Renal Flashcards

1
Q

UTI

Definitions (6)

A

Bacteriuria: bacteria in the urine, may be asymptomatic or symptomatic
UTI: presence of a pure growth of >10^5 organisms per ml of fresh MSU
Lower UTI: urethra (urethritis), bladder (cystitis), prostate (prostatitis)
Upper UTI: renal pelvis (pyelonephritis)
Pyuria: presence of pus cells in urine, inflammatory response
Sterile pyuria: -ve culture but +ve pus (eg. undeclared antibiotics, renal TB, GU infections, stones/malignancy)

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

UTI

Aetiology (3)

A

Mostly E.coli
Proteus mirabilis
Klebsiella pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
UTI 
Risk factors (8)
A

Female: short urethra and close to rectum
Trauma to female urethra in sex/birth
Pregnancy: progesterone dilates ureters and pressure from fetus
Anatomical: VUR, pelvi-ureteric junction obstruction, chronic retention
Pre-existing renal conditions: renal cysts, parenchymal damage, stones
Spermicide activity
Immunosuppression
Foreign body: catheter, cystoscopy, stent

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

UTI

Uncomplicated (3)

A

Healthy, young, sexually active women
E.coli or Staph saprophyticus
Require no further investigation

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

UTI

Complicated (8)

A
In children 
In men 
In patients with abnormal renal tract 
In immunosuppressed 
In patients with foreign body in renal tract 
Bladder tumour 
Chronic retention 
Abnormal bladder outflow tract (BPH, urethral stricture, phimosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

UTI

Symptoms (9)

A
Dysuria 
Frequency 
Urgency 
Haematuria 
Suprapubic pain 
Fever
Hesitancy 
Nocturia
Pyelonephritis: fever, rigors, N&V, back and flank pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

UTI

Signs (3)

A

Fever
Abdominal/loin tenderness
Foul-smelling urine

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

UTI

Investigations (5)

A

Urinalysis: no further investigation if +ve for nitrites and leucocytes (uncomplicated)
Urine MC&S of MSSU: bacteria, WBC, RBC (send immediately if male, child, immunosuppressed)- diagnostic >10^5
Culture for antibiotic sensitivity
Bloods: FBC, U&E, CRP, cultures if systemic unwell
Imaging: USS + referral to urology if child/man/no treatment response/recurrent/pyelonephritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
UTI 
Dipstick testing (6)
A

Nitrate (metabolic byproduct of bacteria)
Protein (sign of inflammation)
Leucocytes (marker of inflammation)
If all 3 are positive- empirical therapy
If leucocytes only positive- doesn’t diagnose or exclude, urine culture recommended
Blood/protein in absence of nitrate/leucocytes should be further investigated

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

UTI

Treatment in women (4)

A

Trimethoprim/nitrofurantoin for 3-6 days
2nd line amoxicillin or co-amoxiclav
If no response do urine culture
If upper UTI: co-amoxiclav IV then oral when afebrile

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

UTI

Treatment in pregnant women (2)

A

Any bacteriuria treat with antibiotic (nitrofurantoin safe)

Dipstick and culture repeated at each antenatal visit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

UTI

Treatment in men (2)

A

If fail to respond to antibiotic must refer to urologist as is often due to anomaly in anatomy/function
Quinolone eg. ciprafloxacin

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

UTI

Treatment of acute pyelonephritis (2)

A

Ciprofloxacin for 7 days

Consider admission for IV co-amoxiclav and gentamicin in 1st 48h if vomiting or septic

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

AKI

Definition (2)

A

Rise in serum creatinine >26 in 48h or rise in creatinine >1.5x baseline or urine output <0.5ml/kg/h for >6h (consecutive hours)
Leads to a failure to maintain fluid, electrolyte and acid-base homeostasis

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

AKI

Pre-renal causes (3)

A
40-70% of cases, due to renal hypoperfusion 
Hypotension (due to hypovolaemia, sepsis, over diuresis) 
Renovascular disease (eg. renal artery stenosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

AKI

Intrinsic renal causes (5)

