nephrology Flashcards
avg. newborn systolic BP
70-75
avg 1 yr old systolic BP
90
avg 5 yr old systolic BP
95
avg 12 yr old systolic BP
100-105
HTN is BP > than 95th percentile for what?
age
gender
ht
HTN is more often_________than_________in CH
secondary than primary (“essential”)
HTN in CH, consider what types of dz first
renal dz
endocrine dz
early HTN in CH is a precursor to what?
serious adult HTN
HTN in CH DDx
renal dz endocrine neurologic psychologic causes vascular causes drugs other
renal dz that may cause HTN in CH
pyelonephritis renal parenchymal dz congenital anomalies reflux nephropathy acute glomerulonephritis Henoch-Schonlein purpura renal trauma hydronephrosis hemolytic-uremic syndrome renal stones nephrotic syndrome Wilms tumor hypoplastic kidney polycystic kidney dz
endocrine dz that may cause HTN in CH
hyperthyroidism congenital adrenal hyperplasia Cushing syndrome primary aldosteronism primary hyperparathyroidism DM hypercalcemia pheochromocytoma
neurologic dz that may cause HTN in CH
increased ICP
Guillain-Barre syndrome
psychologic causes in HTN in CH
mental stress
anxiety
vascular causes of HTN in CH
renal artery abnormalities renal vein thrombosis coarctation of the aorta patent ductus arteriosus arteriovenous fistula
some drugs that may cause HTN in CH
anabolic steroids
corticosteroids, OCPs
PCP, cocaine
other causes of HTN in CH
pain
collagen vascular dz
neurofibromatosis
Henoch-Schonlein purpura pneumonic
NAPA
Nephritis
Abdominal pain
Purpura-non blanching rash over buttocks & calves/ankles
Arthralgias
test urine initially weekly, then monthly to monitor for kidney failure
Hx taking in eval of HTN in CH
CNS- HA, seizures hearing impairment CV- palpitations renal- edema, UTI, urine output meds neonatal hx- hx of central cath early CV dz
eval of HTN cause
intracranial HTN Alport syndrome catecholamine nephropathy (HUS, SLE, GN, tumor, ADPKD, etc) OCPs renal artery or aortic stenosis obesity, essential HTN
Labs for evaluation of HTN in CH
BP measurements w/ approp. cuff size
electrolytes, BUN, cretinine, UA, urine cx
consider: CBC, uric acid, C3 level, FBG, lipid levels, urine catecholamines, renal ULS, echocardiogram & EKG
HTN tx in CH
treatable causes must 1st be r/o- much more common to have a treatable cause in CH than adults
exercise
diet changes to address obesity & co-morbidities
medical therapy- diuretics, ACEi, B-blockers, CCB
Hematuria DDx in CH
DOGSHIT
Drugs Oncologic Glomerulonephritis Stones Hematologic Infection Trauma
Fever in a neonate
blood
CSF
urine
UTI labs in kids <2yo in addition to basics, like CBC
renal ULS- visualizes upper UT
VCUG (voiding cystourethrogram)- visualizes lower UT
what clinches the dx of kidney stones in CH
UA w/ micro to get WBC & RBC count (elevated)
the clincher is….CT w/o contrast
what are some of the causes of red urine w/o urinalysis evidence of blood
red dye
food
meds
chemicals excreted in urine
causes of red urine w/ urinalysis evidence of blood but no RBC on microscopy
free Hgb- hemolysis, DIC
free myoglobin-crush injury, burns, myositis, asphyxia
red urine w/ urinalysis & microscopy evidence of blood but no RBC casts
bleeding from urinary tract distal to renal tubules
red urine w/ blood & casts in urine
glomerular dz
- immunologic dz (e.g. post-streptococcal glomerulonephritis)
- inherited dz (e.g. Alport syndrome)
- vascular injury (e.g. ATN, cortical necrosis)
hematuria work up
hx & PE
confirm true hematuria
-if microscopic w/ benign H&P=>recheck
-if repeatedly + or +H&P=>workup
