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39 Cards in this Set
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If a healthy patient presents with persistent proteinuria on urine dipstick, what would you do?
Q18; P2014 |
Obtain a first moring urine sample to evaluate for orthostatic proteinuria.
Know that persistent dipstick positive proteinuria urine protein:creatinine ratio > 0.2 indicates renal disease.
Know that a urine protein:creatinine ratio in a 1st morning urine sample is as sensitive as a 24H urine collection. |
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What is orthostatic proteinuria?
Q18; P2014 |
Orthostatic proteinuria occurs during eth day with the patient is active and disappears when the patient is supine/asleep for at least 2H.
To confirm OP, a first morning urine sample is needed. It is important that the patient collect the first urine sample immediately on waking because even a small amount of activity can lead to proteinuria. |
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What are girls and young women at risk of developing if they have a narrow urethra?
Q36; P2014 |
Girls and young women with a narrow urethra are at risk of developing "spinning top urethral (STU)" deformity. STU is caused by dilation of the proximal muscular urethra against a closed or narrowed distal urethral sphincter. It is diagnosed by VCUG. It is associated with bladder dysfunction (detrusor-sphincter dyssynergia: contraction of the detrusor muscle against a closed urethral sphincter). This produces the classic "spinning top urethral (STU) deformity on VCUG.
Commonly seen in female infants and young children due to immature voiding reflexes causing an overactive bladder. Usually the detrusor-sphincter dyssynergia will likely resolve with mturation and development of normal voiding habits.
Once identified, prophylactic antibiotics are not required.
No treatment is necessary; it will resolve with time. |
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Know that skin abnomalities of the spine, such as tuft of hair, vascular lesions (hemangioma), or discoloration of the skin overlying the spine, suggests an underlying vertebral or spinal lesion. Spinal lesions can be associated with bladder dysfunction.
Obtain MRI spine to evaluate for spinal lesions.
Q54; P2014 |
Enuresis is diagnosed in kids > 5yo who PEE in the bed or on their clothes 2X or more/wk for 3 conseutive months.
Primary enuresis occurs in kids with NO period of sustained dryness.
Secondary enuresis occurs in kids with a sustained period of dryness for 6m (nocturnal enuresis) OR 3m (diurnal enuresis).
Know that bladder dysfuction leads to chronic renal failure if NOT identified and treated early.
Patients with spina bifida need detailed and regular evalution of bladder capacity and pressures. |
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Know that enterococcus UTI should be suspected in children with indwelling catheters and urine dipstick analysis showing negative nitrites.
Start empiric ABX, Ampicillin and 3rd generation cephalosporin or aminoglycoside in patients suspected of having enterococcal UTI.
Q72; P2014 |
Enterococci are typically isolated from the urinary tract and there is an inceased risk for enterococl UTI associated with catheterization, instrumentation, and obstruction.
Empiric ABX coverage should cover E. coli, the most common cause of community acquired UTI and Enterococcus.
Amoxicillin, Ampicillin, Linezolid and Vancomycin - treats Enterococcus
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Patients with NF1 are at increased risk for renal artery stenosis (that can lead to renovascular HTN).
Renal disease and renovascular anomalies are the most common causes of secondary HTN in children.
Q90; P2014 |
Diagnose RAS: - Intra-arterial angiography (gold standard) - MRA or CTA - Duplex doppler U/S
If the workup for RAS in a patient with NF1 and HTN is negative, consider "pheochromocytma." |
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Know that cerebral aneursyms that measure less than 7mm in diameter, saccular in shape, and present in the anterior cerebral circulation have low risk for rupture. Factors associated with a high risk of aneurysm rupture: size: aneurysms measuring > 7mm; poorly controlled HTN; age < 50y. Cerebral aneursyms are a serious complication of APKD. The prevalance of intracranial aneurysms is low in children and it increases with age. Patients with a family history of APKD and cerebral aneurysms are at an increased risk of developing intracranial aneurysms or SAH. Q107; P2014 |
Routine screening for cerebral aneurysms is indicated for high risk patients only. Screen Q 5y if the initial imaging study is negative. If known aneurysms or history of intracerebral bleeding, then ANNUAL screening for 2 to 3y, and Q 2 to 5y thereafter if the neurysm is stable. |
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Charcterize Renal Vein Thrombosis.
