI workup (from lecture)
urinalysis
urine protein/creatinine ratio
urine myoglobin/hemoglobin
Fe (fractional excretion) of Na, FeUrea (Diuretic)
CPK, uric acid, free hemoglobin
Urine microscopy: muddy brown casts in ATN, RBC casts in AGN
Renal US
Bladder Catheterization
Bladder pressure
completely filtered at the glomerulus, taken up and metabolized by proximal convoluted tubule
filtration marker
no affected by muscle mass, age or hydration status
used in critically ill patients to predict AKI development
used for CF patients to predict aminoglycoside associated nephrotoxic AKI
Cystatin C
used for CF patients to predict aminoglycoside associated nephrotoxic AKI
Cystatin C
Peritoneal dialysis uses ______ ____ solution to infuse into the peritoneal cavity to facilitate the removal of _____, _____ and ________.
hyperosmolar dialysate solution
electrolytes
toxins
free water
Peritoneal dialysis uses the peritoneal space as the
semipermeable membrane filter
solutes move from the intravascular space into the peritoneal space over a prescribed period of time referred to as the _____ ______ and then are passibley drained into an external drainage collection system
dwell time
percutaneous or surgically inserted flexible single-lumen catheter allows for peritoneal dialysis fluid into the peritoneal space, dwells for a prescribed period of time and then drains into an external collection bag
Tenckhoff catheter
for the Tenckhoff catheter healing takes approximately
2 weeks
Typical volumes for a Tenckhoff catheter of __________may be used immediately after insertion; after peritoneal lining is healed, _________ may be used
10mL/kg/cycle
20-40 mL/kg/cycle
2 settings on the cycler machines for peritoneal dialysis
CCPD - continuous cycling peritoneal dialysis via machine
CAPD - continuous ambulatory peritoneal dialysis
which setting for cycler machine used in peritoneal dialysis is used to maximize fluid and toxin removal
CAPD - continuous ambulatory peritoneal dialysis
which setting for cycler machine used in peritoneal dialysis is used in either Nighttime-only therapy or nighttime and periodic day treatment
CCPD - continuous cycling peritoneal dialysis via machine
how many cycles with what dwell time for CCPD
8-10 cycles with dwell times of 30 - 45 minutes
what are the types of peritoneal dialysis fluid
1.5%
2.5%
4.25%
glucose solutions
dialysis fluid is _______ to serum and contains a high concentration of ______
hyperosmolar
carbohydrates
peritoneal dialysis promotes _______
ultrafiltration
higher the percentage of carbohydrate solution, greater the volume of
fluid removed
benefits of peritoneal dialysis
fluid removal
urea, creatinine and potassium clearance
clearance of toxins
treatment may be provided at home, outpatient or inpatient
may be used in neonates and infants
complications of peritoneal dialysis
abd discomfort
peritonitis
electrolyte imbalance, hyperglycemia, protein loss
inguinal/abd hernia
resp compromise
long term peritoneal fibrotic tissue may limit functional dialysis
Peritoneum may lose its selectivity over time (decreased clearance, increased proteinemia)
contraindicated in patients with significant abd pathology
in peritoneal dialysis when should the pt be weighed
prior to and immediately after therapy
Peritoneal dialysis must end with _____ cycle
drain cycle
For a pt who is on peritoneal dialysis, what should you monitor
fluid
electrolytes
hemodynamic status
for peritoneal dialysis access the peritoneal catheter using ____ or ___ technique
aseptic
sterile
for peritoneal dialysis monitor for _____
sepsis
may treat peritonitis for someone who receives peritoneal dialysis
by adding abx to dialysis fluid
kidney biopsy is most commonly performed _______; needle inserted through ____, through _____ and into _____
percutaneously
skin
tissue
kidney
kidney biopsy may be performed ____ using_____ or with the assistance of
blindly
landmarks
imaging guidance using ultrasound, CT or fluoroscopy
occasionally through an open procedure
contraindications to a kidney biopsy
coagulation disorders with increased risk of procedural bleeding
operative kidney tumors (could spread the malignant cells)
hydronephrosis - risk of perforating large renal pelvis r/i urine leak requiring surgical repair
UTI: risk of spreading infection
Potential complications of kidney biopsy
hemorrhage - kidney is highly vascular
unintended puncture of surrounding organ (liver, lung, bowel, inferior vena cava)
Preop for kidney biopsy
NPO coag studies CBC type and cross/type and screen Sedation may not be required in older cooperative children
postop kidney biopsy
pressure over puncture site for 20 min followed by a pressure dressing
limited movement/activity for 24 hours after procedure
monitor for signs of hemorrhage
evaluate abd for signs of hemorrhage or bowel perforation
indications for kidney transplant
irreversible kidney failure
most common etiologies are congenital, urologic and inherited disorders
evaluation for kidney transplant begin when the estimated creatinine clearance is
<60 mL/min/1.73m2
if circumstances allow ________ prior to dialysis requirement is ideal to avoid associated morbidities