A

10-50% of cases, due to direct parenchymal injury and may require renal biopsy for diagnosis
Acute tubular necrosis: commonest, often result of pre-renal damage or nephrotoxins eg. drugs (gentamicin, NSAIDs, ACE-i, lithium), contrast and myoglobinuria in rhabdomyolysis
Glomerular: primary glomerulonephhritis, SLE, drugs, infections
Interstitial: drugs, lymphoma infiltration, tumour lysis syndrome
Vascular: vasculitis, malignant hypertension, cholesterol emboli

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

AKI

Post-renal causes (4)

A

10-25% of cases, caused by obstruction
Luminal: stones, clots
Mural: malignancy (eg. ureteric, bladder, prostate), BPH, strictures
Extrinsic compression: malignancy, retroperitoneal fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q
AKI 
Risk factors (8)
A
>75 
CKD 
Heart failure 
Peripheral vascular disease 
Diabetes 
Drugs/other nephrotoxins (especially recently started) 
Sepsis 
Poor fluid intake or increased losses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

AKI

Signs + symptoms (10)

A

May be asymptomatic
Systemic: rash, arthralgia, fever
Haemoptysis (vasculitis/anti-GBM disease)
LUTS or anuria (obstruction)
Red-brown urine (rhabdomyolysis)
Fluid overload: hypertension, elevated JVP, lung crackles, peripheral oedema
Fluid deplete: reduced urine volume, non-visible JVP, poor turgor
Palpable percussible bladder or pelvic/abdominal mass (obstruction)
Palpable kidneys (polycystic)
Renal bruits (renovascular disease)

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

AKI

Investigations (9)

A

U&E + creatinine: assess severity
Urine: urinalysis (nitrites- infection, protein- intrinsic renal, leucocytes- acute interstitial nephritis, blood- glomerulonephritis), Na concentration (low if pre-renal, high in acute tubular necrosis), Bence Jones protein (exclude myeloma)
ECG: exclude hyperkalaemia
VBG: exclude hyperkalaemia
FBC + film: exclude HUS
Anti-dsDNA and ANA: SLE
Urea:creatinine ratio (>100:1= pre renal, <40:1= intrinsic)
Renal USS: obstruction, hydronephrosis, cysts
ABG: acid-base balance

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

AKI

Classification (3)

A

Stage 1: creatinine increases >1.5x baseline, <0.5ml/kg/h urine output for >6 consecutive hours
Stage 2: serum creatinine rises 2-2.9x baseline, <0.5ml/kg/h urine for >12 hours
Stage 3: serum creatinine >3x baseline or commenced on RRT, <0.3ml/kg/h urine for >24 hours or anuria for 12h

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

AKI

Treatment (6)

A

Fluid therapy
Stop nephrotoxic drugs
Treat pre-renal causes: correct volume depletion, treat sepsis
Treat intrinsic causes: refer
Treat post-renal causes: catheterise if obstruction, consider retrograde stents or insertion of nephrostomy
RRT if complications or drug overdose

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

AKI

Indications for RRT (5)

A

Pulmonary oedema
Persistent hyperkalaemia
Severe metabolic acidosis
Uraemic complications eg. encephalopathy or pericarditis
Drug overdose- BLAST (Barbiturates, Lithium, Alcohol, Salicylates, Theophyline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

CKD

Definition (2)

A

Impaired renal function for >3 months based on abnormal structure/function or GFR <60 for >3 months without evidence of kidney damage
End-stage renal failure: GFR <15 or need for RRT

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

CKD

Aetiology (6)

A
Diabetes 
Glomerulonephritis: usually IgA 
Hypertension 
Renovascular disease 
Pyelonephritis 
Polycystic kidney disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

CKD

Pathology (2)

A

Renal injury causes kidney to adapt to nephron loss by increasing intraglomerular pressure to maintain filtration
Glomerulus becomes more permeable to molecules causing mesangial cell expansion, fibrosis and glomerular scarring

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

CKD

Pathology of complications (5)

A

Anaemia: low erythropoietin production by kidney interstitial fibroblasts leads to lack of RBC growth
Renal osteodystrophy: kidney is site of phosphate excretion and hydroxylation of vit D, low levels of 1,25 dihydroxyvitamin D occurs due to renal scarring and reduced phosphate levels leads to hyperphosphataemia, this causes hypocalcaemia and huge increase in PTH, promoting calcium resorption, changing bones
Cardiovascular risk: hypertension, high lipids, high phosphate
Hyperlipidaemia: reduced lipoprotein lipase and hepatic triglyceride lipase = less lipid uptake
Malnutrition: altered metabolism of protein, water, salt and potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q
CKD
Risk factors (8)
A
Nephrotoxins 
Diabetes 
Hypertension 
Cardiovascular disease 
Structural renal disease, stones or BPH 
Recurrent UTI/childhood history of vesicoureteric reflux 
Multisystem disease such as SLE 
Family history of ESRF or known hereditary disease eg. PKD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