Q178; P2014 |
Renal Vein Thrombosis is characterized by FLANK MASS, THROMBOCYTOPENIA, HEMATURIA.
Dx: Renal U/S with color flow doppler
Risk factors: - prematurity - perinatal asphyxia - shock - CCHD - dehydration - sepsis - polycythemia - maternal DM |
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Know that bright red hematuria with clots and dysuria are suggestive of an underlying cystitis.
Nonglomerular hematuria is usually described as red or pink urine on a patient's history.
Glomerular hematuria is usually described as cola-colored, tea-colored, or brown.
Hemoglobinuria and myglobinuria shows a urine dipstick positive blood but urine microscopy shows NO RBCs. |
Q196; P2014 |
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To differenctiate cystits from pyelonephritis: pyelonephritis is a clinical diagnosis based on the presenting symptoms of fever, vomiting, and flank pain. |
Q196; P2014 |
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Know that patients with VUR must be screened for VOIDING DYSFUNCTION. Voiding dysfunction may cause 2ndary VUR because of abnormally high bladder pressures causing incompetency of the UVJ leading to reflux.
VUR may resolve SPONTANEOUSLY (50%). |
Spontaneous resolution of VUR: - lower grade of reflux 1-3 - unilateral reflux - prenatal hydronephrosis - diagnosis of VUR < 1yo |
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Patients presenting with facial puffiness and periorbital swelling suggests nephrotic syndrome and should have a U/A for evaluation for proteinuria.
Patients with facial puffiness due to nephrotic syndrome are often mistaken as having an allergic reaction.
nEPHrotic syndome is characterized by edema, proteinuria, and hypoalbuminenmia.
Patients with idopathic nephrotic syndrome are initially treated with oral steroids (60mg/m2 per day x 4-6wks followed by weaning over 4-6wks). |
Hereditaray angioedema is associated with low C1 esterase inhibitor, recurrent episodes of nonpruritic, nonpitting edema without urticaria.
1st episode occurs before 5yo. |
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Exposure to nephrotoxic agents should be minimized because of decreaesd nephron mass in patients with a solitary kidney. |
Know that the GFR increases progressively from day 1 after birth up to near adult-level function by 2 yo. The most frequently used method to estimate the GFR of a child is by serum Cr level.
Know that the the serum Cr is elevated for the 1st 10 dol. This reflects Mom's serum Cr levels which has not been eliminated by the NBs kidneys.
By 2-4wks of age, an infant's Cr should be about 0.2-0.3mg/dL.
By 3m of age, the Cr should DECREASE to 0.2 to 0.3mg/dL, where it should remain until about 1-2y. After 2yo, adult level GFR has been reached but the serum Cr may begin to rise slightly because Cr conc also reflects increasing muscle mass in a growing child.
The NML Cr level ranges from 0.8 to 1.1 for adult females; 1.0 to 1.3 for young adult males. Higher values correspond with the muscle mass of the patient. |
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Know that a young girl, ie, 1yo, with febrile UTI or pyelonephritis should be evaluated for uterocele and hydronephrosis.
Uteroceles present as a ureteral obstruction associated with a febrile UTI in female patients. Uteroceles are discovered incidentally through U/S or VCUG, where a filling defect is dicovered within the bladder. They are 5X more frequent in females. They are more often associated with a duplicated collecting system - the upper pole drains into the obstructed ureterocele and the lower pole is associatd with an ectopic ureter with a high likelihood of VUR.
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Know that acute pyelonephritis is associated with an underlying urinary tact abnormality in 30-50% of cases. The most common anatomic abnormality associated with pyelonephritis is VUR.
