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Renal Flashcards

1
Q

What is acute kidney injury (AKI) and how is it diagnosed ?

A

Its is defined as an acute drop in kidney function. It is diagnosed by measuring the serum creatinine.

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2
Q

NICE criteria for diagnosing AKI ?

A

Use any of the following:

  • Rise in creatinine of 26 micromol/L or greater within 48 hrs
  • Rise in creatinine of 50% or more in 7 days
  • Urine output of < 0.5ml/kg/hour for more than 6 hours
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3
Q

Consider the possibility of an AKI in pts that are suffering with an acute illness, such as infection or having a surgical operation. Risk factors that would predispose to developing AKI include ?

A
  • CKD
  • Heart failure
  • Diabetes
  • Liver disease
  • Older age (above 65 years)
  • Cognitive impairment
  • Nephrotoxic medications such as NSAIDS and ACE inhibitors
  • Use of a contrast medium such as during CT scans
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4
Q

TOM TIP

A

Whenever someone asks you the causes of renal impairment always answer “the causes are pre-renal, renal or post-renal”. This will impress them and allow you to think through the cases more logically.

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5
Q

Pre-renal causes of AKI ?

A

Pre-renal pathology is the most common cause of acute kidney injury. It is due to inadequate blood supply to the kidneys reducing the filtration of blood. Inadequate blood supply may be due to:

  • Dehydration
  • Hypotension (shock)
  • Heart failure
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6
Q

Renal causes of AKI ?

A

This is where intrinsic disease in the kidney is leading to reduced filtration of blood. It may be due to:

  • Glomerulonephritis
  • Interstitial nephritis
  • Acute tubular necrosis
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7
Q

Post renal causes of AKI ?

A

Post renal AKI is caused by obstruction to outflow of urine from the kidney, causing back-pressure into the kidney and reduced kidney function. This is called an obstructive uropathy. Obstruction may be caused by:

  • Kidney stones
  • Masses such as cancer in the abdomen or pelvis
  • Ureter or urethral strictures
  • Enlarged prostate or prostate cancer
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8
Q

Investigations for AKI ?

A

Urinalysis for protein, blood, leucocytes, nitrites and glucose:

  • Leucocytes and nitrites suggest infection
  • Protein and blood suggest acute nephritis (But can be positive in infection)
  • Glucose suggests diabetes

US of the urinary tract is used to look for obstruction. It is not necessary if an alternative cause is found for the AKI.

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9
Q

Management of AKI ?

A

Prevention of AKI is important. This is achieved by avoiding nephrotoxic medications where possible and ensuring adequate fluid input in unwell pts, including IV fluids if they are not taking enough orally.

The first step to treating AKI is to correct the underlying cause:

  • Fluid rehydration with IV fluids in pre-renal AKI
  • Stop nephrotoxic medications such as NSAIDS and antihypertensives that reduce the filtration pressure (i.e. ACE inhibitors)
  • Relieve obstruction in post-renal AKI, for example insert a catheter for a pt in retention from a large prostate.

In severe AKI, where there is doubt about the cause or where complications develop, input from a renal specialist is required. They may need dialysis.

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10
Q

Name 4 complications of AKI ?

A
  • Hyperkalaemia
  • Fluid overload, heart failure and pulmonary oedema
  • Metabolic acidosis
  • Uraemia (high urea) can lead to encephalopathy or pericarditis.
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11
Q

What is chronic kidney disease ?

A

CKD describes a chronic reduction in kidney function. this reduction in kidney function tends to be permanent and progressive.

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12
Q

Causes of CKD ( 6 bullet points) ?

A
  • Diabetes
  • HTN
  • Age related decline
  • Glomerulonephritis
  • Polycystic kidney disease
  • Medications such as NSAIDs, PPIs and lithium
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13
Q

Name 5 risk factors for CKD

A
  • Older age
  • HTN
  • Diabetes
  • Smoking
  • Use of medications that affect the kidneys
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14
Q

Presentation of CKD ?

A

Usually CKD is asymptomatic and diagnosed on routine testing. A number of signs and symptoms might suggest CKD:

  • Pruritis (itching)
  • Loss of appetite
  • Nausea
  • Oedema
  • Muscle cramps
  • Peripheral neuropathy
  • Pallor
  • HTN
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15
Q

Investigations for CKD ?

A
  • eGFR can be checked using a U&E blood test. Two tests are required 3 months apart to confirm a diagnosis of CKD
  • Urine albumin:creatinine ratio (ACR) can be used to check for proteinuria. A result of ≥ 3mg/mmol is significant.
  • A urine dipstick can be used to check for haematuria. A significant result is 1+ of blood. Haematuria should prompt investigation for malignancy (i.e. bladder cancer)
  • Renal US can be sued to investigate pts with accelerated CKD, haematuria, FH of polycystic kidney disease or evidence of obstruction
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16
Q

Staging CKD : G score ?