CKD

Signs + symptoms (6)

A
Usually asymptomatic until stage 4/5 
Uraemia: anorexia, vomiting, restless legs, fatigue, weakness, pruritus, bone pain 
Amenorrhoea/impotence 
Oliguria 
Dyspnoea 
Ankle swelling
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

CKD

Investigations (4)

A

Blood: Hb (normochromic normocytic anaemia), U&E, creatinine, glucose, Ca (low), phosphate (high), alk phos (high- renal osteodystrophy), PTH (high if >stage 3)
Urine: urinalysis (proteinuria, haematuria), MC&S (exclude UTI), albumin:creatinine ratio
Ultrasound: check size and anatomy, usually small (<9cm) in CKD but may be enlarged in amyloid, myeloma, APKD, DM
Renal biopsy if rapidly progressive or if unclear cause and normal sized kidneys

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

CKD

Staging (6)

A

Stage 1: GFR >90 (normal/high GFR but other evidence of renal damage)
Stage 2: GFR 60-89
Stage 3A: GFR 45-59
Stage 3B: GFR 30-44
Stage 4: GFR 15-29
Stage 5: GFR <15 (established renal failure)

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

CKD

Treatment of reversible causes (4)

A

Relieve obstruction
Stop nephrotoxins
Address cardiovascular risk factors
Tight glucose control in diabetes

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

CKD

Treatment to limit progression and complications (3)

A

BP: target <130/90 use ACE-i or ARB
Renal bone disease: check PTH and treat if raised (eg. calcitriol and alfacalcidol), restrict phosphate and give binders (eg. Calcichew)
Cardiovascular modification: statins and aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

CKD

Treatment to control symptoms (5)

A

Anaemia: replace iron/B12/folate if necessary, consider recombinant human erythropoietin if still anaemic
Acidosis: consider sodium bicarbonate supplements if low serum bicarbonate
Oedema: high dose loop diuretics and fluid and sodium restriction
Restless leg: clonazepam/gabapentin
RRT if GFR 8-10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q
Haemodialysis
Mechanism (4)
A

Blood is passed over a semi-permeable membrane against dialysis fluid flowing in the opposite direction
Thus blood is always meeting a less concentrated solution and diffusion of small solutes occurs down the concentration gradient
Larger solutes don’t clear as effectively
Ultrafiltration creates a negative transmembrane pressure to clear excess fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Haemodialysis

Problems (4)

A

Disequilibration syndrome
Hypotension
Time consuming
Access problems (AV fistula: thrombosis/stenosis, tunnelled venous access line: infection/blockage/recirculation of blood)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q
Haemofiltration
Mechanism (3)
A

Blood filtered across a highly permeable membrane
Allowing movement of small and large solutes by convection at almost the same rate
The ultrafiltrate is replaced with an equal volume of fluid, so there is less haemodynamic instability

38
Q

Haemofiltration

Use (2)

A

Critically ill patients

Impractical as long-term RRT as it takes much longer than haemodialysis to achieve the same clearance

39
Q

Peritoneal Dialysis

Mechanism (5)

A

Uses the peritoneum as a semi-permeable membrane
Catheter inserted into peritoneal cavity and fluid infused
Allows solutes to diffuse slowly across
Ultrafiltration by adding osmotic agent eg. glucose
Simple to perform, can be carried out continuously and at home, so allows freedom

40
Q

Peritoneal Dialysis

Problems (3)

A

PD peritonitis
Exit site infection
Loss of membrane function over time

41
Q
Kidney Transplant
Absolute contraindications (3)
A

Active infection
Cancer
Severe comorbidity

42
Q

Kidney Transplant

Types of graft (3)

A

DCD: donor after cardiac death, high risk of delayed graft function due to long warm ischaemic time
DBD: donor after brainstem death, much reduced risk of delayed graft function
LD: living donor grafts, planned surgery and minimal ischaemic time, related/unrelated

