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CP3 Medicine > Renal Medicine > Flashcards

Renal Medicine Flashcards

1
Q

What is the function of the kidneys?

A

Kidneys function to regulate plasma ion concentrations, specifically to decrease plasma creatinine, urea, K+, and H+ concentration

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2
Q

Describe the structures in the kidney?

What does each one do?

A

Renal Corpuscle: produces the glomerular filtrate

PCT: reabsorbs ions, water and organic nutrients

Loop of Henle: Further reabsorption of water (desc limb) and reabsorption of Na+/Cl- (asc limb)

DCT: secretion of ions, acids, drugs and toxins
Variable reabsorption of water/sodium under the control of aldosterone

Collecting duct: Variable reabsorption of water under control of ADH
Variable solute reabsorption

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3
Q

What are the secondary functions of the kidney?

A

Secretion of EPO (to stimulate erythropoiesis in the bone marrow

Secretion of renin (to increase blood pressure)

1-alpha-hydroxylation of calcidiol to form calcitriol (vitamin D)

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4
Q

What is AKI?

A

Acute kidney injury:
essentially describes an acute deterioration in kidney function

Urine output: <0.5ml/kg/hr for 6 hours
>50% rise in creatinine over 7 days
>26 micromol rise in creatinine over 48 hours

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5
Q

What is stage 1, 2 and 3 AKI?

A

1: 150-200% increase or 25umol/l increase in 48 hours OR
<0.5ml/kg/hr for 6 hour

2: 200-300% increase OR
<0.5ml/kg/hr for 12 hours

3: >300% increase or >350umol/l with acute rise of >45umol/l in 48 hr OR
<0.3ml/kg/h for 24h or anuria for 12h

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6
Q

Who is AKI most common in?

A

Men, elderly, and those with pre-existing CKD

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7
Q

What are the symptoms of AKI?

A

Symptomless with oliguria (0.5ml/kg/hr) detected by nursing staff
If severe:
uraemia (vomiting, pruritus, pericarditis, encephalitis)
hyperkalaemia (do an ECG)
Pulmonary oedema due to fluid overload (unless pre-renal cause)

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8
Q

What are the causes of AKI?

A

Pre-renal
Renal
Post-renal

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9
Q

What is pre-renal AKI?

A

When blood supply to the kidney is interrupted

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10
Q

What are the main causes of pre-renal AKI?

A

SHOCK: hypovolaemic, cardiogenic, distributive

RENOVASCULAR OBSTRUCTION: embolus, aortic dissection, renal artery stenosis and thrombosis, or ACEis given in bilateral RAS

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11
Q

What happens if there is prolonged interruption to blood supply in pre-renal AKI?

A

Acute tubular necrosis, where ischaemia leads to necrosis of the cells that line the Renal tubules

This leads to porous tubular membranes (leading to a loss of concentrating power) and also a blockage of the tubules by necroses cells

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12
Q

Describe the urine osmolality and sodium in initial pre-renal AKI?

How does this change as ATN develops?

A

Osmolality is high (>500mosmol/kg) and urine sodium is low, as concentrating powers are retained

As ATN develops, urine is isotonic with plasma (<400mosmol/kg) and has high sodium, as concentrating powers are lost

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13
Q

What is post-renal AKI caused by?

A

When there is obstruction to the outflow of the urinary tract

This leads to back flow of urine, damage to the kidney architecture and resultant organ failure

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14
Q

What is the cause of the blockage in post-renal AKI caused by?

A

often in the ureters e.g. stones, strictures, clots, external/internal malignancy

Bladder outlet obstruction can also cause post-renal AKI e.g. prostatic enlargement, urethral strictures or phimosis / paraphimosis

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15
Q

What are the renal causes of AKI?

A 
Acute tubular necrosis (85%) 
Interstitial nephritis (10%)
Glomerular disease (5%)
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16
Q

Which drugs cause ATN?

Which toxins cause ATN?

A

aminoglycosides, cephalosporins, radiological contrast mediums

Toxins: heavy metal poisoning, myoglobulin or HUS

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17
Q

How does myoglobinuria occur?