hematuria DDx
UTI/cystitis/urethritis hypercalcemia urolithiasis trauma post-streptococcal glomerulonephritis IgA nephropathy Henoch Schonlein purpura (HSP) SLE nephrotic syndrome membranoproliferative glomerulonephritis Alport syndrome- sensorineural deafness, progressive renal failure sickle cell trait/dz structural abnormality renal/urinary tract tumor
hematuria benign DDx
benign familial hematuria
post exercise
phase I workup for hematuria
UA w/ microscopic exam CBC urine cx chem 8 (including BUN, Cr) 24 hr urine collection for Cr, protein, Ca2+ serum C3 level renal ULS
phase II workup for hematuria
ANA titer throat culture for Step pyogenes ASO titer or DNAse B titer or streptozyme urine erythrocyte morphology coagulation studies sickle cell screen VCUG (voiding cystourethrogram)
hematuria & when a renal bx is indicated
persistent high grade microscopic hematuria;
microscopic hematuria & diminished renal function, proteinuria exceeding 150 mg/ 24 hrs, 2nd episode of gross hematuria
post streptococcal glomerulonephritis clinical presentation
5-21 days (avg 10) post streptococcal infxn gross hematuria (65% of cases) edema (75% of cases) HTN (HA, visual changes) 50% of cases
post streptococcal glomerulonephritis labs
elevated ASO titer
group A B-hemolytic streptococcal infxn
decreased C3 level
tx of post-streptococcal glomerulonephritis
Abx for streptococcus pyogenes supportive care for renal function -reduce salt intake -tx w/ diuretics -anti-HTN drugs
IgA Nephropathy pathogenesis
glomerulonephritis w/ IgA immunoglobulin in mesangial deposits
absence of systemic dz
IgA nephropathy clinical manifestations
episode of gross hematuria 1-2 days after a viral upper respiratory infxn
may be picked up by UA showing microscopic hematuria
IgA nephropathy tx
usually resolves w/ minimal intervention in CH. some progress to have HTN, diminshed renal function, proteinuria. 25% of adults progress to end-stage renal dz
clinical manifestations of SLE
malar rash discoid rash photosensitivity oral ulcers arthritis serositis renal d/o-variable: minimal to end-stage neurologic d/o hematologic d/o immunologic \+ANA
proteinuria
nml CH exretion <4 mg/m2/hr
proteinuria is a urinary protein loss of 50 mg/kg per 24 hrs
proteinuria may be the result of normal activity such as
exercise
febrile illness
upright posture
some non-renal causes of proteinuria
Fanconi syndrome
drug & heavy metal intoxication
processes that increase glomerular filtration such as physical damage, abnormal hemodynamics
Clinical diagnostic criteria for nephrotic syndrome
generalized edema
hypoproteinemia ( 1g/m2/24 hrs
hypercholesterolemia (>250 mg/dL)
pathophysiology of nephrotic syndrome
loss of basement membrane sialoproteins (loss of nml neg. charge)
allows glomerular permeability to proteins
protein loss in urine
complications of protein loss in urine
hypoalbuminemia
loss of plasma oncotic pressure- fluid shifts from vascular to interstitial compartment
increases risk of thromboembolism
hepatic lipoprotein synthesis stimulated by hypoproteinemia
most common presentation of nephrotic syndrome
sudden onset of pitting edema, wt gain or ascites
onset < 6 yo
DDx of nephrotic syndrome
transient proteinuria postural (orthostatic) proteinuria glomerular proteinuria glomerular proteinuria minimal change dz (typical nephrotic syndrome) congenital nephrotic syndrome focal segmental glomerulosclerosis meangial nephropathy membranous nephropathy
transient proteinuria (w/ fever, dehydration, etc.)
