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RACP paeds Qld Group > Renal > Flashcards

Renal Flashcards

1
Q

What is the nephrotic syndrome triad

A

Proteinuria 3+ or PCR>200
Hypoalbuminemia <25
Oedema

Can also have microscopic haematuria, mild transient hypertension, or high triglycerides

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2
Q

Presentation nephrotic syndrome

A

Often initially mistaken for allergies- periorbital oedema
Volume depletion- dizziness, abdo cramps, tachycardia, reduced UO, prolonged cap refill, cold peripheries, hypotension late sign
Oedema- periorbital oedema, up to gross peripheral oedema, pleural effusion and ascites
Anemia- as excreting EPO
Fever- SBP, cellulitis ( high infection risk as urinating immunoglobulins + complement)
Thrombosis - high risk as excreting clotting factors
Hypothyroidsm

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3
Q

Management nephrotic syndrome

A

Admit for 1st presentation
Treat sepsis if needed
Oedema- no added salt diet, daily weight, fluid restriction
Albumin 20% over 4 hours with frusemide half way if significant overload
Prednisolone 60mg/m2 4 weeks with slow wean over next 4 weeks (alternate daily pred)
Consider penicillin prophylaxis (phenoxymethylpenicillin- if severe oedema and unimmunised) + PPI while on steroids for gastric protection
Delay live vaccines while on high dose steroids

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4
Q

Nephrotic syndrome
Defining disease types

A

Response to therapy-
Steroid sensitive
Steroid dependant
Steroid resistant

Pattern- frequently relapsing

Histology- MCD, FSGN

Genetics- gene pos or neg

If gene pos, unlikely to respond to immunosuppressive and progress quickly to ESRF, need transplant;but low recurrence risk post transplant

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5
Q

What percentage of nephrotic syndrome is idiopathic?

A

90%- MCD, FSGS
May be secondary to SLE, HSP etc - usually have atypical features

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6
Q

What percentage of children with nephrotic syndrome are steroid sensitive??

A

80-90% will respond to initial steroid therapy
Of those with steroid sensitive NS, 80% will have one or more relapses

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7
Q

When would you give prophylactic penicillin V in nephrotic syndrome

A

If risk of pneumococcal infection- gross or symptomatic oedema, and unimmunised

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8
Q

What do you tell parents post discharge with nephrotic syndrome?

A

Check urine protein daily for 1-2 years in order to quickly identify relapse (=3 + protein for 3 consecutive days) at which they should contact their Dr and start prednisolone prior to onset of oedema

Daily weights while nephrotic for signs fluid over load

Convey that 80% chance relapse - most commonly triggered by inter current infection

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9
Q

Functions of kidney

A

a. Excretion of waste products
b. Regulation of water and electrolytes
c. Regulation of fluid osmolality
d. Regulation of BP
e. Regulation of acid base
f. Synthesis/ excretion of hormones - EPO , activation of vitamin D , renin

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10
Q

Level of kidneys

A

T12-L3

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11
Q

Renin produced by which cells?

A

Juxtaglomerular cells
Specialised smooth muscle cells located in walls of afferent arteriole

secrete renin in response to a drop in pressure detected by stretch receptors in the vascular walls, or when stimulated by macula densa cells a

renin catalyses conversion of angiotensinogen produced by liver to ang I (then ACE from lungs converts to Ang 2)

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12
Q

Describe production of Ang II

A

Angiotensinogen produced in liver
Converted to Angiotensin I, catalysed by renin (rate limeting step)
ACE (produced by lungs) catalyses conversion of Ang I to Ang II

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13
Q

Actions of Angiotensin II

A

Arterioles: Vasoconstriction –>increase BP
Brain: increased thirst
Adrenal cortex: Increased aldosterone production –> increased sodium reabsorbtion, increased potassium excretion –> increased water retention –> increased blood volume –> increased BP
Posterior pituitary: Increased ADH secretion –> increased water reabsortion in the collecting duct –> increased blood volume
Kidney: Efferent arteriole constriction –> increased GFR (at low dose)

Net effect: salt and water retention and increased effective circulating volume, to increase perfusion of the juxtaglomerular apparatus (negative feedback to reduce renin release)

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14
Q

Stimulus for renin release

A

SNS input (beta adrenergic stimulation) in response to low BP
Hypotension - sensed by baroreceptors in the afferent arterioles
Low renal blood flow- sensed by macula densa (distal tubule) as reduced Na+ concentration
Drugs- ACEI, ARB
Chronic diseases w oedema
Renal artery stenosis (due to hypoperfusion state)

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15
Q

Inhibition of renin release

A

Ang II
ADH
Hypernatremia
Hyperkalemia
NASAIDs

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16
Q

Aldosterone

A

secreted by zona glomerulosa of adrenal cortex (outermost layer)
Acts on principal cells of collecting duct - mineralocorticoid receptor
Upregulates ENAC channels in collecting duct to increase permeability to Na+ (and water follows)
Also acts on a intercalated cells to increase hydrogen excretion (increased expression H-ATPase)
Also stimulates Na/K/ATPase pump on basolateral side of membrane –> increased excretion of potassium

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17
Q

ADH

A

Synthesised in hypothalamus
Release triggered by hyperosmolarity and hypotension (ie dehydration)–> end goal is to reabsorb more water to bring BP and osmolarity back to normal
Binds to V2 receptor at DCT+ CD –> CAMP -> G protein coupled receptor –> insertion of aquaporin 2 at luminal membrane –> water reabsorption
Concentrated urine and lowering of serum sodium

Also binds to V1 receptor on vessels –> peripheral vasoconstriction –> increased BP

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18
Q

ANP

A

Secreted by R atrium
Triggered by HTN (increased blood volume) in response to atrial stretch Actions to decrease blood volume and increase excretion of sodium
i. Dilates afferent + constricts efferent arterioles = ↑ GFR, ↑ natriuresis
ii. Inhibits aldosterone + renin secretion
iii. Inhibits Na Cl reabsorption in CD
iv. Inhibits ADH action on kidney

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19
Q

PTH

A

Trigger: low calcium
Acts on distal tubules + LOH to increase calcium reabsorption
Inhibits phosphate reabsorption proximal tubule

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20
Q

Action prostaglandins

A

Trigger: hypoperfusion of nephron
Action: dilate afferent arteriole –> increase GFR

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21
Q

Action endothelins

A

Vasoconstriction
reduce renal blood flow and reduce GFR

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22
Q

NSAIDs action on kidney

A

Inhibit prostaglandin release
–> reduced GFR

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23
Q

Reduced renal blood flow sensed by:

