Renal Learning Points CSV Flashcards

(125 cards)

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
What are the bacteria in bacterial peritonitis in a child with PD? Antibiotics?
Treat if WBC >50 and symptomatic or WBC >100 Bacteria = staph epi, staph aureus Antibiotics = Cefazolin, ceftazidime OR vancomycin & ciprofloxacin
26
Causes of PD peritonitis
1. Intraluminal (touch contamination), 2. Periluminal (tunnel infections), 3. Intestinal translocation 4. Systemic, 5 Ascending (rare)
27
Benefits transplant over dialysis
1. Mortality, 2. CVD, 3. Growth, 4. Neurodevelopment, 5. QOL
28
Absolute contraindications to renal transplant
1. active malignancy, 2. severe neurological dysfunction, 3. terminal illness / multiorgan failure, 4. psychiatric illness impairing consent
29
6 causes of allograft dysfunction
1. Dehydration, 2. Medication 3. Infection, 4. Obstruction 5. Rejection (biopsy) 6. Perfusion problem
30
Hypertension Treatment post renal transplant
Ca channel blockers (early), Diuretics (if hypervolaemic) ACEi once 2-3 months post t/p
31
Tacrolimus SE
``` nephrotoxicity, HTN, hepatic dysfunction, glucose intolerance, hyperkalaemia, hypomagnesaemia, alopecia ```
32
Tacrolimus mechanism of action
calcineurin inhibitor > inhibits nuclear activation
33
Cyclosporin SE
neprotoxicity, HTN, gigival hyperplasia, hirsutism, hyperuricaemia, hypercholestoraemia
34
Pulmonary renal syndrome causes
``` [Pneumonic AA STD] - Anti-GBM, ANCA, SLE, Thrombotic disease (antiphospholipid, TTP, HSP), Drugs ```
35
RIFLE criteria
``` For renal insult - Risk dysfunction (Crx1.5), Injury (Crx2), Failure (Crx3), Loss (>4weeks), ESKD (>3months) ```
36
Causes hypochloraemic metabolic acidosis
``` pyloric stenosis, prolonged vomiting, diuretics, Bartter, CF, Choride diarrhoea ```
37
RTA type 1
``` DISTAL, can’t excrete acid, hypercalciuria (stones), urine is alkaline (ph >5.5) loin pain Low K CAUSES: obstructive uropathy, marfan, wilsons, drugs (amphotericin) ```
38
RTA type 2
PROXIMAL, can’t resorb bicarb, hypercalcaemia / low calcium in urine acidic urine (pH <5.5) Low K CAUSES: cystinosis, fanconi
39
Fanconi
``` 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 ```
40
RTA type 4
normal urine anion gap, hyper aldosteronism High K, Low Na CAUSES: CAH, tacro, NSAIDS, tubular aldosterone def
41
Bartter Syndrome
``` Na/K/2Cl Channel defect in LOH - hypochloraemic hypokalaemic metabolic alkalosis Hypercalciruia, hyperchloride uria Prone to hypernatraemic dehydration Manage with NSAIDS > slow GFR ```
42
Gitelman syndrome
NaCl defect in distal tubule hyPOcalciuria present later in childhood with cramps - LOW Mg
43
metabolic alkalosis with volume contraction (normal/low BP)
``` ABCD - Anorexic (vomiting/laxatives), Bartter, CF, Diuretics. ```
44
metabolic alkalosis with volume expansion (high BP)
Anything that activates RAAS: - Aldosteronism, - Renal artery stenosis, - Renin producing tumour, - Adrenal carcinoma,
45
what level are the kidneys? Which kidney is larger? How much size discrepancy is normal?
Level T12-L3, Left larger than Right, 10% difference in size is normal.
46
What percentage of cardiac output reaches kidneys?
20-30%
47
what part of the LOH is high permeable to water?
(thin Loop of Henle) highly permeable to water;
48
Glomerular basement membrane structure
Capillary > endothelium > Basement membrane > podocyte
49
3 Factors affecting filtration through basement membrane
(1) Size <3nm (2) charge negative (repels albumin), (3) protein binding
50
When does GFR reach adult levels?
2 years of age
51
3 activators of renin-angiotensin system
Sympathetic nervous system; hypotension / low RBF, Oedema
52
6 suppressors of renin-angiotensin
``` Angiotensin 2; ADH; Hypernatraemia/Hyperkalaemia; NSAIDs; Betablockers; ACEi ```
53
Renin-angiotensin system
renin (kidneys) converts angiotensinogen (liver) to angiotensin 1 which is then converted to angiotensin 2 (via ACE from lungs).