A

The G score is based on the eGFR:

G1 = eGFR>90
G2 = eGFR 60-89
G3a = eGFR 45-59
G3b = eGFR 30-44
G4 = eGFR 15-29
G5 = eGFR < 15 (known as "end-stage renal failure"
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17
Q

Staging CKD: A score ?

A

The A score is based on the albumin:creatinine ratio:

A1= < 3mg/mmol
A2 = 3-30mg/mmol
A3 = > 30mg/mmol
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18
Q

When would a pt not have CKD/ have CKD ?

A

The pt does not have CKD if they have a score of A1 combined with G1 or G2. They need at least an eGFR of less than 60 (G3a and above) or proteinuria for a diagnosis of CKD.

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19
Q

Name 5 complications of CKD ?

A 
Anaemia 
Renal bone disease
Cardiovascular disease
Peripheral neuropathy
Dialysis related problems
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20
Q

When do NICE suggest referral to a specialist in CKD ?

A

Any of the following:

  • eGFR < 30
  • ACR ≥ 70mg/ mmol
  • Accelerated progression defined as a decrease in eGFR of 15 or 25% or 15ml/min in 1 year
  • Uncontrolled HTN despite 4 or more antihypertensives
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21
Q

Aims of management of CKD ?

A
  • Slow the progression of the disease
  • Reduce the risk of cardiovascular disease
  • Reduce the risk of complications
  • Treating complications
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22
Q

Management of CKD (use headings) ?

A

Slowing the progression of the disease:

  • Optimise diabetic control
  • Optimise hypertensive control
  • Treat glomerulonephritis

Reducing the risk of complications:

  • Exercise, maintain a healthy weight and stop smoking
  • Special dietary advice about phosphate, sodium, potassium and water intake.
  • Offer atorvastatin 20mg for primary prevention of cardiovascular disease

Treating complications:

  • Oral sodium bicarbonate to treat metabolic acidosis
  • Iron supplementation and erythropoietin to treat anaemia
  • Vit D to treat renal bone disease
  • Dialysis in end stage renal failure
  • Renal transplant in end stage renal failure
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23
Q

Treating HTN in CKD ?

A

ACEi are the first line in pts with CKD. These are offered to all pts with:

  • Diabetes plus ACR > 3mg/mmol
  • HTN plus ACR > 30mg/mmol
  • All pts with ACR > 70mg/mmol

Aim to keep BP < 140/90 (or 130/80 if the ACR > 70mg/mmol)

Serum potassium needs to be monitored as CKD and ACEi both cause hyperkalaemia.

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24
Q

How can CKD cause anaemia ?

A

Healthy kidney cells produce erythropoiein. Erythropoietin is the hormone that stimulates production of red blood cells. Damaged kidney cells in CKD cause a drop in erythropoietin Therefore, there is a drop in RBCs and a subsequent anaemia.

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25
Q

How can anaemia of CKD be treated ?

A

With erythropoiesis stimulating agents, such as exogenous erythropoietin. Blood transfusions should be limited as they can sensitise the immune system (“allosensitisation”) so that transplanted organs are more likely to be rejected.

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26
Q

What should be treated before offering EPO in anaemia of CKD, with what and why does this happen ?

A

Iron deficiency should be treated before offering EPO. IV iron is usually given, particularly in dialysis pts. Oral iron is an alternative. This happens as CKD causes a rise in hepcidin which reduces iron absorption from the GI tract.

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27
Q

What is renal bone disease also known as ?

A

Chronic kidney disease-mineral and bone disorder (CKD-MBD)

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28
Q

Features of renal bone disease ?

A
  • Osteomalacia
  • Osteoporosis
  • Osteosclerosis
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29
Q

Xray changes of renal bone disease ?

A

Spinal xray shows sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white). This is classically known as “rugger jersey” spine after the stripes found on a rugby shirt.

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30
Q

Pathophysiology of renal bone disease ?

A

HIGH SERUM PHOSPHATE due to reduced phosphate excretion. LOW ACTIVE VIT D occurs because the kidney is essential in metabolising vit D to its active form. ACTIVE VIT D is essential in calcium absorption from the intestines and kidneys, therefore there is a low serum calcium. Vit D also regulates bone turnover.

SECONDARY HYPERPARATHYROIDISM occurs because the PT glands react to the low serum calcium and high serum phosphate by excreting more PTH. This leads to increased osteoclast activity. Osteoclast activity leads to the absorption of calcium from bone.

