Based on 2010 Content Specs

2. Normal function

3. Know age related changes in GFR and the impact of the serum creatinine concentration

4. Adult level of GFR usually not reached until about 18 -24 months of age

5. Ate age 3 months it is roughly 50% of adult GFR and by age 1 year about 80%

6. Know age related normal serum cre concentrations

7. The Schwartz formula is used to derive GFR in kids

8. eGFR = kL/SCr (L=length)

9. k is a constant based on age

10. 0.45 for up to one year of age

11. 0.55 age 1 to 13 years in males and to age 17 in females

12. 0.7 for males age 13-17

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

15. Recognize the limitations of 24 hour urine collections in pediatric patients

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

18. Proteinuria

19. Plan the appropriate evaluation of a child with proteinuria

20. See above

21. Recognize that fever and exercise are causes of transient proteinuria

22. Transient proteinuria can be caused by fever and vigorous exercise; other inciting factors include stress, dehydration and cold exposure

23. Transient proteinuria is a benign phenomenon so the approach is reassurance and re-eval with repeat UA after the inciting event has resolved

24. Recognize that a dipstick examinations of an alkaline urine might yield a false positive result for proteinuria

25. Benign conditions that can cause proteinuria:

26. Concentrated urine (SG >1.020)

27. Alkaline urine (pH >7.5)

28. Presence of mucoproteins

29. Acute illness

30. * rarely will these ever have more than 1+ protein

31. also consider orthostatic proteinuria, which is ruled out bt a clean first AM void and a spot urine protein to cre ratio of <0.2

32. Hematuria

33. Know the ddx for a child with gross hematuria

34. Broken down into categories of

35. Gross hematuria

36. Symptomatic microscopic hematuria

37. Asymptomatic microscopic hematuria with proteinuria

38. Isolated asymptomatic microscopic hematuria

39. Plan the appropriate eval and management of a child with microscopic hematuria

40. Further eval not recommended unless has hematuria present on at least 2 of 3 urine samples; repeat a UA every 2 weeks is okay

41. Plan the eval of a child with persistent microscopic hematuria

42. Eumorphic RBCs

43. Check a urine Ca/Cr

44. Hypercalciuria is frequently associated with asymptomatic hematuria

45. Rule out meatal stenosis

46. Do family screening

47. Assesses for benign familial hematuria (this basement membrane disorder)

48. Dysmorphic RBCs

49. Evaluate for proteinuria

50. Check serum lytes, CBC

51. Check C3, C4 and ANA, ANCA

52. Check strep antibodies

53. Evaluate for HSP and other vasculitides

54. Recognize the ddx and px of patients with persistent microscopic hematuria with and without persistent proteinuria

55. WITH persistent proteinuria: see above for evaluation; more indicative of a glomerular process

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

58. Recognize the importance of the family hx in a child with persistent microscopic hematuria

59. Want to eval for benign familial hematuria (this basement membrane disease)

60. Know that structural abnormalities should be ruled out in patients with gross hematuria

61. Cola or tea colored urine usually have painless hematuria without clots

62. Disease usually a nonglomerular renal cause, lower urinary tract, rarely a hematologic problem

63. Cola colored urine needs monitoring of BP and renal function and an eval for possible underlying glomerulonephritis

64. Best single diagnostic test in eval of acute glomerulonephritis is C3

65. Additional testing = C4, ANA, dsDNA, albumin

66. Bright red urine with clots

67. Need to eval for structural causes of the hematuria

68. Nonglomerular renal causes: ruptured cyst in the kidney, renal mass, stone, renal vein thrombosis, papillary necrosis, hypercalciuria

69. Lower urinary tract: hemorrhagic cystitis, bladder calculi, tumor on the lower urinary tract (rare)

70. Evaluation to look for cysts, stones or tumors = ultrasound (not a CT)

71. Know that myoglobin can yield false positive results for hematuria on UA

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)

75. Dysuria

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

78. Leukocyte esterase reflects pyuria. Other causes of pyuria can be vaginitis, cervicitis, urethritis

79. Nitite AND leuko esterase = bacteruria, but an also have concurrent STI

80. Some UTIs (esp s. saprophyticus) won’t give a nitrite pos result

81. Understand the importance of taking an hx regarding sexual activity when considering the ddx of abd pain and dysuria

82. Always have to take an hx and ascertain whether they have sexually active/abused

83. Recognize the importance of perineal inspection in girls with dysuria

84. Incontinence

85. Recognize that children with secondary nocturnal enuresis rarely have serious underlying disease

86. Primary enuresis = kid was never dry at night

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

89. Know that ectopic ureteral opening can cause incontinent in females

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

94. Recognize unstable (overactive) bladder in children with urinary frequency and negative urine cultures

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)

