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MEDICINE NEW > Renal > Flashcards

Renal Flashcards

1
Q

A patient today has a creatinine of 130, when they arrived in hospital it was 62. What stage AKI do they have?

A

Stage 2:

2x creatine of baseline
Or 0.5mL/kg/hour for 12 hours

If the patient weighed 60kg and had produced < 360mL in the last 12 hours it would also be stage 2

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2
Q

Causes of acute kidney injury:

A

Pre-renal: hypoperfusion- low BP or renal artery stenosis

Intrinsic:
Tubular- necrosis from contrast, nephrotoxic drugs, myoglobin, stones or myeloma
Glomerular- glomerulonephritidies, autoimmune, infections
Interstitial- infiltration from lymphoma, infection, tumour lysis syndrome
Vascular- vasculitis, hypertension, emboli, HUS/TTP

Post-renal:
Blockage- stones, clots, strictures, malignancy
Compression- malignancy, retroperitoneal fibrosis

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3
Q

Bedside tests to do in an AKI:

A

Dipstick (blood + protein = glomerulonephritis, or leukocytes)
MC+S (crystals)
Culture
Bence Jones protein

Bloods (including CK-myoglobin, ESR + ANCA, ANA if suspect autoimmune cause)

Renal USS- small kidneys suggest CKD

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4
Q

Patient with an AKI starts getting chest pain, why is an ECG warranted?

A

They may have hyperkalaemia or uraemia causing pericarditis

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5
Q

Indications for dialysis in AKI

A

Refractory pulmonary oedema or hyperkalaemia (>7mmol)
Severe metabolic acidosis
Uraemia causing encephalopathy or pericarditis
Drug overdose- BLAST (barbituates, lithium, alcohol, salicylates, theophylline)

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6
Q

Emergency management of hyperkalaemia

A

10mL of 10% calcium gluconate IV, repeated until ECG improves

IV 10U actrapid + 20% glucose

Ultimately: Rx cause of AKI- catheterise, give fluids, haemodialysis/haemofiltration

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7
Q

Stages of AKI

A

1: 1.5 x baseline of creatinine
or creatinine rise >26mmol/L in 48 hours
<0.5mL/kg/hr for 6 hours

2: 2 x baseline of creatinine
<0.5mL/kg/hr for 12 hours

3: 3 x baseline of creatinine
Or >350 umol rise
Or renal replacement therapy commenced
<0.3mL/kg/hr for 24 hours
Anuria for 12 hours
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8
Q

What are the 3 layers that comprise the glomerular filtration surface in the kidney?

A 
Endothelial cells (prevents red cell + platelet passage)
Basement membrane
Epithelial cell layer of podocytes
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9
Q

Which hormone is catabolised by the kidney?

A

Insulin

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10
Q

Histological patterns of nephrotic syndrome:

A

Primary and Secondary causes will give rise to one of the following patterns:

Minimal change
Membranous (silver membrane spikes)
Membrano-proliferative (Mesangiocapillary, tram line capillary walls)
Focal Segmental Glomeulosclerosis (diabetes, amyloid)
SLE

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11
Q

Hepatitis is associated with which histological patterns of nephrotic syndrome?

A

Membranous nephropathy- Hep B

Immune complex mediated mesangiocapillary- Hep C

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12
Q

Common secondary causes of nephrotic syndrome and the histological change associated?

A

NSAIDs + gold + penacillamine
Hepatitis + SLE + paraneoplastic- normally membranous
HIV + amyloid + diabetes- FSGS

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13
Q

Membrane spikes on silver stains and subepithelial dense deposits seen on histology. What type of nephrotic syndrome is it?

A

Membranous nephropathy

May also see diffuse IgM

Other types: minimal change, focal segmental glomerulosclerosis (also IgM seen), mesangiocapillary

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14
Q

Kimmelstein wilson nodules are associated with which cause of nephropathy?

A

Diabetes

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15
Q

HIV and heroin causing nephrotic syndrome produce what histological pattern of glomerular damage?

A

Focal segmental glomerulosclerosis

Focal- some glomeruli, segmental- some parts of the glomerulus

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16
Q

Features of nephrotic syndrome?