A
  1. Baroreceptors (carotid/cardiac/afferent arteriole)–> SNS stimulation
  2. Juxtaglomerular cells (in walls of afferent arterioles)–> release renin
  3. Macula densa cells in DCT–> communicates with JG cells and mesangial cells to stimulate renin release
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24
Q

Renal embryology

A

Metanephric mesenchyme (mesodermal layer)
Bowmans capsule
Prox tubule
LOH
Distal tubule

Ureteric bud (from Wolfian duct):
Collecting duct
Renal pelvis
Ureter

first nephron develops at 8-9 weeks of age
Urine production starts at 10 weeks
Complete by 36 weeks BUT GFR continues to increase for years - doesnt approximate adult values until ~ age 3 (so cant make more nephrons after birth can can compensate somewhat)

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25
Q

Alports disease

A

Most commonly X linked
Absent/abn collagen 4, replaced by immature glomerular basement membrane

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26
Q

Vasoconstriction of afferent/efferent arteriole leads to …

A

constriction afferent: reduced GFR (eg due to NSAIDs, noradrenaline, high dose Ang2
constriction efferent: increased GFR (eg ANP, Ang2 (low dose)

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27
Q

Vasodilation of afferent/efferent arteriole leads to..

A

dilation afferent : increased GFR (eg prostaglandins, ANP)
dilation efferent: reduced GFR (eg ACE-I, ARB)

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28
Q

Triple whammy

A

· ACE-I = Dilates the efferent arteriole reducing the GFR
· NSAID = Prevents PG mediated vasodilation of the afferent arteriole to maintain GFR; thereby further reducing GFR
Diuretics = reduce plasma volume and GFR

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29
Q

Proximal convoluted tubule

A

BULK OF REABSORPTION
-65% sodium
- 70% bicarbonate
- 30-50% potassium
-chloride
-100% glucose + amino acids
- 70% H2O

Secretion of:
-H+
-organic ions (urate, citrate, penicillins)

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30
Q

Loop of Henle

A

Creates concentration differences
i. Thin = squamous epithelium with high water permeability (reabsorbs 20% water)
Thick = cuboidal epithelium –> lots of mitochondria for active transport, no water permeability
iii. 25-30% of sodium absorption (NKCC2 co transporter)
iv. Sodium absorption important in making the countercurrent system with hyperosmotic medulla

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31
Q

Distal convoluted tubule

A

FINE TUNING SALT AND WATER

Reabsorbs 5% of Na Cl and bicarbonate
Reabsorbs Mg and calcium

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32
Q

Collecting duct

A

Concentrates urine - ADH mediated
Aquaporins inserted to allow H2O reabsorption when plasma is too concentrated/low blood volume

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33
Q

Major transporter in proximal convoluted tubule

A

Na/H (antiporter)
Na/glucose (symporter) = SGLT2 (remember SGLT1 is in the intestine)
Paralell transport of Mg etc

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34
Q

Thin loop Henle main tranporters

A

Trick Q!
i. Permeable to sodium
ii. Water is reabsorbed freely – 20%
Everything transported via simple diffusion

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35
Q

Thick loop of Henle main transporters

A

Luminal NKCC2 transporter (Na, K, 2 x Cl) co transporter
Back leak of K+ via ROMK
Na/H+ antiporter
IMPERMEABLE to water
Reabsorption of Ca and Mg (paracellular) via electrochemical gradient created by Na+ reabsorption
therefore inhibition of NKCC transporter will lead to reduced Ca and Mg reabsorption

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36
Q

Distal convoluted tubule - main transporters

A

Impermeable to water and urea
Permeable to Na, also small amount Ca and Mg reabsorbtion

NCC (Na, Cl co trnasporter)
NCC defect= Gitelmans disease

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37
Q

What is the significance of principle cells and intercalated cells in the collecting duct

A

Principle cells – site of aldosterone action
Intercalated cells – site of acid base balance

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38
Q

Main sodium channel in collecting duct

A

ENAC channel
- upregulated by aldosterone
- creates gradient to drive K+ and H+ secretion

Mutations:
inactivating ENAC mutation –> pseudohypoaldosteronism type 1 (neonatal salt wasting, hyperkalemia)
Activating mutation ENAC = Liddels disease

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39
Q

Aldosterone secretion is stimulated by…

A
  1. angiontensin 2
  2. increased serum potassium
  3. acidosis

Aldosterone stimulates reabsorbtion of salt (and water), secretion of K+, as well as H+ via the H+/ATPase in the intercalated cells–> increasing blood volume/pressure, reducing serum potassium and reducing plasma acidosis

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40
Q

Primary hyperaldosteronism

A

Primary = overproduction of aldosterone by the adrenal glands, when not a result of excessive renin secretion. eg Conns syndrome (aldosterone producing adenoma)

–> HTN + hypokalemia (due to excessive excretion of potassium), usually a diagnostic clue. (same presentation as Liddels)

Secondary hyperaldosteronism is due to overactivity of the renin–angiotensin system.

Rx: surgical (if adenoma), or medical w spironolactone

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41
Q

Only type of diarrhea that causes metabolic alkalosis rather than metabolic acidosis

A

congenital chloride diarrhoea

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42
Q

chloride responsive vs chloride resistant metabolic alkalosis

A

Chloride responsive - loss of H+
· Low ECFV
· Low urine chloride (<25 mEQ/L), hyperaldosteronism secondary to dehydration leading to sodium retention and potassium loss, and excretion of bicarbonate
· Alkalosis likely to improve fairly easily with chloride supplementation- fluids with NaCl (ie. non-renal chloride loss)
Examples:
· Vomiting
· Diuretic
· Congenital chloride diarrhoea
· Volume depletion (contraction alkalosis)
· CF
· Non-absorbable anion eg. imipenem
· Stool chloride loss – laxative abuse
· Post-hypercapnoea

Chloride resistant, retention of HCO3/shift of H+ into cells:
· High ECFV
· High urine chloride (>40 mEQ/L)
· Alkalosis likely to persist despite NaCl containing fluids (ie. likely renal chloride/ hydrogen loss)
Examples:
· Hypokalemia - shift of potassium out of cells, leading to H+ shift into cells
· Hyperaldosteronism/Conns syndrome
§ Increased RAAS activity
· Bartter’s/ Gitelman’s syndrome
· Liddle syndrome