transplantation
contraindications to kidney transplant
malignancy
chronic illness with shortened life expectancy
severe brain damage
inability to improve quality of life
evaluation of someone looking at kidney transplant
diagnosis of kidney failure or ESRD and eval for multisystem involvement
- Lab sampling
- Anti-human leukocyte antigen antibodies and panel-reactive antibodies: evaluated for sensitization to determine which donor antigens should be avoided to prevent rejection
- Radiologic eval
- US - look for urinary tract abnormalities
- Echocardiogram
- electrocardiogram
invasive studies
- cardiac cath in select patients
- angiogram in select patients
discussion of prognosis and appropriateness of transplantation
Psychosocial eval - ability to adhere to posttransplant therapies and f/u appts, readiness, religious or cultural beliefs that may impact transplant, resources, barriers
what lab is used to evaluated for sensitization to determine which donor antigens should be avoided to prevent rejection
Anti-human leukocyte antigen antibodies and panel-reactive antibodies
what type of donors are preferred in kidney transplant and why
live - improved graft survival unless high suspicion of recurrent disease
when a live donor is used for kidney transplant focus on
overall donor health
must be>=18 years of age unless an identical twin
may be exceptions with the evaluation by an ethics team
Preparing for tranplantation
achieve optimal physical and mental health state prior to transplant with financial planning
living donor eval
preliminary labs for
blood type
human leukocyte antigen typing, crossmatch
referral to unbiased physician
Posttranplant care
maintenance immunosuppression
calcineurin inhibitor, usually in conjunction with a second agent such as an antiproliferative agent (mycophenolate mofetil) or mTOR inhibitor (rapamune)
Calcineurin inhibitors (mycophenolate mofetil) are
nephrotoxic
levels require monitoring
Cadaveric kidney differences
graft function - poor initial graft function is more common - can indicate acute tubular necrosis
dialysis may be required in the first few weeks after transplant; typically only temp
starting of immunosuppression often differs between living and cadaveric donors
common kidney rejection signs and symptoms
HTN fever proteinuria oliguria graft nonfunction
must always be on your differential list of transplant patients
definitive diagnosis of kidney rejection is
biopsy
type of rejection that occurs minutes to hours after transplant
hyperacute
type of rejection that occurs 3-90 days post tranplant
acute
type of rejection that occurs >60 post tranplant
chronic
Posttranplant infection
fever days after transplant think
atelectasis
posttransplant infection
fever
weeks after transplant think
foreign objects
posttransplant infection
fever
2-6 weeks post transplant think
fungal
posttransplant infection
fever
6-8 weeks post transplant think
viral
signs and symptoms of post-transplant infection these 2 staples then varies
fever
elevated WBC
when you think post-transplant infection
think ____ vs ____ vs _____
primary
reactivation
reinfection
result of an inherited or acquired defect that affects the kidneys ability to filter bicarbonate or excrete ammonia
renal tubular acidosis
can be a genetic cause of renal tubular acidosis
Sickle cell anemia
Acquired cases of renal tubular acidosis
certain medications
obstructive uropathy
autoimmune diseases
often associated with presence of UTI
renal tubular acidosis
relatively uncommon clinical syndrome characterized by defects in the renal tubules as a result of failure to maintain a normal serum bicarbonate level despite the consumption of a regular diet and normal metabolism and acid production
renal tubular acidosis
in renal tubular acidosis the defects in renal tubules lead to a ______ __________ __________ with a normal to moderately decreased GFR and normal anion gap
hyperchloremic metabolic acidosis
decrease in acid excretion
Type I RTA (distal)
failure of bicarbonate reabsorption with decreased ammonium absorption
Type II RTA (proximal)
Aldosterone deficiency or impairment of its effects, resulting in reduced potassium excretion, hyperkalemia and acidosis
Type IV RTA
what types of renal tubular acidosis are most common in children
types I and II
clinical presentation of renal tubular acidosis
Polyuria
polydipsia
preference of savory foods
hypokalemia
refractory rickets
metabolic acidosis
RTA that is linked to multiple genetic disorders (sensorineural hearing loss and nephrocalcinosis); FTT or short stature, anorexia, vomiting, dehydration
type I RTA
RTA with FTT, hyperchloremic acidosis with hypokalemia
rarely nephrocalcinosis
rickets or osteomalacia may indicate _____ _______
Type II RTA
Fanconi Syndrome
RTA - HTN common if child has underlying _____ syndrome, renal parenchymal disease or mineralocorticoid dysfunction
Type IV RTA
Gordon syndrome
RTA type linked to multiple genetic disorders
Type I RTA
diagnostic evaluation of renal tubular acidosis
serum and urine electrolytes
fractional excretion of bicarbonate and urine pH
Urine glucose and protein, calcium-to-creatinine ratio.