A

HOP

Hypoalbuminaemia, oedema, proteinuria

Adults should undergo renal biopsy

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17
Q

3 Complications of nephrotic syndrome:

A

Infection susceptibility- loss of Ig and complement
Thromboembolism- increase in clotting factors (stimulated in the liver by a loss of albumin)
Hyperlipidaemia- hepatic response to low oncotic pressure is to produce more cholesterol + triglycerides

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18
Q

Rx of nephrotic syndrome

A
  1. Steroids
  2. Cyclophosphamide or ciclosporin

Loop diuretics, salt + fluid restrict
ACEi to reduce proteinuria

Hepatic response to low oncotic pressure is higher clotting factors + cholesterol so start a statin + anticoagulate

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19
Q

Which cause of glomerulonephritis do you not treat with immunosupression or plasma exchange?

A

Post-streptococcal GN

Just supportive care, as tends to be self-limiting eventually

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20
Q

Pneumonic for remembering causes of glomerulonephritis?

A

A Hen SLEeps in the PASTURE as the COCK was MEAN and AGGRESSIVE

IgA
Henoch Shonlein + vasculitidies
SLE
Goodpastures
Post-streptococcal
Mesangio-capillary GN
Rapidly progressive GN
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21
Q

Which glomerulonephritidies demonstrate deposition of the following Ig on immunofluorescence:

  1. IgG
  2. IgM
  3. IgA
A
  1. Post-strep and Anti-GBM
  2. Focal segmental glomerulosclerosis
  3. IgA nephropathy + Henoch Schonlein vasculitis
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22
Q

What is the definition of CKD?

A 
Impaired renal function for 3 months evidenced by:
Abnormal structure (ie <9cm in size)
GFR <60mL/min/1.73
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23
Q

Top 5 causes of chronic kidney disease

A
  1. Diabetes
  2. Glomerulonephritis (commonly IgA)
  3. Unknown- too late to biopsy
  4. Hypertension or renovascular disease
  5. Pyelonephritis/reflux nephropathy
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24
Q

Difference in histology on renal biopsy between a patient with post-streptococcal GN and IgA nephropathy GM?

A

IgA nephropathy: mesangial proliferation (lots of pink)

Post-strep: mesangial + capillary proliferation (lots of nuclei + pink)

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25
Q

Different types of bladder tumour

A

90% transitional cell Ca
7% squamous cell Ca- associated with chronic irritation (UTIs, schistosoma haematobium, catheters)
2% adenocarcinoma - urachas remnant

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26
Q

4 main different types of primary kidney cancer:

A
  1. Renal cell carcinoma
  2. Transitional cell ca- renal pelvis
  3. Nephroblastoma (Wilms)
  4. Epithelial- sarcomas
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27
Q

IHx to rule out suspected bladder cancer

A 
Flexible cystoscopy ± protoporphyrin (to highlight neoplasms)
Urine cytology (sterile pyuria)

Staging:
MRI pelvis
CT chest, abdo, pelvis
bone scan

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28
Q

For prostate and bladder cancer TNM staging, what T grade is given if the cancer has extended beyond the bladder or prostate?

A

T3

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29
Q

Treatment of bladder cancer that has not invaded the muscle of the bladder wall (T1)

A

For low grade: transurethreal resection of bladder tumour

For higher grade or relapse: resection
+ intravesical BCG or chemo (mitomycin C, doxorubicin, cisplatin)

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30
Q

Treatment of bladder cancer that has invaded the muscular bladder wall (T2-T3 no mets)

A

Gold standard:
Radical cystectomy
Neoadjuvant chemotherapy improves survival

Conservative:
Transurethral resection + radiotherapy + chemotherapy

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31
Q

Patient presents with haematuria, loin pain and fever (of unknown origin), what tests should be done for suspected renal cell carcinoma?

A

Urine MC+S- RBCs, cytology
US scan

CT- pre and post contrast will show an enhancing mass

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32
Q

What is unusual about the treatment of renal cell carcinoma?

How is it treated?