Q33; P2013 |
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To diagnose HTN, you must obtain an elevated BP during at least 3 office visits separated by at least 1wk.
Q38; P2013 |
COA presents with HTN, different BP in UE compared to LE and DELAYED pulses in the LE. Measure BP in all 4 extremities.
Pre-HTN is BP beween the 90th and 95th%. |
Q38; P2013 |
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Think RENAL STONES if you see flank pain, gross hematuria, > 100 RBC/HPF and occassional CRYSTALS!
Screening test: U/A with microscopy. To evaulate for secondary causes of renal stones, ie, metabolic disease, hypercalciuria, hyperoxaluria, hypocitraturia, hyperuricosuria, and cystinuria; obtain a 24H urine collection.
Q50; P2013 |
The most common symptoms of renal stones: renal colic and gross hematuria. DX: Noncontrast CT to evaluate for calcifications in adults; renal U/S in children. |
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Preadolescent child with COLA COLORED URINE, well several days ago when he developed runny nose and cough, BP 106/62, nml C3/C4 levels; Cr 0.9, U/A with protein +3, blood +2 BUT family history with an uncle on HD.
Think: Alport syndrome.
Obtain a hearing test to evaluate for bilateral sensorineural hearing loss. |
Q67; P2013 |
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What are the types of familial nephritis?
Q67; P2013 |
Alport syndrome Thin glomerular basement disease
80% of Alport syndrome cases are XLR. The affected male patient inherits the abnormal X gene from his mother, who is heterozygous for the condition or, basically, a CARRIER, who passes the defective gene to 50% of her offspring.
Women who are carriers have microscopic hematuria.
Most cases are characterized by hematuria (cola colored urine) at disease onset followed by the development of proteinuria, and lter, renal failure and bilateral sensorineural hearing loss (80%). |
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RHABDOMYOLYSIS is suggested by a history of strenous exercise, reddish brown urine with U/A with + blood but urine microscopy shows LESS THAN 5RBC/HPF.
Hemoglobinuria and myoglobinuria produces red colored urine; these conditions can give false + dipstick results because NO RBCs.
Q101; P2013 |
Rhabdomyolysis results from muscle injury and breakdown leading to the release of free myoglobin in the plasma and ultimately, myoglobinuria and re-colored urine.
Labs: - high CPK - |
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U/S findings of bilateral hydronephrosis, bladder thickening; and, PE findings of suprapubic mass suggests OBSTRUCTIVE UROPATHY secondary to PUV. PUV is caused by residual valve tissue in the prostatic urethra.
Patients with PUV have an increased risk of developing: - VUR - RTA Type 4, characterized by a NAG metabolic acidosis, hyperkalemia, Urine Cl < 15, Urine pH < 5.5.
Q118; P2013 |
Male infants in the NB period, with PUV often present with a weak urinary stream.
Know that patients with renal tubular damage, ie, hydronephrosis, secondary to PUV are at increased risk of dehydration more than expected in the setting of acute gastroenteritis. |
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Elevated C3 levels in PSGN should NORMALIZE by 8wks. If C3 remains persistently LOW after 8wks, consider MPGN (low C3 & C4).
- Microscopic hematuria may persist for 1-3y after disease resolution.
Q154; P2013 |
Treatment: - supportive care - IVF +/- ACE-I or ARB if HTN - low Na diet - diuretics if edematous |
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Think NEPHRITIC SYNDROME: hematuria, proteinuria, edema, HTN, and azotemia.
Think Acute Glomerulonephritis if a sudden, new onset of cola colored urine.
Classify GN by hypocomplementemic (low C3) or normocomplementic (nml C3).
Q154; P2013 |
Hypocomplementemic causes: PSGN - MPGN (2/3 cases) - Lupus nephritis (also low C4) - Shunt (ventriculoatrial shunt) nephritis - Subacute bacterial endocarditis
Normocomplementemic causes: - IgA Nephritis - HSP - ANCA-associated GN - MPGN (1/3 cases) |
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What is RTA type 1?
