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Renal > Renal Learning Points CSV > Flashcards

Renal Learning Points CSV Flashcards

1
Q

Renal differences in the neonate (6)

A

(1) nephron number multiplies until 36/40 (increased risk hypertension in preterm)
(2) decreased GFR in preterm
(3) oliguria then polyuria (K wasting in polyuric phase)
(4) ADH increases at birth and can be very high in HIE
(5) renal wasting of bicarb - can be acidotic
(6) renal wasting Calcium

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2
Q

what are nephropathies have low C3

A 
5 S’s: 
1. post Strep, 
2. MeSangioProliferative/Membranous GN, 
3. SLE, 
4 Septic (SBE, HBV, HCV) 
5. Shunt nephritis
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3
Q

Normal complement nephropathies

A 
4 A’s and H: 
1. Alport 
2. Anti-GBM (Goodpastures) 
3. IgA, 
4. ANCA associated (Wegeners) & 
HSP
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4
Q

When will children with HSP develop nephritis by?

A

by 6-8 weeks but need to be monitored for 6 months

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5
Q

renal biopsy indications

A

nephritic/nephrotic at presentation,
persistently impaired/deteriorating renal function,
C3 low at 3 months

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6
Q

IgA nephropathy characteristics

A

Not inherited
gross haematuria with illness, recurrent,
flank pain,
persistent microscopic haematuria
benign in childhood but HTN in adult - treat with ACEi

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7
Q

Alport syndrome characteristics

A

hearing loss (age 10),
EYE abnormalities (macular flecks)
recurrent gross haematuria post viral ilness persistent microscopic haematuria,
ESRD late teens

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8
Q

With nephropathies are rapidly progressive?

A 
crescents >50% glomeruli
ANCA associated (pauciimmune)
Anti-GBM (Goodpastures - pulm-renal syndrome)
SLE (systemic symptoms)
Membranoproliferative (low complement)
HSP (IgA)
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9
Q

Definition nephrotic syndrome & most common cause

A

Oedema,
Proteinuria (uPCR >200, 3+ protein),
Low Alb <25 .

Most common cause = minimal change disease

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10
Q

what explains oedema in minimal change disease

A

reduced oncotic pressure and increased sodium reabsorption

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11
Q

Complications of nephrotic syndrome

A 
hypothyroidism, 
rickets, 
thrombosis, 
short stature, 
anaemia
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12
Q

best way to calculate GFR in clinical setting

A

plasma disappearance of radio-isotope

**inulin gold standard but only in research setting

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13
Q

when does GFR reach adult values

A

age 2

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14
Q

Triad of HUS

A

Thrombocytopenia,
Haemolytic anaemia,
Acute kidney injury

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15
Q

Typical HUS - causes

A

diarrhoea related - E.Coli 0157:H7 - verotoxin/shiga toxin

Shigella – shiga toxin

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16
Q

HUS Atypical causes

A

Pneumococcal
*Complement (C3, CD46, factor B, H inhibitors) , *ADAMTS13,
Cobalamin deficiency
*lead to activation of alternative complement

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17
Q

what does ADAMTS13 do

A

acts to cleave vWF multimers and prevent thrombus formation

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18
Q

Long term sequelae HUS

A

“Microangiopathy” diabetes,
Hypertension,
Proteinuria
CKD

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19
Q

What is the most predictive risk factor for long term sequelae in HUS

A

duration anuria >10 days,

prolonged dialysis >7 days

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20
Q

Duration follow-up of HUS? ** need to know

A

at least 5 years as long term sequelae can occur up to 5 years post apparent recovery

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21
Q

Clues to chronic glomerular causes to CKD

A

Oligouria,
Haematuria/proteinuria,
Hypertension

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22
Q

Clues to tubular disease for CKD

A

Polyuria, Polydipsia
Sodium loss,
Enuresis

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23
Q

Progression of CKD can be slowed by?

A

Control HTN,
Control proteinuria,
Treatment anaemia,
Treatment hyperlipidaemia

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24
Q

Complications CKD

A
  1. Growth failure
  2. Osteopenia
  3. Anaemia,
  4. Acidosis (impairs GH release),
  5. Water and electrolyte imbalance,
  6. Delayed puberty,
  7. Social and cognitive.
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25
Q

What are the bacteria in bacterial peritonitis in a child with PD? Antibiotics?

