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AKT > Renal Medicine > Flashcards

Renal Medicine Flashcards

1
Q

Pre-renal causes of AKI

A

Due to inadequate blood supply to kidneys reducing the filtration of blood. Inadequate blood supply may be due to:

Dehydration
Hypotension (shock)
Heart failure

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2
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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3
Q

Post-renal causes of AKI

A

Caused by obstruction to the 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 uretral strictures
Enlarged prostate or prostate cancer

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4
Q

Nephrotoxic drugs include

A

NSAIDS and ACE inhibitors

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5
Q

What gives GFR better than creatinine

A

Cystatin C - produced in the body at a constant rate

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6
Q

Creatine clearance calculation

A

U (urine concentration) x V (urine flow rate) / P (plasma concentration) x 24 x 60 = creatinine clearance

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7
Q

G Score of ranking kidney failure

A

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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8
Q

What is needed for diagnosis of CKD

A

eGFR of < 60 or proteinuria for a diagnosis of CKD.

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9
Q

Albumin creatine ratio?

A

Measures proteinuria
A1 = < 3mg/mmol
A2 = 3 – 30mg/mmol
A3 = > 30mg/mmol

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10
Q

Drug for patients with CKD

A

ACE inhibitors

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11
Q

Xray changes in CKD

A

Spine xray shows sclerosis of both ends of the vertebra (denser white) and osteomalacia in the centre of the vertebra (less white)

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12
Q

Indications for acute dialysis in patients with a severe AKI

A

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 reduced consciousness

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13
Q

Peritoneal Dialysis

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.

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14
Q

What is a Tenckhoff catheter?

A

This is a plastic tube that is inserted into the peritoneal cavity with one end on the outside. It allows access to peritoneal cavity. This is used for inserting and removing the dialysis solution.

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15
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 is inserted into the peritoneum and changed four times a day.

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16
Q

What is automated dialysis ?

A

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

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17
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 patient 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.

Psychosocial 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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18
Q

Options for blood supply for haemodialysis

A

Tunnelled cuffed catheter
Arterio-venous fistula

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19
Q

Positioning of a tunnelled cuffed catheter

A

Tube inserted into the subclavian or jugular vein with a tip that sits in the superior vena cava or right atrium

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20
Q

Examine an AV fistula

A

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

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21
Q

What is STEAL syndrome

A

STEAL syndrome 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 is was supposed to supply and flows straight into the venous system.

This causes distal ischaemia.

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22
Q

What is high output heart failure?

A

Where there is an A-V fistula blood is flowing very quickly from the arterial to the venous system through the fistula. This means there is rapid return of blood to the heart. This increases the pre-load in the heart (how full the heart is before it pumps). This leads to hypertrophy of the heart muscle and heart failure.

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23
Q

Procedure of kidney transplant

A

The patient’s own kidneys are left in place.

The donor kidney’s blood vessels are connected (anastomosed) with the patient’s pelvic vessels, usually the external iliac vessels.

The donor kidney’s ureter is anastomosed directly with the patient’s bladder.

The donor kidney is placed anterior 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”.