54
6 Actions angiotensin 2
(1) systemic vasoconstriction (2) Thirst (3) ADH release (4) Aldosterone release (5) constriction efferent >afferent arterioles (6) Proximal tubule sodium absorption
55
what undergoes sodium co-transport in the proximal tubule?
Glucose, AA, lactate, Cl, Phos
56
Actions Loop of Henle
countercurrent mechanism thin descending loop = passive movement of water thick ascending limb = active pump Fluid changes from isotonic > hypertonic > hypotonic
57
Action aldosterone
increase Na reabsorption | excretion K and H
58
Actions ANP
triggered by hypertension tries to oppose it dilates afferent and contracts efferent arterioles > Increased GFR and diuresis inhibits aldosterone, renin, ADH
59
Actions of PTH on kidney
increase Ca reabsorption and phosphate excretion
60
Actions prostaglandins
dilate afferent arteriole
61
Polyhydramnios associations
Maternal GDM, GIT obstruction (TOF, atresia), Increased output (Bartters, congenital Cl and Na diarrhoea), CNS failed swallowing
62
Raised AFP associated with
neural tube defect, congenital nephrotic syndrome, epidermolysis bullosa
63
Radiology tests for renal function
MCU - PUV voiding dysfunction DMSA (M=Meat) renal scarring, DTPA (T=tubules) split renal function MAG3 best for VUR
64
What layers do nephrotic and nephritic syndrome affect?
Nephrotic - podocyte layer and GBM Nephritic affects ALL layers hence haematuria, proteinuria, hypertension, AKI, oedema
65
Diagnosis and bacteria in spontaneous peritonitis in nephrotic syndrome
strep pneumonia | Diagnosis = WCC >250, PMN>50, pH <7.35
66
Features congenital nephrotic syndrome
``` 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
Most common cause of idiopathic nephrotic syndrome, features and treatment.
``` Minimal change disease, 2-3 years of age, NORMAL complement, treatment with steroids 90% respond, ACEi, 2nd line cyclosporine, also immunisation, penicillin, aspirin ```
68
What is definition of relapse of nephrotic syndrome?
2+ proteinuria for 3 days
69
Features of FSGS
``` Nephrotic syndrome, steroid resistant >6yoa, tea coloured urine, proteinuria, glycosuria, IgM and C3 ```
70
Features masangiocapillary/membranoproliferative GN
Nephrotic syndrome, Older child LOW complement Poor response to steroids
71
Features membranous GN
Nephrotic syndrome older children, Associated Hep B, SLE, malignancy
72
Most common causes haemanturia
Post strep GN | IgA nephropathy
73
Acute glomerular injury pneumonic
HOOHUP - haemanturia, oligouria, oedema, hypertension, uraemia, proteinuria
74
Rapidly progressive GN
ANCA, Anti-GBM disease (Good pastures), Membranoproliferative GN HSP SLE
75
Features thin BM disease
AD but no chronic issues in family | Excellent prognosis
76
Features Good pastures
Anti GBM, Older child pulmonary renal syndrome
77
Features Shunt nephritis
Due to staph aureus most, Subacute LOW complement
78
Features Post Strep GN
``` 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
Features SLE nephritis
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
Types ANCA associated nephritis
(1) granulomatosis with polyangiitis cANCA (2) churg strauss eosinophillic pANCA (3) microscopic polyangitis pANCA (4) polyarteritis nodosa (5) takagasu arteritis
81
differences between pre-renal and ATN
urine osmolality higher in pre-renal, High urine Na in ATN urine sediment is normal in pre-renal
82
indications for dialysis
``` hyperkalaemia, fluid overload resistant to frusemide, acidosis, urea >40, prolonged anuria, multi-system failure ```
83
fractional excretion of sodium
``` low is salt retaining, high if salt wasting 100 x (sodium in urine x creatinine in plasma)/(sodium plasma x creatinine urine) ```
84
features cystinosis
AR, cystine accumulation in lysosomes hypophosphataemic rickets growth failure fanconi syndrome
85
most common renal stones are?
calcium oxalate
86
what factor is most important in managing persons with renal stones?