24 hour urine sample
radiographies of long bone or wrists for eval of rickets
abd us (kidneys)
genetic or chromosomal eval
mgmt of RTA
emergent or inpatient mgmt for children with hyperchloremic, non-anion gap acidosis requiring bicarbonate replacement IV
slow rehydration and electrolyte replacement, sodium bicarbonate or citrate, diuretic, phosphate replacement in children with rickets
without proper therapy, chronic acidity in the blood results in
growth retardation
nephrolithiasis
bone disease
chronic renal failure
which type of RTA - a lot of bicarbonate lost through the urinary tract
Type II Renal tubular acidosis
which type of RTA are too many hydrogen ions retained
Type I and IV renal tubular acidosis
In Type I RTA, there is a build up of ___ ions in the blood leading to _____ which causes _____ _____. There is an increase of _____ excretion
H+
Acidemia
Metabolic acidosis
potassium
metabolic acidosis will increase ____ excretion w/o increasing calcium ____
urine calcium excretion
calcium absorption
which RTA involves osmotic diuresis -> mild hypovolemia -> activates RAAS -> sodium reabsorption and K excretion -> hypokalemia
Type II RTA
which RTA is r/t a aldosterone deficiency or resistance in the collecting ducts
Type IV
what is the most common cause of GN in older children and adults
Membranoproliferative glomerular nephritis (MPGN)
this form of nephritis results in ongoing glomerular injury that leads to glomerular destruction and ESRD
Membranoproliferative glomerular nephritis (MPGN)
Etiology of Membranoproliferative glomerular nephritis (MPGN)
Autoimmune disease (SLE, scleroderma, Sjogren syndrome, sarcoidosis)
malignancy (leukemia, lymphoma)
infectious (hepatitis B, C, endocarditis, malaria)
clinical presentation of Membranoproliferative glomerular nephritis (MPGN)
nephrotic syndrome
gross hematuria or asymptomatic microscopic hematuria
Proteinuria
Renal function may be normal or decreased
HTN is common
Serum C3 may be low
diagnostic eval for Membranoproliferative glomerular nephritis (MPGN)
kidney biopsy is gold standard for diagnosis
mgmt Membranoproliferative glomerular nephritis (MPGN)
systemic steroids for children and antiplatelets for adults
additional therapies include plasmapheresis and plasma infusion
an extracorporeal blood purification therapy intended to substitute for impaired renal function over an extended period of time.
continuous renal replacement therapy
Continuous renal replacement therapy is used to treat
fluid overload acute renal failure chronic renal failure life threatening electrolyte imbalances intoxications (molecule size dependent) concomitant sepsis multiorgan failure
continuous renal replacement therapy is used only in what setting?
administered for _____ hours
can be given for how much time?
only in critical care setting
administered continuously, 24 hours a day
administered for days or weeks but not a long term therapy
what criteria for AKI is used for necessitating use of continuous renal replacement therapy
RIFLE
estimated creatinine clearance decreased by 50% urine output <0.5mL/kg/hour x 16 hours
In sepsis with hemodynamic instability what is continuous renal replacement therapy used for
cytokine removal reduces hemodynamic instability allows precise volume control toxin removal effective control of uremia, hypophosphatemia, hyperkalemia
in uremia with encephalopathy, how does continuous renal replacement therapy help
removal of urea and toxins
what criteria for Acute renal failure is used for necessitating the use of continuous renal replacement therapy
RIFLE
estimated creatinine clearance by 75% or urine output <0.3ml/kg/hour for 24 hours or anuric for 12 hours
for continuous renal replacement therapy to be effective in the case of intoxication, the molecular size must be able to
be cleared by filter for effective treatment
complications of continuous renal replacement therapy
hypotension
hypothermia
bleeding
electrolyte imbalance
central line infection (hemodialysis catheter)
venus thrombus
-consider PRBCs transfusion prior to start of continuous renal replacement therapy (CRRT) - esp if <=10kg
Hyperthermia unit may be added to CRRT machine to warm the blood being returned to the pt
what placement of the hemodialysis catheter can be temp or permanent?