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24
Q

Immunosuppressants for kidney transplant

A

Most common
Tacrolimus
Mycophenolate
Prednisolone

Other possible immunosuppressants:
Cyclosporine
Sirolimus
Azathioprine

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25
The most common cause of nephrotic syndrome in adults
Focal segmental glomerulosclerosis.
26
What is the most common cause of primary glomerulonephritis (not caused by another disease)?
IgA nephropathy
27
Most common type of glomerulonephritis overall
Membranous glomulonephritis
28
Membranous glomulonephritis histology
IgG and complement deposits on the basement membrane
29
Classic presentation of Post streptococcal glomerulonephritis (AKA diffuse proliferative glomerulonephritis)
Patients are typically under 30 years. It presents as: 1-3 weeks after a streptococcal infection (e.g. tonsillitis or impetigo) They develop a nephritic syndrome There is usually a full recovery
30
Goodpasture syndrome presentation
Patient that presents with acute kidney failure and haemoptysis (coughing up blood). Anti-GBM (glomerular basement membrane) antibodies attack glomerulus and pulmonary basement membranes. This causes glomerulonephritis and pulmonary haemorrhage.
31
What two conditions may cause both haemoptysis and acute renal failure?
Goodpasture syndrome and granulomatosis with polyangiitis (AKA Wegener’s granulomatosis).
32
Granulomatosis with polyangiitis
Type of vasculitis associated with anti-neutrophil cytoplasmic antibodies (ANCA).
33
Acute interstitial nephritis presents with
Acute kidney injury and hypertension. There is acute inflammation of the tubules and interstitium.
34
Cause of acute interstitial nephritis
Usually caused by a hypersensitivity reaction to: Drugs (e.g. NSAIDS or antibiotics) Infection
35
What can cause direct damage to kidney tubules
Radiology contrast dye Gentamycin NSAIDs
36
Urinalysis unique to kidney tubular necrosis
Muddy brown casts and renal tubular epithelial cells
37
Renal tubular acidosis
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.
38
What is Type 1 Renal Tubular Acidosis?
Type 1 renal tubular acidosis is due to pathology in the distal tubule. The distal tubule is unable to excrete hydrogen ions.
39
Causes of type 1 renal tubular acidosis
Genetic. There are both autosomal dominant and recessive forms. Systemic lupus erythematosus Sjogren’s syndrome Primary biliary cirrhosis Hyperthyroidism Sickle cell anaemia Marfan’s syndrome
40
Signs type 1 renal tubular acidosis
Failure to thrive in children Hyperventilation to compensate for the metabolic acidosis Chronic kidney disease Bone disease (osteomalacia)
41
Lab results for type 1/2 tubular acidosis
Hypokalaemia Metabolic acidosis High urinary pH (above 6)
42
Treatment for type 1/2 renal acidosis
Treatment is with oral bicarbonate. This corrects the other electrolyte imbalances.
43
What is Type 2 Renal Tubular Acidosis?
Type 2 renal tubular acidosis 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.
44
Main cause of type 2 renal tubular acidosis
Fanconi's syndrome
45
What is Type 4 Renal Tubular Acidosis?
Type 4 renal tubular acidosis is caused by reduced aldosterone. Reduced urine buffering capacity
46
Cause of type 4 renal tubular acidosis
This can be due to adrenal insufficiency, medications such as ACE inhibitors and spironolactone or systemic conditions that affect the kidneys such as systemic lupus erythematosus, diabetes or HIV.
47
Lab results for type 4 renal tubular acidosis
Hyperkalaemia High chloride Metabolic acidosis Low urinary pH
48
Management of type 4 renal tubular acidosis
Management is with fludrocortisone. Sodium bicarbonate and treatment of the hyperkalaemia may also be required.
49
Triad of haemolytic uraemia syndrome
Haemolytic anaemia Acute kidney injury Low platelet count (thrombocytopenia)
50
Cause of HUS
Most common cause is a toxin produced by the bacteria e. coli 0157 called the shiga toxin. Shigella also produces this toxin and can cause HUS.
51
Classic presentation of HUS, timeline and symptoms
E. coli 0157 causes a brief gastroenteritis often with bloody diarrhoea. Around 5 days after the diarrhoea the person will start displaying symptoms of HUS: Reduced urine output Haematuria or dark brown urine Abdominal pain Lethargy and irritability Confusion Hypertension Bruising
52
What component of muscle cells in rhabdomyolysis causes AKI
Myoglobin in particular is toxic to the kidney in high concentrations.
53
Causes of rhabdomyolysis
Prolonged immobility, particularly frail patients that fall and spend time on the floor before being found Extremely rigorous exercise beyond the person’s fitness level (e.g. ultramaraton, triathalon, crossfit competition) Crush injuries Seizures
54
Rhabdomyolysis investigations
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 until 12 hours, then remains elevated for 1-3 days, then falls gradually. A higher CK increases the risk of kidney injury. Myoglobinurea is myoglobin in the urine. It gives urine a red-brown colour. This will cause a urine dipstick to be positive for blood. Urea and electrolytes (U&E) blood tests for acute kidney injury and hyperkalaemia. ECG is important in assessing the heart’s response to hyperkalaemia.
