13. in the newborn period cr is elevated and reflects maternal cre; until about 10 days of age and then decrease to the normal newborn range of 0.2 – 0.4
14. preterm infants have been demonstrated to have slightly high cre than term babies
16. Basically its just too hard to get a god 24 hour collection that is very accurate, so now we just collect a spot urine protein:cre ratio to further eval proteinuria
17. proteinuria on a dilute sample (SG <1.015) needs more workup and the spot urine as above is the starting point
56. Ddx includes postinfectious acute glomerulonephritis (PIAGN), secobdary causes of renal dz like SLE, small vessel vasculitis, HBV, HCV, HIV, sickle cell disease or trait
57. In most cases in which patient has both hematuria and proteinuria, serial UAs will show resolution of one or both of them
72. Always look at the micro to see if there are actually any RBCs, need to have >5 per HPF in order to have the RBCs be the cause of the positive UA
73. Determine by hx and lab evaluation the etiology of red urine
74. Ddx for causes of red urine = hematuria, hemoglobinuria, myoglobinuria, prophyrinuria; certain pathogens (serratia) can cause red urine, certain foods/dyes (beets, blackberries, food dyes) may cause red urine and some meds (deferoxamine, rifampin, phenolphthalein)
76. Recognize the etiologies of dysuria may be age-related and that numerous other etiologies include vaginitis, chemical irritation, and trauma
77. Can presumptively treat for UTI without necessarily getting a urine cx with adolescent females who have dysuria, pyuria, and normal findings on genitalia inspection and have not been sexually active
87. Secondary enuresis = kid had previously sustained dryness and then subsequently resumed bedwetting
88. Only 2-3% of kids with nocturnal enuresis actually have a physical problem contributing to it; usually is due to diminished bladder capacity or inability to ake up in respone to a full bladder or get to the toilet to pee
90. A history of constant wetness in an otherwise healthy female who is toilet trained is indicatove of ectopic ureter
91. US often misses the ectopic ureter, so when suspected need to get an excretory urograpghy or an MRU (MR urography) – the latter is now the preferred modality
92. Know the importance of skin abnormalities in the sacral area when evaluating a patient with primary enuresis
93. Look for dimples, etc as clues to presence of a spina bifida type problem; to further eval bladder dysfunction would get abd ultrasonography
95. Often experience urgency due to uninhibited bladder contractions and have frequent day and night time enuresis (the night time enuresis distinguishes them form the kids with pollakiuria)
96. They often compensate for their uninhibited bladder contractions by doing things to activate the external sphincter (squatting, leg crossing, Vincent curtsy)
103. A renal US can confirm the dx, and then do need to further eval for other problems like VUR, which can occur in the contralateral kidney. Do this by getting VCUG
106. The kidney anomalies can be agenesis, dysplasia, hypoplasia and therefore the kidneys must be evaluated
107. Know that abd ultrasonogrpahy is the preferred diagnostic procedure in children suspected of having autosomal dominant polycystic kidney disease
108. Recognize the association of bilateral renal aplasia or severe dysplasia with pulmonary hypoplasia (Potter syndrome)
109. Renal aplasia/dysplasia in the fetus results in oligohydramnios that alters amniotic fluid dynamics and interrupts the normal development of the fetal lung, especially during cannicular development in 16-24 weeks; results on pulmonary hypoplasia that may be fatal
114. Usually congenital abnormalities: ureteral hypoplasia and asymmetry of the utreteral wall musculature, stenosis of scarred ureteral valves, abberant vessels in the lower renal pole, renal ectopy, horseshoe kidney, duplex collecting systems
115. Duplex collecting system is the most common urinary tract anomaly, with varying grades of obstruction due to them
117. PUV is the leading cause of severe urinary obstruction in children (males)
118. Plan the evaluation of an infant with anuria more than 48 hours after birth
119. If there is no voiding after 24 horus, then need to get a thorough hx, including prenatal hx and any imaging that was done, assess for any evidence of perinatal asphyxia or sepsis, and family hx of renal disease
120. Examine the genitalia, flanks, abdomen and look at baby for any signs of edema or oligohydramnios sequence
122. Also need to attempt to pass a urinary catherter: allows to obtain urine for studies, see if there has even been any urine produced, and also to see of the tract is patent
123. If no urine can be obtained then need to do a US of kidneys, ureters, bladder
125. Know the urologic findings associated with prune belly (Eagle-Barret) syndrome
126. Hydronephosis, which is usually due to an obstructive cause (PUV, vesicoureteral relfux, UPJ obstruction)
127. Renal outcome for thee kids is usually poor, most develop renal insufficiency
128. Know that a ureterocele may lead to urinary tract obstruction
129. A ureterocele is a cystic dilation of the ureter where is inserts into the bladder. It can be contained entirely within the bladder (intravesicular) or can be beyond the bladder into the urethra or bladder neck (extravesicular)
131. Know that natural hx (e.g. etiology, familial association, outcome) of vesicoureteral reflux
132. Is the most common urologic abnormality in children
133. Rates are elevated among siblings and offspring with higher rates in Caucasians, females and kids under age 2
134. By 5 years of age, grade I an II spontaneously resolve in 80% of children; those with high grade VUR are about 5x more likely to have renal scarring than those with low grade, and 9x more than those with none
140. Recognize the necessity for long term evaluation of renal and bladder function in patients with PUV
141. Know that urethral strictures in boys almost always result from urethral trauma (iatrogenic or accidental)
142. Previous trauma or instrumentation. Other causes can include infection (gonorrhea), congenital abnormality, idiopathic cause, complication of balanitis
143. Tx depends on the length, location and persistence of the stricture