internal jugular
what placement of the hemodialysis catheter is temp access only
femoral vein
during CRRT maintenance of anticoagulation
sodium citrate
how does sodium citrate work in anticoagulation for CRRT
it combines with calcium ion to render clotting factors inactive within the filter
how is citrate processed
through the liver
when using sodium citrate for anticoagulation during CRRT, what must you have continually infusing and why
calcium outside of the circuit to maintain normal calcium levels
Prior to initiating sodium citrate in the CRRT circuit, the patients ionized calcium should be
> =1.1 mmol/L
benefits of using sodium citrate
minimal bleeding risks
extended filter life
risk of using sodium citrate for anticoagulation during CRRT
metabolic alkalosis
-citrate is buffered into bicarbonate
citrate lock
- rising total calcium with dropping ionized calcium
- delivery of citrate exceeds hepatic metabolism and CRRT clearance
hypocalcemia
hypernatremia
hyperglycemia
-monitor CRRT ionized calcium levels, serum ionized and total calcium, sodium and glucose levels
treatment for metabolic alkalosis for someone on CRRT (risk when using sodium citrate for anticoagulation)
eliminate acetate and bicarbonate sources
treatment for citrate lock during CRRT
increase dialysis by 20-30%
decrease or stop citrate for 3-4 hours and restart at 70% of prior rate
what levels must be monitored closely during CRRT
CRRT ionized calcium levels
serum ionized calcium
serum total calcium
sodium
glucose
how does heparin work in anticoagulation for CRRT
acts indirectly at multiple sites in both intrinsic and extrinsic coagulation pathways to prolong coagulation
goal for heparin in CRRT
achieve activated clot time (ACT) 180-220 milliseconds (commonly used to maintain the circuit)
benefits for using heparin in CRRT
may be used in liver failure
risks for using heparin in CRRT
bleeding
monitoring heparin in CRRT
anticoagulation (ACT, protime, prothrombin time)
kidney dysfunction results in
electrolyte imbalance
anasarca
accumulation of uremic toxins
blood and dialysis fluid enter hemodialysis filter in a _____ approach which does what??
countercurrent
maximizes the concentration gradient between the blood and dialysis fluid
typically hemodialysis will run for __- __ hours each session
3-4
indications for hemodialysis
hypervolemia: resp compromise, heart failure, HTN, hyponatremia and/or anasarca
electrolyte abnormalities: Hyperkalemia, hyperphosphatemia, hypocalcemia
and/or acidosis
symptomatic azotemia or uremia: confusion, bradycardia, platelet dysfunction, pericardial effusion
asymptomatic azotemia or uremia (ie-acute or chronic renal failure)
toxicity of non-protein bound medications, poisons or ammonia
malnutrition: decreased intake due to volume restriction, increased metabolic demands, catabolic metabolism or malabsorption
placement options for hemodialysis catheter
short term
tunneled (internal jugular or superior vena cava)
arteriovenous fistula or graft - internal vascular access surgical connection joining an artery and a vein for hemodialysis use
Blood flow rate and dialysis rate for hemodialysis treatment
150-350mL/min
500mL/hour
Hemodialysis treatment requires at least a __Fr catheter to allow appropriate flood flow rate
7
ideally a pt receiving hemodialysis weighs more than
10kg
hemodynamic stability is optional or required prior to initiation of hemodialysis treatment
required
Hemodialysis can be done where and by who
inpatient (acute or critical care) or outpatient facility by a hemodialysis technician
benefits of hemodialysis
fluid removal urea creatinine potassium toxin clearance
complications of hemodialysis
disequilibrium syndrome
hypotension
bleeding
electrolyte imbalance
catheter infection
vessel thrombosis
baroreceptor dysfunction
what is disequilibrium syndrome
dialysis induced cerebral edema
symptoms of disequilibrium syndrome
nausea
headache
confusion
seizures
in someone who is receiving dialysis
treatment for disequilibrium syndrome
mannitol infusion (poorly cleared by dialysis) and short session with low blood flow rate without ultrafiltration
why is hypotension a potential complication of hemodialysis
caused by rapid removal of fluid from intravascular space
symptoms of hypotension listed for hemodialysis prior to the hypotension
tachycardia
nausea
crampy abd pain
emesis
treatment for hypotension with hemodialysis
small fluid boluses
decrease in ultrafiltration
if shock occurs, treat with fluid and discontinue dialysis
how do you monitor for electrolyte imbalances for hemodialysis
pre- and post dialysis weights
fluid, electrolyte and hemodynamic monitoring
how do you prevent vessel thrombosis for hemodialysis pt
heparinize catheter after use
symptoms of baroreceptor dysfunction
this may happen with chronic renal failure
bradycardia
treatment for baroreceptor dysfunction in hemodialysis pt
atropine
or
epinephrine
to restore perfusion
when kidneys have sustained damage in structure or function for over 3 months, this is referred to as
chronic kidney disease
causes of CKD are divided into 3 categories
Prerenal
intrarenal
postrenal
prerenal cause of CKD is due to?