55
Management of rhabdomyolysis
IV fluids are the mainstay of treatment. The aim is to rehydrate the patient and encourage filtration of the breakdown products. 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 on this is not clear and there is some debate about whether to use it. Consider IV mannitol. This aims to increase the glomerular filtration rate 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.
56
ECG hyperkalemia
Tall peaked T waves Flattening or absence of P waves Broad QRS complexes
57
Hyperkalemia management
Insulin (e.g. actrapid 10 units) and dextrose (e.g. 50mls of 50%) drives carbohydrates into cells and takes potassium with it, reducing the blood potassium. Calcium gluconate stabilises the cardiac muscle cells and reduces the risk of arrhythmias.
58
Extra-renal manifestations of PKD
Cerebral aneurysms Hepatic, splenic, pancreatic, ovarian and prostatic cysts Cardiac valve disease (mitral regurgitation) Colonic diverticula Aortic root dilatation
59
Autosomal recessive polycystic kidney disease (ARPKD) presents in pregnancy with
Oligohydramnios as the fetus does not produce enough urine. Leads to underdevelopment of the lungs resulting in respiratory failure shortly after birth. 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.
60
Treatment for PKD
Tolvaptan (a vasopressin receptor antagonist) can slow the development of cysts and the progression of renal failure in autosomal dominant polycystic kidney disease.
61
What is Alport syndrome ?
Alport syndrome is a genetic disorder leading to mutations on collagen type 4. This type of collagen is found in the basement membrane of the kidney, the eye, and the cochlear leading the renal, hearing and eye problems.
62
Genetics of Alport syndrome
It is commonly X-linked but may be seen in a less severe, lyonization pattern in affected females. It can also present in a dominant or recessive fashion. Diagnosis is made on tissue biopsy and genetic testing.
63
Drug to reduce phosphate
Calcium carbonate Sevelamer (non calcium phosphate binder)
64
What does the 4-parameter Modification of Diet in Renal Disease (MDRD) formula include?
Creatinine, ethnicity, gender and age only CAGE
65
What does base excess tell us ?
Indicates metabolic component Positive base excess - metabolic alkalosis Negative base excess - metabolic acidosis Then use anion gap to work out cause
66
Paracetamol overdose
Paracetamol overdose tends to be indolent at the beginning of the syndrome with general nausea and vomiting. Right upper quadrant pains can be seen when liver damage occurs.
67
Acute interstitial nephritis causes findings of
An 'allergic' type picture consisting usually of raised urinary WCC, IgE, and eosinophils, alongside impaired renal function
68
Hyaline casts may be seen in the urine of patients taking
Loop diuretics
69
Dialysis disequilibrium syndrome
Array of neurological manifestations that are seen during or following dialysis, primarily after the new initiation of dialysis. Due to cerebral oedema
70
Why is sarcoidosis a RF for diabetes insipidus
Sarcoidosis can result in the formation of granulomas in the pituitary gland which leads to neurogenic diabetes insipidus.
71
What is the key indication that kidney disease is chronic and not acute
Hypocalcaemia
72
KDIGO staging of
Stage 1 Increase in creatinine to 1.5-1.9 times baseline, or Increase in creatinine by ≥26.5 µmol/L, or Reduction in urine output to <0.5 mL/kg/hour for ≥ 6 hours Stage 2 Increase in creatinine to 2.0 to 2.9 times baseline, or Reduction in urine output to <0.5 mL/kg/hour for ≥12 hours Stage 3 Increase in creatinine to ≥ 3.0 times baseline, or Increase in creatinine to ≥353.6 µmol/L or Reduction in urine output to <0.3 mL/kg/hour for ≥24 hours, or The initiation of kidney replacement therapy, or, In patients <18 years, decrease in eGFR to <35 mL/min/1.73 m2
73
What is used as a vitamin D supplement in end-stage renal disease because it does not require activation in the kidneys
Alfacalcidol
74
Diagnosis of Post-streptococcal glomerulonephritis
Raised anti-streptolysin O titres are used to confirm the diagnosis of a recent streptococcal infection
75
Distinguishing between prerenal uraemia and acute tubular necrosis
Look the urine sodium and osmolality and the serum urea : creatinine ratio. In prerenal uraemia, the body is trying to retain fluids. Hence, it is going to retain sodium to increase them, resulting in high blood sodium and low urine sodium. In ATN normal serum urea:creatinine ratio would be expected. On urine tests, sodium levels higher than 40 mmol/, low osmolality, and muddy brown casts would be expected.
76
What does urea:creatine ratio tell us about AKI?
Urea to creatinine ratio above 100 is a landmark characteristic of a pre-renal acute kidney injury.

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