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Renal disorders copy Document Transcript

  • 1. RENAL DISORDERS<br />
    • General
    • 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