A

Follows an episode of rhabdomyolysis (muscle breakdown from trauma, strenuous exercise or medications), releasing myoglobin, which is rapidly filtered by the glomerulus

This gives classical dark urine, but in high quantities will precipitate out within the tubules to cause damage

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18
Q

What is HUS?

A

Haemolytic uraemiac syndrome
Occurs in children, following a diarrhoeal illness caused by verotoxin-producing E.Coli O157 or following URTI in adults

It leads to thrombocytopenia (can cause purpura), haemolysis and ATN

Children usually recover in a few weeks, but prognosis poor in adults
Treatment is supportive, including dialysis

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19
Q

What is the cause of interstitial nephritis?

A

Most commonly, drugs
Antibiotics = most common cause
other agents = diuretics, allopurinol, and PPIs

Treated by withdrawal of drugs and short course of oral steroids

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20
Q

Describe the approach to the patient with Oliguria (or raised creatinine / decreased GFR)

A

AKI or CKD?
CKD if history of co-morbidities (HTN, DM) and long duration of symptoms (confirm with USS showing small kidneys)

If AKI - pre-renal, renal or post-renal

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21
Q

How do you tell if its pre-renal, renal or post-renal?

A

Pre-renal: look for signs of shock and treat appropriately
listen for renal bruits and take a vascular history if suspecting arterial pathology

Post-renal: USS to show distended bladder/hydronephrosis
Examine prostate

Renal: Take a meticulous drug history and enquire about recent infections, joint pains and rashes
Order a urine dip to look for positive blood/protein
Red cell casts on urine microscopy diagnostic for glomerulonephritis

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22
Q

How is AKI investigated?

A

Observations: hypotension in pre-renal causes/HTN in CKD
Examination: palpable bladder

Bloods: FBC, U&Es, bicarbonate, CRP, clotting, CK, nephritis screen

ABG
Urine dip and MCS
ECG: risk of hyperkalaemia

RENALS USS: look for post-renal causes

Non-contrast CT
Echo

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23
Q

What is the nephritic screen?

A 
ANCA & anti-GBM (RPGN) 
ANA, dsDNA & complement studies (SLE) 
Immunoglobulins, serum electrophoresis (myeloma)
Rheumatoid factor (RA-associated GN) 
Hepatitis B/C screen (MCGN)
ASO (post-streptococcal)
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24
Q

What is the management of AKI?

A

A-E assessment
Stop any potentially damaging drugs (NSAIDs, ACEi)

Restrict potassium intake

Pre-renal causes: treat shock
Post renal causes: refer to urology
Renal causes: assess fluid status, CVP measurements, ?furosemide stress tests

emergency managements - pulmonary oedema, acute hyperkalaemia

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25
Q

What are the indications for dialysis in AKI?

A 
refractory hyperkalaemia
pulmonary oedema 
acidosis
uraemic pericarditis / encephalopathy
complete anuria 
drug OD
26
Q

What is the furosemide stress test and how is it used?

A

Used to assess AKI severity
Furosemide 1mg/kg given after fluid resuscitation and the urine output measured and replaced at 2 Hours

The volume of fluid output at 2 hours can then be used to demonstrate likelihood of progression to AKI stage III

Generally, after a week of oliguria, if the AKI is improving, there will be one week of polyuria before return to normal kidney function at week 3

27
Q

What are the common electrolyte abnormalities in AKI?

A

Rapidly progressive uraemia: anorexia, vomiting and pruritus –> encephalopathy and haemorrhagic episodes

Hyperkalaemia
Hypernatreamia
Metabolic acidosis
Hypocalcaemia / hypophosphatemia (more common in CKD)

28
Q

What are the causes of hyperkalaemia?

A

Pseudohyperkalaemia: haemolysis, incorrect order of blood draw, sample taken from drip arm

AKI/CKD

DRUGS: supplements, K+ sparing diuretics, ACEis, NSAIDs

ACIDOSIS: Including DKA

Others: Addison’s / tumour-lysis syndrome / burns

29
Q

What are the signs of hyperkalaemia on ECG?

A

Tall, peaked T-waves
Widened QRS complex
Flattened P waves / prolonged PR interval

30
Q

What can happen if hyperkalaemia goes untreated?