43
Q

Kidney Transplant

Immunosuppression (2)

A

Induction: basiliximab/alemtuzumab
Maintenance: triple therapy- calcineurin inhibitor (tacrolimus), antimetabolite (mycophenalate) and prednisolone

44
Q

Kidney Transplant

Complications (6)

A

Delayed graft function (affects approx. 40%)
Rejection (acute/chronic)
New onset diabetes after transplant
Increased infection risk
Increased malignancy risk, particularly skin and viral associated
Cardiovascular disease (increased bP in >50% of transplant patients)

45
Q

Glomerulonephritis

Pathology (4)

A

Inflammation of glomerulus and nephrons
Damage to the glomerulus restricts blood flow, leading to a compensatory rise in BP
Damage to filtration mechanism allows protein and blood to enter the urine
Loss of the usual filtration capacity leads to AKI

46
Q

Glomerulonephritis

Presentation (2)

A

Nephrotic syndrome: BP- normal to mildly high, urine- proteinuria, GFR- normal to mildly low
Nephritic syndrome: BP- moderate to severely high, urine- haematuria, GFR- moderately to severely low

47
Q

Glomerulonephritis

Causes (4)

A

Primary causes of nephrotic syndrome: membranous, minimal change, FSGC, mesangiocapillary
Secondary causes of nephrotic syndrome: diabetes, SLE (class V nephritis), amyloid, hep B/C
Primary causes of nephritic syndrome: IgA nephropathy, mesangiocapillary
Secondary causes of nephritic syndrome: post-Streptococcal, vasculitis, SLE nephritis, anti-GBM

48
Q

Glomerulonephritis

Investigations (10)

A

Blood: FBC, U&E, LFT, ESR, CRP
Immunoglobulines
Electrophoresis
Complement (C3+C4)- sign of inflammation (SLE)
Autoantibodies: ANA, ANCA, anti-dsDNA, anti-GBM
HBV & HCV serology
Urine: RBC casts, MC&S, Bence Jones protein, ACR
CXR
Renal ultrasound
Renal biopsy: what is affected (mesangial cells, capillaries, basement membrane, endothelium), how much kidney involved (focal vs diffuse), how much glomerulus involved (segmental vs global)

49
Q
Nephrotic Syndrome 
Primary causes (4)
A

Membranous glomerulonephritis
Minimal change disease
Focal segmental glomerulosclerosis
Mesangiocapillary glomerulonephritis

50
Q
Nephrotic Syndrome 
Secondary causes (5)
A
Hep B/C
SLE (class V lupus nephritis) 
Diabetic nephropathy 
Amyloidosis (myeloma) 
Drug related (NSAIDs, penicillamine, anti-TNF)
51
Q

Nephrotic Syndrome

Signs + symptoms (2)

A

Classic triad: proteinuria, hypoalbuminaemia, oedema Hyperlipidaemia

52
Q
Nephrotic Syndrome 
General treatment (4)
A

Reduce oedema: loop diuretics and fluid restriction and salt restriction
Reduce proteinuria: ACE-i or ARB for all patients
Reduce risk of complications: anticoagulate if large proteinuria, statin to reduce cholesterol, treat infections promptly and vaccinate
Treat underlying cause

53
Q
Nephrotic Syndrome 
Membranous nephropathy (3)
A

20-30% of nephrotic syndrome in adults
Mostly idiopathic but can be associated with malignancy, hep B, drugs (penicillamine, NSAIDs) and autoimmunity (thyroid, SLE)
On biopsy: diffusely thickened GBM with IgG and C3 deposits

54
Q

Nephrotic Syndrome

Minimal change disease (4)

A

Commonest cause in children
Rapid onset oedema
Normal biopsy
Treat with steroids

55
Q

Nephrotic Syndrome

Focal segmental glomerulosclerosis (2)

A

May be primary or secondary (vesicoureteric reflux, IgA nephropathy, Alport’s syndrome, vasculitis)
Biopsy: glomeruli have scarring at certain segments with IgM and C3 deposits on immunofluorescence

56
Q
Nephrotic Syndrome 
Mesangiocapillary glomerulonephritis (3)
A

Immune complex mediated or complement mediated
Biopsy: thickened capillary basement membrane, mesangial and endocapillary proliferation
Overlapping nephrotic and nephritic syndromes