OSTEOMALACIA occurs due to increased turnover of bones without adequate calcium supply

OSTEOSCLEROSIS occurs when the osteoblasts respond by increasing their activity to match the osteoclasts, creating new tissue in the bone. Due to the low calcium level this new tissue is not properly mineralised.

OSTEOPOROSIS can exist alongside the renal bone disease due to other risk factors such as age and use of steroids.

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31
Q

Management of renal bone disease ?

A

A combination of:

  • Active forms of vit D (alfacalcidol and calcitriol)
  • Low phosphate diet
  • Biphosphonates
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32
Q

What is dialysis, which pts is it used in and what does it involve ?

A

A method of performing the filtration tasks of the kidneys artificially. It is used in pts with end stage renal failure or complications of renal failure. It involves removing excess fluid, solutes and waste products.

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33
Q

Indications for acute dialysis in pts with severe AKI ?

A

AEIOU

A - Acidosis (Severe and not responding to treatment)
E - Electrolyte abnormalities (severe and unresponsive hyperkalaemia)
I - Intoxication (overdose of certain medications)
O - Oedema (severe and unresponsive pulmonary oedema)
U - Uraemia symptoms such as seizures or reduces consciousness

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34
Q

Indications for long term dialysis ?

A
  • End stage renal failure (CKD stage 5)

- Any of the acute indications continuing long term

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35
Q

Options for maintenance dialysis ?

A
  • Continuous ambulatory peritoneal dialysis
  • Automated peritoneal dialysis
  • Haemodialysis
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36
Q

Decision about which form of dialysis to use is based on ? (4 bullet points)

A
  • Patient preference
  • Lifestyle factors
  • Co-morbidities
  • Individual differences regarding risks
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37
Q

How does peritoneal dialysis work ?

A

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

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38
Q

How does dialysis solution get into and out of the peritoneal cavity ?

A

By using a Tenckhoff catheter. This is a plastic tube that is inserted into the peritoneal cavity with one end on the outside.

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39
Q

What is continuous ambulatory peritoneal dialysis ?

A

This is where the dialysis solution is in the peritoneum at all times. There are various regimes for changing the solution. One example is where 2 litres of fluid are inserted into the peritoneum and changed four times a day.

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40
Q

What is automated peritoneal dialysis ?

A

This involves peritoneal dialysis occurring overnight. A machine continuously replaces the dialysis fluid in the abdomen overnight to optimise ultrafiltration. It takes 8-10 hours.

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41
Q

Complications of peritoneal dialysis ?

A
  • BACTERIAL PERITONITIS - Infusions of glucose solution make the peritoneum a great place for bacterial growth. 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 pt starts to absorb the dextrose in the filtration solution. This reduces the filtration gradient making ultrafiltration less effective. This becomes more prominent over time.
  • WEIGHT GAIN can occur as they absorb the carbohydrates in the dextrose solution
  • PSYCHOLOGICAL EFFECTS - there are huge social and psychological effects of having to change dialysis solution and sleep with a machine every night.
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42
Q

What is haemodialysis + what is needed for this to work ?

A

Pts have their blood filtered by a haemodialysis machine. Regimes can vary but a typical regime might be 4 hours day for 3 days a week.

They need good access to an abundant blood supply. The options for this are:

  • Tunnelled cuffed catheter
  • Arterio-venous fistula
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43
Q

What is a tunnelled cuffed catheter ?

A

A tube inserted into the subclavian or jugular vein with a tip that sits in the superior vena cava or right atrium. It has two lumens, one where blood exits the body (red) and one where blood enters the body (blue).

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44
Q

What is a Dacron cuff ?

A

Part of a tunnelled cuffed catheter. It is a ring that surrounds the catheter. It promotes healing and adhesion of tissue to the cuff, making the catheter more permanent and providing a barrier to bacterial infection. These can stay in long term and be used for regular haemodialysis.

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45
Q

Main complications of a tunnelled cuffed catheter ?

A

Infection and blood clots within the catheter

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46
Q

What is an AV fistula, how does it work + why is this useful and how are they created ?

A

An artificial connection between an artery and 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.

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47
Q

Where are AV fistulas usually made ?

A

They are typically formed between an artery and vein in the pts forearm:

  • Radio-cephalic
  • Brachio-cephalic
  • Brachio-basilic (less common)
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48
Q

Examining an AV fistula is a common exam question. Look for ?

A
  • Skin integrity
  • Aneurysms
  • Palpable thrill (a fine vibration felt over the anastomosis)
  • Stereotypical “machinery murmur” on auscultation
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49
Q

Complications of an AV fistula ?