144. Severe stricture in males may damage the bladder and even cause hydronephrosis
145. Know that a girl with a narrow urethra needs no tx
173. Renal scarring increases the risk for development of hypertension and kids with VUR, or any cause for renal scarring, need to be carefully monitored for development of htn
182. In the first 3 post natal months it is more common in boys, and 5-10 times more common in uncircumcised than circumcised boys; after the first 3 post natal months it is far more common in girls
183. Know that UA alone is often insufficient to dx UTI
184. UA can be low sensitivity; findings like nitrite are less likely to be positive in the younger patients, for example. Negative nitrite, leuko esterase are not sufficient to r/o UTI
187. Can cause detrusor instability, which can lead to incontinence, large bladder capacity, and dyscoordinated voiding
188. Urinary retention is common due to dyscoordinated voiding or outflow tract obstruction caused by large rectal fecal masses
189. If all imaging, work up and other thigns about the kid are normal then treat underlying things like constipation before referring them to urologist, nephrologist, etc
193. cephalosporins and FQs are ideally reserved for use as second line treatment or with documented resistance to TMP-SMX (i.e. C/S results)
194. standard duration of tx of 7-14 days, though a recent met analysis cited in the question critique does support 2-4 days courses of treatment – not sure if this is best answer on the exam, though
197. Suspicion of PIAGN increases when gross hematuria is accompanied by a h/o antecedent illness, especially GAS or impetigo. Also often have edema and HTN
198. Interval beyween pharyngitis and PIAGN is about 1-2 weeks where latency between skin infection and PIAGN is 3-6 weeks
199. A positive GAS throat swab, elevated ASO, hypocomplementemia (low C3) and urinary RBC casts
200. Know the lab evaluation of acute post-streptococcal glomerulonephritis
201. Lab work up as above; need to check a UA, serum lytes and renal function tests, check complement levels, ANA and anti-dsDNA
202. hypocomplementemia occurs in more than 90% of cases and looking for complement levels is the most important dx test after initial assessment (low C3 and normal C4) (initial assessment = UA and the serum lytes.creatinine.BUN)
203. Complement value normalize in 6-8 weeks, but microscopic hematuria may persist for 6-12 months (even years per the question critique); gross hematuria and htn resolve in a few weeks and proteinuria in a few months
204. Understand that acute post strep nephritis rarely progresses to chronic renal failure
205. Can have acute renal failure (azotemia in 1/3 of cases)
206. Acute renal failure may require treatment with corticosteroids, cyclophosphamide and even dialysis if the renal failure persists; for those pts the renal prognosis is guarded
215. Plan the initial management of acute post strep glomerulonephritis
216. Initial management needs to focus on supportive treatment, management of sodium and fluid retention (diuretics), as well as Na and fluid restriction; management of hypertension, which may require vasodilators. Abx can reduce the risk of transmission of nephritogenic strains of strep to close contacts
217. Initial lab should be a UA, then check serum lytes and renal function. Additional serologic tests are complement levels, ANA and anti-dsNDA
218. Must assess renal function to determine if it is a rapidly progressive GN that warrants renal consult for possible renal bx and urgent tx
221. Most pts have gravity dependent edema, might have abd ascites, shoes too tight; sx may be triggered by a preceeding infection although actually contribution of infection to disease is unknown
226. After initial eval, then look for secondary causes of the NS: includes ANA, anti-dsDNA, HBV core and surface antibodies, HCV ab and HIV, CBC to look for evidence of blood malignancy or sickle cell; need to also check a PPD in case need to start steroids
227. Plan the initial treatment for a child with an initial episode of nephrotic syndrome
229. Corticosteroids are the mainstay of treatment, if this fails they might need cyclophosphamide, cyclosporine or chloramphenicol (“off label”)
230. If relapse is not achieved with steroids within 8-10 weeks then need a renal bx for further studies and for possible other dxes (i.e. FSGS, membranous nephropathy)
232. Pts and parents need to be taught to check urine for protein with dipsticks as most pts have a chronic, relapsing course and have “flares” with URIs
234. In an acute setting in which the patient has evidence of complications (anasarca, volume depletion, etc) then need to assess and restore intravascular volume status and replete with albumin (1mg/kg of 25% albumin)
235. Know the ddx of nephrotic syndrome with and without hematuria
240. Create an increased risk of thrombosis; also aggressive diuretic use can induce hypovolemia with secondary renal failure, thromboembolism or electrolyte disturbances.
241. If diuretics are needed for treatment of sever ascites, peritonitis, resp distress or heart failure then you can prevent or treat volume depletion with albumin admnistration
245. Acute renal failure: can usually be corrected with intravascular volume correction
246. Thromboembolic complications, which can cause the acute renal failure in cases of renal thrombosis, also can have thromtoic events that affect the lungs, brain and peripheral vessels – the increased risk of thrombosis is due to the loss of antithrombin III and protein S in the urine
256. Recognize that response to therapy is one of the best indicators of prognosis in nephrotic syndrome
257. Recognize that the prognostic significance of a decreased serum C3 concentration in a patient with nephrotic syndrome is an indication of a dx other than MC disease
270. Monitor volume status; although fluid administration is a difficult balance as patient may be euvolemic but oliguric, therefore recommend insensible losses plus urine output in this kind of patient
282. Renal manifestations in 40-50% of cases of HSP and usually occur within 4 months after the rash (usually in one month)
283. Involvement ranges from microscopic hematuria, mild proteinuria but may have sx as severe as nephritic or nephrotic syndromes and chronic renal disease
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