57
Q
Nephritic Syndrome 
Primary causes (2)
A

IgA nephropathy

Mesangiocapillary glomerulonephritis

58
Q
Nephritic Syndrome 
Secondary causes (4)
A

Post streptococcal
Vasculitis
SLE (lupus nephritis- except class V)
Anti-GBM disease (Goodpasture’s disease)

59
Q

Nephritic Syndrome

Signs + symptoms (1)

A

Classic triad: hypertension, haematuria, mild proteinuria

60
Q
Nephritic Syndrome 
IgA nephropathy (3)
A

Commonest cause of glomerulonephritis
Presentation: macro/microscopic haematuria, occasionally nephritic syndrome, usually young person following a recent URTI
Biopsy: mesangial proliferation, IgA + C3 deposits

61
Q

Nephritic Syndrome

Henoch-Schonlein Purpura (2)

A

Systemic variant of IgA nephropathy causing a small vessel vasculitis
Presentation: purpuric rash on extensor surfaces, polyarthritis, nephritic syndrome

62
Q

Nephritic Syndrome

Anti-GBM disease (3)

A

Caused by autoantibodies to type IV collagen (which is a component of the GBM)
AKI may occur within days of symptom onset (it is a type of rapidly progressive glomerulonephritis)
Treat with plasma exchange and immunosuppression

63
Q

Nephritic Syndrome

Post-streptococcal glomerulonephritis (3)

A

Diffuse proliferative glomerulonephritis
Occurs 1-12 weeks after a sore throat or skin infection
A streptococcal antigen is deposited on the glomerulus, causing a host reaction and formation of immune complex

64
Q

Acute Interstitial Nephritis

Aetiology (5)

A

Mediated by an immune reaction to drugs, infections or autoimmune disorders
Drugs: NSAIDs, antibiotics, diuretics, allopurinol, omeprazole, phenytoin
Infections: Staph, Strep, Brucella
Autoimmune: SLE, sarcoidosis
Idiopathic

65
Q

Acute Interstitial Nephritis

Pathology (1)

A

Acute inflammation of the renal interstitium, often a hypersensitivity reaction

66
Q

Acute Interstitial Nephritis

Signs + symptoms (4)

A

Usually just mild renal impairment
High BP
Oliguria
Drugs reactions: often ‘allergic’ picture with fever, rash and eosinophilia

67
Q

Acute Interstitial Nephritis

Treatment (2)

A

Stop/treat cause/causative agent

Trial of prednisolone if renal function slow to improve

68
Q

Chronic Interstitial Nephritis

Aetiology (3)

A

Structural: reflex nephropathy, cystic kidney disease
Drugs: NSAIDs
Haematological: myeloma, sickle cell disease

69
Q

Chronic Interstitial Nephritis

Pathology (1)

A

Chronic inflammation of the renal interstitium

70
Q

Chronic Interstitial Nephritis

Signs + symptoms (3)

A

Often asymptomatic
Painless haematuria
Signs of CKD

71
Q
Rhabdomyolysis 
Aetiology (9)
A
Post ischaemia: embolism, clamped artery
Prolonged immobilisation 
Burns 
Crush injury 
Excessive exercise 
Infection: EBC, influenza 
Drugs/toxins: statins, alcohol, ecstasy, heroin 
Metabolic: low K, low phosphate, myositis 
Duchenne's muscular dystrophy
72
Q
Rhabdomyolysis 
Pathology (2)
A

Skeletal muscle breaks down and releases its contents into the circulation (myoglobin, phosphate, potassium, urate and creatinine kinase)
Myoglobin is filtered by glomeruli and precipitates into the renal tubule which it obstructs

73
Q

Rhabdomyolysis

Signs + symptoms (4)

A

Muscle pain
Swelling
Tenderness
Red-brown urine

74
Q
Rhabdomyolysis 
Investigations (6)
A

Plasma CK >10,000 (then have to exclude MI with troponin)
Urine +ve for blood on dipstick but without RBC on microscopy
U&E + creatinine: AKI occurs 12-24 hours later
K (high)
Phosphate (very high)
Ca (low because it enters muscle)

75
Q
Rhabdomyolysis 
Treatment (4)
A

Treat hyperkalaemia
IV fluids to prevent AKI
Sometimes need IV sodium bicarbonate to alkalinise urine to stabilise a less toxic form of myoglobin
Dialysis may be needed

