Renal Flashcards

1
Q

3 endocrine roles of the kidney

A

Renin (vasoconstriction as part of RAAS)

EPO

vit D metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What stimulates EPO?

A

hypoxia
anaemia
renal ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

When is EPO increased?

A

PKD and RCC

causes polycythaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When is EPO decreased?

A

CKD

causes normocytic normochromic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe metabolism of vit D

A

natural vit D (cholecalciferol) –> goes to liver, becomes 25(OH)D3 —> in proximal tubule, under 1a hydroxylase becomes 1,25 (OH)2 D3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is vit D needed for?

A

bone mineralisation

absorption of calcium and phosphate from gut

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What regulates the formation of 1,25 (OH)2 D3?

A

PTH, phosphate and negative feedback

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What causes agenesis of the kidney?

A
collecting duct (from ureteric buds) fails to fuse with nephrons (from metanephric mesoderm)
can be unilateral (or bilateral - Potter's syndrome -> death)

remaining kidney hypertrophies, may have abnormalities (hydronephrosis, malrotation)
renal function may be normal

often associated with other congenital abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are common problems with congenital kidney issues, eg hypoplasia, horse-shoe kidney?

A

Often issues with malrotation and prone to reflux, obstruction, infection and stones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 3 general causes of glomerulonephritis?

A

Hereditary (Alport’s, Fabry’s)
Primary
Secondary (SLE, DM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

5 levels of severity of glomerular disease

A
  1. asymptomatic haematuria/ proteinuria
  2. nephrotic syndrome
  3. nephritic syndrome
  4. rapidly progressive glomerulonephritis
  5. CKD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Clinical features of nephrotic syndrome

A

Proteinuria, hypoalbuminaemia, oedema, hyperlipidaemia (hepatic lipoprotein secondary to protein losses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical features of nephritic syndrome

A

Oliguria/ anuria, HTN, fluid retention, haematuria, uraemia, some proteinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Clinical features of rapidly-progressive glomerulonephritis?

A

Haematuria, oliguria, hypertension –> renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Examples of primary glomerulonephritis typically giving nephrotic syndrome

A

Minimal change disease

Membranous glomerulonephropathy

Focal segmental glomerulosclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Who usually gets minimal change disease?

A

typically kids under 6
seen on electron microscopy
cause unknown, maybe circulating immune-complexes

good prognosis in kids, variable in adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Most common cause of nephrotic syndrome in adults?

A

Membranous glomerulonephropathy

chronic - causes 40% nephrotic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is membranous glomerulonephropathy?

A

widespread glomerular basement thickening caused by Ig deposition - causes hyalinisation and death of individual nephrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Causes of membranous glomerulonephropathy

A

85% are idiopathic

secondary causes:
infections (hep B, malaria, syphilis)
tumours (melanoma, Ca bronchus, lymphoma)
drugs
systemic (SLE)

Prognosis depends on cause - 1/3 get CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Examples of primary glomerulonephritis typically giving nephritic syndrome

A

Berger’s disease (IgA nephropathy)
Rapidly progressive glomerulonephritis
Focal proliferative glomerulonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Most common cause of primary glomerulonephritis?

A

Berger’s

no effective treatment - 20% > CKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What causes Berger’s disease?

A

IgA nephropathy

usually affects young men after an URTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the causes of secondary glomerulonephritis?

A
Post-streptococcal GN
Non-strep GN
SLE
Henoch-Schonlein purpura
Bacterial endocarditis
Diabetic glomerulosclerosis
Amyloidosis
Goodpasture's syndrome
Microscopic polyarteritis nodosa
Wegener's granulomatosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

When does post-strep GN occur?

A

1-3 weeks after group A beta-haemolytic strep infection (tonsils, pharynx, skin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How is post-strep GN treated?

A

Conservative/ abx for remaining infection

Kids recover well but 40% adults develop HTN/ renal impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What % SLE have kidney involvement?

A

75% - often most significant of lesions

caused by immune-complex deposition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What causes HSP?

A

can follow URTI - immune-mediated systemic vasculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Which organs does HSP affect?

A

Skin (purpuric rash over legs, arms, arse)
Joints (pain)
Intestine (abdo pain, vomiting, bleeding)
Kidney (third develop lesions identical to IgA nephropathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How does bacterial endocarditis cause glomerulonephritis?

A

Emboli
Immune-complex deposition

Presents with haematuria and fluid retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Why can Alport’s not get Goodpasture’s?

A

Lack the Goodpasture’s antigen - abnormality of BM collagen IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Clinical features of Alport’s syndrome

A

ocular abnormalities - sensorineural deafness - renal failure

X-linked
(female carriers may have microscopic haematuria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Clinical features of Fabry’s syndrome

A

X-linked

metabolic defects due to missing enzyme
deposits accumulate in kidney, skin, vascular system (associated with angina + HF)
most die in 50s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does acute tubular necrosis present?

A

Cause of AKI - high mortality, full recovery with prompt fluid/ electrolytes and dialysis

34
Q

Causes of acute tubular necrosis

A

Ischaemic ATN
Toxic ATN
Rhabdomyolysis

35
Q

When does PKD present?

A

30-40 years

36
Q

What causes acquired cystic disease?

A

Dialysis

Small cysts throughout cortex and medulla

37
Q

Are simple renal cysts painful?