A

It is resistant to chemotherapy and radiotherapy

Localised:
radical nephrectomy ± nephron sparing, robotic or laparoscopic

Advanced:
Immunotherapy- Interleukin 2 or VEGF tyrosine kinase inhibitor (as RCC’s are very vascular)

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33
Q

Child has haematuria and an abdominal mass, what tests are warranted to rule out suspicious cause?

A

US + CT/MRI to diagnose Wilms tumour

From mesodermal cells
Prognosis 90% long term survival

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34
Q

How does Wilms tumour management differ to renal cell carcinoma Rx?

A

RCC is radiotherapy and chemo-resistant

Wilms is treated with chemotherapy

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35
Q

Stages of CDK

A

Stage 1: GFR >90 + renal damage:
Proteinuria, haematuria, abnormal anatomy

Stage 2: 60-89 + renal damage
Stage 3a: above 45
Stage 3b: above 30
Stage 4: above 15 
Stage 5: <15

Can factor in ACR to determine risk

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36
Q

What rate of fall in eGFR shoudl prompt referral to the nephrologist?

A

> 5mL/min over a year

Or >10mL/min over 5 years

37
Q

What is the target BP for a patient with CKD ± diabetes or Albumin Creatinine Ratio >70

A

CKD 130/80

Diabetes + CKD 125/75

38
Q

Rx for CKD that limits progression or complications

A

If diabetic or >130/80: ACEi or ARB (even if BP is normal)

If PTH is high: phosphate binders, Ca+ supplements, vit D analogues

Aspirin- reduces CVS risk

39
Q

Symptomatic Rx of CKD:

A

Anaemia: iron, B12, folate, recombinant erythropoietin

Acidosis: failure to reabsorb bicarbonate leads to low pH and serum HCO3 levels > sodium bicarbonate (caution- BP)

Oedema: loop diuretics

Resless legs: benzodiazepines + increase ferritin levels

40
Q

In what unique circumstance would you consider biopsying a kidney if it was the patient’s only working one?

A

For kidney transplant

41
Q

3 categories of rapidly progressive glomerulonephritis

A

Immune complex: post-strep, SLE, IgA/Henoch Schönlein

Pauci-immune: ANCA+ (Wegners), microscopic polyangiitis, Churg-Strauss (no complement or IgG with immunofluorescence)

Anti-GBM: Goodpasture’s

42
Q

What symptoms might indicate a patient has a rapidly progressive form of glomerulonephritis?

A

AKI + systemic features: fever, myalgiaa, weight loss, haemoptysis

Goodpastures and vasculitidies may cause pulmonary haemorrhage

43
Q

What screening test helps identify those with diabetes mellitus at risk of renal damage?

A

Annual check for albumin levels in 24 hour urine
Microalbuminaemia (30-300mg/24 hours) gives early warning.

All patients with microalbuminaemia should be given ACEi, irrespective of BP

44
Q

Renal causes of hypertension

A

Kidneys produce renin (AT2) and may retain salt and water

Intrinsic renal disease:
glomerulonephritis, polyarteritis nodosa, systemic sclerosis (anti-scl70 and anti-RNA), chronic pyelonephritis, polycystic kidneys
Can do urine dipstick to look for blood, protein, nitrates, leukocytes

Renovascular disease:
Atheromatous artery stenosis
or fibromuscular dysplasia (non-inflammatory, non-atherosclerotic thickening of artery wall)

45
Q

How is renal artery stenosis investigated?

A

Renal Doppler ultrasound

CT or MR angiography is more sensitive

RENAL ANGIOGRAPHY IS GOLD STANDARD (more invasive)

46
Q

How much protein in the urine suggests nephrotic syndrome proteinuria (over a day)?

A

3g/day

47
Q

What is the definition of microalbuminuria?

A

30-300mg in 24 hour urine collection

Indicates those with diabetes at risk of kidney deterioration = need ACEi

48
Q

A patient has found to have proteinuria on a urine dipstick, they have no symptoms. What would prompt a referral to urology or nephrology?

A

Urology:
over 40
persistent protein +++

Nephrology:
hypertensive >140/90
EGFR <60
Albuminuria (ACR >30 or PCR >50)

49
Q

Recommended investigations for a 45 year old patient with haematuria discovered on urine dipstick?