76
Q
Rhabdomyolysis 
Complications (3)
A

AKI
Hyperkalaemia
Compartment syndrome from muscle injury

77
Q

Renal Artery Stenosis

Aetiology (3)

A

Atherosclerosis
Fibromuscular dysplasia
Thromboembolism

78
Q

Renal Artery Stenosis

Pathology (2)

A

Narrowing of renal artery leads to reduced renal perfusion
Activates renin-angiotensin-aldosterone system leading to hypertension (mediated by angiotensin II) and hypokalaemia and hyponatraemia (secondary hyperaldosteronism)

79
Q

Renal Artery Stenosis

Signs + symptoms (6)

A
Asymptomatic 
Hypertension resistant to treatment 
Worsening renal function after ACE-i/ARB
'Flash' pulmonary oedema (sudden onset, without LV impairment on cardiac echo) 
Abdominal +/- carotid/femoral bruits 
Weak leg pulses
80
Q

Renal Artery Stenosis

Investigations (3)

A

USS: renal size asymmetry (affected side smaller)
MR/CT angiography followed by invasive renal angioplasty
U&E + creatinine

81
Q

Renal Artery Stenosis

Treatment (2)

A

Manage hypertension

Transluminal angioplasty +/- stent placement or revascularisation surgery

82
Q

Renal Tubular Acidosis

Definition (2)

A
Metabolic acidosis (normal anion gap) due to impaired acid secretion by the kidney 
There are 4 types (but 3 is a rare combination of types 1 +2)
83
Q

Renal Tubular Acidosis

Aetiology (3)

A
Type 1 (distal): idiopathic (usually inherited), genetic (Marfan's, Ehlers-Danlos), autoimmune (SLE) 
Type 2 (proximal): idiopathic, tubulointerstitial disease (myeloma, interstitial nephritis) 
Type 4 (hyperkalaemia): Addison's disease, diabetic nephropathy, drugs (K-sparing diuretics, NSAIDs)
84
Q

Renal Tubular Acidosis

Signs + symptoms (3)

A
Type 1 (distal): rickets/osteomalacia (buffering of H with Ca in bone), nephrocalcinosis with calcium phosphate stones 
Type 2 (proximal): hypokalaemia (due to osmotic diuretic effect of bicarbonate reabsorption, causing an increased flow rate to distal tubule and therefore increased K excretion) 
Type 4: hyperkalaemia
85
Q

Renal Tubular Acidosis

Investigations (6)

A

Urine pH
U&E + creatinine
ABG
Type 1: urine pH >5.5 despite metabolic acidosis
Type 2: urine pH <5.5 with hypokalaemia and metabolic acidosis, diagnose with IV sodium bicarbonate lead
Type 4: urine pH <5.5, hyperkalaemia + metabolic acidosis

86
Q

Renal Tubular Acidosis

Treatment (3)

A

Type 1: oral sodium bicarbonate or citrate
Type 2: high dose sodium bicarbonate
Type 4: remove any cause, fludrocortisone/furosemide/calcium resonium to control high K

87
Q

Polycystic Kidney Disease

Epidemiology + genetics (4)

A

1:1000
Autosomal dominant
Almost all have mutations in PKD1 (chromosome 16) and reach ESRF by 50s
If mutation is on PKD2 (chromosome 4) reach ESRF by 70s

88
Q

Polycystic Kidney Disease

Signs + symptoms (9)

A

Renal enlargement with cysts (cysts replace renal tissue)
Abdo pain
Haematuria if haemorrhage into a cyst
Cyst infection
Renal calculi
Hypertension
Progressive renal failure
Development of liver cysts/ovarian cysts
Intracranial aneurysm which can rupture and cause subarachnoid haemorrhage

89
Q

Polycystic Kidney Disease

Investigations (2)

A
Renal USS (also for screening) 
Screening for SAH: MR angiography for 1st degree relatives of SAH and APKD
90
Q

Polycystic Kidney Disease

Treatment (6)

A
BP control (<130/80 target) with ACE-i 
Reduce Na intake 
Increase water intake 
Treat infections 
Laparoscopic cyst removal or nephrectomy for painful cysts 
Dialysis/transplant for ESRF