CLIPP 31: 5yo - Hematuria, proteinuria Flashcards
10yo female presents with gross hematuria (tea-colored)
diffdx of periorbital swelling = “puffy eyes”
DDX: glomerular
==> systemic sxs, brown/black urine, RBC casts, dysmorphic RBCs
- glomerulonephritis TYPES ==> post-infectious, MPGN, SLE, IgA nephropathy, HSP, HUS, Alport’s thin BM dz
DDX: non-glomerular
==> localized sxs; pink/red urine +/- clots; eumorphic RBCs
- tumors (=Wilm’s in toddlers; RCC in adults)
- trauma (fall, voiding dysfunction b/c don’t want to pee)
- infection (+ pain, discomfort, dysuria, freq, urgency, secondary enuresis)
- inflammation
- cystic dz
- congenital anomaly (esp. after minor trauma), crystalluria (calciuruia)
- stones =pain, painless hematuria (if in kidney/tract and not obstructing) ==> 50% due to underlying urinary metabolic condition
- sickle cell
10yo female presents with gross hematuria (tea-colored)
distinguish between and initiate an evaluation for glomerular and non-glomeruar hematuria
glomerular
==> systemic sxs, brown/black urine, RBC casts, dysmorphic RBCs
non-glomerular
==> localized sxs; pink/red urine +/- clots; eumorphic RBCs
MANAGEMENT
1) confirm true hematuria = UA + blood (if -blood –> beets, meds)
2) confirm RBC in urine = microscopy + RBCs (if -RBCs –> myo/hemo-globinuria; old specific; other false +)
acute glomerulonephritis
- indications for management
- management
for microhematuria ALONE
- monitor for persistence
for persistent GROSS hematuria, microscopic hematuria:
1) HEMATURIA alone ==> outpatient eval
2) HEMATURIA + sxs and/or elevated Cr, HTN==> immediate supportive management
MANAGEMENT
1) evaluate signs of severity
- electrolytes, BUN, Cr
- quantitate proteinuria
2) evaluate for etiology (depending on hx)
- CBC, C3, C4, Strep titers, ANA, ANCA, and/or anti-GBM titers
- Renal Ultrasound –> r/o other etiologies (cysts, congenital anomalies)
acute glomerulonephritis
- indications for management
- management
for microhematuria ALONE
- monitor for persistence
for persistent GROSS hematuria, microscopic hematuria:
1) HEMATURIA alone ==> outpatient eval
2) HEMATURIA + sxs and/or elevated Cr, HTN==> immediate supportive management
MANAGEMENT
1) evaluate signs of severity
- electrolytes, BUN, Cr
- quantitate proteinuria
2) evaluate for etiology (depending on hx)
- CBC, C3, C4, Strep titers, ANA, ANCA, and/or anti-GBM titers
- Renal Ultrasound –> r/o other etiologies (cysts, congenital anomalies)
3) Indications for renal biopsy
- significant proteinuria (>1gram/24hrs; or Pr/Cr > 1.0)
- significant hypertension
- elevated creatinine
Serology interpretation
low C3
(stays los)
Serology interpretation: MPGN
Serology interpretation
low C3, then nml C3 (in 8-12w)
Serology interpretation: post-infectious glomerulonephritis (PIGN)
Serology interpretation:
nml C3, C4
+ strep titers
Serology interpretation:
- recent strep infection NOT causing the concurrent glomerulonephritis
Serology interpretation:
nml C3, C4
+ strep titers
Serology interpretation:
- recent strep infection NOT causing the concurrent glomerulonephritis
- A 6 year old girl presents with red colored urine. A urinalysis with microscopy will be important because
a. If it tests positive for blood, but microscopy does not reveal RBCs, then this indicates a non-glomerular etiology
b. It may test negative for blood, indicating that this is not hematuria, but rather an ingestion, such as beets, which is discoloring the urine
c. The presence of RBC casts would mean a kidney biopsy must be performed
d. Hemolysis could be the etiology, in which case the microscopy would be positive for RBCs, but the urine dip will test negative for blood
B
b/c even with red colored could be ingesiton
If it tests positive for blood, but microscopy does not reveal RBCs ==> hemoglobinuria or myoglobinuria
== these are still glomerular etiologies
- Glomerular etiologies of hematuria can be distinguished from non-glomerular ones in that
a. Glomerular causes will have RBC casts and dysmorphic RBCs, whereas non-glomerular causes will lack casts and usually have eumorphic RBCs
b. Non-glomerular causes usually have systemic manifestations such as hypertension or edema, or may be associated with rashes or arthritis
c. Glomerular causes will often involve pink appearance and if heavy hematuria, may include passage of blood clots
d. They are difficult to distinguish on history, exam, or urinalysis which is why blood tests and renal ultrasounds are usually needed
A