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43
Q

Dent disease

A

Think Fanconi syndrome /(but mostly just protein) with renal stones

X linked recessive
CNL5 gene mutation
Disorder of proximal tubules
Triad: proteinuria, hypercalciuria, nephrocalcinosis and/or nephrolithiasis
Fanconi syndrome
Polyuria, microscopic hematuria

Phenotype of Lowe syndrome overlaps with Dent disease - LMW proteinuria + hypercalciuria
Lowe syndrome: + renal tubular acidosis, cataracts, intellectual disability

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44
Q

Lowe Syndrome

A

X linked recessive
Congenital cataracts
Mental retardation
Fanconi syndrome
- progresses to renal failure

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45
Q

Proximal RTA features

A

Impaired ability of proximal tubule to reabsorb filtered bicarb
Often occurs as global proximal tubulopathy - Fanconi syndrome

Non anion gap metabolic acidosis
HYPOkalemia - worsens with bicarb therapy
Urinary pH <5.5
No stones

Presentation:
Polyuria, polydypsia, dehydration
Growth failure
Rickets

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46
Q

Distal RTA features (type 1)

A

Impaired hydrogen secretion in distal tubule
Urine pH >5.5
HYPOkalaemia - improves with therapy
HYPERcalciuria
Hyperammoniaemia
Nephrolithiasis/nephrocalcinosis (think- high urinary calcium)

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47
Q

Type 4 RTA features

A

Urine pH >5.5
HYPERkalemia

causes:
most common - impaired renal response to aldosterone (pesudohypoaldosteronism)
Hypoaldosteronism
RAAS blockage
Drugs- spironolactone, amiloride, calcinurin inhibitors

pseudohypoaldosteronism: during pyelonephritis, urinary obstruction/obstructive uropathy

polyuria, dehydration due to salt wasting
growth failure

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48
Q

what is the effect of low aldosterone on K+ and H+?

A

↓ aldosterone action = ↓ sodium reabsorption = ↓ H+ and K + secretion = acidosis and hyperkalemia

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49
Q

Similarities bw Bartter and Gitelman syndromes?

A

Inherited tubulopathies
Both HYPOkalaemic metabolic ALKALOSIS
w NORMAL renal function

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50
Q

Bartter syndrome

A

AR mutations in transporters in the TAL Henle
Usually present in prenatal period - childhood
Recurrent episodes polyuria + dehydration
FTT
Growth + mental retardation
*same biochemical anomalies as loop diuretics

HYPOkalemia
HYPOchloremia
Metabolic ALKALOSIS
Magenesium low/NORMAL
Renin and aldosterone ELEVATED but normal BP
Prostaglandins ELEVATED

Urine- hYPERcalciuria –> renal stones

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51
Q

Gitelman syndrome

A

AR mutations in transporters in DCT (NCC transporter)
Present in adolescence/adulthood
Hx recurrent muscle cramps
Polyuria without dehydration
*same biochemical anomalies as thiazide diuretics

HYPOkalemia
HYPOmagnesemia
Metabolic ALKALOSIS
Renin and aldosterone NORMAL
Prostoglandins NORMAL
HYPOcalciuria (hypercalciuria in Barterrs) + high Mg in urine

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52
Q

When to suspect either Bartter or Gitelman syndrome

A

The two inherited hypokalemic salt-wasting tubulopathies, BS and GS, are clinically suspected in individuals who present with hypokalemic hypochloremic metabolic alkalosis, high urinary chloride excretion and normal to low blood pressure (BP) despite elevated renin and aldosterone levels.

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53
Q

congenital chloride diarrhea vs Bartter syndrome differentia investigation findings

A

Both present with hypokalemic metabolic alkalosis

CD can be differentiated from BS as it is associated with low urinary chloride excretion, whereas BS is characterized by high urinary chloride excretion

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54
Q

Pseudohypoaldosteronism vs Bartter syndrome differential investigation findings

A

Pseudohypoaldosteronism: hyperkalemia and metabolic acidosis
Normal aldosterone but impaired response

BS: hypokalemic metabolic alkalosis.
Elevated aldosterone/renin

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55
Q

Loop diuretics

A

Act on thick ascending loop of Henle
NaK2Cl transporter- reabsorption of Na down its concentration gradient allows movement of C into the cell
Na/K ATPase drives the concentration gradient (low Na inside cell)
Loop diuretics bind and block the chloride part of NaK2Cl–> excretion of Na, K, and Cl
Calcium and magensium are also excreted as they depend on the concentration gradient for reabsorption

Side effects:
Ototoxicity
Hypomagnesemia
Hypocalcemia
Hypokalemia
Metabolic alkalosis

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56
Q

Thiazide diuretics

A

Distal convoluted tubule
Blocks Na/Cl symporter
The sodium/calcium exchanger on the basolateral side works overtime to pump more Na into cell (as Na/CL symporter not pumping Na into cell on apical side) thus increasing movement of Ca out of cell into interstitium –> more calcium is reabsorbed from the urine

A/E:
Hypokalemia
Metabolic alkalosis
Hypercalcemia
Hyperuricemia
Hyperglycemia
Hyperlipidemia

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57
Q

Potassium sparing diuretics

A

Act on distal convoluted tubule and collecting duct
Principal cells: Aldosterone binds on mineralocroticoid receptor in cytoplasm –> increased synthesis of ENacs and Na/K ATPase transporters to increase Na reabsorbption into blood and K secretion into urine
In alpha intercalated cells: aldosterone increases synthesis of H/K transporters to increase H+ secretion

Spironolactone directly inhibits aldosterone receptors
Uses: hyperaldosteronism

Amiloride blocks Enac channals –> reduced synthesis of Na/K ATPase on basolateral membrane

Total effect: increase excretion of sodium, decrease excretion of hydrogen and potassium

A/E-
Hyperkalemia
Acidosis

***Liddle syndrome- increased activity of ENAC channels —>too much sodium retention, too much potassium excretion , HTN

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58
Q

Carbonic anhydrase inhibitors

A
  • End in “zolomide”
    • Inhibit carbonic anhydrase in proximal convoluted tubule
    • Leads to reduced bicarbonate reabsorption in the proximal tubule –> water follows
    • Also causes urine alkalinization - used in cystinuria
    • Also used in the treatment of idiopathic cerebral HTN and glaucoma (reduced aqueous humor production)
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59
Q