Q169; P2013 |
RTA type 1 is due to a defect in the ?????. It is characterized by HYPERCHLOREMIC NAG METBOLIC ACIDOSIS: - high urine pH > 5.5 - NAG metabolic acidosis - low serum K - high serum Cl - high urine Ca - high urine PO4 (low serum PO4 because you are excreting and losing PO4 in the urine) - STONES!!!
Causes: - SLE - Sjorgren's disease - RA - meds: amphotericin b, ifosfamide |
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What are the most common causes of an abdominal mass during the newborn period?
Q186; P2013 |
Multicystic kidney disease (MCDK) Hydronephrosis (most likely due to UPJ obstruction)
Most NB abdominal masses are found during prenatal U/S.
First, obtain a renal U/S. - MCKD shows "noncommunicting renal cysts with minimal parenchyma" - 30% increased risk of VUR in the contralateral (nml) kidney
Then, check a VCUG. If VUR is found on VCUG, then start prophylactic ABX immediately (Amoxicillin 10mg/kg/day) |
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Do NOT use bactrim in infants < 2m. |
Q186; P2013 |
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Know that the kidney affected with MCDK is nonfunctiong due to the multiple noncommunicting cysts. The nml kidney is at risk for VUR (30%) and UPJ obstruction (15%). MCDK is associated with an excellent prognosis. Q186; P20113 |
MUST monitor MCDK with renal U/S Q3-6m in the 1st year for progressive renal disease, then ANNUALLY until 5yo because it is associated with an increased risk of WILMs TUMOR. |
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What is the difference between nephritic syndrome and synpharyngitic syndrome?
Q203; P0213
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When patient's present with acute onset of cola colored urine, hematuria, proteinuria, HTN, elevated BUN/Cr, and edema....THINK: Nephritic process.
When associated with URTI, pharyngitis or skin infections, the etiology may be either Nephritic Syndrome or Synpharyngitic Syndrome.
Nephritic syndrome: is associated with NML complement levels - For example: IgA nephropathy, Alport Synddrome, MPGN - Onset within days of URTI symptoms - IgA Nephropathy is associated with a URTI 1-2 days before the onset of renal symptoms
Synpharyngitic syndrome is associated with LOW C3 levels - For example: PSGN - Onset of PSGN: 7-21d prior to the onset of renal symptoms |
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What is microscopic hematuria? Q220; P2013 |
Microscopic hematuria is RBC > 5 per HPF; it is usually an incidental finding. It can be transient or persistent. If hematuria persists on 3 consecutive urine samples, then begin a workup for the following: Cr, C3/C4 levels, ANA (dsANA), CBC, ESR, U/A with micro, urine protein and Cr, renal and bladder U/S If ALL is negative, then recheck U/A Q 3m. |
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What is Minimal Change Nephrotic Syndrome? Q237; P2013 |
Minimal Change Disease: - Normotensive - Edema - NO microscopic hematuria (but may be resent in 15-20%) - HTN (20%) - Steroid responsive during treatment Nephrotic syndrome in general: - Marked proteinria +3 to +4 - Hypoalbuminemia/Protein loss in urine - Edema - Normal BP - Minimal microscopic hematuria - Nml serum Cr |
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Know that fever and exercise are common causes of transient proteinuria.