A
  • Aneurysms
  • Infection
  • Thrombosis
  • Stenosis
  • STEAL syndrome
  • High output heart failure
50
Q

What is STEAL syndrome ?

A

It is where there is inadequate blood flow to the limb distal to the AV fistula. The AV fistula “steals” blood from the distal limb. The blood is diverted away from where it was supposed to supply and flows straight into the venous system. This causes distal ischaemia

51
Q

How can an AV fistula cause high output heart failure ?

A

Blood is flowing very quickly from the arterial to the venous system through an A-V fistula. This means there is rapid return of blood to the heart. This increases the pre-load in the heart. this leads to hypertrophy of the heart muscle and heart failure

52
Q

TOM TIP

A

Never take blood from a fistula !! This is a lifeline for the pt, providing access to dialysis. If it gets damaged it will set them back and you will be in big trouble.

53
Q

Patients and donor kidneys are matched based on what ?

A

The human leukocyte antigen (HLA) type A, B and C on chromosome 6.

Note: 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.

54
Q

What happens during a renal transplant procedure ?

A

The pts own kidneys are left in place. The donor kidney’s blood vessels are connected (anastomosed) with the pts pelvic vessels, usually the external iliac vessels. The ureter of the donor kidney is anastomosed directly with the pts bladder. The donor kidney is placed anteriorly in the abdomen and can usually be palpated in the iliac fossa area. They typically use a “hockey stick incision” and there will be a “hockey stick scar”

55
Q

When will the new kidney start functioning post transplant ?

A

Immediately

56
Q

What will the pts require to reduce the risk of transplant rejection ? (Give an example regime)

A

Life long immunosuppression. The usual immunosuppressant regime is:

  • Tacrolimus
  • Mycophenolate
  • Prednisolone

Other possible immunosuppressants:

  • Cyclosporine
  • Sirolimus
  • Azathioprine
57
Q

Name 3 complications relating to a renal transplant ?

A
  • Transplant rejection (hyperacute, acute, chronic)
  • Transplant failure
  • Electrolyte imbalances
58
Q

Name 6 complications related to immunosuppressants?

A
  • 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)
59
Q

What is “nephritis” ?

A

A very generic term that means inflammation of the kidneys. It is a very non-specific descriptive term and is not a diagnosis or syndrome that has any criteria.

It is easy to get confused and think that when a pt is described as having “nephritis” this is a diagnosis. It is not, they are simply saying that the pt has inflammation of the kidney.

60
Q

What is a nephritic syndrome ?

A

This term refers to a group of symptoms not a diagnosis. When we say a pt has “nephritic syndrome” it simply means they fit a clinical picture of having inflammation of their kidney and it does not represent a specific diagnosis or give the underlying cause. Unlike nephrotic syndrome there are no set criteria however there are the following features of nephritic syndrome:

  • Haematuria - microscopic or macroscopic
  • Oliguria
  • Proteinuria - In nephritic syndrome there is less than 3g per 24hrs of urine. Any more and it starts being classified as nephrotic syndrome
  • Fluid retention
61
Q

What is a nephrotic syndrome ?

A

It refers to a group of symptoms without specifying the underlying cause. Therefore nephrotic syndrome is not a disease, but is a way of saying “the pt has these symptoms”. To have a nephrotic syndrome a pt must fulfil the following criteria:

  • Peripheral oedema
  • Proteinuira (more than 3g per 24 hrs)
  • Serum albumin (less than 25g per litre)
  • Hypercholesterolaemia
62
Q

What is glomerulonephritis ?

A

An umbrella term applied to conditions that cause inflammation of or around the glomerulus. Therefore, there are many conditions that can be described as a glomerulonephritis.

63
Q

What is interstitial nephritis ?

A

A term to describe a situation where there is inflammation of the space between cells and tubules (the interstitium) within the kidney.

It is important not to confuse this with glomerulonephritis. Under the umbrella term of interstitial nephritis there are two key specific diagnoses: acute interstitial nephritis and chronic tubulointerstitial nephritis.

64
Q

What is glomerulosclerosis ?

A

A term to describe the pathological process of scarring of the tissue in the glomerulus. It is not a diagnosis in itself and is more a term used to describe the damage and scarring done by other diagnoses

65
Q

What can cause glomerulosclerosis ?

A

It can be caused by any type of glomerulonephritis or obstructive uropathy (blockage of urine outflow), and by focal segmental glomerulosclerosis.

66
Q

Different types of glomerulonephritis ?

