Renal disorders copy


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Renal disorders copy

  1. 1. RENAL DISORDERS<br /><ul><li>General
  2. 2. Normal function
  3. 3. Know age related changes in GFR and the impact of the serum creatinine concentration
  4. 4. Adult level of GFR usually not reached until about 18 -24 months of age
  5. 5. Ate age 3 months it is roughly 50% of adult GFR and by age 1 year about 80%
  6. 6. Know age related normal serum cre concentrations
  7. 7. The Schwartz formula is used to derive GFR in kids
  8. 8. eGFR = kL/SCr (L=length)
  9. 9. k is a constant based on age
  10. 10. 0.45 for up to one year of age
  11. 11. 0.55 age 1 to 13 years in males and to age 17 in females
  12. 12. 0.7 for males age 13-17
  13. 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. 14. preterm infants have been demonstrated to have slightly high cre than term babies
  15. 15. Recognize the limitations of 24 hour urine collections in pediatric patients
  16. 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. 17. proteinuria on a dilute sample (SG <1.015) needs more workup and the spot urine as above is the starting point
  18. 18. Proteinuria
  19. 19. Plan the appropriate evaluation of a child with proteinuria
  20. 20. See above
  21. 21. Recognize that fever and exercise are causes of transient proteinuria
  22. 22. Transient proteinuria can be caused by fever and vigorous exercise; other inciting factors include stress, dehydration and cold exposure
  23. 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. 24. Recognize that a dipstick examinations of an alkaline urine might yield a false positive result for proteinuria
  25. 25. Benign conditions that can cause proteinuria:
  26. 26. Concentrated urine (SG >1.020)
  27. 27. Alkaline urine (pH >7.5)
  28. 28. Presence of mucoproteins
  29. 29. Acute illness
  30. 30. * rarely will these ever have more than 1+ protein
  31. 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. 32. Hematuria
  33. 33. Know the ddx for a child with gross hematuria
  34. 34. Broken down into categories of
  35. 35. Gross hematuria
  36. 36. Symptomatic microscopic hematuria
  37. 37. Asymptomatic microscopic hematuria with proteinuria
  38. 38. Isolated asymptomatic microscopic hematuria
  39. 39. Plan the appropriate eval and management of a child with microscopic hematuria
  40. 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. 41. Plan the eval of a child with persistent microscopic hematuria
  42. 42. Eumorphic RBCs
  43. 43. Check a urine Ca/Cr
  44. 44. Hypercalciuria is frequently associated with asymptomatic hematuria
  45. 45. Rule out meatal stenosis
  46. 46. Do family screening
  47. 47. Assesses for benign familial hematuria (this basement membrane disorder)
  48. 48. Dysmorphic RBCs
  49. 49. Evaluate for proteinuria
  50. 50. Check serum lytes, CBC
  51. 51. Check C3, C4 and ANA, ANCA
  52. 52. Check strep antibodies
  53. 53. Evaluate for HSP and other vasculitides
  54. 54. Recognize the ddx and px of patients with persistent microscopic hematuria with and without persistent proteinuria
  55. 55. WITH persistent proteinuria: see above for evaluation; more indicative of a glomerular process
  56. 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. 57. In most cases in which patient has both hematuria and proteinuria, serial UAs will show resolution of one or both of them
  58. 58. Recognize the importance of the family hx in a child with persistent microscopic hematuria
  59. 59. Want to eval for benign familial hematuria (this basement membrane disease)
  60. 60. Know that structural abnormalities should be ruled out in patients with gross hematuria
  61. 61. Cola or tea colored urine usually have painless hematuria without clots
  62. 62. Disease usually a nonglomerular renal cause, lower urinary tract, rarely a hematologic problem
  63. 63. Cola colored urine needs monitoring of BP and renal function and an eval for possible underlying glomerulonephritis
  64. 64. Best single diagnostic test in eval of acute glomerulonephritis is C3
  65. 65. Additional testing = C4, ANA, dsDNA, albumin
  66. 66. Bright red urine with clots
  67. 67. Need to eval for structural causes of the hematuria
  68. 68. Nonglomerular renal causes: ruptured cyst in the kidney, renal mass, stone, renal vein thrombosis, papillary necrosis, hypercalciuria
  69. 69. Lower urinary tract: hemorrhagic cystitis, bladder calculi, tumor on the lower urinary tract (rare)