A

Treat if WBC >50 and symptomatic or WBC >100
Bacteria = staph epi, staph aureus
Antibiotics = Cefazolin, ceftazidime OR vancomycin & ciprofloxacin

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26
Q

Causes of PD peritonitis

A
  1. Intraluminal (touch contamination),
  2. Periluminal (tunnel infections),
  3. Intestinal translocation
  4. Systemic,
    5 Ascending (rare)
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27
Q

Benefits transplant over dialysis

A
  1. Mortality,
  2. CVD,
  3. Growth,
  4. Neurodevelopment,
  5. QOL
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28
Q

Absolute contraindications to renal transplant

A
  1. active malignancy,
  2. severe neurological dysfunction,
  3. terminal illness / multiorgan failure,
  4. psychiatric illness impairing consent
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29
Q

6 causes of allograft dysfunction

A
  1. Dehydration,
  2. Medication
  3. Infection,
  4. Obstruction
  5. Rejection (biopsy)
  6. Perfusion problem
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30
Q

Hypertension Treatment post renal transplant

A

Ca channel blockers (early),
Diuretics (if hypervolaemic)
ACEi once 2-3 months post t/p

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31
Q

Tacrolimus SE

A 
nephrotoxicity, 
HTN, 
hepatic dysfunction, 
glucose intolerance, 
hyperkalaemia, hypomagnesaemia, 
alopecia
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32
Q

Tacrolimus mechanism of action

A

calcineurin inhibitor > inhibits nuclear activation

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33
Q

Cyclosporin SE

A

neprotoxicity, HTN, gigival hyperplasia, hirsutism, hyperuricaemia, hypercholestoraemia

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34
Q

Pulmonary renal syndrome causes

A 
[Pneumonic AA STD] - 
Anti-GBM, 
ANCA, 
SLE, 
Thrombotic disease (antiphospholipid, TTP, HSP), 
Drugs
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35
Q

RIFLE criteria

A 
For renal insult - 
Risk dysfunction (Crx1.5), 
Injury (Crx2), 
Failure (Crx3), 
Loss (>4weeks), 
ESKD (>3months)
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36
Q

Causes hypochloraemic metabolic acidosis

A 
pyloric stenosis, 
prolonged vomiting, 
diuretics, 
Bartter, 
CF, 
Choride diarrhoea
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37
Q

RTA type 1

A 
DISTAL, can’t excrete acid, 
hypercalciuria (stones),  
urine is alkaline (ph >5.5)
loin pain  
Low K 
CAUSES: obstructive uropathy, marfan, wilsons, drugs (amphotericin)
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38
Q

RTA type 2

A

PROXIMAL, can’t resorb bicarb, hypercalcaemia / low calcium in urine
acidic urine (pH <5.5)
Low K
CAUSES: cystinosis, fanconi

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39
Q

Fanconi

A 
ALL of proximal tubule 
short child no growth and vomiting.
Renal >GI losses
occurs at time that transitions from breast milk to cows milk ~6 months age 
- hypophosphataemic ricketts
- amino acid uria, glycosuria, 
- normal glucose in plasma
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40
Q

RTA type 4

A

normal urine anion gap,
hyper aldosteronism
High K, Low Na
CAUSES: CAH, tacro, NSAIDS, tubular aldosterone def

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41
Q

Bartter Syndrome

A 
Na/K/2Cl Channel defect in LOH - 
hypochloraemic hypokalaemic metabolic alkalosis 
Hypercalciruia, hyperchloride uria
Prone to hypernatraemic dehydration
Manage with NSAIDS > slow GFR
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42
Q

Gitelman syndrome

A

NaCl defect in distal tubule
hyPOcalciuria
present later in childhood with cramps - LOW Mg

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43
Q

metabolic alkalosis with volume contraction (normal/low BP)

A 
ABCD - 
Anorexic (vomiting/laxatives), 
Bartter, 
CF, 
Diuretics.
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44
Q

metabolic alkalosis with volume expansion (high BP)

A

Anything that activates RAAS:

  • Aldosteronism,
  • Renal artery stenosis,
  • Renin producing tumour,
  • Adrenal carcinoma,
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45
Q

what level are the kidneys? Which kidney is larger? How much size discrepancy is normal?