A

Check if recent UTI, menstruation, vigorous exercise

Serum creatinine, spot ACR
BP
Bloods- including ESR, clotting
Urine MC+S
USS + renal referral if also getting proteinuria, GFR decline or casts seen
50
Q

Drugs that can cause microscopic haematuria?

A

Cephalosporin + ciprofloxacin (both broad spectrum)
Furosemide + captopril (ACEi)
NSAIDs

51
Q

What are the pro’s and con’s of PSA testing?

A

Around 70% of 70 year olds are likely to have prostate ca
Test may not mean you live longer, even if you have prostate ca- likely to die of something else
False +ve leads to more tests- biopsies etc
False -ve unnecessary worry

52
Q

Patient keeps getting UTIs and has pain around his bladder, on DRE a boggy prostate is felt (swollen). Likely cause and eitiology?

A

Prostatitis (acute or chronic)

Due to: E Coli, Strep faecalis or chlamydia

53
Q

What’s the difference between haemodialysis and haemofiltration?

A

Haemodialysis: semi-permeable membrane, with blood flowing in opposite direction to dialysis fluid.
Problems: large fluid shifts, larger solutes clear less well

Haemofiltration: permeable membrane, with dialysis fluid flowing in same direction.
Problems: very slow, less fluid shifts

54
Q

Pros and cons of peritoneal dialysis:

A

Peritoneum = semi-permeable membrane used to filter fluids across it by infusing fluids into the peritoneal cavity.

Pros: can be done more slowly, at home, less fluid shifts
Cons: Peritonitis or infection of the catheter site, blockage or loss of membrane function.

55
Q

6 long term complications occurring in patients on renal replacement therapy?

A

CAP BMI

CVS disease: MI + stroke
Amyloidosis: arthralgia, carpel tunnel
Protein calorie malnutrition: reduce intake

Bone disease: osteodystrophy + osteitis fibrosa (fibrosis replaces calcium)
Malignancy: commoner
Infection: sepsis, related to mode of dialysis (ie peritonitis)

56
Q

Contraindications to renal transplant:

A

Active infection
Cancer in the last 5 years
Comorbidity

57
Q

How is immunosuppression induced and maintained in kidney transplants?

A

Induction: anti-IL 2R antibody or anti-CD52 (on lymphocytes)

Maintenance:

  1. Calcineurin inhibitor (tacrolimus, ciclosporin)
  2. Antimetabolite (azathioprine, mycophenolate)
  3. Prednisolone
58
Q

Types of graft rejection in kidney transplants

A

Hyperacute: within 2 days, mediated by pre-existing antibodies

Acute: weeks - months later, cellular-mediated lymphocyte infiltration
High dose IV methylprednisolone + more immunosupression

Chronic allograph nephropathy: vessel walls thicken, tubules atrophy + interstitial fibrosis is seen

59
Q

What side effects occur in kidney transplant immunosuppression regimes?

A

Calcineurin inhibitors- tremor, confusion
Ciclosporin- gum hypertrophy, hirsutism
Antimetabolites (azathioprine)- hepatitis, agranulocytosis

60
Q

Patient has loin pain, what tests can identify if there is urinary tract obstruction and what level it is?

A

US- hydronephrosis or hydroureter

If +ve
CT- determines the level of obstruction
Radionucleotide imaging- functional assessment

61
Q

Rx for upper urinary tract obstruction:

A

Nephrostomy (artificial ureter implanted that drains to skin surface)
Stent ± alpha blocker to reduce ureteric spasms

62
Q

Patient has been getting progressively reduced kidney function, blood tests show:
Raised urea + creatinine
Raised ESR + CRP

US shows dilated ureters
CT shows periaortic mass
Diagnosis + Rx?

A

Periaortitis / Retroperitoneal fibrosis

Ureters get embedded in dense fibrous tissue around the aorta, which fibroses in response to vasculitis/SLE, drugs or idiopathically.

Rx: stent to relieve obstruction
±Dissection of the ureters from retroperitoneal tissue + immunosupression

63
Q

Rx for retroperitoneal fibrosis compressing the ureters bilaterally?