A

Ventricular fibrillation / tachycardia

31
Q

What are the principles of hyperkalaemia management?

A

Stabilise the heart: calcium gluconate

drive potassium intracellularly - insulin & dextrose / salbutamol

calcium resonium (orally or enema)

Treat underlying cause

32
Q

State the steps of hyperkalaemia management

A

If potassium >6.5mmol/L or ECG changes, start management:

  1. Start continuous ECG monitoring
  2. 10ml of 10% calcium gluconate IV to stabilise myocardium
    Repeat at 5 minute intervals until a maximum of 3 doses until ECG normal
  3. 50ml of 50% glucose with 10U ACTRAPID insulin into larger vein to decrease K+ concentration
    Onset 1-4h, monitor BMs
  4. Consider 10mg salbutamol neb
  5. If pH <7.2, consider sodium bicarbonate IV if advised by renal registrar
  6. Recheck K+ after 2 Hrs
  7. Calcium resonium can then be given orally/rectally, however, this is a long term management option, taking days to reduce potassium concentration
  8. Ensure underlying cause is treated
33
Q

What is CKD?

A

Chronic kidney disease - when any two tests 3 months apart show reduced eGFR, and can be staged 1-5 depending on level of function

34
Q

What are the 5 stages of kidney disease?

A

1: GFR 90+ and normal kidney function, urine findings/structural abnormalities or genetic traits point to kidney disease
2: GFR 60-89 and mildly reduced kidney disease
3: GFR 30-59: and moderately reduced kidney function
4: GFR 15-29: severely reduced kidney function
5: <15 very severe / ESRD

35
Q

What is eGFR?

A

Estimate of GFR based on a plasma level of creatinine Can be inaccurate in certain situations, so a 24 hour urinary creatinine may be collected to calculate true creatinine clearance

36
Q

Describe the aetiology of CKD?

A 
Diabetes Mellitus 20-40%
HTN
Chronic glomerulonephritis
Chronic pyelonephritis
Obstructive uropathy 
Renovascular disease
Drugs (long term NSAIDs)
PKD
37
Q

What are the symptoms of chronic renal failure?

A 
vague fatigue and anorexia
polyuria, nocturia
restless legs syndrome
sexual dysfunction 
nausea and pruritus (early uraemia)
yellow pigmentation, encephalopathy, pericarditis (severe uraemia)

pedal oedema and pulmonary oedema

38
Q

What are the signs of chronic renal failure?

A

Pallor, due to anaemia
Excoriations (pruritus)
HTN / fluid overload signs

Pericardial rub (rare)

39
Q

What ix can be done for chronic renal failure?

A

Bloods: FBC, U+Es, LFTs, Calcium, phosphate, PTH levels, glucose

Urinalysis and MCS: quantify proteinuria, exclude infection and look for casts

24hr urinary protein / creatinine clearance
assess severity/for nephrotic syndrome

CXR: If suspecting pulmonary oedema

Renal USS: if suspecting obstructive causes

DTPA to investigate vascular supply, renal biopsy, bone imaging

40
Q

What is the management of CKD?

A

Treat reversible causes (obstruction, nephrotoxic drugs)

First line: Blood pressure/diabetic control

Second line: control of complications

Renal replacement therapy if ESRD

41
Q

How is blood pressure controlled in CKD?

A

BP controlled to 130/80
If proteinuria, 125/75

ACEi first line
Primary CV prevention - statin and low dose aspirin

42
Q

How are CKD complications controlled?

A

Recombinant EPO if signs of anaemia
Calcium/vitamin D supplementation for those with bone disease
K+ restriction if any signs of hyperkalaemia

43
Q

How does renal anaemia occur?

A

Kidney normally secretes EPO in response to hypoxia
In CKD, kidney partially loses this secretory function, leading to anaemia

Recombinant EPO can be given to those with ESRD

Other factors implicated are bone marrow toxins, increased blood loss and abnormal red cell membranes

44
Q

What is the role of the kidneys in calcium regulation?