. When a patient presents with glomerulonephritis, the following are indicators of severity and a need for immediate management
a. hypertension, proteinuria, gross hematuria
b. hypertension, elevated creatinine, low C3
c. elevated creatinine, hypertension, proteinuria
d. elevated creatinine, proteinuria, low C3
e. gross hematuria, abnormal ultrasound, low C3
C == more intense injury to the basement membrane
not a problem with the podocytes directly
nephritis = basement membrane problem
nephrotic sydrome = podocyte disease
- A 12 yo boy presents with an acute glomerulonephritis. Evaluation revealed a low C3 but normal C4. 3 months later, the nephritis persists, as does the low C3. The most likely etiology is:
a. Post-infectious glomerulonephritis
b. Membranoproliferative glomerulonephritis
c. Lupus nephritis
d. IgA Nephropathy
e. Alport Syndrome
B
low 3, nml C4
would be persistently low
PIGN should normalize within 6-8w (at most by 3mo)
- Hypercalciuria is the most common cause of non-glomerular gross hematuria in children. It’s clinically relevant because:
a. Recurrent episodes of gross hematuria, no matter the etiology, is not desirable
b. It results in an increased risk for nephrolithiasis
c. On a chronic basis, it can result in tubulointerstitial damage and progressive loss of kidney function
d. All of the above
D.
- IgA Nephropathy can be mistaken for Postinfectious glomerulonephritis because
a. both can be associated with upper respiratory infections—IgA Nephropathy concurrently, though Post-infectious a few weeks afterwards
b. both can be associated with a low C3, though only transiently with post-infectious GN
c. both can be associated with a hemolytic anemia, though only transiently with post-infectious GN
d. neither are associated with clinically significant proteinuria
e. neither are associated with long-term risk for progressive renal insufficiency
A
- A child presents with peri-orbital edema. To confirm nephrotic syndrome, the provider should illustrate
a. nephrotic range proteinuria, lack of hematuria, coagulopathy
b. nephrotic range proteinuria, hypoalbuminemia, coagulopathy
c. nephrotic range proteinuria, lack of hematuria, hypercholesterolemia
d. nephrotic range proteinuria, coagulopathy, hypercholesterolemia
e. nephrotic range proteinuria, hypoalbuminemia, hypercholesterolemia
E
1) nephrotic range proteinuria = d/t leakage through BM
2) hypoalbuminemia = d/t leaking thru BM
- evidence: problems with renal tubular absorption/metabolism; decreased synthesis of protein in liver
3) hypercholesterolemia = d/t decreased albumin –> liver stimulated to make lipoproteins + albumin
= decreased lipid clearance from circulation
==> later increased risk of atherosclerosis & CAD with persistent nephrotic syndrome
coagulopathy is a part of nephrotic syndrome, but not a part of the definition
lack of hematuria only suggests SOLELY nephrotic syndrome, but could have both nephrotic and nephritic in one
Asymptomatic proteinuria is most often a benign etiology. Which of the following would be more suggestive of a concerning etiology
a. An orthostatic pattern in which the first morning urine is normal or near normal for protein
b. A history of intense exercise on the day of testing
c. A 24 hour urine protein that is only 1.5 grams/day
d. A history of a concurrent febrile illness
e. A concentrated urine (spG 1.020 or higher)
C
others = are reasurring that it would resolve
- Minimal Change Disease is the most common cause of nephrotic syndrome in children. When a child presents with nephrotic syndrome, the following would suggest further evaluation would be needed rather than treating presumptively for minimal change
a. Age between 1 and 10
b. Hypertension
c. Presence of RBC casts on urine microscopy
d. A and B
e. B and C
B, C = more concerning
minimal change usually between 1-10
- In addition to edema and complications directly attributable to fluid overload (e.g. anasarca, pleural effusions, ascites and resulting peritonitis), children with nephrotic syndrome are at greater risk for
a. Infection due to T cell dysfunction
b. Anemia due to decreased erythropoiesis
c. Fractures due to secondary hyperparathyroidism
d. Non-anion gap metabolic acidosis
e. Thrombotic risk due to loss of anti-coagulants in urine
E == definitely hypercoagulable
if treated with steroids, then would be at infection risk. but nephrotic syndrome itself would not lead to higher risk of infection
the rest are related to renal failure.