A

Upper urinary tract obstruction

Rx: stent to relieve obstruction
±Dissection of the ureters from retroperitoneal tissue + immunosupression

64
Q

In children under 6 months, found to have an atypical or recurrent UTI, what tests should be done to look for renal abnormalities?

A

Ultrasound (during the acute phase or within 6 weeks if responding to ABx)
DMSA 4 months later (functional test for scarring)
MCUG- injects contrast + xrays to see reflux

DMSA= dimercaptosuccinic acid scintigraphy
MCUG= micturating cystourethrogram
65
Q

In a child aged 6months-3 years, how does investigation of atypical and recurrent UTIs differ to such UTIS in infants under 6 months?

A

Atypical UTI: any age gets acute USS (or within 6 weeks if quickly resolving)
Under 3 years: DMSA (scarring)
Under 6 months: add MCUG (reflux)

Recurrent UTI:
All get DMSA
Over 6 months: add USS at 6 weeks
Under 6 months: add MCUG

66
Q

How is a typical UTI resolving in 48 hours investigated differently in children aged under 6 months vs those aged 6 months to 3 years?

A

No follow up IHx routinely needed for children aged 6 months to 3 years, if under 6 months USS at 6 weeks warranted

67
Q

In a child aged 6 months to 3 years who has a non E Coli UTI, what features would prompt a micturating cystourethrogram?

A

PC: poor urine flow
FHx: vesicoureteric reflux
IHx: dilatation on ultrasound
non-E Coli infection (atypical infection)

68
Q

What is vesicouteric reflux and why is it a problem?

A

Retrograde backflow of urine to the kidneys, thought to cause pyelonephritis and scarring, leading to hypertension + end stage renal failure ultimately.

69
Q

What features constitute an atypical UTI in a child/infant?

A

PC: seriously ill, poor urine flow, bladder mass, septicaemia
HPC: failure to respond to suitable Abx within 48 houra
IHx: non E Coli organism, raised creatinine

70
Q

How is recurrent UTI defined in children/infants?

A

1 pyelonephritis + 1 UTI/pyelonephritis
Or
3 UTI

71
Q

Prevention of renal scarring in children waiting for imaging to exclude or diagnose vesicoureteral reflux?

A

Trimethoprim prophylaxis to reduce chance of infection being transmitted to kidneys

72
Q

A hypertensive patient is on some antihypertensive meds, after starting an ACEi, their renal function worsens, what needs to be investigated?

A

Renal artery stenosis (loss of angiotensin mediated afferent dilatation worsens function)

Can do a doppler USS
CT or MR angiography are more sensitive
Renal angiography is gold standard

73
Q

7 year old boy has been getting bloody diarrhoea and has not weed much for the last 6 hours.

Bloods: anaemia, low platelets
Blood film shows schistocytes

Diagnosis?

A

Haemolytic uraemic syndrome:
E Coli 0157 strain produces verotoxin which attacks endothelial cells.

Endothelial damage = thrombosis, platelet consumption + fibrin strand deposition (which mechanically destroys RBCs- schistocytes)

74
Q

Rx of haemolytic uraemic syndrome?

A

AKI + bloody diarrhoea + haematuria

Dialysis for AKI may be needed
Plasma exchange to remove venotoxin from E Coli 0157 strain may be needed

75
Q

Patieent is jaundiced, has reduced consciousness and has stopped seizuring, they have an AKI brewing. What could be the cause?

A

Thrombotic thrombocytopenic purpura
Lack of ADAM13 protease that normally cleaves von Willebrand factor meaning large vWF multimers form and aggregate platelets.

IHx: dipstick (protein ++ blood++), blood film (schistocytes), low platelets + Hb

76
Q

Treatment for thrombocytopenic purpura?

A

Low platelets and Hb > blood film

Rx: Urgent plasma exchange
Steroids

Biologics in development (targeting C5 pathway)

77
Q

Difference between type 1 and type 2 renal tubular acidoses?