  70. 70. Evaluation to look for cysts, stones or tumors = ultrasound (not a CT)
  71. 71. Know that myoglobin can yield false positive results for hematuria on UA
  72. 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. 73. Determine by hx and lab evaluation the etiology of red urine
  74. 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. 75. Dysuria
  76. 76. Recognize the etiologies of dysuria may be age-related and that numerous other etiologies include vaginitis, chemical irritation, and trauma
  77. 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. 78. Leukocyte esterase reflects pyuria. Other causes of pyuria can be vaginitis, cervicitis, urethritis
  79. 79. Nitite AND leuko esterase = bacteruria, but an also have concurrent STI
  80. 80. Some UTIs (esp s. saprophyticus) won’t give a nitrite pos result
  81. 81. Understand the importance of taking an hx regarding sexual activity when considering the ddx of abd pain and dysuria
  82. 82. Always have to take an hx and ascertain whether they have sexually active/abused
  83. 83. Recognize the importance of perineal inspection in girls with dysuria
  84. 84. Incontinence
  85. 85. Recognize that children with secondary nocturnal enuresis rarely have serious underlying disease
  86. 86. Primary enuresis = kid was never dry at night
  87. 87. Secondary enuresis = kid had previously sustained dryness and then subsequently resumed bedwetting
  88. 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. 89. Know that ectopic ureteral opening can cause incontinent in females
  90. 90. A history of constant wetness in an otherwise healthy female who is toilet trained is indicatove of ectopic ureter
  91. 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. 92. Know the importance of skin abnormalities in the sacral area when evaluating a patient with primary enuresis
  93. 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. 94. Recognize unstable (overactive) bladder in children with urinary frequency and negative urine cultures
  95. 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. 96. They often compensate for their uninhibited bladder contractions by doing things to activate the external sphincter (squatting, leg crossing, Vincent curtsy)
  97. 97. May be associated with UTIs and urinary retention
  98. 98. Treatment is timed voiding, possibly anticholinergic agents
  99. 99. Congenital
  100. 100. Renal dysplasia
  101. 101. Recognize that multicystic dysplastic kidney frequently presents with unilateral flank mass in neonates/infants
  102. 102. Eventually most dysplastic kidneys or MDKs involute and atrophy
  103. 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. 104. Recognize the association of the VATER syndrome with renal dysplasia
  105. 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. 106. The kidney anomalies can be agenesis, dysplasia, hypoplasia and therefore the kidneys must be evaluated
  107. 107. Know that abd ultrasonogrpahy is the preferred diagnostic procedure in children suspected of having autosomal dominant polycystic kidney disease
  108. 108. Recognize the association of bilateral renal aplasia or severe dysplasia with pulmonary hypoplasia (Potter syndrome)
  109. 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. 110. Abnormalities of the collecting system, kidney, and bladder
  111. 111. Know the differntial dx of urinary tract obstruction
  112. 112. Ureteropelvic junction obstruction is most common cause, and includes:
  113. 113. Aberrant structres or positions of the ureter, kidney or renal blood vessels
  114. 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. 115. Duplex collecting system is the most common urinary tract anomaly, with varying grades of obstruction due to them
  116. 116. Obstruction outside the UPJ: infundibular stenosis, congenital obstructive megaureter, ectopic ureter, ureterocele, posterior urethral valves
  117. 117. PUV is the leading cause of severe urinary obstruction in children (males)
  118. 118. Plan the evaluation of an infant with anuria more than 48 hours after birth
  119. 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. 120. Examine the genitalia, flanks, abdomen and look at baby for any signs of edema or oligohydramnios sequence
  121. 121. Lab eval should include serum lutes, BUN and creatinine
  122. 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. 123. If no urine can be obtained then need to do a US of kidneys, ureters, bladder