A
  • Minimal change disease
  • Focal segmental glomerulosclerosis
  • Membranous glomerulonephritis
  • IgA nephropathy (AKA Berger’s disease)
  • Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)
  • Mesangiocapillary glomerulonephritis
  • Rapidly progressive glomerulonephritis
  • Goodpasture syndrome
67
Q

Most types of glomerulonephritis are treated with ?

A
  • Immunosuppression (e.g. steroids)

- Blood pressure control by blocking the renin-angiotensin system (i.e. ACE inhibitors or angiotensin receptor blockers)

68
Q

Nephrotic syndrome usually presents with oedema. Pts might notice frothy urine (proteinuria). Nephrotic syndrome predisposes pts to what ?

A
  • Thrombosis
  • HTN
  • High cholesterol
69
Q

What is the most common cause of nephrotic syndrome in children is + what is it normally caused by + how is it treated ?

A

Minimal change disease .

This is normally idiopathic and treated successfully with steroids.

70
Q

The most common cause of nephrotic syndrome in adults is ?

A

Focal segmental glomerulosclerosis

71
Q

3 facts about IgA nephropathy (AKA Berger’s disease) ?

A
  • The most common cause of primary glomerulonephritis
  • Peak age at presentation is in the 20s
  • Histology shows “IgA deposits and glomerular mesangial proliferation”
72
Q

5 facts about membranous glomerulonephritis ?

A
  • Most common type of glomerulonephritis overall
  • There is a bimodal peak in age in the 20s and 60s
  • Histology shows “IgG and complement deposits on the basement membrane”
  • The majority (about 70%) are idiopathic
  • Can be secondary to malignancy, rheumatoid disorders and drugs (e.g. NSAIDs)
73
Q

Key fact about post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis) and how does it present ?

A

Pts are typically under 30 years old.

It presents as:

  • 1 to 3 weeks after a streptococcal infection (e.g. tonsillitis or impetigo)
  • They develop a nephritic syndrome
  • There is usually a full recovery
74
Q

Goodpasture syndrome ?

A

Anti-GBM (glomerular basement membrane) antibodies attack the glomerulus and pulmonary basement membranes. This causes glomerulonephritis and pulmonary haemorrhage. In my exam there may be a pt that presents with acute kidney failure and haemoptysis

75
Q

3 facts about rapidly progressive glomerulonephritis ?

A
  • Histology shows “crescentic glomerulonephritis”
  • It presents with a very acute illness with sick pts but it responds well to treatment
  • Often secondary to Goodpasture syndrome
76
Q

Most common cause of glomerular pathology and CKD in the UK ?

A

Diabetic nephropathy

77
Q

What is diabetic nephropathy ?

A

The chronic high level of glucose passing through the glomerulus causes glomerulosclerosis.

78
Q

Key feature of diabetic nephropathy and why does this happen ?

A

Proteinuria. This is due to damage to the glomerulus allowing protein to be filtered from the blood to the urine.

79
Q

Pts with diabetes should have regular screening for diabetic nephropathy with what tests ?

A
  • Urine albumin:creatinine ratio

- U&Es

80
Q

Management of diabetic nephropathy ?

A

Treatment is through optimising blood sugar levels and blood pressure. ACEi are the treatment of choice in diabetics for BP control. They should be started in pts with diabetic nephropathy even if they have a normal BP.

81
Q

What is acute interstitial nephritis ?

A

Acute inflammation of the tubules and interstitium

82
Q

How does acute interstitial nephritis present, what is it caused by and any other features that can occur ?

A

AKI and HTN

It is usually caused by a hypersensitivity reaction to:

  • Drugs (e.g. NSAIDS or antibiotics)
  • Infection

Other features of a generalised hypersensitivity reaction can accompany the acute kidney injury:

  • Rash
  • Fever
  • Eosinphilia
83
Q

Management of acute interstitial nephritis ?

A

Treating the underlying cause. Steroids have a role in reducing inflammation and improving recovery.

84
Q

What is chronic tubulointerstitial nephritis, how does it present, what are the causes and management?

A

Chronic inflammation of the tubules and interstitium.

It presents with CKD.

It has a large number of underlying autoimmune, infectious, iatrogenic and granulomatous disease causes.

Management involves treating the underlying cause. Steroids have a role when guided by a specialist

85
Q

Brief description of acute tubular necrosis ?

A

It is damage and necrosis of the epithelial cells of the renal tubules. Damage to the kidney cells occurs due to ischaemia and toxins. The epithelial cells have the ability to regenerate making acute tubular necrosis reversible. It usually takes 7 to 21 days to recover.

86
Q

Causes of acute tubular necrosis ?