Cystinuria

A

AR
High cystine in urine –> cystine kidney stones
- type aminoaciduria

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60
Q

Nephrogenic DI

A

Inability to concentrate urine in presence of ADH
Inherited- usually X linked recessive, AVPR2 gene (ADH receptor)
Acquired- obstructive uropathies, nephrocalcinosis, intersitital kidney disease, lithium, acute or chronic kidney disease etc

Presentation: polyuria, hypernatremia

Ix: paired serum + urine osmolality, serum osmolality >290 mOsm/kg with urine of <290 mOsm/kg diagnostic (ie concentrated plasma with inappropriately dilute urine)
No/minimal improvement with desmopressin

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61
Q

Acute interstitial nephritis

A

Classic triad: fever, rash, eosinophilia

AKI + sterile pyuria, white cell casts, eosinphilia
Wide range depending on cause- rash, joint pain, fever, nausea, weight loss , hematuria, HTN
Can be caused by any drugs, but most commonly penicillins or NSAIDs

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62
Q

Acute tubular necrosis

A

Oedema + muddy brown casts
Can be toxic or ischemic
Toxic- medications such as aminoglycosides, statins, cisplatin, ethylene glycol
Ischaemic- caused when the kidneys are not sufficiently perfused for a long period of time (i.e. renal artery stenosis) or during shock.

if underlying cause address- revovery in 1-2 weeks as cells grow back

fractional excretion of sodium is >2%, used to differentiate from prerenal AKI

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63
Q

Tubulointerstitial nephritis

A

Inflammatory infiltrate in kidney interstitial, sparing glomeruli and vessels
Usually drug induced - penicillin, cephalosporins, carbemazepine, infections

usually occurs 1-2 weeks post drug exposure

Fever, rash and arthralgia, rising creatinine
May have rash
Haematuria, proteinuria, WBC casts

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64
Q

VCUG/MCUG used for…

A

Distal obstruction
Vesicoureteric reflux
Posterior urethral valves

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65
Q

MAG3/DTPA used for …

A

Functional scan - info about uptake (blood flow through kidney) + excretion (obstruction)
Assess tubular function/GFR and proximal obstruction (PUJ)
in a duplex kidney, lower pole is associated with VUR, and upper pole with obstruction–> obstruction needs MAG3 to diagnose

66
Q

DMSA used for..

A

STATIC imaging
- structure, scarring, ectopic tissue

67
Q

transient proteinuria can be caused by…

A
  1. Typically, after vigorous exercise, fever, dehydration, seizures and adrenergic agonist therapy. can also be postural/orthostatic (proteinuria when upright)
    2. Usually mild, glomerular in origin, and always resolves within a few days
    3. Does NOT indicate renal disease
    4. ALWAYS follow up with early morning urine when well/rested
68
Q

What is the cause of idiopathic nephrotic syndrome

A

Minimal change disease (85%) - usually age 3+ years
Focal segmental glomerulosclerosis (FSGS)- 15%- usually age 6+ years
Overall 90% of nephrotic syndrome in kids is ideopathic

69
Q

Significance of gene positive nephrotic syndrome

A

unlikely to be steroid responsive
progress quickly to ESRF
very low risk recurrence post renal transplant

70
Q

Definition of remission in nephrotic syndrome

A

urine protein excretion < 4 mg/hr/m2(<30 mg/mmol PCR) 3 consecutive days

71
Q

Definition relapse nephrotic syndrome

A

urine protein excretion > 40 mg/hr/m2(>200 mg/mmol PCR), OR dipstick >=3 for 3 consecutive days

72
Q

Nephrotic syndrome can be secondary to ..

A

SLE
HSP
MPGN
Hep B membranous nephropathy
Denys Drash ( nephrotic syndrome, ambiguous genitalia, Wilms tumor)
Pierson syndrome (nephrotic syndrome, eye probems)
Nail patella syndrome
Fabry disease (X linked lysosomal storage disorder - angiokeratomas, peripheral burning pain)

73
Q

Where is the aldosterone receptor located

A

As with all steroid hormones, aldosterone passes through cell membranes to bind to cytoplasmic receptors which translocate to the nucleus to influence mRNA transcription and subsequently protein synthesis
Located DCT and collecting duct

74
Q

Differential diagnosis oedema

A

Heart failure
Liver failure
Renal - nephrotic syndrome
Protein losing enteropathy
Protein malnutrition

75
Q

Minimal change disease

A

most common cause nephrotic syndrome
100% of those with MCD present with nephrotic syndrome
Age: 2-3 years

76
Q

is there likley to be ongoing haematuria in IgA nephropathy?

A

there is often microscopic haematuria in between episodes of macroscopic haematuria
often triggered by intercurrent illness

77
Q

features associated with ESKD in IgA nephropathy

A

Proteinuria >1g/day
HTN
Reduced baseline GFR
Persistent hematuria
Biopsy findings = glomerulosclerosis,

78
Q

Key features of IgA nephropathy

A

Usually presents as haematuria(+/- pain/proteinuria), or nephritic syndrome. Nephrotic syndrome rare

Usually occurs 1-2 days post onset URTI symptoms
May have recurrent episodes macroscopic haematuria with illness, with microscopic haematuria in between

NORMAL C’levels
<20% have elevated IgA

Rx: control BP and proteinuria with ACEI/ARB
If severe- imunnosuppress with steroids

20-30% will develop ESKD 20 years after disease onset
RF: proteinuria >1g/day, HTN, reduced GFR, persistant haematuria, biopsy markers

79
Q

Alport syndrome

A

X linked (but can be AD and AR less commonly)- Mutations in COL4A5 gene - for type IV collagen (major component of GBM)

Multisystem disorder – includes nephritis, sensorineural deafness and eye abnormalities

Renal:
Micoroscopic haematuria, some episodes of macroscopic (from infancy)
Proteinuria

Hearing:
Bilat SN hearing loss
50% deaf by age 15, 90% end up deaf
HTN by mid teens
Microhaematuria –> gross haematuria with urti –> proteinuria –> renal failure
50% have ESRD by age 25

Eyes:
ANTERIOR LENTICONUS 2nd to 3rd decade

Diagnosis:
Normal C’ levels
Opthal- anterior lenticonus pathognemonic
Genetic testing - COL4A5 x linked (also COL4A3-4 in autosomal)
Skin biopsy
Renal biopsy
FHX and urinalyisis of relatives