what are 2 examples
decrease in renal perfusion
heart failure
cirrhosis
Intrarenal cause of CKD
renal vascular disease
- HTN
- Renal artery stenosis
Glomerular disease
- Nephritic disease
- nephrotic disease
Tubulointerstitial disease
-polycystic kidney disease
nephrotoxic substances
Postrenal cause of CKD
prostatic disease
repeated episodes of pyelonephritis
stages of CKD based on GFR
Stage 1 (G1) - >=90 mL/min/1.73m2 (underlying kidney disease)
Stage 2 (G2) - 60-89 mL/min/1.73m2 (mildly decreased)
Stage 3a(G3a) - 45-59
mL/min/1.73m2
(mild-moderately decreased)
Stage 3b (G3b) - 30-44
mL/min/1.73m2
(moderately-severely decreased)
Stage 4(G4) - 15-29
mL/min/1.73m2
(severely decreased)
Stage 5 (G5) - <15
mL/min/1.73m2
ESRD
if on dialysis its staged as G5D
what is referred to as G stages
eGFR for staging of chronic kidney disease
CKD can cause anemia, why
kidney not making enough erythropoietin
hemodialysis - regular blood loss
prone to iron deficiency anemia
- diet low in iron
- blood loss
- impaired absorption of iron
CKD can cause mineral and bone disorder (CKD-MBD)
tell me about it
hyperphosphatemia
hypocalcemia
skeletal abnormalities
extra -skeletal calcifications such as coronary artery calcifications
kidneys cannot excrete the phosphate so this leads to hyperphosphatemia and improper conversion of 25-hydroxyvitamin D to activate calcitriol (active version of vit D) -> leads to hypocalcemia ->
hyperphosphatemia + hypocalcemia = increased levels of parathyroid hormone (leads to secondary - as these increase more (hypertrophied parathyroid) this can lead to hypercalcemia
hyperkalemia symptoms
palpitations
paresthesias
muscle weakness
medications listed in book to cause AKI
prostaglandin synthetase inhibitors (naproxen, ibuprofen, mefenamic acid, indomethacin)
ACE inhibitors (-pril)
Cyclosporin A (immunosuppressive drug)
Diuretics
another found in video
aminoglycosides (-mycin)
leading causes of anemia in CKD
iron deficiency
Erythropoietin (EPO) defieciencies
what type of failure is most common cause of AKI
prerenal failure
(book lists the following as prerenal causes of AKI) gastroenteritis gastrointestinal damage DKA hypoproteinemia hemorrhage third space losses
peripheral vasodilation
impaired cardiac output
bilat renal vessel occlusion
medications that can be used to reduce serum potassium level or stabilize the cardiac membrane
sodium bicarb
albuterol
glucose
insulin
all of the above work by shifting potassium into cell
sodium polystyrene exchanges sodium for potassium in the colonic mucosa
emergency dialysis is needed if serum potassium level is above ____ with ____
6-7 mEq/L with tall peaked T waves, prolongation of PR interval, flattening of P waves or widening of the QRS complex on ECG
continued hyperkalemia will result in
ventricular tachycardia
ventricular fibrillation
chronic metabolic acidosis which is a bicarb level of
22
bicarbonate
acids
In CKD, metabolic acidosis contributes to bone disease by
acidosis also causes a resistance to ____ hormone and _____ factors
releasing calcium in an attempt to buffer the acidosis
growth
insulin - like growth
____ and _____ intake should be limited in kidney insufficiency. Special formulas with low _____ and ____ can help with nutrition mgmt in infants.
potassium
phosphorous
potassium
phosphorous
what factors affect growth in children with CKD
malnutrition
persistent metabolic acidosis
end organ growth hormone resistance
renal bone disease
even with correction of malnutrition and acidosis children with CKD grow poorly
optimizing ____ and managing ____ abnormalities in early childhood allows for the greatest linear growth when supplementing with recombinant growth hormone.
nutrition
metabolic
pediatric patients with CKD and HTN have greater variation in _______ and decreased variation in_______.