A

Ischaemia can occur secondary to hypoperfusion in:

  • Shock
  • Sepsis
  • Dehydration

Direct damage from toxins can occur due to:

  • Radiology contrast dye
  • Gentamicin
  • NSAIDs
  • Lithium
  • Heroin
87
Q

What will urinalysis show in acute tubular necrosis ?

A

“Muddy brown casts” found on urinalysis if a pathognomic finding specific to acute tubular necrosis. There can also be renal tubular cells in the urine.

88
Q

Management of acute tubular necrosis ?

A

Same as other other causes of acute kidney injury:

  • Supportive management
  • IV fluids
  • Stop nephrotoxic medications
  • Treat complications
89
Q

What is renal tubular acidosis ?

A

Where there is a metabolic acidosis due to pathology in the tubules of the kidney. The tubules are responsible for balancing the hydrogen and bicarbonate ions between the blood and urine and maintaining a normal pH. There are four types, each with a different pathophysiology.

Type 1 and type 4 are the two that may come up in exams and are most relevant to clinical practice.

90
Q

What happens in type 1 renal tubular acidosis, what causes it, how does it present, what does it result in and how is it treated ?

A

It is due to pathology in the distal tubule. There is failure of H+ secretion into lumen of nephron by the alpha intercalated cells.

There are many causes

  • Genetic. There are both autosomal dominant and recessive forms
  • Systemic lupus erythematosus
  • Sjogrens sydnrome
  • Primary biliary cirrhosis
  • Hyperthyroidism
  • Sickle cell anaemia
  • Marfan’s syndrome

Presentation:

  • Failure to thrive in children
  • Hyperventilation to compensate for the metabolic acidosis
  • CKD
  • Bone disease (osteomalacia)

Results:

  • Hypokalaemia
  • Metabolic acidosis
  • High urinary pH (above 6)

Treatment is with oral bicarbonate. This corrects the other electrolyte imbalances as well as the acidosis.

91
Q

Why does type 1 renal tubular acidosis cause hypokalaemia ?

A

The alpha interecalated cells cannot secrete hydrogen ions thus cannot reabsorb potassium.

In other words, the intercalated cells’ apical H+/K+ antiporter is non-functional.

92
Q

What happens in type 2 renal tubular acidosis, what is the main cause + name some features of this, what does it result in and how is it treated ?

A

It is due to pathology in the proximal tubule. The proximal tubule is unable to reabsorb bicarbonate from the urine into the blood. Excessive bicarbonate is excreted in the urine.

Fanconi’s syndrome is the main cause. This is a genetic condition commonly associated with Ashkenazi Jews, that causes bone marrow failure, acute myeloid leukaemia and other cancers. There are certain features on examination such as cafe au lait spots, certain facial featurs and an absence of the radius bone bilaterally.

Results:

  • Hypokalaemia
  • Metabolic acidosis
  • High urinary pH (above 6)

Treatment is with oral bicarbonate.

93
Q

Type 3 renal tubular acidosis ?

A

A combination of type 1 and 2 with pathology in the proximal and distal tubules.

This is rare and unlikely to appear in exams or clinical practice

94
Q

What is type 4 renal tubular acidosis caused by, what happens, what causes this, what does it result in and how is it managed ?

A

It is caused by reduced aldosterone. Aldosterone is responsible for stimulating sodium reabsorption and potassium and hydrogen ion excretion in the distal tubules. This leads to insufficient potassium and hydrogen ion excretion causing a hyperkalaemic renal tubular acidosis. Normally ammonia is produced in the distal tubules to balance the excretion of hydrogen ions and prevent the urine from becoming to acidotic (ammonia is a base). Hyperkalaemia suppresses the production of ammonia so the urine is acidotic in type 4 RTA.

Low aldosterone or low aldosterone activity can be due to adrenal insufficiency, mediactions such as ACEi and spironolactone or systemic conditions that affect the kidneys such as SLE, diabetes or HIV.

Results

  • Hyperkalaemia
  • High chloride
  • Metabolic acidosis
  • Low urinary pH (due to reduced ammonia production)

Management is with fludrocortisone. Sodium bicarbonate and treatment of hyperkalaemia may also be required.

95
Q

What is haemolytic uraemic syndrome ?

A

It is when there is thrombosis in small blood vessels throughout the body. This is usually triggered by a bacterial toxin called the shiga toxin. It leads to the classic triad of:

  • Haemolytic anaemia
  • Acute kidney injury
  • Low platelet count (thrombocytopenia)
96
Q

What is the most common cause of haemolytic uraemic syndrome and what increases the risk of developing it ?