  124. 124. Know that hydronephrosis is one of the causes of abd masses in infants
  125. 125. Know the urologic findings associated with prune belly (Eagle-Barret) syndrome
  126. 126. Hydronephosis, which is usually due to an obstructive cause (PUV, vesicoureteral relfux, UPJ obstruction)
  127. 127. Renal outcome for thee kids is usually poor, most develop renal insufficiency
  128. 128. Know that a ureterocele may lead to urinary tract obstruction
  129. 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. 130. Associated with duplex collecting system over 80% of the time
  131. 131. Know that natural hx (e.g. etiology, familial association, outcome) of vesicoureteral reflux
  132. 132. Is the most common urologic abnormality in children
  133. 133. Rates are elevated among siblings and offspring with higher rates in Caucasians, females and kids under age 2
  134. 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. 135. Abnormalities of the urethra
  136. 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. 137. Recognize that renal failure may develop in boys with posterior urethral valves despite repair of the valves
  138. 138. Evidence about age at diagnosis and likelihood of developing later renal failure is conflicting
  139. 139. Urinary incontinence is also a common problem (about 20%)
  140. 140. Recognize the necessity for long term evaluation of renal and bladder function in patients with PUV
  141. 141. Know that urethral strictures in boys almost always result from urethral trauma (iatrogenic or accidental)
  142. 142. Previous trauma or instrumentation. Other causes can include infection (gonorrhea), congenital abnormality, idiopathic cause, complication of balanitis
  143. 143. Tx depends on the length, location and persistence of the stricture
  144. 144. Severe stricture in males may damage the bladder and even cause hydronephrosis
  145. 145. Know that a girl with a narrow urethra needs no tx
  146. 146. “narrow urethra” is now recognized as a normal variant
  147. 147. Hereditary nephropathy (eg, familial nephritis)
  148. 148. Know that deafness is bilateral and sensorineural in Alport syndrome
  149. 149. Acquired
  150. 150. Infection of the urinary tract
  151. 151. Know that symptomatic pyelonephritis may occur in patients with <100,000 organisms/mL of urine
  152. 152. Any growth of gram negative bacteria in urine obtained by suprapubic aspiration indicates UTI
  153. 153. For urine obtained from children via transurethral cath more than 50,000 colonies has been proposed as diagnostic for UTI
  154. 154. Know the predominant organisms causing UTI in children
  155. 155. E. coli is the most common pathogen (90% of initial UTIs and 2/3 of recurrent UTIs)
  156. 156. Community acquired UTI can also come from enterbacter, proteus, klebsiella, strep agalactiae (esp in neonates), s. saprophyticus
  157. 157. Recognize that children with reflux nephropathy are often asymptomatic
  158. 158. Evaluate a child who is not toilet trained following an initial upper urinary tract infection
  159. 159. ALL first UTIs need to have a renal/bladder ultrasound to rule out structural abnormalities
  160. 160. i.e. hydronephrosis, renal cysts, nephrolithiasis, urolithiasis, ureteral dilatation, duplex collecting system, bladder wall thickening, ureteroceles
  161. 161. First FEBRILE UTIs in a :
  162. 162. Male or females with suspicion for dysfunctional voiding fluoroscopic VCUG
  163. 163. Other females, or those in whom prior fluoro VCUG was normal voiding cystourethrogram (radionucleotide cystography)
  164. 164. Know the indication for long-term antibiotic prophylaxis against UTI
  165. 165. VUR grades II through V or recurrent UTI abx prophylaxis
  166. 166. Long term prophylactic medical management is as effective as surgical therapy for those who have primary VUR
  167. 167. Daily nitrofurantoin, TMP, TMP-SMX
  168. 168. With VUR, recurrent UTI and progressive renal damage despite abx then surgery is indicated for correction of the VUR
  169. 169. Know the appropriate initial antimicrobial drugs for acute pyelonephritis before urine culture results are available
  170. 170. TMP-SMX is standard for initial therapy UNLESS e. coli resistance rates in the area exceed 20-30%
  171. 171. First, second and third generation cephalosporins, a pcn-beta lacatamase combo, or FQ if older than 12 months (?)