97. May be associated with UTIs and urinary retention

98. Treatment is timed voiding, possibly anticholinergic agents

99. Congenital

100. Renal dysplasia

101. Recognize that multicystic dysplastic kidney frequently presents with unilateral flank mass in neonates/infants

102. Eventually most dysplastic kidneys or MDKs involute and atrophy

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

104. Recognize the association of the VATER syndrome with renal dysplasia

105. VATER – vertebral anomalies, anal atresia, tracheo-esophagela fistula,renal/radial defects; or VACTERL – vertebral anomalies, anal atresia, cardiac defects, tracheoesophageal fistula, renal anomalies, limb (radial) anomalies

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

110. Abnormalities of the collecting system, kidney, and bladder

111. Know the differntial dx of urinary tract obstruction

112. Ureteropelvic junction obstruction is most common cause, and includes:

113. Aberrant structres or positions of the ureter, kidney or renal blood vessels

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

116. Obstruction outside the UPJ: infundibular stenosis, congenital obstructive megaureter, ectopic ureter, ureterocele, posterior urethral valves

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

121. Lab eval should include serum lutes, BUN and creatinine

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

124. Know that hydronephrosis is one of the causes of abd masses in infants

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)

130. Associated with duplex collecting system over 80% of the time

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

135. Abnormalities of the urethra

136. Recognize that a palpably distended bladder and a weak urinary stream in a newborn or infant boy are suggestive of posterior urethral valves

137. Recognize that renal failure may develop in boys with posterior urethral valves despite repair of the valves

138. Evidence about age at diagnosis and likelihood of developing later renal failure is conflicting

139. Urinary incontinence is also a common problem (about 20%)

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

146. “narrow urethra” is now recognized as a normal variant

147. Hereditary nephropathy (eg, familial nephritis)

148. Know that deafness is bilateral and sensorineural in Alport syndrome

149. Acquired

150. Infection of the urinary tract

151. Know that symptomatic pyelonephritis may occur in patients with <100,000 organisms/mL of urine

152. Any growth of gram negative bacteria in urine obtained by suprapubic aspiration indicates UTI

153. For urine obtained from children via transurethral cath more than 50,000 colonies has been proposed as diagnostic for UTI

154. Know the predominant organisms causing UTI in children

155. E. coli is the most common pathogen (90% of initial UTIs and 2/3 of recurrent UTIs)

156. Community acquired UTI can also come from enterbacter, proteus, klebsiella, strep agalactiae (esp in neonates), s. saprophyticus

157. Recognize that children with reflux nephropathy are often asymptomatic

158. Evaluate a child who is not toilet trained following an initial upper urinary tract infection

159. ALL first UTIs need to have a renal/bladder ultrasound to rule out structural abnormalities

160. i.e. hydronephrosis, renal cysts, nephrolithiasis, urolithiasis, ureteral dilatation, duplex collecting system, bladder wall thickening, ureteroceles

161. First FEBRILE UTIs in a :

162. Male or females with suspicion for dysfunctional voiding fluoroscopic VCUG

163. Other females, or those in whom prior fluoro VCUG was normal voiding cystourethrogram (radionucleotide cystography)

164. Know the indication for long-term antibiotic prophylaxis against UTI

165. VUR grades II through V or recurrent UTI abx prophylaxis

166. Long term prophylactic medical management is as effective as surgical therapy for those who have primary VUR

167. Daily nitrofurantoin, TMP, TMP-SMX

168. With VUR, recurrent UTI and progressive renal damage despite abx then surgery is indicated for correction of the VUR

169. Know the appropriate initial antimicrobial drugs for acute pyelonephritis before urine culture results are available

170. TMP-SMX is standard for initial therapy UNLESS e. coli resistance rates in the area exceed 20-30%

171. First, second and third generation cephalosporins, a pcn-beta lacatamase combo, or FQ if older than 12 months (?)

172. Recognize the association between vesicoureteral reflux and htn

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

174. Recognize the association of UTI and unexplained fever in infants

175. Approximately 5-7% of febrile infants under 8 weeks of age have UTI

176. Know the importance of antibiotic sensitivity testing in the treatment of acute pyelo

177. Urine cultures are an absolute must, and appropriate abx must be used

178. Know the epidemiology of UTI: age of onset, gender

179. In newborns, preterm babies are more like ly than term babies to get UTIs

180. More common in preschool age children than school age children

181. During adolescene sexually active girls and homosexual boys are more likely to get UTI

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

185. Always have to run a culture if suspected

186. Recognize the association between UTI and constipation

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

190. Know the appropriate abx tx for and follow-up management of acute cystitis

191. 90% of cases are due to e.coli and should be empirically treated with TMP-SMX