7yo boy presents with tea colored urine. cold sxs 1 mo ago, now better. has a headache
- hx of T1DM (on insulin) for 4y
- increased weight from a week ago
- next step?
- management?
1) next step: UA and microscopy (==> showing red cell casts, dysmorphic RBCs)
2)
- severity: BMP (Cr, Albumin) with protein:creatinine ratio
- etiology: complement levels; Strep titers
If pos Strep titers, nml C3, C4
- IgA nephropathy
If pos Strep titers, low C3, nml C4
- post-infectious strep nephropathy
non-glomerular causes of hematuria
TICKS
- tumors, trauma
- infection, inflammation
- cystic dz, congenitalanomaly, crystalluria (calciuruia)
- stones, sickle cell
GN associated with hemolytic anemia (Coomb’s positive)
PIGN
Indications for renal biopsy
- by epidemiology, history, acute sxs, nonresponse to treatment
EPIDEMIOLOGY
- pts <6mo ==> increased chance of congenital nephrotic syndrome
- pts 3-18mo + hematuria
- pts >10yo if NOT drug rxn, or PIGN
HISTORY
- pts <18yo + hematuria, protein + Fhx mom with hematuria (Alport syndrome)
- HSP
- SLE + proteinuria, nephrotic syndrome’
- chronic renal insufficiency + persistent elevation of serum BUN, Cr
ACUTE SXS
- significant proteinuria (>1gram/24hrs; or Pr/Cr > 1.0)
- significant hypertension
- elevated creatinine
- severe AKI
- nml C3, C4 ==> b/c need to determine etiology
- NOT PIGN + low C3 at presentation
LONG-TERM
- steroid-resistance nephrotic syndrome - lack of response to steroids after 8w
- NOT PIGN + progressive decline in renal fx and UOP
- suspected lupus, + ANA, high anti DS DNA, low C3 persisting >3mo
kiddo has iga nephropathy. also been having HA. what can you do for his HTN of 150/80. which of the following would you do
a. provide reassurance. if this is post-strep GN, it will get better on its own so it does not requirement tx
b. it is severely elevated for a 7yo so warrants treatment wiht a low sodium diet and an ACE inhibitor until the GN resolves
c. it is severely elevated for a 7yo so warrants treatments with a low sodium diet, and thiazide diuretic until the GN resolves
B
if BP+5 >99%ile ==> SEVERE HYPERTENSION
ACE-inhibitor > diuretics, CCB
==> less pressure from the medication (more protective to the kidney)
= maintains GFR better
ACE-I contraindicated if had hyperkalemia, AKI in the acute setting
if had milder HTN –> would:
1) reassure
2) low-sodium diet
kiddo has iga nephropathy. also been having HA. what can you do for his HTN of 150/80. why did he gain weight?
a. with his acute GN and HTN he was more sedentary, so this is increased body fat
b. with his acute GN, his GFR may be decreased so thsi is likely fluid weight from renal failure
c. with his acute GN, renin is stimulated and his nephrons are likely absorbing salt and water, so this is fluid weight.