A

Level T12-L3,
Left larger than Right,
10% difference in size is normal.

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46
Q

What percentage of cardiac output reaches kidneys?

A

20-30%

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47
Q

what part of the LOH is high permeable to water?

A

(thin Loop of Henle) highly permeable to water;

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48
Q

Glomerular basement membrane structure

A

Capillary > endothelium > Basement membrane > podocyte

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49
Q

3 Factors affecting filtration through basement membrane

A

(1) Size <3nm
(2) charge negative (repels albumin),
(3) protein binding

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50
Q

When does GFR reach adult levels?

A

2 years of age

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51
Q

3 activators of renin-angiotensin system

A

Sympathetic nervous system;
hypotension / low RBF,
Oedema

52
Q

6 suppressors of renin-angiotensin

A 
Angiotensin 2; 
ADH; 
Hypernatraemia/Hyperkalaemia; 
NSAIDs; 
Betablockers; 
ACEi
53
Q

Renin-angiotensin system

A

renin (kidneys) converts angiotensinogen (liver) to angiotensin 1 which is then converted to angiotensin 2 (via ACE from lungs).

54
Q

6 Actions angiotensin 2

A

(1) systemic vasoconstriction
(2) Thirst
(3) ADH release
(4) Aldosterone release
(5) constriction efferent >afferent arterioles
(6) Proximal tubule sodium absorption

55
Q

what undergoes sodium co-transport in the proximal tubule?

A

Glucose, AA, lactate, Cl, Phos

56
Q

Actions Loop of Henle

A

countercurrent mechanism
thin descending loop = passive movement of water
thick ascending limb = active pump

Fluid changes from isotonic > hypertonic > hypotonic

57
Q

Action aldosterone

A

increase Na reabsorption

excretion K and H

58
Q

Actions ANP

A

triggered by hypertension tries to oppose it
dilates afferent and contracts efferent arterioles > Increased GFR and diuresis
inhibits aldosterone, renin, ADH

59
Q

Actions of PTH on kidney

A

increase Ca reabsorption and phosphate excretion

60
Q

Actions prostaglandins

A

dilate afferent arteriole

61
Q

Polyhydramnios associations

A

Maternal GDM,
GIT obstruction (TOF, atresia),
Increased output (Bartters, congenital Cl and Na diarrhoea),
CNS failed swallowing

62
Q

Raised AFP associated with

A

neural tube defect,
congenital nephrotic syndrome,
epidermolysis bullosa

63
Q

Radiology tests for renal function

A

MCU - PUV voiding dysfunction
DMSA (M=Meat) renal scarring,
DTPA (T=tubules) split renal function
MAG3 best for VUR

64
Q

What layers do nephrotic and nephritic syndrome affect?

A

Nephrotic - podocyte layer and GBM

Nephritic affects ALL layers hence haematuria, proteinuria, hypertension, AKI, oedema

65
Q

Diagnosis and bacteria in spontaneous peritonitis in nephrotic syndrome

A

strep pneumonia

Diagnosis = WCC >250, PMN>50, pH <7.35

66
Q

Features congenital nephrotic syndrome

A 
AR, NPHS1 gene, 
antenatal increase AFP, 
low birth weight and large placenta, 
heavy proteinuria, 
tubular dilatation with microcytic change, 
baby can have Potter syndrome

OR AR NPHS2 gene (podocin), presents 3-5 years of age with steroid resistant nephrotic syndrome.

67
Q

Most common cause of idiopathic nephrotic syndrome, features and treatment.

A 
Minimal change disease, 
2-3 years of age, 
NORMAL complement, 
treatment with steroids 90% respond, ACEi, 
2nd line cyclosporine, 
also immunisation, penicillin, aspirin
68
Q

What is definition of relapse of nephrotic syndrome?