  172. 172. Recognize the association between vesicoureteral reflux and htn
  173. 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. 174. Recognize the association of UTI and unexplained fever in infants
  175. 175. Approximately 5-7% of febrile infants under 8 weeks of age have UTI
  176. 176. Know the importance of antibiotic sensitivity testing in the treatment of acute pyelo
  177. 177. Urine cultures are an absolute must, and appropriate abx must be used
  178. 178. Know the epidemiology of UTI: age of onset, gender
  179. 179. In newborns, preterm babies are more like ly than term babies to get UTIs
  180. 180. More common in preschool age children than school age children
  181. 181. During adolescene sexually active girls and homosexual boys are more likely to get UTI
  182. 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. 183. Know that UA alone is often insufficient to dx UTI
  184. 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. 185. Always have to run a culture if suspected
  186. 186. Recognize the association between UTI and constipation
  187. 187. Can cause detrusor instability, which can lead to incontinence, large bladder capacity, and dyscoordinated voiding
  188. 188. Urinary retention is common due to dyscoordinated voiding or outflow tract obstruction caused by large rectal fecal masses
  189. 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. 190. Know the appropriate abx tx for and follow-up management of acute cystitis
  191. 191. 90% of cases are due to e.coli and should be empirically treated with TMP-SMX
  192. 192. amoxicillin should not be sued due to high resistane rates
  193. 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. 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. 195. Acute glomerulonephritis
  196. 196. Differentiate acute post-streptococcal glomerulonephritis from other forms of glomerulonephritis
  197. 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. 198. Interval beyween pharyngitis and PIAGN is about 1-2 weeks where latency between skin infection and PIAGN is 3-6 weeks
  199. 199. A positive GAS throat swab, elevated ASO, hypocomplementemia (low C3) and urinary RBC casts
  200. 200. Know the lab evaluation of acute post-streptococcal glomerulonephritis
  201. 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. 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. 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. 204. Understand that acute post strep nephritis rarely progresses to chronic renal failure
  205. 205. Can have acute renal failure (azotemia in 1/3 of cases)
  206. 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. 207. Recognize the immediate complications of acute post strep nephritis
  208. 208. Immediate complications are:
  209. 209. Hypertension (70%), azotemia (33%)
  210. 210. Need to give supportive care for the sodium and fluid retention (diuretics)
  211. 211. Know the time sequence of resolution of hypocomplementemia, hematuria, and proteinuria in post strep glomerulonephritis
  212. 212. Hypocomplementemia: 6-8 weeks
  213. 213. Hematuria: gross resolves in a few weeks, microscopic may not resolve for months to years
  214. 214. Proteinuria: a few months
  215. 215. Plan the initial management of acute post strep glomerulonephritis
  216. 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. 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. 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. 219. Nephrotic syndrome
  220. 220. Know the presenting si/sx of minimal change nephrotic syndrome
  221. 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. 222. Recognize the lab findings in children with MCNS
  223. 223. Proteinuria with oval fat bodies (maltese crosses), commonly have waxy or hyaline casts; elevated cre, hyponatremia, C3 normal or high
  224. 224. May have microscopic hematuria, but not gross hematuria (think of a different dx of this is present)
  225. 225. Hypercholesterolemia and hypoalbuminemia
  226. 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. 227. Plan the initial treatment for a child with an initial episode of nephrotic syndrome
  228. 228. Initial treatment is often EMPIRIC and is done without a renal bx
  229. 229. Corticosteroids are the mainstay of treatment, if this fails they might need cyclophosphamide, cyclosporine or chloramphenicol (“off label”)
  230. 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. 231. Also need salt restriction to manage the edema
  232. 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. 233. Understand the appropriate initial management of a nephrotic patient
  234. 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. 235. Know the ddx of nephrotic syndrome with and without hematuria
  236. 236. With hematuria: basically rules out a process like MCNS, FSGS and membranous nephropathy
  237. 237. Without hematuria: and lots of proteinuria more likely to be one of the above
  238. 238. Understand the MCNS is a relapsing disease
  239. 239. Understand the complications of diuretic tx in a child with nephrotic syndrome
  240. 240. Create an increased risk of thrombosis; also aggressive diuretic use can induce hypovolemia with secondary renal failure, thromboembolism or electrolyte disturbances.
  241. 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. 242. Understand the etiology of hyponatremia in a child with nephrotic syndrome
  243. 243. ?