low salt diet - increase bone deposition and decreases calcium urine excretion
87
causes hypercalciuria and hypercalcaemia
``` hyperparathyroidism, vit D excess, immobilisation, hypophosphataemia, williams syndrome ```
88
causes hypercalciuria and normocalcaemia
``` idioapathic, immobilisation, medullary sponge kidney, drugs (frusemide, steroids), ketogenic diet, genetic ```
89
what decreases calcium in urine
potassium and citrate
90
features cystinuria
AR urine hexagonal crystals, raised COAL (cystine, ornithine,argentine,lysine) in urine, treat with fluids, low salt, penecillamine, alkalinise the urine
91
rhabdomyolysis features, and treatment
high CK, K, Phos, Ur, LOW Ca. | Treat with fluids and allopurinol
92
conditions with cysts seen on USS of kidneys
``` multicystic kidney disease (dysplastic) autosomal dominant kidney disease, renal cysts associated with diabetic syndromes (MODY 5) simple cysts Tuberous sclerosis ```
93
features ADPCKD
PKD1/2, cannot be excluded until 30 years of age, cysts in other areas (liver), cerebral aneurysms, disease progression related to HTN.
94
features ARPCKD
PKHD1, Large kidneys hyper echoic Potter syndrome (contractures, pulmonary hypoplasia, typical facies), hepatic Caroli syndrome - intrahepatic bile duct dilatation, fibrosis
95
features nephronophthisis
``` Ciliopathy, tubular disorder salt wasting > polydipsia, polyuria Anaemia Small smooth echogenic kidneys growth failure ```
96
features bardet biedl
``` 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
what immunosuppressives act in the S phase?
Prednisolone, Methotrexate, MMF, Azathioprine, cytarabine, doxorubicin, thioguanine
98
What does Sirolimus act on
mTOR, G1 phase
99
what immunosuppressives are cell cycle indepamdant
cyclophosphamide (alkylating agents) Cisplatin etoposide ifosfamide
100
What monoclonal antibodies act as TNF inhibitors?
Adalimumab, Ertanecept, Infliximab
101
What monoclonal antibody acts on B cells?
Rituximab - Anti-CD20
102
Tocilizumab action
anti-IL6
103
Anakinra
Anti-IL1
104
Basilixumab
Anti-CD25 Treg cells
105
Multi-cyctic dysplastic kidney
No function Contralateral kidney hypertrophy, Low risk Wilms, Nephrectomy cures hypertension.
106
Horseshoe kidney associations
``` VACTERL, Trisomies, fetal alcohol syndrome, infant diabetic mother. Associated renal carcinoma ```
107
Imaging for PUJ obstruction
MAG 3 scan
108
Posterior urethral valves
poor stream, bilateral dilatation UTI male, MCUG at diagnosis then DMSA + MCU 3 months. Don't use Foley catheter!!!
109
Poor prognostic factors obstruction
oligohydramnios hydronephrosis 100 after decompression cortical cysts diurnal incontinence >5yoa
110
Prune belly syndrome features
absence abdominal wall muscles, megaureter/cysts, Undescended testes infertility also other abnormalities
111
antenatal hydronephrosis
APD >15mm = severe | APD >10mm = mod
112
indications circumcision
balanitis obliterans, paraphimosis, recurrent balanitis/UTI, phimosis failing steroid treatment
113
complications circumcision
UTI, wound infection, stenosis
114
contraindications to circumcision
hypospadia, micropenis, dorsal hood deformity
115
How does pneumococcal cause HUS?
Produces Neuroimidase > T cell attack Direct Coombs test + Treat with Abx
116
Pitfalls of GFR
screwed by tubules & more secreted as GFR falls (inaccurate, overestimates function) creatnine doesn't rise until <50% function
117
actions prostaglandins
dilate afferent arteriole
118
actions caffeine
dilates afferent arteriole
119
actions calcium channel blockers
increase GFR > diuresis
120
what is the strongest markers for chronic kidney disease?
proteinuria
121
Indications for biopsy with Post Strep GN
Cr elevated at 6 weeks Complement low at 3 weeks Proteinuria ongoing at 6 weeks
122
How to calculate plasma anion gap
(Na + K) - (Cl + Bicarb) >14 abnormal Normal Anion Gap Addisons GI losses RTA
123
Stones and chance of passage
5mm will pass 5-7mm 50% pass 7mm need to be removed
124
what rise in creatnine is considered acceptable in chronic renal failure treated with ACEinhibitors
20-25%
125
in obstructive uropathy what correlates with prognosis
Creatnine at 12 months