Rx: ACE/ARB

Female carriers can be affected, just later in life

80
Q

Acute Post Streptococcal GN

A

Post GAS infection
2 weeks post throat infection
3-6 weeks post skin infection

Haematuria (tea/cola), oliguria, HTN, oedema - nephritic syndrome (but can be just isolated hematuria)
Nephrotic syndrome rare (~5%)

Most common kids 2-12 years

Immune complex mediated

Ix:
throat swab, ASOT (3 weeks post infection), ANti-DNAse (6 weeks post infection),
low C3 –> returns to normal in 6-8 weeks
C4 normal

If C3 doesnt normalise at 6 weeks consider MPGN or SLE

Renal biopsy indicated for : RPGN, persistent proteinuria >6 mo, low C3 at 8 weeks

Rx:
Oral penicillin
Fluid restrict to 400ml/m2
HTN- frusemide 1st line (as fluid overloaded)

NOT ACE-I

Persistent haematuria can persist for 2 years, need to follow up to ensure resolution

3-5% have rapidly progressive GN

95% resolve spontaneously
gross haematuria and HTN should resolve by 1 week

81
Q

SLE Nephritis

A

GN is the most important cause of morbidity and mortality in SLE
kidney disease is present in up to 80% of kids
Deficiency C1q s strongest genetic factor

Immune complex mediated

Clinical manifestations
a. Mild lupus nephritis (class I-II, some class III) = haematuria, normal renal function, proteinuria <1 g/24 hours
b. Class III (some) and ALL patients with class IV nephritis = haematuria, proteinuria, hypertension, reduced renal function, nephrotic syndrome, or acute renal failure
c. class V nephritis = nephrotic syndrome

Ix: ANA, dsDNA, anti smith

Rx:
Class >3 (reduced renal function, proteinuria, HTN)= prednisolone, mycophenolate, other immunsuppression, depending on subtype
Also need ACE-I

everyone with SLE needs hydroxychloroquine

82
Q

HSP nephritis

A

Most common small vessel vasculitis in childhood
PURPURIC RASH, ARTHRITIS, ABDOMINAL PAIN
100% have rash - can be maculopapular initially, later purpuric
GIT- abdo pain, N/V, GI bleed, intussuception
50% have renal manifestations, asymptomatic microscopic haematuria–> severe progressive GN
If renal manifestations will occur, they usually develop by first 3 months

Rx:
Supportive- NSAIDS
Steroids for abdo pain (1 week then slow wean), not for renal
ACEI if HTN/proteinuria

Systemic manifestation of IgA nephropathy

Refer reanl team if nephrotic or nephritc syndrome at presentation, or persistent proteinuria

If untreated, risk renal failure 2-5%

83
Q

RPGN

A
  1. Key points
    a. Nephritic syndrome with rapidly deteriorating renal function – commonly dialysis requirement
    b. Crescents on biopsy
  2. Etiology
    a. Primary
    i. IgA nephropathy
    ii. MPGN
    iii. Anti-GBM
    b. Secondary
    i. ANCA-mediated
    ii. SLE nephritis
    iii. Post-streptococcal GN – note rarely proceeds to CGN but as it is the most common cause of GN in childhood accounts for significant percentage of patients with CGN
    iv. IgAV/HSP nephritis
  3. Pathology + pathogenesis
    Hallmark = crescents in glomeruli
  4. Prognosis + management
    a. Children with crescentic post-infectious GN can spontaneously recover
    b. Natural course of other forms of RPGN = ESRF in weeks to months
    c. Poor prognosis = fibrous crescents (irreversible)
    Immunosuppression needed
84
Q

Goodpastures disease

A

Pulmunary renal syndrome

Pulumunary haemorrhage + cresenteric GN

Antibodies against type 4 collagen –> GBM
(type 2 hypersensitivity)
Hemoptysis + acute GN–> rapid progress to ESRF

Cresenteric GN on biopsy, C3 normal
Poor prognosis

Needs immunosuppression

85
Q

ANCA Vasculitis

A

Chronic, often relapsing, multi organ involvement

Ab directed against neutrophil cytoplasmic Ag
ANCA = PR3 ANCA = granulomatosis with polyangiitis (GPA or Wegners)—> granulmoas of respiratory tract, sinusitis
pANCA = MPO ANCA = microscopic polyangiitis (MPA) –> no granulomas but can have resp involevement with pulm haemorrhage, interstitial nephritis

High mortality if untreated
Treat with immunosuppression

86
Q

Haemolytic uraemic syndrome

A
  1. Microangiopathic haemolytic anemia (DAT-) (due to microvasuclar injury/endothelial damage/platelet aggregation)
  2. Thrombocytopenia
  3. Acute renal injury

Presentation:
pallor
irritabiility –> can have more severe CNS involvement with seizures, encephalopathy
lethargy
haematuria
fever
anemia, thrombocytopenia
Often post gastro illness with bloody diarrhoea OR very unwell with a pneumonia

Most often secondary to shiga toxin producting E.coli (shigella dystenteriae)
Strep pneumoniae - usually very unwell with this

Ix:
FBE + film: low Hb, platelets, SHISTIOCYTES on film
Normal coags
Markers of haemolysis
Negative coombs
AKI
Urine- haematuria, proteinuria
Stool MCS
Pneumonocccal PCR

Rx:
Supportive- fluid and electrolytes
Dialysis
No antibiotics for STEC

30% have long term CKD

87
Q

Renal vein thrombosis

A

a. Occurs in 2 distinct clinical settings
i. Newborns and infants – associated with asphyxia, dehydration, shock, sepsis, congenital hypercoagulable states, maternal diabetes
ii. Older children – nephrotic syndrome, cyanotic heart disease, inherited hypercoagulable states, sepsis, following kidney transplantation
2. Clinical manifestations
a. Typical = sudden onset gross haematuria and unilateral or bilateral flank masses
b. Other features
i. Hypertension
ii. Microscopic haematuria
iii. Oliguria

USS: renal enlargement
Doppler to confirm

Rx: supportive, anticoagulation, thrombolysis only if bilateral
if unilateral without AKI, can be monitored

88
Q

Idiopathic hypercalciuria

A

AD
Cause of haematuria, dysuria, abdo pain

Ix: 24 hr urinary calcium excretion, or calcium/creatinine ratio

Can lead to nephrolithiasis if untreated

Rx: thiazide diuretics, sodium restriction, potassium citrate

89
Q

Management frequently relapsing nephrotic syndrome

A

1st line: Cyclosporin (calcinurin inhibitor)
2nd line: rituximab

90
Q

Microangiopathic haemolytic anemia

A

Destruction of RBC in small blood vessels
Anemia, evidence of hemolysis (bili, LDH elevated), DAT neg, schistocytes on blood film

eg HUS, DIC

The endothelial layer of small vessels is damaged with resulting fibrin deposition and platelet aggregation. As red blood cells travel through these damaged vessels, they are fragmented resulting in intravascular hemolysis.