192. amoxicillin should not be sued due to high resistane rates

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

195. Acute glomerulonephritis

196. Differentiate acute post-streptococcal glomerulonephritis from other forms of glomerulonephritis

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

207. Recognize the immediate complications of acute post strep nephritis

208. Immediate complications are:

209. Hypertension (70%), azotemia (33%)

210. Need to give supportive care for the sodium and fluid retention (diuretics)

211. Know the time sequence of resolution of hypocomplementemia, hematuria, and proteinuria in post strep glomerulonephritis

212. Hypocomplementemia: 6-8 weeks

213. Hematuria: gross resolves in a few weeks, microscopic may not resolve for months to years

214. Proteinuria: a few months

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

219. Nephrotic syndrome

220. Know the presenting si/sx of minimal change nephrotic syndrome

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

222. Recognize the lab findings in children with MCNS

223. Proteinuria with oval fat bodies (maltese crosses), commonly have waxy or hyaline casts; elevated cre, hyponatremia, C3 normal or high

224. May have microscopic hematuria, but not gross hematuria (think of a different dx of this is present)

225. Hypercholesterolemia and hypoalbuminemia

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

228. Initial treatment is often EMPIRIC and is done without a renal bx

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)

231. Also need salt restriction to manage the edema

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

233. Understand the appropriate initial management of a nephrotic patient

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

236. With hematuria: basically rules out a process like MCNS, FSGS and membranous nephropathy

237. Without hematuria: and lots of proteinuria more likely to be one of the above

238. Understand the MCNS is a relapsing disease

239. Understand the complications of diuretic tx in a child with nephrotic syndrome

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

242. Understand the etiology of hyponatremia in a child with nephrotic syndrome

243. ?

244. Recognize the complications of nephrotic syndrome

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

247. Antiphospholipid syndrome is also implicated with NS and increased risk of thromboembolic dz

248. Infections due to urine loss of immunoglobulins and other immune mediating proteins as well as impaired T cell function

249. Strep pneumo is particularly risky, need to make sure and give all of these patients pneumovaccine

250. Think about spontaneous bacterial peritonitis when there is ascites abd pain, etc.

251. Anasarca and pulmonary edema

252. Growth problems

253. Recognize peritonitis as a major complication of MCNS

254. Know the factors that predict the prognosis of nephrotic syndrome

255. Response to steroid therapy

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

258. C3 is NORMAL in minimal change

259. C3 is low at the onset of PIAGN, MPGN and usually in lupus nephritis

260. In PIAGN it normalizes by about 3 months, but does not normalize in lupus nephritis and MPGN; so a persistently low C3 indicates LN or MPGN

261. C4 is usually normal in PIAGN but low in MPGN and LN

262. HUS

263. Know the diagnostic and lab findings in children with HUS

264. Microangiopathic hemolytic anemia, thrpmbocytopenia, renal insufficiency

265. MaHA = anemia, schistocytes and helmet cells; increased indirect bilirubin, decreased haptoglobin, increased LDH

266. TCP, note that PT and PTT are normal

267. Renal failure: increased BUN and Cre

268. Know the appropriate initial management of child with HUS

269. Supportive care

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

271. Might need dialysis

272. PRBC transfusion

273. NO ANTIBIOTICS OR ANTIMOTILITY AGENTS

274. Know the appropriate management of a child with HUS (see above)

275. Recognize the si/sx and diarrheal prodrome of a child with HUS

276. HUS usually develops 2-14 days after the onset of diarrhea, with avg of 6 days

277. Know the association between e. coli O157:H7 and HUS

278. Strongly associated

279. Clinical note – to test for this strain you need to use MacConkey agar because it won’t ferment on sorbitol

280. HSP

281. Recognize the renal manifestations of HSP

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

284. Understand that HSP nephritis rarely progresses to chronic renal failure

285. Overall progression to end stage renal failure is only seen in about 1-5% of kids with HSP

286. But in those with both nephritic and nephrotic syndromes about 50% go on to develop chronic renal dz

287. After HSP 4 months of follow up with UA and blood pressure evals is recommended

288. IgA nephropathy

289. Recognize the si/sx of IgA nephropathy (aka Berger’s disease)

290. Classic presentation: brief h/o painless gross hematuria following and URI

291. UA has lots of blood but NO PROTEIN

292. Renal function normal

293. Proteinuria can eventually develop, and agents to reduce this are ARB and ACEi

294. Other Renal conditions

295. Renal failure

296. Recognize the causes of acute renal failure in infants and children

297. Prerenal: Generally caused by extracellular volume deficits like

298. GI losses / decreased intake

299. Increased urinary loss of fluids (diuresis, DI, adrenal insufficiency, loss of concentrating ability)

300. Blood loss

301. Redistribution of ECF (hypoalbuminemia, nephrotic syndrome, liver disease)

302. Vasodilation (sepsis and anaphylaxis)

303. Skin losses (including third spacing)

304. Cardiac dysfunction such as congenital heart disease, cardiomyopathy, arrhytmia, acquired valvular disease, tamponade)