A

Kidneys produce 1-alpha-hydroxylase, which enables conversion of calcidiol from the liver to calcitriol (activated vitamin D)

Vitamin D normally increases intestinal calcium absorption, increases renal reabsorption of calcium and has complex bone protective actions, stimulating both resorption and formation

45
Q

How does CKD affect bones?

A

Lower vitamin D in CKD –> hypocalcaemia and hypophosphataemia

Low vitamin D levels lead to osteomalacia.

46
Q

What is the effect of osteomalacia in CKD?

A

leads to a secondary hyperparathyroidism, with raised PTH acting to increase calcium reabsorption from bones and renal tubules

Increased bone osteoclast activity leads to cyst formation and marrow fibrosis –> osteitis fibrosis cystica

47
Q

What are the long term effects of osteomalacia in CKD?

A

Tertiary hyperparathyroidism and the hypercalcaemia leads to osteosclerosis of the spine

End result of all processes is osteopenia, which can be detected radiologically (pseudo fractures, subperiosteal erosions)

48
Q

What is the management of renal bone disease?

A

Restricting dietary phosphate and giving phosphate binders (calcichew) with AdCal (calcium and vitamin D supplementation)

49
Q

What are the options for renal replacement therapy?

A

haemo-dialysis, peritoneal dialysis or transplantation

50
Q

What is haemo-dialysis?

A

Diffusion of solutes between blood and dialyse which flow in opposite directions with a semi-permeable membrane between them

They need good access to an abundant blood supply. The options for this are:
Tunnelled cuffed catheter
Arterio-venous fistula

51
Q

How many times is dialysis needed per week?

A

4 hours / 3 times/weekly
normally at hospital
home treatment available but requires support and training

52
Q

What is haemofiltration?

A

A variant of haemodialysis where blood is continuously filtered across a highly permeable membrane

More efficient, so more haemo-dynamically stable, so is used in critically ill patients, but is more expensive

53
Q

How is an AV fistula formed?

A

artificial connection between an artery to a vein.

It bypasses the capillary system and allows blood to flow under high pressure from the artery directly into the vein. This provides a permanent, large, easy access blood vessel with high pressure arterial blood flow. Creating an A-V fistula requires a surgical operation and a 4 week to 4 month maturation period without use.

54
Q

What are the complications of AV fistulas?

A 
Aneurysm
Infection
Thrombosis
Stenosis
STEAL syndrome
High output heart failure
55
Q

How is peritoneal dialysis done?

A

Peritoneal dialysis uses the peritoneal membrane as the filtration membrane. A special dialysis solution containing dextrose is added to peritoneal cavity. Ultrafiltration occurs from the blood, across the peritoneal membrane, in to the dialysis solution. The dialysis solution is then replaced, taking away the waste products that have filtered out of the blood into the solution.

56
Q

What are the complications of peritoneal dialysis?

A

Bacterial peritonitis.Bacterial infection is a common and potentially serious complication of peritoneal dialysis.

Peritoneal sclerosis involves thickening and scarring of the peritoneal membrane.

Ultrafiltration failure can develop. This occurs when the patient starts to absorb the dextrose in the filtration solution.

Weight gain can occur as they absorb the carbohydrates in the dextrose solution.

Psychosocial effects

57
Q

Why Is renal transplant good?

A

Adds 10 years to life of renal failure patient compared to just dialysis

58
Q

How are donors matched for renal transplant?

A

Patients and donor kidneys are matched based on the human leukocyte antigen (HLA) type A, B and C on chromosome 6. They don’t have to fully match. Recipients can receive treatment to desensitise them to the donor HLA when there is a living donor. The less they match, the more likely the transplant is to fail.

59
Q

What immunosuppression do transplant patients need?

A

Tacrolimus
Mycophenolate
Prednisolone

60
Q

What are the complications of renal transplant?

A

Complications relating to the transplant:

Transplant rejection (hyperacute, acute and chronic)
Transplant failure
Electrolyte imbalances

Complications related to immunosuppressants:
Ischaemic heart disease
Type 2 diabetes (steroids)
Infections are more likely and more severe
Unusual infections can occur (PCP, CMV, PJP and TB)
Non-Hodgkin lymphoma
Skin cancer (particularly squamous cell carcinoma)

CP3 Medicine (19 decks)

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