91
Q

Nephritic syndrome

A

Haematuria
HTN
Oedema
Oliguria/AKI

most common cause in childhood is post strep GN

92
Q

Simple cysts

A

Usually asymptomatic
occasionally cause pain, haematuria, obstruction

USS- thin wall, no septations, no calcifications
usually solitary and unilateral
If above features present- increased risk of malignancy

complications: rupture, infection, haemorrhage

Conservative management

Surgery should be restricted to symptomatic large compressive cysts, increase in cyst size on follow-up imaging, and when there is uncertainty about the underlying diagnosis

Laparoscopic marsupialization may be considered for a simple renal cyst in a symptomatic child

93
Q

Multicystic dysplastic kidney (MCDK)

A

Most severe form of cystic renal dysplasia - non hereditory
Numerous non communicating cysts separated by dysplastic tissue. No identifiable kidney tissue.
Usually detected antenatally
Usually unilateral
Natural history: involution of affected kidney (60% completely involute by age 5)
Contralateral kidney undergoes compensatory hypertrophy –> monitor with serial USS to ensure this occurs appropriately
No/minimal increased risk of HTN or malignant transformation
Usually no long term complications, but more at risk of ESKD if any insult to remaining kidney
Increased risk of VUR in remaining kidney (30%)
No specific management apart from long term follow up up ensure remaining kidney ok

94
Q

Autosomal Recessive Polycystic Kidney Disease (ARPCKD)

A

THINK BILATERAL KIDNEY AND LIVER INVOLVEMENT

Presentation:
Perinatal: oligohydramnios, Potter sequence, pulmunary hypoplasia
Neonatal: bilat flank masses, HTN, USS: enlarged echogenic kidneys, cystic changes develop over time (microscopic –> macroscopic)
50% with early presentation develop ESRF by age 10
Some patients present in adolescence- typically present with hepatomegaly, portal hypertension
Liver disease always present but clinical complications may become obvious at any point in childhood or adulthood

Rx:
Supportive
Treat HTN
Dialysis
Liver-kidney transplant

DDx – other causes of bilateral renal enlargement
a. Multicystic dysplasia
b. Hydronephrosis
c. Wilm’s tumour
d. Bilateral renal vein thrombosis

95
Q

Autosomal Dominant Polycystic Kidney Disease (ADPCKD)

A

Most common hereditary form of CKD
Rare in kids, often only presents in adulthood
Most commonly an incidental finding during USS for other causes
THINK- CYSTS EVERYWHERE in adults

Symptoms- very variable
Asymptomatic, haematuria, proteinuria, HTN, polyuria/polydypsia

Adults will develop cysts in liver, pancreas, spleen, intracranial aneurysms, bowel divirtucular disease, abdo wall hernia
Mitral valve prolapse in 12% kids

Diagnosis: enlarged kidneys with bilateral macroscopic cysts in patient with affected 1st degree relative (may need to check parents)
however kids often have normal kidney size and unilateral disease

Rx: supportive, regular review, ACE-I for HTN, avoid NSAIDs, high fluid intake, avoid high protein diet
CKD usually develops in late adulthood

96
Q

Nephronophthisis

A

Group of AR cystic kidney diseases which progress to CKD

Characterized by impaired urinary concentrating ability (polyuria, polydypsia), a bland urinalysis (no proteinuria or mild tubular proteinuria, no hematuria or cellular elements), chronic tubulointerstitial disease, and progression to end-stage kidney disease (ESKD) generally by 20 years of age.

Infantile: ESRF by 3 years
Severe HTN
Extra renal: hepatic, cardiac, valve/septal, recurrent lung infections

Juvenile: most common
ESRF by adolescence
Present with polyuria/polydypsia in middle childhood, enuresis (impaired urine concentrating ability)
BP normal
Nephrogenic DI- dilute urine, no improvement with ADH
Sodium wasting, poor growth
Retinitis pigmentosa

Progression to ESRF universal by age 20 yrs

b. Renal USS
	i. Increased echogenicity of kidneys with loss of corticomedullary differentiation 
	ii. Normal/ slightly reduced size  + no dilation of urinary tract Renal cysts NOT typically identified on initial USS – may appear later
97
Q

Renal anomalies in Tuberous sclerosis

A

Angiomyolipoma
Simple cysts
Renal cell carcinoma

98
Q

Joubert Syndrome

A

Cerebellar- delay motor milestones, ataxia, hypotonia, abnormal eye moebments
Retinitis pigmentosa
Syndromic cause of Nephronopthisis

99
Q

Bardet-Biedl Syndrome

A

Syndromic cause of Nephronopthisis
Retinitis pigmentosa
polydactyly
Hypogonadism
Dev delay, low IQ
Ataxia
Craniofacial dyphmorphism

100
Q

WAGR syndrome

A

Wilms tumor
Andridia
Genitourinary abnormalities
Retardation (mental)

101
Q

Denys Drash syndrome

A

Wilms tumor -90% will develop (compared to 5-10% in BWS, 50% in WAGR)
Ambiguous genitalia (male)
Progressive nephropathy

102
Q

Calculating Fractional Excretion of Sodium

A

(urine sodium x serum creatinine) / (serum sodium x urine creatinine)

103
Q

Kidney largely formed from the

A

Metanephros

all except the collecting duct, renal pelvis, and ureters

104
Q

What does the mesonephros become

A

vas deferens in males
broad ligament in females

105
Q

Liddle Syndrome

A

AD
Gain of function mutation of ENAC channel - too much Na and water reabsorbtion
HTN
High sodium, low potassium, metabolic alkalosis

Rx; amiloride, blocks the channel

106
Q

Most accurate measure of glomerular filtration is by..