A

The most common cause is a toxin produced by the bacteria e. coli 0157 called the shiga toxin. Shigella also produces this toxin. The use of antibiotics and anti-motility medications such as loperamide to treat gastroenteritis caused by these pathogens increases the risk of developing HUS

97
Q

Presentation of haemolytic uraemic syndrome ?

A

E. coli 0157 causes a brief gastroenteritis, often with bloody diarrhoea.

Around 5 days after the diarrhoea the person will start displaying S+S of HUS:

  • Reduced urine output
  • Haematuria or dark brown urine
  • Abdominal pain
  • Lethargy and irritability
  • Confusion
  • HTN
  • Bruising
98
Q

Management of HUS ?

A

It is a medical emergency and has a 10% mortality rate. The condition is self limiting and supportive management is the mainstay of treatment:

  • Antihypertensives
  • Blood transfusions
  • Dialysis

70-80% of pts make a full recovery.

99
Q

What is rhabdomyolyis + what happens ?

A

It is a conditon where skeletal muscle tissue breaks down and releases breakdown products into the blood. This is usually triggered by an event that causes the muscle to break down, such as extreme underuse or overuse or a traumatic injury.

The muscle cells (myocytes) undergo apoptosis. the apoptosis results in muscle cells releasing:

  • Myoglobin (causing myoglobinuria)
  • Potassium
  • Phosphate
  • Creatine kinase

These breakdown products are filtered by the kidney and cause injury to the kidney. Myoglobin in particular is toxic to the kidney in high concentrations. This results in AKI. The AKI results in the breakdown products accumulating further in the blood.

100
Q

Most immediaetly dangerous breakdown product in rhabdomylosis and why ?

A

Potassium is the most immediately dangerous breakdown product, as hyperkalaemia can cause cardiac arrhythmias that can potentially result in a cardiac arrest.

101
Q

Causes of rhabdomyolysis ?

A

Anything that causes significant damage to muscle cells can cause rhabdomylosis:

  • Prolonged immobility - particularly frail pts that fall and spend time on the floor before being found
  • Extremely rigorous exercise beyond the person’s fitness level (e.g. ultramarathon, triathlon or crossfit competiton)
  • Crush injuries
  • Seizures
102
Q

Signs and symptoms of rhabdomylosis ?

A
  • Muscle aches and pain
  • Oedema (fluid accumulating in damaged muscle)
  • Fatigue
  • Confusion (particularly in elderly frail pts)
  • Red-brown urine
103
Q

Investigations for rhabdomyolysis ?

A
  • CREATINE KINASE (CK) blood test is a key investigation in establishing the diagnosis. It will be in the thousands to hundreds of thousands of Units/L. CK typically rises in the first 12 hours, then remains elevated for 1 to 3 days, then falls gradually. A higher CK increases the risk of kidney injury.
  • MYOGLOBINURIA. It gives urine a dark red-brown colour. This will cause a urine dipstick to be positive for blood.
  • U&E blood tests for AKI and hyperkalaemia
  • ECG is important in assessing the heart’s response to hyperkalaemia
104
Q

Management of rhabdomyolysis ?

A

Suspect rhabdomyolysis in pts with trauma, crush injury, prolonged immobilisation or excessive exercise.

  • IV fluids are the mainstay of treatment. The aim is to rehydrate the pt and encourage the filtration of the breakdown products.
  • Treat complications particularly hyperkalaemia. Hyperkalaemia can be immediately life threatening as it can cause arrhythmias (particularly ventricular fibrillation).
  • Consider IV sodium bicarbonate. This aims to make the urine more alkaline (pH ≥ 6.5), reducing the toxicity of the myoglobin on the kidneys. The evidence of this is not clear and there is some debate about whether to use it.
  • Consider IV mannitol. This aims to increase the GFR to help flush the breakdown products and to reduce oedema surrounding muscles and nerves. Hypovolaemia should be corrected before giving mannitol. The evidence on this is not clear and there is some debate about whether to use it.
105
Q

Main complication of hyperkalaemia ?

A

Cardiac arrhythmias such as ventricular fibrillation. These can be fatal .

106
Q

Causes of hyperkalaemia ?

A

Conditions:

  • Acute kidney injury
  • Chronic kidney disease
  • Rhabdomyolysis
  • Adrenal insufficiency
  • Tumour lysis syndrome

Medications :

  • Aldosterone antagonists (spironolactone and eplerenone)
  • ACEi
  • Angiotensin II receptor blockers
  • NSAIDs
  • Potassium supplements
107
Q

Relevance of U&Es for suspected hyperkalaemia ?

A

Hyperkalaemia is diagnosed on a formal U&E blood test. Pay attention to creatinine, urea and eGFR. Acute or chronic renal failure is important as they will need discussion with the renal team and consideration of haemodialysis.