blood pressure
heart rate
recommended cardiovascular management in CKD includes
24 hour ambulatory BP measurements
dyslipidemia screening as a part of their cardiovascular risk assessment
RAAS inhibitors for HTN mgmnt
In G3 CBC is checked to look for
normocytic anemia
normochromic anemia
the lack of EPO is a reflection of
dysfunctional kidney and poor GFR
what is a good indicator of iron stores
calculating the serum transferrin saturation
divide serum iron by total iron binding capacity and multiply by 100
labs for iron deficiency
serum iron (low)
TIBC (high)
ferritin (low)
to evaluate CKD-MBD what levels are checked
phosphate
calcium
PTH
vit D
At stage 3 what do the following levels look like
Phosphate and calcium remain normal
high PTH
low vit D
at what G level do you start to see hyperphosphatemia and hypocalcemia
G4
US used in CKD - what do they US and what are they looking for
abd US to check size of kidneys and look for signs of hydronephrosis
Parathyroid US to look for large parathyroid
anemia for CKD
elemental iron replacement should be delivered
2-3mg/kg (up to 6mg/kg) with the ferritin level at least 100ng/mL and a transferrin saturation of 20%
dont give iron with _____ due to decreases gi aborption
calcium binders
Recombinant EPO should be started at -___-____ units/kg weekly by subcutaneous or IV injection adjusted to reach a desired hgb level of 11-12 gm/dL
80-120
The correction of anemia has been associated with
better exercise tolerance
physical performance
school attendance
improved quality of life
caloric intake to slow progression of renal disease
30-35kCal/kg/day
this is to help manage body weight
protein restriction for an CKD pt who is not on dialysis
0.8g/kg/day
CKD with HTN/volume overload
sodium restriction
2g/day (roughly 1/3 of a tablespoon of salt daily)
calcium intake to prevent tissue deposition should be
<1g/day
if the eGFR < 30mL/min/1.732 then the max potassium intake is
4g/day
at what G stage should the pt be on a statin
G3
pediatric hypertension is defined as
systolic or diastolic BP measurement exceeding the 95% percentile for gender age and height on 3 occasions
book for children 1-12
normal BP
<90th percentile
book for children 1-12
elevated BP
BP>=90th percentile to <95th percentile or 120/80 to <95th (whichever is lower)
book for children 1-12
stage 1 HTN
> = 95th percentile to <95th percentile +12mmHg, or 130/80-139/89 (whichever is lower)
book for children 1-12
stage 2 HTN
> =95th percentile + 12mmHg, or >140/90 (whichever is lower)
book for children >= 13
normal BP
<120/<80
book for children >= 13
elevated BP
120/<80 - 129/<80
book for children >= 13
Stage 1 HTN
130/80 - 139/89
book for children >= 13
Stage 2 HTN
> = 140/90
if the initial bp measurement is >=90% what should you do?
auscultatory bp should be measured 2 additional times at the same visit and the average of the 2 readings should be used to categorize the BP
Patients with elevated BP should have theri BP rechecked by auscultation every ___ months for ___ yr(s)
6 months
1 year
Stage 1 HTN is re-evaluated on repeated visits on ??? to confirm
1-2 weeks after initial check and then again 3 months later to confirm
if elevated still -> further eval and/or referral to specialist is warranted
Stage 2 HTN should have a repeat bp measurement within _____ and be referred for further eval if their bp remains within stage 2 criteria
1 week
determinants of BP
cardiac output
peripheral vascular resistance
the most common type of HTN in children and adolescents in the US
primary HTN
what can you take iron supplements with in improve absorption
orange juice
secondary HTN is most commonly seen with
kidney disease
most common cardiac cause of HTN
coarctation of aorta
most common endocrine cause of HTN
hyperthyroidism
genetic disorders associated with HTN
Liddle syndrome
Gordon syndrome
neoplasms associated with HTN
Wilms tumor
pheochromocytoma
neonatal HTN can be due to factors such as
umbilical catheter-associated thromboembolism
congenital lesions of the renal vasculature or parenchyma
bronchopulmonary dysplasia
exposure to medications
maternal drug use
education for fistula arm
should not use for Blood draw
Should not use for BP checks
should not sleep on that arm
should not carry anything >5lbs
when should a healthy child over the age of 3 have their bp checked
annually
pretty much everyone else is at every visit
comorbidities associated with HTN
obesity
kidney disease
diabetes
aortic coarctation
History that predisposes to HTN
prematurity
congenital heart disease
kidney disease
transplant