A

51 Cr EDTA clearanace
Freely filtered, not reabsorbed or secreted in tubules

**gold standard= inulin, but only used in research

107
Q

Causes nephrotic syndrome

A

Primary/idiopathic (most children)
minimal change disease (most common)
focal segmental glomerulosclerosis
membranoproliferative glomerulonephritis
membranous nephropathy
diffuse mesangial proliferation
Iga nephrotpathy
Post strep GN

Secondary
SLE
HSP
malignancy (lymphoma/leukaemia)
infections (hepatitis, HIV, malaria)

AD thin membrane disease causes isolated hematuria , NOTT nephrotic syndrome

108
Q

What is the natural history for rapidly progressive/cresenteric glomeruopnephritis

A

Often recover spontaneously if post strep
Use steroids, cyclophosphamide with SLE, IgA nephropathy, HSP
In other conditions, prognosis is worse

109
Q

Pseudohypoaldosteronism type 1 presents with

A

Collecting duct resistance to aldosterone
High aldosterone levels
Low sodium reabsorbtion, low K excretion
–>Low plasma sodium, high potassium

110
Q

Pseudohypoaldosteronism type 2

A

AKA Gordons syndrome
Low sodium, high potassium
but low aldosterone/renin (unlike type 1)
+ arthrogyposis

111
Q

Most common cause HTN in NF1

A

Essential HTN

Less common- renal artery stenosis
Phaemochromocytoma

112
Q

most common drug related cause of nephrogenic DI

A

lithium

113
Q

Differentiating glomerular bleeding from non glomerular bleeding

A

Glomerular: tea colourerd or coca cola
No clots
May have proteinuria
Dysmorphic RBC
RBC may be present

Non glomerular: red or pink, may have clots, no proteinuria, normal RBC morphology, no casts

114
Q

Lower urinary tract and parenchymal causes of haematuria

A

infection- haemorrhagic cystitis (eg adenovirus), urtethitis, bacterial UTI
injury- urethral trauma, stone
tumor
polyp
malformation

pyelonephritis
interstitial nephritis
cyst rupture
Wilms tumor
obstruction
renal trauma
sickle cell disease
nutcracker syndrome
renal vein thrombosis
hypercalciuria

115
Q

What if there is red urine but no blood on urine mcs?

A

Haemaglobinuria from haemolytic anemia (intravscular hemolysis)
Myoglobinuria from rhabdomyolysis

116
Q

what is thin basement membrane disease

A

aka benign familal haematuria
usually presents with microscopic haematuria
gross haematuria uncommon
part of nephritic syndromes, never nephrotic
no treatment needed

117
Q

medications causing haematuria

A

aspirin
cyclophosphamide
diuretics
anticonvulsants
aminoglycosides

118
Q

Membranoproliferative disease (MPGN)

A

HYPOCOMPLEMENTEMIA (deposition of circulating immune complexes, or deranged complement regulation)
c3 low, C4 usually normal (but can also be low)

Presentation- isolated haematuria +/- proteinuria to nephritic/nephrotic syndrome
Diagnosis can be made when child previosly diagnosed with post strep GN and complement fails to rise after 6-8 weeks

Biopsy diagnostic- tram track appearance

Without treatment (immunosuppression), 50% develop ESKD within 10 years

119
Q

Which diabetic med can be used for non diabetic CKD including IGA nephropathy

A

SGLT2 inhibitor
eg dapaglifzolin
not yet approved in aus yet for kids

120
Q

Electron microscopy findings in Alport syndrome

A

Thickened basement membrane
Basket weave pattern

121
Q

Nephrotic range proteinuria

A

> 40mg/m2/hr
Urine PCR >200mg/mmol

122
Q

Treatment of steroid resistant nephrotic syndrome

A

Persistant proteinuria after 4 weeks of daily prednisolone 60mg/kg/day
Do genetic testing
Commenced ACE-I
Cyclosporin or tacrolimus for 6 months; 2nd line rituximab

123
Q

what is the definition of frequently relapsing nephrotic syndrome

A

2+ relapses in first 6 months
4+ relapses in any 12 month period

if frequent relapses, can trial low dose alternate day steroids, or increased steroids during URTI (dont need to taper)

124
Q

PUJ obstruction

A

Most common cause antenatally detected hydronephrosis
Most common obstructive lesion
Presentation: intermittent flank pain, hematuria, renal calculi, UTI –> scarring of kidney if untreated

Rx: pyeloplasty to relieve obstruction

125
Q

Grades of VUR

A
  1. Reflux into the ureter but not into collecting system
  2. Reflux into ureter without mild ureteric and renal pelvis dilatation
  3. Reflux into the ureter and collecting system with mild-mod ureteric and renal pelvis dilatation
  4. Gross dilation of the ureter and collecting system, causing significant blunting of the calyces and ureteric turturosity
    5.Gross dilation of the ureter and collecting system, causing significant blunting of the calyces as well as loss of papilllary impressions; intrarenal reflux may be present
126
Q

Duplex kidney

A

a. Classification
i. Upper moiety
ii. Lower moiety

VUR – usually into lower
Obstruction – usually of upper

127
Q

Ectopic ureter

A

more common in girls
2nd ureter drains outside kidney
if drains distal to sphincter–> continous urinary incontinence “always wet”

128
Q

What are the differences in renal function between 32 week neonate and 38 week neonate

A

Prem neonate will have reduced GFR, lower renal excretion of K+ (thus higher serum K+) and lower acid excretion (thus lower plasma pH)

129
Q

in salt loaded person, the main mechanism by which salt is excreted involves..

A

Increased ANP
Dilates afferent + constricts efferent arterioles = ↑ GFR, ↑ natriuresis
ii. Inhibits aldosterone + renin secretion
iii. Inhibits Na Cl reabsorption in CD
iv. Inhibits ADH action on kidney

130
Q

Renal fanconi syndrome - genetic conditions

A

cystinosis
dent disease
tyrosinemia type 1 (presents very early)
galactosemia
wilsons disease
hereditory fructose intolorence

131
Q

Drugs associated with development renal fanconi syndrome

A

aminoglycosides
cisplatin
ifosphamide
tacrolimus
valproate
heavy metals

132
Q

Signs/symptoms fanconi syndrome

A

Growth failure
Polyuria (due to salt wasting)
Rickets, osteopenia
Muscle cramps, weakness, constipation

Ix: glucosuria, proteinuria
Metabolic acidosis
hypophosphatemia
hypokalemia

133
Q

Prune belly syndrome

A

Cryptorchidism, abdominal wall defects and genitourinary defects
Urinary tract abnormality such as unusually large ureters, distended bladder, vesicoureteral reflux

134
Q

most common abnormality associated with renal stones

A

hypercalciuria

associated with:
dent disease
glycogen storage disease type 1
bartter syndrome
wilsons syndrome

135
Q

most common type of stones in kids

A

calcium oxolate 60-90%
calcium phosphate 10%
struvite 1-10%
uric acid 1-5%
cystine 1-5%