305. Intrarenal: due to parenchymal injury in the kidney

306. Usually ATN, interstitial nephritis, HUS, glomerulonephritis, nephotoxins

307. Postrenal: obstructive issues in the lower GU tract

308. Congenital like bladder outlet obstruction (PUV) or ureteropelvic obstruction

309. Acquired causes (clots, tumors, stones)

310. Plan the initial treatment for a child with renal failure

311. Goal is to maintain renal perfusion, fluid/electrolye balance, control BP

312. Recognize the utility of the urine sodium concentration and FeNa in children with oliguria

313. FeNa can help elucidate the cause of the renal failure

314. <1% indicates a prerenal cause

315. >3% indicates intrarenal or postrenal

316. Understand the principles of initial treatment of a child with acute renal failure: fluid admin, correction of hyperkalemia and acidosis

317. Know the transient effect of bicarbonate, glucose, insulin, and calcium on hyperkalemia associated with renal failure

318. Drive K intracellularly and therefore decrease circulating K

319. Recognize the complications of acute renal failure

320. Know that drug dosages must be modified in acute renal failure

321. Recognize that the risk of tetany is increased during bicarb tx when serum calcium concentration is decreased

322. Chronic kidney dz (chronic renal failure)

323. Understand the major complications of chronic kidney disease

324. Recognize that volume and salt depletion may develop in an infant with renal dysplasia and hydronephrosis

325. Know that growth failure is common in children with CKD and that growth hormone therapy may be useful in those with growth failure

326. Know that acidosis contributes to growth failure in CKD

327. Understand the alterations in calcium, vitamin D and phosphorous metabolism seen in CKD

328. Understand the value and risks of epo tx in anemia associated with CKD

329. End stage kidney disease and transplantation

330. Recognize that immunizations should be given to pts prior to transplantation

331. Recognize that pts with ESRD need to attend school or be home schooled

332. Trauma

333. Evaluate a child with blunt abd trauma with and without hematuria

334. Understand that gross urethral bleeding is a contraindication to cath following acute trauma

335. Toxins

336. Know the drug classes that can cause renal toxicity (e.g. antibiotics, NSAIDs, chemotx agents, cyclosporine, tacrolimus)

337. Know that chemotx agents can cause renal toxicity

338. Know that cyclosporine and tacrolimus cause renal toxicity

339. Urinary tract stones

340. Recognize the sx of urinary tract stones in children

341. Plan the evaluation of a child with urinary tract stones

342. Know the value of increasing fluid intake in a child with urinary tract stones

343. Recognize the association between hypercalciuria and the formation of urinary tract stones

344. Renal tubular acidosis

345. Know that growth failure is a common presentation of RTA

346. Formulate a ddx for RTA including the association with tubular defects

347. Hereditary conditions with renal manifestations (e.g. nephrogenic DI)

348. Recognize the si/sx of DI in children

349. Know how to interpret urine and serum osmols in a child with DI

350. Recognize the association between cranial injury/surgery and DI, and that it is an inherited d/o

351. Hypertension

352. General

353. Know the tx of hypertension

354. Know the nonpharmacologic management of htn in children

355. Identify stupor, seizures, and vomiting as sx of htnsive encephalopathy

356. Know the initial eval of htn

357. Formulate a ddx of htn in children and adolescents

358. Recognize the different mechanisms of action of doffernt classes of antihtnsive drugs

359. Recognize the causes of false blood rpessure measurements in relation to age and size

360. Renal

361. Know the causes of renal htn

362. Vascular

363. Recognize that htn is asscoated with NF

364. Adrenal

365. Recognize the si/sx of htn in children with pheo

366. Know that htn in a short, obese child may be due to Cushing

367. Misc causes

368. Understand the ddx of essential htn

369. Recognize the most common causes of htn in adolescents

370. Understand the tx of essental htn

371. Know that certain drugs can cause htn in children

372. Understand the development of acute htn in a child placed in traction