protein to creatinine ratio reveals mild proteinuria, ratio <1
postural (orthostatic) proteinuria
benign condition of moderate proteinuria while upright
rationale for 1st morning samples
glomerular proteinuria
associated w/ acute illnesses involving kidney
clinical findings of nephrotic syndrome
edema
periorbital swelling
oliguria
fluid shifts- ascites, pleural effusion, scrotal/ labial edema
labs in nephrotic syndrome
low albumin
UA (proteinuria)- 1+ proteinuria on 2+ random specimens warrants quantitative measure or proteinuria (1st a.m. void spot protein/Cr ratio, ratio>0.5 prompts lab & radiographic workup)
C3 level
renal bx
C3 level in nephrotic syndrome
a low C3 level is the most sensitive & specific test to imply a presence OTHER than minimal change dz
renal bx in nephrotic syndrome
generally unremarkable
foot processes of glomerular basement membrane fused
nephrotic syndrome tx
corticosteroids (80% of pts respond)
low Na+ diet to prevent massive fluid shifts
can try immunosuppressive agents
renal bx if no response to either above (this would typically preced steroids if C3 level was low- implying dz other than minimal change dz)
complications of nephrotic syndrome
infection (peritonitis, bacteremia/sepsis- S. pneumoniae, E. coli), cellulitis
hypercoagulability
pleural effusion
renal insufficiency- BP instability
what accounts for renal cysts as well as tuberous sclerosis
ADPKD (1:1000)
ARPKD (1:10k-40k)
ADPKD can present in infancy & CH
urinary tract obstructions that can lead to nephropathy
ureteropelvic junction (UPJ) obstruction posterior urethral valves
clinical manifestations of posterior urethral valves
poor urine stream
urethra dilates, VUR may develop, kidneys swell & become dysplastic
rupture of the renal pelvis may cause urinary ascites
hopefully caught on fetal ULS (as obstruction)
what is the MCC of newborn ascites
rupture of the renal pelvis d/t posterior urethral valves
hypospadias
ventral malposition of urethral meatus
10% have undescended testes
severe cases of hypospadias prompt suspicion of what?
congenital adrenal hyperplasia & masculinization of female genotype
hypospadias is often associated w/ what?
chordee (ventral curve in penile shaft)
phimosis
unretractable foreskin
90% can retract by 16 yo
tx w/ serial stretching/ steroid cream
circumcision in severe cases
paraphimosis
trapped retracted foreskin in coronal sulcus
foreskin becomes swollen, red, painful
reduce manually w/ lubrication & plenty of analgesia
rarely proceeds to circumcision
testicular torsion
torsion of the testis twists the spermatic cord, causing vascular compromise of involved testicle
S&S of testicular torsion
acute onset of severe scrotal & testicular pain n/v swelling & color change of scrotum transverse lie to testicle vascular flow absent in scrotal ULS
tx of testicular torsion
address in 1st 6 hrs of symptoms & 90% of testes will survive
surgical- detorsion, orchiopexy
torsion of the appendix testis
appendix of the epididymis may torse & undergo vascular compromise
S&S of torsion of the appendix testis
insidious onset of pain
n/v
“blue dot” sign- pain at upper pole of testicle w/ appearance of blue dot
point tenderness at epididymis
minimal swelling
torsion of testis needs to be r/o if pain is moderate or severe
epididymitis
inflammation of the epididymis usually 2/2 infxn or inciting agent- STI, UTI/structural anomaly, trauma, chemical inflammation, often w/ antecedent sexual activity or UTI
clinical presentation of epididymitis
pain & swelling of the epididymis
frequency, dysuria, urethral d/c
fever
PE of epididymitis
normal vertical lie of testis
normal cremasteric reflex
scrotal edema, redness
labs for epididymitis
UA, urine cx
urine nucleic acids for N. gonorrhoeae, C. trachomatis
gram stain & cx of urethral d/c
consider screening for other UTIs in high risk pts
tx of epididymitis
Abx to address UTI/STI
further work up if age or circumstances suggest a structural anomaly- scrotal or renal ULS, VCUG
hydrocele
trapped fluid around the testis located in the tunica vaginalis
what are the 2 types of hydrocele
communicating- precursor to inguinal hernia
non-communicating
tx of hydrocele
observation 1st 2 years of life
earlier if underlying problem (adj. testis becomes inflamed), not resolving, compromise to the testicle
varicocele
tortuous collection of veins around the spermatic cord
clinical sx’s of varicocele
fullness
may be asymptomatic
“bag of worms”
tx of varicocele
tx to preserve function of testes
observation- testicular vol., LH, FSH levels
surgical intervention- embolization, ligation
spermatocele
sperm-containing cyst distinct from the testis. may arise from epididymis, rete testis, or ductulis efferentes
dx of spermatocele
transilluminates
ULS
tx of spermatocele
surgical excision for comfort
undescended testes
more common in premies
present in 3.4% of newborns, remains in 0.7% at 1 yo
if no descent by 1 yo, testes are located (if present) & surgically corrected/removed
retractile testes
retract from scrotum when cold
present in scrotum by parent’s report
testes retained in the abdomen are at higher risk for what
progression to testicular cancer. rates higher for infertility & torsion