  244. 244. Recognize the complications of nephrotic syndrome
  245. 245. Acute renal failure: can usually be corrected with intravascular volume correction
  246. 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. 247. Antiphospholipid syndrome is also implicated with NS and increased risk of thromboembolic dz
  248. 248. Infections due to urine loss of immunoglobulins and other immune mediating proteins as well as impaired T cell function
  249. 249. Strep pneumo is particularly risky, need to make sure and give all of these patients pneumovaccine
  250. 250. Think about spontaneous bacterial peritonitis when there is ascites abd pain, etc.
  251. 251. Anasarca and pulmonary edema
  252. 252. Growth problems
  253. 253. Recognize peritonitis as a major complication of MCNS
  254. 254. Know the factors that predict the prognosis of nephrotic syndrome
  255. 255. Response to steroid therapy
  256. 256. Recognize that response to therapy is one of the best indicators of prognosis in nephrotic syndrome
  257. 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. 258. C3 is NORMAL in minimal change
  259. 259. C3 is low at the onset of PIAGN, MPGN and usually in lupus nephritis
  260. 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. 261. C4 is usually normal in PIAGN but low in MPGN and LN
  262. 262. HUS
  263. 263. Know the diagnostic and lab findings in children with HUS
  264. 264. Microangiopathic hemolytic anemia, thrpmbocytopenia, renal insufficiency
  265. 265. MaHA = anemia, schistocytes and helmet cells; increased indirect bilirubin, decreased haptoglobin, increased LDH
  266. 266. TCP, note that PT and PTT are normal
  267. 267. Renal failure: increased BUN and Cre
  268. 268. Know the appropriate initial management of child with HUS
  269. 269. Supportive care
  270. 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. 271. Might need dialysis
  272. 272. PRBC transfusion
  274. 274. Know the appropriate management of a child with HUS (see above)
  275. 275. Recognize the si/sx and diarrheal prodrome of a child with HUS
  276. 276. HUS usually develops 2-14 days after the onset of diarrhea, with avg of 6 days
  277. 277. Know the association between e. coli O157:H7 and HUS
  278. 278. Strongly associated
  279. 279. Clinical note – to test for this strain you need to use MacConkey agar because it won’t ferment on sorbitol
  280. 280. HSP
  281. 281. Recognize the renal manifestations of HSP
  282. 282. Renal manifestations in 40-50% of cases of HSP and usually occur within 4 months after the rash (usually in one month)
  283. 283. Involvement ranges from microscopic hematuria, mild proteinuria but may have sx as severe as nephritic or nephrotic syndromes and chronic renal disease
  284. 284. Understand that HSP nephritis rarely progresses to chronic renal failure
  285. 285. Overall progression to end stage renal failure is only seen in about 1-5% of kids with HSP
  286. 286. But in those with both nephritic and nephrotic syndromes about 50% go on to develop chronic renal dz
  287. 287. After HSP 4 months of follow up with UA and blood pressure evals is recommended
  288. 288. IgA nephropathy
  289. 289. Recognize the si/sx of IgA nephropathy (aka Berger’s disease)
  290. 290. Classic presentation: brief h/o painless gross hematuria following and URI
  291. 291. UA has lots of blood but NO PROTEIN
  292. 292. Renal function normal
  293. 293. Proteinuria can eventually develop, and agents to reduce this are ARB and ACEi
  294. 294. Other Renal conditions
  295. 295. Renal failure
  296. 296. Recognize the causes of acute renal failure in infants and children
  297. 297. Prerenal: Generally caused by extracellular volume deficits like
  298. 298. GI losses / decreased intake
  299. 299. Increased urinary loss of fluids (diuresis, DI, adrenal insufficiency, loss of concentrating ability)
  300. 300. Blood loss
  301. 301. Redistribution of ECF (hypoalbuminemia, nephrotic syndrome, liver disease)
  302. 302. Vasodilation (sepsis and anaphylaxis)
  303. 303. Skin losses (including third spacing)
  304. 304. Cardiac dysfunction such as congenital heart disease, cardiomyopathy, arrhytmia, acquired valvular disease, tamponade)
  305. 305. Intrarenal: due to parenchymal injury in the kidney
  306. 306. Usually ATN, interstitial nephritis, HUS, glomerulonephritis, nephotoxins
  307. 307. Postrenal: obstructive issues in the lower GU tract