malignancy
evidence of Intracranial pressure
recurrent UTIs
medications with HTN side effects
BP should be measured with an appropriately sized cuff, after ___ min of rest in what position
5
seated position with feet resting on the floor and with the R arm supported at the level of the heart and uncovered above the BP cuff
what is the preferred device/method for BP measurement
auscultation because oscillometric devices use proprietary algorithms to calculate BP from measured MAP and can vary in accuracy
Patient history on an H&P for HTN should include
gestational age
birth weight
complications for preg, delivery
nutritional
physical activity
psychosocial factors such as anxiety and situational stressors
familial history
HTN can be secondary to medications such as
steroids
decongestants
oral contraceptives
chronic NSAID use
drug use
caffeine
stimulants
what labs should be ordered for all patients with confirmed HTN
UA and chemistry panel
those less than 6 years old with HTN or have abnormal UA or kidney function should also have a
renal US
an ____ should be obtained at the time of consideration of pharmacologic therapy for HTN
echocardiogram
HTN….in addition to the evaluation for underlying causes and end organ damage, evaluation for comorbidities such as _____ and ______ should be considered
dyslipidemia
obstructive sleep apnea (OSA) - associated with HTN independent of obesity status
other symptoms of Obstructive sleep apnea
HTN
snoring
daytime tiredness in older children
hyperactivity in younger children
lifestyle changes for HTN
weight reduction
regular physical activity
diet modification
pharm treatment for HTN is indicated in children with
symptomatic HTN
stage 2 HTN without an identified modifiable factor
comorbidities such as DM or CKD
or who remain Hypertensive after a trial of lifestyle modifications
Treatment for HTN should be initiated with a ___ at a ___ dose with dose adjustments every __-___ weeks
single
low
2-4
pharm classes for treating pediatric HTN
ACE inhibitor
ARB
Long acting CCB
or Thiazide diuretic
what antihypertensives are not recommended as initial treatment in children
B blockers
____ and _____ are renoprotective and are preferred in pt with HTN and CKD, proteinuria or diabetes unless there is a contraindication (what are those)
(Book)
ACE and ARBs
use with caution in children with volume depletion, bilat renal artery stenosis or hyperkalemia
contraindicated in pregnancy and angioedema
what race may need a higher dose of ACE due to possible decreased response
African American children
elfin faces think
when eval for HTN
Williams syndrome
moon face think
when eval for HTN
cushing syndrome
thyroid enlargement think
when eval for HTN
hyperthyroidism
webbed neck think
when eval for HTN
Turner syndrome
tonsillar hypertrophy think
when eval for HTN
OSA,
retinal changes think
when eval for HTN
severe HTN and secondary etiology
papilledema think
when eval for HTN
intracranial HTN
Acne, hirsutism, striae think
when eval for HTN
cushing syndrome
steroid use
cafe -au-lait spots and/or neurofibromas
when eval for HTN
neurofibromatosis
ash leaf spots and/or adenoma sebaceum
when eval for HTN
tuberous sclerosis
rash think
when eval for HTN
secondary kidney disease
Lupus erythematosus
henoch-schonlein purpura
acanthosis nigricans think
when eval for HTN
Type 2 DM
murmur think
when eval for HTN
coarctation of aorta
apical heave think
when eval for HTN
L ventricular hypertrophy
abdominal bruit think
when eval for HTN
renovascular disease
abd mass think
when eval for HTN
hydronephrosis
polycystic kidney disease
kidney tumors
neuroblastoma
Pulse in lower extrem
coarctation of aorta
asymmetry of limbs think
when eval for HTN
Beckwith-Weideman syndrome
Arthritis think
when eval for HTN
henoch-schonlein purpura
collagen vascular disease
lupus erythematosus
muscle weakness think
when eval for HTN
Liddle syndrome
Hyperaldosteronism
Ascending paralysis
when eval for HTN
guillain - barre syndrome
diminished pain response
when eval for HTN
familial dysautonomia
Pt should be seen every __-_ weeks while titrating medications and every ___ -___ months thereafter if on medications for HTN
4-6 weeks
3-4 months
Pt attempting lifestyle mods for HTN should be seen every _-__
3-6 months
The AHA recommends restricting competitive sports participation in athletes with
LVH beyond what is seen with typical athletic Heart until BP is controlled and restriction those with stage 2 HTN even without LVH from participating in high static sports (weight lifting, boxing, wrestling) until BP is controlled.