A

Only if haemorrhages

38
Q

Clinical features of AKI

A

Reduced renal function in days/ weeks

increased urea
increased creatinine
usually oliguria
usually reversible

39
Q

Dangerous consequences of AKI

A
Fluid overload/ pulm oedema
metabolic acidosis
high K+
high phosphate
low calcium (less marked than CKD)
low Na
40
Q

Causes of AKI

A
PRE-RENAL
reduced kidney perfusion
dehydration
shock
renal artery stenosis or emboli
NSAIDs and ACEi (impair renal autoreg)
RENAL
ATN
acute interstitial nephritis
glomerular disease
vascular disease
POST-RENAL
bladder outflow obstruction (BPH, strictures)
tumour (prostate, bladder, gynae)
stones (bilateral)
retroperitoneal fibrosis
41
Q

Who does NICE suggest have screening for CKD?

A

DM - HTN - CVD - obstruction - SLE - family hx - nephrotoxic drugs

42
Q

How is the increased risk of CVD managed in CKD?

A

lifestyle, statin, aspirin

43
Q

Indications for RRT in AKI

A

hyperkalaemia
pulmonary oedema
acidosis
uraemic pericarditis

44
Q

Where is the fistula usually for haemodialysis?

A

radial artery and cephalic vein

45
Q

Triad for presentation of renal cell carcinoma

A

loin pain
loin mass
haematuria

(rarely all 3)

46
Q

Example of osmotic diuretic. Where does it act?

A

Mannitol

Proximal tubule

47
Q

Example of loop diuretic

A

Furosemide, bumetanide

48
Q

How much stronger is bumetanide?

A

x40

49
Q

Example of thiazides/ thiazide-like diuretics. Where does it act?

A

Bendroflumethiazide
Thiazide-like: indapamide, chlortalidone
Distal tubule

50
Q

Example of potassium-sparing diuretics. Where does it act?

A

Amiloride: distal tubule
Spiro: collecting duct - alodosterone antagonist

51
Q

Indications for osmotic diuretic

A

Increase urine volume/ prevent anuria
Decrease ICP
Decrease intraocular pressures before opthalmic surgery

52
Q

Indications for loop diuretics

A

Relief of symptoms of fluid overload: pulm oedema, CHF, renal/ liver disease

53
Q

What side-effects can happen with high furosemide doses?

A

Tinnitus, hearing loss

54
Q

Indications for thiazides?

A

HTN only

55
Q

What should be avoided with thiazides?

A

Loop diuretics (hypokalaemia)

56
Q

ADRs thiazides

A

Low sodium

Exchange for K+ can lead to low potassium

57
Q

Indications for potassium-sparing diuretics?

A

Treatment of hypokalaemia from loop or thiazide therapy
(weak as diuretic alone)

Spiro also used in:

  • ascites and oedema due to liver cirrhosis
  • HF
  • primary HYPERaldosteronism
58
Q

In whom should potassium-sparing diuretics not be given?

A

severe renal impairment

hyperkalaemia

59
Q

ADRs of spiro?

A

hyperkalaemia
gynaecomastia
stevens-Johnson syndrome

60
Q

Normal urea

A

2.5 to 6.6

61
Q

Normal creatinine

A

60 to 120

creatinine is reciprocal relationship to GFR

62
Q

When is urea increased?

A

renal disease, dehydration, high protein intake

63
Q

Normal albumin

A

35 - 50

64
Q

When might you see hypoalbuminaemia and hyperalbuminaemia in renal disease?

A

Hypo: nephrotic syndrome

Hyper: dehydration

65
Q

When might Hb be affected in renal disease?

A

Decreased: chronic renal failure, blood loss

Increased: polycythaemia in renal tumours, renal cysts

66
Q

Normal eGFR

A

Above 90

67
Q

What should always be done in suspected UTI?

A

Urine culture

> 100, 000 CFU/mL is diagnostic (otherwise prob contamination of sample)

68
Q

When might urine be brown?

A

Concentrated cholestatic jaundice

69
Q

What can discolour urine making it appear to be haematuria?

A

Beetroot
Myoglobinuria
Porphyria
Phenolphthalein

70
Q

eGFR in end-stage renal failure

A

less than 15

71
Q

How to calculate anion gap?

A

[Na] - [Cl] + [HCO3]

72
Q

What is MUDPILES?

A

Causes of high anion gap metabolic acidosis

Methanol
Uraemia
DKA
Paraldehyde
Isoniazid
Lactic acidosis
Ethylene glycol
Salicylates
73
Q

Causes of bilat enlarged kidneys

A

APKD
bilateral hydronephrosis
amyloidosis

74
Q

causes of unilateral enlarged kidney

A

hydronephrosis
renal ca
renal cyst

75
Q

cannonball mets associated with

A

RCC most common

76
Q

contraindications catheter insertion

A

Trauma patient with suspected urethral injury as evidenced by:
Blood at the urethral meatus
High-riding prostate on rectal examination
Penile, scrotal, perineal hematoma
Radiographic evidence of urethral/bladder trauma (in many centers a gentle attempt at urethral catherisation by an experienced doctor is accepted practice)
Postoperative urological patients. Always consult the urologist first if the patient has had bladder neck or prostate surgery.
Known stricture or ‘impossible insertion‘ last time

77
Q

What is haemolytic uraemic syndrome?
Cause?
Ix?
mx?

A

combination of haemolysis with red cell fragmentation, thrombocytopenia, acute renal failure
caused post-infections, esp E.coli
FBC, blood film, u&e
mx supportively: fluids/ transfusion - may need dialysis

78
Q

how is contrast-induced nephropathy managed?

A

fluid bolus

79
Q

define aki

A

creatinine x1.5

fall in urine to 0.5 mL/kg/h for 6h+ in adults

80
Q

what should pregnant patients be offered for stones?

A

uteroscopy