136
Q

which bacteria are most associated with stone formation

A

e.coli
proteus - struvite stones, staghorn calculi

137
Q

medical management of stones

A

tamsulosin (alpha blocker)
stones <5mm will usually pass spontaneously

138
Q

risk factors for stone formation

A

a. High salt diet= biggest risk factor
b. 50% have underlying metabolic condition
c. 25% due to UTI
d. 20% due to urinary obstruction/stasis
e. Strong genetic factors
Geography = hot climate

139
Q

management renal stones

A

a. Dietary
i. High fluid intake - daily intake of 2-2.5L
ii. Low salt intake (to reduce urinary Ca) – high Na increases urinary excretion of Ca
b. Medical
i. Alpha-adrenergic blockers
c. Metabolic defects
i. Potassium supplements – to reduce urinary Ca excretion
ii. Citrate forms soluble complexes with Ca; supplemental potassium citrate - prevents calcium stones
iii. Bicarbonate supplementation increases urinary citrate
iv. Allopurinol – prevents uric acid stones
v. Cystinuria/oxalosis = surveillance USS, urine 3-6/12
vi. Monitor bloods on penicillamine
d. Assess likelihood of spontaneous passage
i. <7mm = wait and repeat USS 3/12
ii. >7mm = surgical referral
e. Surgical
Percutaneous nephrostomy OR stent – if acute obstruction

140
Q

risk factor for calcium oxolate stones

A
  • genetic
    -malabsorptive syndromes- IBD, CF, pancreatic insufficiency if not taking creon
  • low calcium diets
141
Q

causes AKI

A

pre renal - dehydration, haemorrhage, sepsis , hypoalbuminemia/oedema, hypovolemia
renal artery/vein thrombosis, HUS
renal- GN, ATN, tumor lysis syndrome, AIN, pyelonephritis
Postrenal- any kind of obstruction

142
Q

AKI- determining if acute or chronic

A

hx antenatal abnormality
previous UTIs
polyuria/polydypsia
family hx
lethargy
short stature
renal osteodystrophy/rickets

143
Q

Treatment of AKI complications

A
144
Q

correction of Na imbalance

A
145
Q

When would AKI lead to poluria

A

tubulointerstitial pathology - impaired reabsorption

Oliguia with glomerular pathology- no filtration

146
Q

features of ATN

A

impaired concentrating ability
muddy brown casts
dilute urine with high urinary sodium > 40- cant reabsorb
high fractional excretion of sodium >1-2

to differentiate from pre renal AKI: can still concentrate urine so higher serum osmolality, sodium <20, fractional excretion sodium <1

147
Q

most common causes non glomerular CKD

A

CAKUT
hyperplasia/dysplasia
obstructive nephropathy
cystic disease
cystinosis
reflux nephropathy

148
Q

glomerular causes of CKD

A

FSGS
congenital nephrotic syndrome
SLE
MPGN
HSP
IGa
Alport
HUS

149
Q

triple immunosuppression for renal transplant

A

tacrolimus
mycophenolate
prednisolone

150
Q

mechanism of HTN in VUR

A

renal parenchymal scarring

151
Q

Infections post transplant

A

post op- bacterial infections related to surgery itself eg UTI, line infections, pneumonia, wound infections
Next 6 months- viral (CMV, BK virus), PJP

152
Q

Features of self induce vomiting

A

BP is low normal. Loss of chloride and hydrogen

metabolic alkalosis, mild renal insufficiency.
Hypochloraemia with urinary chloride close to zero. Secondary hyperaldosteronism and renal loss of potassium.
Urinary potassium usually >10mmol/L. Metabolic alkalsosis - renal excretion of sodium bicarbonate, so urinary sodium higher than chloride. So urine will have reasonably elevated sodium, very low chloride, high potassium, and be alkaline

153
Q

Juvenile nephronophthisis

A

Presents with
- polyuria, polydypsia, dehydration
- growth failure
- anemia
- chronic renal failure by adolescence
Imaging - small kidneys with cysts

The clinical manifestations are related to tubular injury that leads to a reduction in urinary concentrating capacity, renal sodium loss, and insidious but inevitable progression to renal failure. The tubular defects precede the decline in renal function and may be present in asymptomatic siblings with the disease.
In most patients, the signs associated with decreased urinary concentration capacity are present by age 5 years.

Because of salt wasting, hypertension is rare, even in patients with severe renal insufficiency.

154
Q

Gold standard for renal artery stenosis

A

Renal arteriography
Renal Doppler ultrasound first line

155
Q

Renal artery thrombosis presentation

A

flank mass + hematuria

156
Q

Peritoneal dialysis

A

Solute moves down concentration gradient across peritoneal membrane by diffusion
Water moves across peritoneal membrane by osmosis (ultrafiltration)
Ultrafiltration causes movement of solutes by drag forces even without concentration gradient

157
Q

Haemodialysis

A

Removes solutes by diffusion, via dialysate fluid. Solutes passively flow from one fluid compartment to the other down their concentration gradient ie urea, creatinine and potassium move from blood to dialysate; calcium and bicarbonate move from dialysate to blood

158
Q

Haemofiltration

A

Solutes removed by convection. Uses hydrostatic pressure to induce filtration of plasma fluid across the filter membrane, so small and mid molecular weight solutes move in same direction as water. No dialysate fluid used.

159
Q

nephrocalcinosis

A

calcification of renal tissue
commonly seen in prem neonates receiving frusemide (causing hypercalciuria) or Barters syndrome
children with Medullary sponge kidney
type 1 distal RTA
hyperparathyroidism

160
Q

what is the main predisposing factor to calcium oxolate stones

A

IBD
pancreatic insufficiency
biliary disease
–> GI malabsorption of fatty acids, which bind intraluminal calcium and form salts. Oxolates therefore dont have calcium to bind to as they do normally, therefore there is increased gut absorption of unbound oxalate

161
Q

main inhibitor of calcium stone formation

A

citrate
citrate forms complexes with calcium –> increasing urinary calcium soluability
inhibitng aggregation of calcium phosphate or calcium oxalate

162
Q

prevention renal stones

A

fluids
low sodium diet
potassium citrate
normal calcium
thiazide diuretics - reduce renal Ca excretion
allopurinol if uric acid stones (inhibits xanthine oxidase)
maintain high urinary pH- sodium bicarb or citratw

RACP paeds Qld Group (46 decks)

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