d. with his acute GN and being sick, he probalby actually lost weight, so this is measurement error
C
renin is JGA ==> most likely retaining the water
HTN is in response to renin stimulation
he is not in renal failure quite yet
6yo male presents with pinkish-red colored urine
- otherwise well, no known trauma, no recent meds, in school but no obvious illness, ROS completely egative
- PMHx, soc hx, family hx all normal
- exam: normal BP and vitals, 50% height and weight (otherwise completely normal)
- UA and microscopy ==> blood, trace protein, many eumorphic RBCs
non-glomerular: TICS
- tumors, trauma
- infection, inflammation
- cystic dz, congenital anomaly, crystalluria (calciuruia)
- stones, sickle cell
most common cause of nonglomerular bloody urine
hypercalciuria
Ca/Cr > 0.2
Renal US neg or positive –> +/- stones
esp. if microscopic
ddx of non-glomerular hematuria
-management
TICS
1) Urine Ca/Cr, renal US
==> if either positive for stones –> 24h urine for stone chemistries
==> signs & sxs of infection –> CBC, CMP
2) electrolytes, BUN, Cr, CBC, Pr/Cr ratio
complications of hypercalciuria
- recurrent gross hematuria is very bad
- risk of nephrolithiasis & stones (PAINFUL)
- nephrocalcinosis == deposits of calcium within tubulointerstitial parenchyma; progressive scarring loss of function
how do you treat idiopathic calciuria
a. drink lots of fluids to make a dilute urine
b. low sodium diet
c. high citrate diet
d. thiazide diuretic
All of the above, in that order
drink plenty of fluids –> to flush through
low sodium diet –> so that don’t reabsorb as much
high citrate diet –> to help be more soluble
C/I in alkaline urine ==> will make more alkaline
thiazide diuretic
C/I if have hypercalcemia ==> will retain Ca
most common types of hypercalciuria?
1) idiopathic = multifactorial (genetics, diet)
2) tubulopathies = Dent’s dz; Bartter’s syndrome
3) medication -induced
14yo boy has maroon-colored urine. otherwise healthy, playing touch football with friends earlier. denies obvious trauma / rough tackle. ROS otherwise NEgative.
soc hx = athlete , 9th grade, doing well, no substance use, not sexually active
FamHx - mother with HTN
exam - HR 60, BP 138/84,tall and thin, athletic build, no abd masses / tenderness
- UA: 1.025, pH 6, trace protein, large blood, many dysmorphic RBCs, no casts
- diffdx
- evaluation
GLOMERULAR
- glomerulonephritis (Alport)
- HUS
NON-GLOMERULAR
- trauma
- congenital anomaly + mild trauma
management
- renal ultrasound
- CBC, BMP, complement
==> Urine Ca/Cr; BMP was normal
==> Renal US revealing b/l enlarged kidneys with multiple cysts
- ADPKD
could be a milder form of it - even if no FHx (mom, even with HTN could be normal)
do lack of RBC casts preclude glomerulonephritis
NO
presentation of ADPKD
1) gross hematuria
2) HTN
management of ADPKD
1) strict BP control == RAAS inhibition (ACE-I +/- ARB): target <120/80 ==> slower deciline of renal fx
2) control of proteinuria == RAAS inhibition (ACE-I +/- ARB): delay oprogression of CKD, prevent future ESRD
3) kidneys >15cm –> restrict from high impact sports/activitys = risk of trauma and cyst rupture == massive bleeding
4) high fluid intake == ADH assoc. with cyst growth, so suppress ADH with super optimal hydration to slow progression of ESRD
5) pt education, connection with resources
6) other symptomatic control (e.g. low sodium)
in a kid with ADPKD, do you screen for berry aneurysm
ONLY if there is a Fhx of massive brain bleed
- screen at age 30yo
16yo female with diarrhea illness x2w presents with brown-colored urine
- no recent travel / new foods, no emesis, but crampy abd pain results in decreased intake
- at first thought urine was super concentrated, but now dark brown
- took cipro after 1w of illness, tylenol and motrin prn pain
- FHx for mom with grave’s disease
- EXAM: Bp normal, vitals normal, Ht 50%, Wt 10%
- otherwise completely normmal, no edema, mild non-specific diffuse abd pain
- UA = blood, proteins, LOTS of RBC casts
diffdx?
- IgA nephropathy = acute mucosal damage
- HUS = from Shigella diarrhea –> sheared RBCs
- systemic autoimmune vasculitis (SLE, polyarthritis)
- HSP - not really diarrhea (abd pain, hematuria) +/- rash (can come on later - within a week)
- post-infectious GN
EVALUATION
- CMP, CBC nml (no HUS)
- 24h urine protein 0.9g
==> diagnosed with C. diff colitis –> treated.
- everything resolved
- C3 levels normalized in 2mo
==> DX:
- post-infectious
- IgA nephropathy (if get another infection - will get nephritis again)
treatment for IgA nephropathy
ACE-I == slow decline of renal fx
SEVERE - steroids