when can children and adolescents with HTN participate in sports
once target organ damage and risks have been assessed
bacterial or fungal infection in any part of the urinary tract (urethra, ureters, bladder, kidney)
UTI
a UTI that migrates to the kidney results in ______ which is what type of UTI
pyelonephritis
upper urinary tract infection
uncircumcised males have the highest incidence in the first 3 months of life
UTI
what is associated with higher incidence of UTI
genetic predisposition
history of dysfunctional voiding or elimination
in otherwise healthy children, UTI may indicate an underlying abnormality in the urinary tract such as
vesicoureteral reflux (VUR) disease
most common etiology of UTI
colonic organisms
pathogens commonly cause UTI
gram neg bacteria
E.Coli
Klebsiella species
Pseudomonas aeruginosa
gram positive bacteria
enterococcus
Staph aureus
group B streptococcus
Candida
adenovirus
herpes simplex
in a UTI pathogens infiltrate the _____ of the ____, resulting in an _____ response
mucosa
bladder
inflammatory
clinical presentation of UTI in infants/young children
fever irritability fussiness decreased appetite lethargy changes in activity level jaundice weight loss
clinical presentations of UTI in preschool/young school age
abd pain
n/v
urinary frequency
clinical presentations of UTI in older children
urinary frequency dysuria urgency suprapubic pain n/v
evaluate history for UTI
structural abnormalities of UT
baths
voiding/elimination dysfunction
sexual activity
maltreatment risk
physical exam evaluation for UTI
evaluate for sacral dimple
costovertebral angle tenderness
suprapubic tenderness
Urinalysis evaluation for UTI
presence of leukocyte esterase
nitrites
> 5 WBCs
bacteria/hpf
Urine culture for UTI
identifies pathogen and evaluates abx sensitivity/resistance
what tests are recommended to determine presence of a UTI
UA and UC
when is a renal US indicated in a UTI
children 2 mos - 2yrs
US evaluates what in UTI
anatomy
kidney size/shape
evidence of hydronephrosis
areas of inflammation and signs of pylelonephritis
when would you order a voiding cystourethrography
if renal and bladder US show hydronephrosis, scarring or evidence of high grade VUR or obstructive uropathy
all infants 2 months to 2 yrs with recurrence of febrile UTI
what is a dimercaptosuccinic acid (DMSA) scintigraphy
nuclear medicine scan used to evaluate for renal scarring
mgmt for UTI- duration is determined by
determined by pt age, severity of illness, local resistance patterns, associated underlying disorders
Uncomplicated UTI duration of therapy is
7-10 days
2-4 days according to some studies
complicated UTI duration of therapy
14 days
initial oral therapy abx selection for UTI
Bactrim
Augmentin
Cefixime
initial parenteral therapy for UTI treatment
ceftriaxone
cefotaxime
gentamicin
in general, oral abx are just as effective or less effective than pareneral
equally
recommended medication for discomfort or fever in UTI
acetaminophen
when is hospitalization recommended for UTI
when unable to tolerate oral meds
or maintain adequate hydration
fail to improve outpatient
evidence of sepsis
underlying medical that may complicate management
Pt family education for UTI
signs of UTI
hygiene
limiting bubble baths
constipation prevention
urination after intercourse if sexually active
close clinical f/u after 7-10 days of abx to evaluate for recurrent UTI
why are underlying urinary tract abnormalities important to recognize early
so they do not lead to renal scarring
prophylactic abx do/do not reduce risk of recurrent UTI,. How about in cases of mild to moderate VUR
do not
even in cases of mild to moderate VUR
1 in = ___ cm
2.54cm
proximal tubule job
water and electrolyte reabsorption
the job of the distal convoluted
primary site of vasopressin response so urine concentration
Sodium Polystyrene aka
kayexalate
eCCl decrease by 25% or decrease in urine output <0.5ml/kg/h for 8 hours
pRIFLE risk
eCCl decrease by 50% or decrease in urine output <0.5ml/kg/h for 16 hours
pRIFLE injury
eCCl decrease by 75% or eCCl <35 ml/min/1.73m2 or decrease in urine output <0.3ml/kg/h for 24 hours or anuric for 12 hours
pRIFLE failure
persistent failure > 4 weeks
pRIFLE loss
persistent failure >3months
pRIFLE End stage renal disease
retrograde flow of urine from the bladder up the ureter, sometimes into the kidney – usually results from congenital incompetence of the ureterovesical junction (matures in early childhood), renal dysplasia, or neurogenic bladder
Vesicoureteral reflux:
Vesicoureteral reflux causes
renal scarring even with one UTI
Vesicoureteral reflux exposes the kidney to increased
hydrodynamic pressure during voiding and increases likelihood of infection d/t incomplete emptying of ureter and bladder
diagnosis Vesicoureteral reflux diagnosis
renal ultrasound (best method) → VCUG (direct measurement of VUR)
us - if there is reflux
VCUG - how severe it is
Treatment Vesicoureteral reflux
+/- prophylactic antibiotic therapy (bactrim) for mild to moderate VUR, monitor for complications (HTN, CKD)
what is the significance of evaluating for the sacral dimple on physical exam in UTI
spina bifida is at increased risk for UTI secondary to neurogenic bladder
more than 50, 000 colony-forming units/mL of a single organism and pyuria
Positive urine culture for a UTI
organism mentioned in UTI but not in pyelonephritis
Group B streptococcus
organisms mentioned in pyelonephritis not mentioned for UTI