A

2+ proteinuria for 3 days

69
Q

Features of FSGS

A 
Nephrotic syndrome, steroid resistant
>6yoa, 
tea coloured urine, proteinuria, 
glycosuria, 
IgM and C3
70
Q

Features masangiocapillary/membranoproliferative GN

A

Nephrotic syndrome,
Older child
LOW complement
Poor response to steroids

71
Q

Features membranous GN

A

Nephrotic syndrome
older children,
Associated Hep B, SLE, malignancy

72
Q

Most common causes haemanturia

A

Post strep GN

IgA nephropathy

73
Q

Acute glomerular injury pneumonic

A

HOOHUP - haemanturia, oligouria, oedema, hypertension, uraemia, proteinuria

74
Q

Rapidly progressive GN

A

ANCA,
Anti-GBM disease (Good pastures), Membranoproliferative GN
HSP
SLE

75
Q

Features thin BM disease

A

AD but no chronic issues in family

Excellent prognosis

76
Q

Features Good pastures

A

Anti GBM,
Older child
pulmonary renal syndrome

77
Q

Features Shunt nephritis

A

Due to staph aureus most,
Subacute
LOW complement

78
Q

Features Post Strep GN

A 
Group A beta haemolytic strep
2 weeks post throat infection
1 month weeks post skin infection, 
ASOT + 1 month, 
DNAase B + 2 months (more specific)
Resolves 2-3 weeks, 95% fully recover
Penecillin prevents spread to contacts
79
Q

Features SLE nephritis

A

teenagers,
females,
systemic = rash, oral ulcers, photosensitivity, arthritis, anti dsDNA +, renal, anaemia
Treat class 3-5 (3=focal glomerulosclerosis, 4=segmental/global proliferative nephritis, 5=nephrotic syndrome)
steroids>cyclophosphamide>ritixumab

80
Q

Types ANCA associated nephritis

A

(1) granulomatosis with polyangiitis cANCA
(2) churg strauss eosinophillic pANCA
(3) microscopic polyangitis pANCA
(4) polyarteritis nodosa
(5) takagasu arteritis

81
Q

differences between pre-renal and ATN

A

urine osmolality higher in pre-renal,
High urine Na in ATN
urine sediment is normal in pre-renal

82
Q

indications for dialysis

A 
hyperkalaemia, 
fluid overload resistant to frusemide, 
acidosis, 
urea >40, 
prolonged anuria, 
multi-system failure
83
Q

fractional excretion of sodium

A 
low is salt retaining, high if salt wasting 
100 x (sodium in urine x creatinine in plasma)/(sodium plasma x creatinine urine)
84
Q

features cystinosis

A

AR, cystine accumulation in lysosomes
hypophosphataemic rickets
growth failure
fanconi syndrome

85
Q

most common renal stones are?

A

calcium oxalate

86
Q

what factor is most important in managing persons with renal stones?

A

low salt diet - increase bone deposition and decreases calcium urine excretion

87
Q

causes hypercalciuria and hypercalcaemia

A 
hyperparathyroidism, 
vit D excess, 
immobilisation, 
hypophosphataemia, 
williams syndrome
88
Q

causes hypercalciuria and normocalcaemia

A 
idioapathic, 
immobilisation, 
medullary sponge kidney, 
drugs (frusemide, steroids), 
ketogenic diet, 
genetic
89
Q

what decreases calcium in urine

A

potassium and citrate

90
Q

features cystinuria

A

AR
urine hexagonal crystals,
raised COAL (cystine, ornithine,argentine,lysine) in urine,
treat with fluids, low salt, penecillamine, alkalinise the urine

91
Q

rhabdomyolysis features, and treatment

A

high CK, K, Phos, Ur, LOW Ca.

Treat with fluids and allopurinol

92
Q

conditions with cysts seen on USS of kidneys

A 
multicystic kidney disease (dysplastic) 
autosomal dominant kidney disease, 
renal cysts associated with diabetic syndromes (MODY 5)
simple cysts
Tuberous sclerosis
93
Q

features ADPCKD

A

PKD1/2,
cannot be excluded until 30 years of age,
cysts in other areas (liver), cerebral aneurysms, disease progression related to HTN.