  308. 308. Congenital like bladder outlet obstruction (PUV) or ureteropelvic obstruction
  309. 309. Acquired causes (clots, tumors, stones)
  310. 310. Plan the initial treatment for a child with renal failure
  311. 311. Goal is to maintain renal perfusion, fluid/electrolye balance, control BP
  312. 312. Recognize the utility of the urine sodium concentration and FeNa in children with oliguria
  313. 313. FeNa can help elucidate the cause of the renal failure
  314. 314. <1% indicates a prerenal cause
  315. 315. >3% indicates intrarenal or postrenal
  316. 316. Understand the principles of initial treatment of a child with acute renal failure: fluid admin, correction of hyperkalemia and acidosis
  317. 317. Know the transient effect of bicarbonate, glucose, insulin, and calcium on hyperkalemia associated with renal failure
  318. 318. Drive K intracellularly and therefore decrease circulating K
  319. 319. Recognize the complications of acute renal failure
  320. 320. Know that drug dosages must be modified in acute renal failure
  321. 321. Recognize that the risk of tetany is increased during bicarb tx when serum calcium concentration is decreased
  322. 322. Chronic kidney dz (chronic renal failure)
  323. 323. Understand the major complications of chronic kidney disease
  324. 324. Recognize that volume and salt depletion may develop in an infant with renal dysplasia and hydronephrosis
  325. 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. 326. Know that acidosis contributes to growth failure in CKD
  327. 327. Understand the alterations in calcium, vitamin D and phosphorous metabolism seen in CKD
  328. 328. Understand the value and risks of epo tx in anemia associated with CKD
  329. 329. End stage kidney disease and transplantation
  330. 330. Recognize that immunizations should be given to pts prior to transplantation
  331. 331. Recognize that pts with ESRD need to attend school or be home schooled
  332. 332. Trauma
  333. 333. Evaluate a child with blunt abd trauma with and without hematuria
  334. 334. Understand that gross urethral bleeding is a contraindication to cath following acute trauma
  335. 335. Toxins
  336. 336. Know the drug classes that can cause renal toxicity (e.g. antibiotics, NSAIDs, chemotx agents, cyclosporine, tacrolimus)
  337. 337. Know that chemotx agents can cause renal toxicity
  338. 338. Know that cyclosporine and tacrolimus cause renal toxicity
  339. 339. Urinary tract stones
  340. 340. Recognize the sx of urinary tract stones in children
  341. 341. Plan the evaluation of a child with urinary tract stones
  342. 342. Know the value of increasing fluid intake in a child with urinary tract stones
  343. 343. Recognize the association between hypercalciuria and the formation of urinary tract stones
  344. 344. Renal tubular acidosis
  345. 345. Know that growth failure is a common presentation of RTA
  346. 346. Formulate a ddx for RTA including the association with tubular defects
  347. 347. Hereditary conditions with renal manifestations (e.g. nephrogenic DI)
  348. 348. Recognize the si/sx of DI in children
  349. 349. Know how to interpret urine and serum osmols in a child with DI
  350. 350. Recognize the association between cranial injury/surgery and DI, and that it is an inherited d/o
  351. 351. Hypertension
  352. 352. General
  353. 353. Know the tx of hypertension
  354. 354. Know the nonpharmacologic management of htn in children
  355. 355. Identify stupor, seizures, and vomiting as sx of htnsive encephalopathy
  356. 356. Know the initial eval of htn
  357. 357. Formulate a ddx of htn in children and adolescents
  358. 358. Recognize the different mechanisms of action of doffernt classes of antihtnsive drugs
  359. 359. Recognize the causes of false blood rpessure measurements in relation to age and size
  360. 360. Renal
  361. 361. Know the causes of renal htn
  362. 362. Vascular
  363. 363. Recognize that htn is asscoated with NF
  364. 364. Adrenal
  365. 365. Recognize the si/sx of htn in children with pheo
  366. 366. Know that htn in a short, obese child may be due to Cushing
  367. 367. Misc causes
  368. 368. Understand the ddx of essential htn
  369. 369. Recognize the most common causes of htn in adolescents
  370. 370. Understand the tx of essental htn
  371. 371. Know that certain drugs can cause htn in children
  372. 372. Understand the development of acute htn in a child placed in traction