A

Both have alkaline urine production pH >5.5 despite metabolic acidosis in blood

Type 1: inability to excrete H+ ions at distal convoluted tubule, osteomalacia occurs as Ca+ from bone tries to buffer high H+ levels

Type 2: bicarbonate leak at proximal tubule- defect in reabsorption. Diagnosed by high fractional urinary excretion of NaHCO3 when given IV, get hypokalaemia also

78
Q

Which type of renal tubular acidosis is associated with a high K+ level?

A

Type 4- hyporeninaemic hypoaldosteronism
Low aldosterone reduces K+ and therefore H+ excretion

Rx: Mineralocorticoid like Fludrocortisone are used

79
Q

Patient has recurrent calcium phosphate stone formation, low K+ and osteomalacia. What is the linking diagnosis?

A

Type 1 renal tubular acidosis
failure to excrete H+ in the distal tubule (despite metabolic acidosis) means more H+ in the blood.
Ca+ leaves bones to buffer high H+ levels- osteomalacia, then the combination of hypercalciuria, low urinary citrate (reabsorbed as H+ buffer) and alkaline urine favours stone formation.

Low pH means more K+ is swapped for Na+ absorption instead
Technically Fanconi syndrome might have similar features (PCT loss of amino acids, glucose, phosphate and bicarbonate)

80
Q

The inherited Bartter syndrome and Gitelman syndrome mimic which types of diuretics?

A

Bartter syndrome- low K+, metabolic alkalosis, hypercalciuria
Inherited mutation in NA+/K+/Cl co-transporter
Like LOOP diuretics, presents in infancy

Gitelman syndrome- low K+, metabolic alkalosis, hypocalciuria, low Mg2+
Inherited mutation in Na+/Cl co-transporter
Like THIAZIDE diuretics, presents with muscle cramps, weakness, low BP

81
Q

How do the metabolic abnormalities differ and compare in Bartter syndrome and Gitelman syndrome?

A

Both have low K+ and metabolic alkalosis

Gitelman will have hypocalciuria- without Na/Cl symporter on tubular side, less Na gets into tubule cell, so on the other basolateral cell side Na/Ca antiporter is more active and more Ca is reabsorbed

Bartter has hypercalciuria- normally K+ is uptaken via the Na/K/Cl cotransporter and then leaks back into the tubule providing a gradient to allow cations (Ca, Mg) to be absorbed

82
Q

Where and what is the genetic defect in most cases of polycystic kidney disease?

A

85%: Autosomal dominant mutations in PKD1 gene on chromosome 16
End stage renal failure in 50s

Other: PKD2 is on chromsosme 4

83
Q

What heart and gynae complications are associated with polycystic kidney disease?

A

Heart: mitral valve prolapse
Gynae: ovarian cyst

84
Q

What is the best test to determine if a patient has polycystic kidney disease?

A

Ultrasound scan

Genetic testing for PKD1 (chromosome 16- 85% of patients) is difficult due to size of the gene and hundreds of mutations

85
Q

Clinical definition of polycystic kidney disease?

A

USS findings
Under 39 years: >3 unilateral or bilateral cysts
40-59 years: >2 cysts in each kidney
>60 years: >4 cysts in each kidney

86
Q

Which inherited syndrome is associated with a constellation of end stage renal failure- with cyst formation, and retinal degeneration, cerebellar ataxia ad retinitis pigmentosa, liver fibrosis?

A

Medullary cystic disease- autosomal recessive

87
Q

Boy is found to have blood +++, protein +++ and rising creatinine on his U+Es. He was born deaf, what is the most likely heritable syndrome?

A

Alport syndrome

X linked type IV collagen mutation

88
Q

What is Fabry disease?

A

X linked lysosomal storage disease (GLA gene abnormalities)

Glycosphingolipids in:
Skin - angiokeratoma, hypohidrosis
Eyes- lens opacities
Heart- angina, MI, syncope, LVH, arrythmias
Kidneys- renal failure
CNS- stroke
Nerves- neuropathies
89
Q

Why are renal transplant patients with Fabry disease at risk of anti-GBM glomerulonephritis post-transplant?

A

The gene abnormality affects type IV collagen, which is the immunogenic antigen in anti-GBM glomerulonephritis

MEDICINE NEW (22 decks)

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