Haemolysis during sampling can result in falsely elevated potassium. The lab might indicate that they have noticed some haemolysis and require a repeat sample to confirm the correct potassium result

108
Q

ECG changes in pts with hyperkalaemia?

A
  • Tall peaked T waves
  • Flattening or absence of P waves
  • Broad QRS complexes
109
Q

Management of hyperkalaemia ?

A

Pts with a POTASSIUM ≤ 6 mmol/L with otherwise stable renal function don’t need urgent treatment and may just require a change in diet and medications (i.e. stopping their spironolactone or ACE inhibitor)

Pts with a POTASSIUM ≥ 6 mmol/L and ECG changes need urgent treatment.

Pts with a POTASSIUM ≥ 6.5 mmol/L need urgent treatment regardless of the ECG

The mainstay of treatment is with an insulin and dextrose infusion and IV calcium gluconate:

  • Insulin and dextrose drive carbohydrate into cells and take potassium with it, reducing the blood potassium
  • Calcium gluconate stabilises the cardiac muscle cells and reduces the risk of arrhythmias.

Other options for lowering the serum potassium:

  • Nebulised salbutamol temporarily drives potassium into cells.
  • IV fluids can be used to increase urine output which encourages potassium loss from the kidneys (but don’t fluid overload pts with renal failure)
  • Oral calcium resonium draws potassium out of the gut and into stools. It works slowly and is suitable for milder cases of hyperkalaemia
  • Sodium bicarbonate (IV or oral) may be considered on the advice of a renal specialist in acidotic pts with renal failure. It drives potassium into cells as the acidosis is corrected.
  • Dialysis may be required in severe or persistant cases associated with renal failure.
110
Q

Note

A

Follow the local policy and protocol for treating hyperkalaemia. Get help from an experienced doctor. Pts with significant hyperkalaemia will need close ECG monitoring to detect changes and arrhythmias. Pts with significant renal impairment should be discussed with renal physicians.

111
Q

What is polycystic kidney disease ?

A

A genetic condition where the kidneys develop multiple fluid filled cysts. Kidney function is also significantly impaired.

112
Q

What may be felt on examination of polycystic kidney disease ?

A

Palpable enlarged kidneys.

113
Q

What are the two types of polycystic disease and which is more common ?

A

Autosomal dominant PKD and autosomal recessive PKD. Autosomal dominant PKD is more common.

114
Q

How is PKD diagnosed ?

A

By kidney US and genetic testing

115
Q

Autosomal dominant PKD genes ?

A

PKD-1: chromosome 16 (85% of cases)

PKD-2: chromosome 4 (15% of cases)

116
Q

Extra renal manifestations of AD PKD ?

A
  • Cerebral aneurysms
  • Hepatic, splenic, pancreatic, ovarian and prostatic cysts
  • Cardiac valve disease (mitral regurgitation)
  • Colonic diverticula
  • Aortic root dilation
117
Q

Complications of AD PKD ?

A
  • Chronic loin pain
  • HTN
  • Cardiovascular disease
  • Gross haematuria can occur with cyst rupture. This usually resolves within a few days
  • Renal stones are more common in pts with PKD
  • End stage renal failure occurs at a mean age of 50 years
118
Q

AR PKD is caused by a gene on which chromosome ?

A

chromosome 6

119
Q

AR PKD is more rare and more severe than AD PKD. How does it often present ?

A

It often presents in pregnancy with oligohydramnios as the fetus does not produce enough urine.

120
Q

Features of AR PKD ?

A

The oligohydramnios leads to underdevelopment of the lungs, resulting in respiratory failure shortly after birth. Pts may require dialysis within the first few days of life. They can have dysmorphic features such as underdeveloped ear cartilage, low set ears and a flat nasal bridge. They usually have end stage renal failure before reaching adulthood.

121
Q

Managment of PKD ?

A

Tolvaptan can slow the development of cysts and the progression of renal failure in AD PKD.

Management of PKD is mainly supportive of the complications:

  • Antihypertensives for HTN
  • Analgesia for renal colic related to stones or cysts
  • Antibiotics for infection. Drainage of infected cysts may be required
  • Dialysis for end stage renal failure
  • Renal transplant for end stage renal failure

Other management steps:

  • Genetic counselling
  • Avoid contact sports due to the risk of cyst rupture
  • Avoid anti-inflammatory medications and anticoagulants
  • Regular US to monitor cysts
  • Regular blods to monitor renal function
  • Regular blood pressure to monitor for HTN
  • MR angiogram can be used to diagnose intracranial aneurysms in symptomatic pts or those with a family history

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