Q30; P011 |
Know that a urine dipstick with proteinuria +2 is always abnormal. Proteinuria can be transient or persistent (fixed) that can be distinguised by orthostatic proteinuria which is common in adolescents. If suspected, obtain a first morning urine specimen. Persistent (fixed) orthostatic is present on random and first morning samples. Transient proteinuria can occur wit stress, dehydrtion, exercise or fever (>38 deg). Proteinuria associated with vigorous exercise is milde (usually +2) and resolves after resting for 48h. |
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Know that patients with sickle cell trait may present with a family history of SCD, hematuria, proteinuria and normal renal function. UA shows specific gravity of 1.010 (this urine suggests Isosthenuria, ie, specific gravity 1.010 and urine osmolality 300mOsm/L; the urine is neither diute nor concerntrated relative to the serum). But, no clinical signs or symptoms of renal disease. Obtain a hemoglobin electrophoresis to confirm the diagnosis of SCD or SCT. |
Q46; P2011 |
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What is HUS (hemolytic uremic syndrome)? What is the most common cause? How do you treat HUS? Q62; P2011 |
TRIAD (THINK - HUS/HAT-DAT) - hemolytic anemia (MAHA with fibrin deposition at the site of renal tubular cellular injury in the kidneys - ARF - thrombocytopenia - diarrhea (90%) Cause: E. coli O157:H7 D+ strain is associated with the shiga toxin that causes diarrhea. Diagnose: peripheral lood smear showing schistocytes, burr cells and minimal platelets Treat with supportive care; AVOID ABX use in these patients. |
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What is HSP (Henoch Scholein Purpura)? Q78; P2011 |
HSP is a small vasculitis involving the joints, skin, GI tract and kidneys. CP: - Skin: purpuric skin rash on the extensor surfaces (often the buttocks and LE) - GI: submucosal bleeding presenting as abdominal pain, hematochezia, intussuception - Bones/Jts: athralgias, arthritis -Renal: hematuria +/- proteinuria Know that patients wiwth HSP and hematuria AND significant proteinuria > +2 must obtain a renal biopsy to assess the severity of GN and the need for immunosuppressant therapy. |
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What is the association between renal disease and Williams syndrome? How does Williams syndrome present?
Q110; P2011 |
Williams syndrome: - hypercalcemia - intellectual disability - HTN - Vascular involvement: supravalvular aortic stenosis, pulmonary ratery stenosis, COA, aortic hypoplasia, renal artery stenosis - systolic murmur - abdominal bruit
Renal disease in Williams syndrome: *** RENAL ARTERY STENOSIS Wiliams syndrome presents with infantile hypercalcemia which can lead to hyercalciuria and nephrocalcinosis that usually resolves by 1-2yo. Often have phobias and anxiety; difficulties with visuospatial relationships and understanding math concepts. |
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What should you think when you hear, "acute glomerulonephritis?" Q190; P2011 |
THINK: - hematuria - proteinuria - mild hypertension - trace edema - history of cola colored urine - azotemia (high BUN and Cr) |
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Patients with poorly controlled seizures may try a ketogenic diet for improved seizure control. These patients have an increased risk of developing hypercalciuria and renal stones. Q222; P2011 |
Other risk factors for stone formation: - hypercalciuria - acidic urine - hypocitraturia Stones are either uric acid or mixed calcium/uric acid stone. When on a ketogenic diet, patients should take POTASSIUM CITRATE irrespective of the presnece of hypercalciuria. |
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What is the initial workup for hypercalciuria? Q222; P2011 |
Obtain a urine Ca to Cr ratio. |
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Know that some children with enuresis ve a functionally reduced bladder capacity and/or frequent uninhibited bladder contractions.
Know that it is expected that children will acheive continence of urine by 5yo. THINK: ENURESIS or 5NURESIS
Do NOT treat for incontinence until 7yo.
What is the treatment for enuresis?
Q238; P2011 |
Treatment consists of behavior modification and pharmacologic therapy.Behavior modification: - bedwetting alarms (auditory or silent, ie, vibratory) and are the most effective strategy for nocturnal enuresisMedications:- anticholinergic agents, ie, oxybutynin chloride, to reduce bladder contractions; very useful to treat nocturnal enuresis with daytime symptoms of incontience, urgency and frequencyAn overactive bladder with syptoms of daytime incontinence, urgency and frequency is effectively treated with an anticholinergic agent. |
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Patients with a UTI diagnosed on U/A must have a Renal/bladder U/S done to evaluate for hydronephrosis and renal stones, both of which are risk factors for a UTI. A DMSA tyically is done as a follow up study to evaluate for renl scarring in a paitent with a history of pyelonephritis. |
Q253; P2011 |
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