94
Q

features ARPCKD

A

PKHD1,
Large kidneys hyper echoic
Potter syndrome (contractures, pulmonary hypoplasia, typical facies),
hepatic Caroli syndrome - intrahepatic bile duct dilatation, fibrosis

95
Q

features nephronophthisis

A 
Ciliopathy, tubular disorder
salt wasting > polydipsia, polyuria
Anaemia
Small smooth echogenic kidneys
growth failure
96
Q

features bardet biedl

A 
obesity, developmental delay
hypogonadism, 
polydactyly, 
Retinal problems
renal nephronophthisis 
can't even eat, can't even see, can't even think, can't even pee
97
Q

what immunosuppressives act in the S phase?

A

Prednisolone, Methotrexate, MMF, Azathioprine, cytarabine, doxorubicin, thioguanine

98
Q

What does Sirolimus act on

A

mTOR, G1 phase

99
Q

what immunosuppressives are cell cycle indepamdant

A

cyclophosphamide (alkylating agents)
Cisplatin
etoposide
ifosfamide

100
Q

What monoclonal antibodies act as TNF inhibitors?

A

Adalimumab,
Ertanecept,
Infliximab

101
Q

What monoclonal antibody acts on B cells?

A

Rituximab - Anti-CD20

102
Q

Tocilizumab action

A

anti-IL6

103
Q

Anakinra

A

Anti-IL1

104
Q

Basilixumab

A

Anti-CD25 Treg cells

105
Q

Multi-cyctic dysplastic kidney

A

No function
Contralateral kidney hypertrophy,
Low risk Wilms,
Nephrectomy cures hypertension.

106
Q

Horseshoe kidney associations

A 
VACTERL, 
Trisomies, 
fetal alcohol syndrome, 
infant diabetic mother. 
Associated renal carcinoma
107
Q

Imaging for PUJ obstruction

A

MAG 3 scan

108
Q

Posterior urethral valves

A

poor stream, bilateral dilatation
UTI male,
MCUG at diagnosis then DMSA + MCU 3 months.
Don’t use Foley catheter!!!

109
Q

Poor prognostic factors obstruction

A

oligohydramnios
hydronephrosis 100 after decompression
cortical cysts
diurnal incontinence >5yoa

110
Q

Prune belly syndrome features

A

absence abdominal wall muscles, megaureter/cysts,
Undescended testes
infertility
also other abnormalities

111
Q

antenatal hydronephrosis

A

APD >15mm = severe

APD >10mm = mod

112
Q

indications circumcision

A

balanitis obliterans,
paraphimosis,
recurrent balanitis/UTI,
phimosis failing steroid treatment

113
Q

complications circumcision

A

UTI, wound infection, stenosis

114
Q

contraindications to circumcision

A

hypospadia, micropenis, dorsal hood deformity

115
Q

How does pneumococcal cause HUS?

A

Produces Neuroimidase > T cell attack
Direct Coombs test +
Treat with Abx

116
Q

Pitfalls of GFR

A

screwed by tubules & more secreted as GFR falls (inaccurate, overestimates function)
creatnine doesn’t rise until <50% function

117
Q

actions prostaglandins

A

dilate afferent arteriole

118
Q

actions caffeine

A

dilates afferent arteriole

119
Q

actions calcium channel blockers

A

increase GFR > diuresis

120
Q

what is the strongest markers for chronic kidney disease?

A

proteinuria

121
Q

Indications for biopsy with Post Strep GN

A

Cr elevated at 6 weeks
Complement low at 3 weeks
Proteinuria ongoing at 6 weeks

122
Q

How to calculate plasma anion gap

A

(Na + K) - (Cl + Bicarb)
>14 abnormal

Normal Anion Gap
Addisons
GI losses
RTA

123
Q

Stones and chance of passage

A

5mm will pass
5-7mm 50% pass
7mm need to be removed

124
Q

what rise in creatnine is considered acceptable in chronic renal failure treated with ACEinhibitors

A

20-25%

125
Q

in obstructive uropathy what correlates with prognosis

A

Creatnine at 12 months

Renal (1 decks)

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