Interstitial Kidney Disease

Question 1

Interstitial nephritis

Answer 1

inflammation of the space between cells and tubules (the interstitium in the kidney)

two types-
acute interstitial nephritis
chronic tubulointerstitial nephritis

Question 2

acute interstitial nephritis

Answer 2

AKI and hypertension
acute inflammation of the tubules and interstitium

usually a hypersensitivity reaction to:
drugs (NSAIDs, antibiotics)
infection

• rash
• fever
• eosinophilia

*Steroids reduce inflammation and improve recovery

Question 3

chronic tubulointerstitial nephritis

Answer 3

chronic inflammation of the tubules and interstitium

CKD

autoimmune
infectious
iatrogenic
granulomatous disease

Question 4

acute tubular necrosis

Answer 4

death of the epithelial cells in the tubules. the most common cause of AKI occurs due to ischaemia or toxins

ATN is reversible as the epithelial cells can regenerate. takes 7-21 days to recover.

causes:
shock, sepsis, dehydration

direct damage:
radiology, gentamycin, NSAIDs

Question 5

acute tubular necrosis investigation and management

Answer 5

urinalysis= muddy brown cast and enal tubular epithelial cells in the urine

management:
supportive
IV fluids
stop nephrotoxic meds
treat complications

Question 6

renal tubular acidosis

Answer 6

metabolic acidosis due to pathology in the tubules of the kidney.

tubules are responsible for balancing H+ and HCO3 between the blood and urine, maintaining a normal pH

4 types of renal tubular acidosis

Question 7

type 1 renal tubular acidosis (pathophysiology)

Answer 7

pathology in the distal tubule
cannot excrete hydrogen ions

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

Question 8

type 1 renal tubular acidosis
presentation
+ treatment

Answer 8

Presentation:
Failure to thrive in children
Hyperventilation to compensate for the metabolic acidosis
Chronic kidney disease
Bone disease (osteomalacia)

Results:
Hypokalaemia
Metabolic acidosis
High urinary pH (above 6)

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

Question 9

type 2 renal tubular acidosis

Answer 9

pathology in the proximal tubule
cannot reabsorb bicarbonate from the urine into the blood

excessive bicarbonate is excreted in the urine

Fanconi’s syndrome is the main cause

Hypokalaemia
Metabolic acidosis
High urinary pH (above 6)

Treatment is with oral bicarbonate.

Question 10

type 3 renal tubular acidosis

Answer 10

Type 3 renal tubular acidosis is a combination of type 1 and type 2 with pathology in the proximal and distal tubule. This is rare and unlikely to appear in your exams or clinical practice.

Question 11

type 4 renal tubular acidosis

Answer 11

reduced aldosterone
most common cause

• adrenal insufficiency
• meds like ACEi, spironolactone
• SLE, diabetes, HIV

Hyperkalaemia
High chloride
Metabolic acidosis
Low urinary pH

management: fludrocortisone
sodium bicarbonate and treat hyperkalaemia

Question 12

Haemolytic uraemic syndrome

Answer 12

thrombosis in the small blood vessels throughout the body

triggered by shiga toxin (E.coli) and shigella (bacterial toxin)

risk factors- loperamide to treat gastroenteritis

Question 13

HUS classic triad

Answer 13

Haemolytic anaemia

Acute kidney injury

Low platelet count (thrombocytopenia)

because there are lots of blood clots being formed, this uses up a lot of platelets (thrombocytopenia) and this causes anaemia

Question 14

presentation of HUS

Answer 14

E.coli - gastroenteritis with bloody diarrhoea

5 days after- develop signs of HUS:
Reduced urine output
Haematuria or dark brown urine
Abdominal pain
Lethargy and irritability
Confusion
Hypertension
Bruising

Question 15

management of HUS

Answer 15

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

Antihypertensives
Blood transfusions
Dialysis

Question 16

Rhabdomyolysis

Answer 16

skeletal muslce tissue breaks down and releases breakdown products into the blood. extreme underuse or overuse or traumatic injury

myocytes undergo apoptosis and release-
myoglobin (toxic in high conditions to the kidneys= AKI)
potassium (!hyperkalaemia!)
phosphate
creatine kinase

Question 17

causes of rhabdomyolysis

Answer 17

anything which causes significant damage to the muscle cells

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

Question 18

signs and symptoms of rhabdomyolysis

Answer 18

Muscle aches and pain
Oedema
Fatigue
Confusion (particularly in elderly frail patients)
Red-brown urine

Question 19

investigations for rhabdomyolysis

Answer 19

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.

Question 20

management of rhabdomyolysis

Answer 20

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

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.

Treat complications, particularly hyperkalaemia. Hyperkalaemia can be immediately life threatening as it can cause arrhythmias (particularly ventricular fibrillation).

Question 21

glomerulosclerosis

Answer 21

pathological process of scarring of the tissue. can be caused by any type of glomerulonephritis / obstructive uropathy and focal segmental glomerulosclerosis

Question 22

acute tubular injury

Answer 22

ischaemia- on going pre renal insult
toxins: sepsis, drugs, pigments, radio contrast
x
If urine output improves immediately with fluids or BP =
pre-renal

If no improvement with fluids or BP = ATNSupportive
Avoid all nephrotoxics
Consider altering doses or stopping other medication
May require dialysis
Almost always recovers

Question 23

tubulointerstitial nephritis

Answer 23

Drugs
NSAID’s
Antibiotics: penicillins, cephalosporins
PPI
‘Herbal remedies’
Acute pyelonephritis
Sarcoidosis
Multiple myeloma

Withdrawal of offending drug
Steroids

Some recovery often seen