Renal medicine conditions Flashcards
Rhabdomyolysis
skeletal muscle tissue breaks down and releases breakdown products into the blood.
triggered by an event that causes the muscle to break down, such as extreme underuse or overuse or a traumatic injury
causes raised CK, dipstick +ve for blood cells.
treat hyperkalaemia and rehydrate.
what did muscle cells (myoctyes) release in cell death?
Myoglobin (causing myoglobinurea)
Potassium
Phosphate
Creatine kinase
K+ dangerous= cardiac arrhythmias
myoglobin= toxic to the kidneys in high concentrations (AKI)
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
signs and symptoms of rhabdomyolysis:
Muscle aches and pain Oedema Fatigue Confusion (particularly in elderly frail patients) Red-brown urine
investigation for rhabdomyolysis
Creatinine kinase: thousands to hundreds of thousands unitsL. rises until 12 hous, remains elevated for 1-3 days
myoglobinurea (in the urine) red brown colour. urine dipstick is +ve for blood
U+E- AKI and hyperkalaemia
ECG
management of rhabdomyolysis
trauma, crash injury, crush injury, prolonged immobilisations, excessive exercise.
IV fluids
IV sodium bicarbonate (makes urine more alkaline, pH >6.5) which reduces the toxicity of the myoglobin on the kidneys
IV mannitol (increase eGFR) and redue oedema
hypovolemia should be corrected before giving mannitol
treat complications (hyperkalaemia)
PKD
autosomal dominant and recessive type genetic condition (PKD1 on chormosome 16)
kidneys develop multiple fluid filled cysts
kidney function is impaired. palpable and enlarged kdineys
hepatic cyst
cerebral aneurysm
Hepatic, splenic, pancreatic, ovarian and prostatic cysts
Cardiac valve disease (mitral regurgitation)
Colonic diverticula
Aortic root dilatation
renal manifestations:
nocturia, loin pain, UTI, hypertension, bilateral kidney enlargement, renal stones, renal failure
extrarenal: male infertility, liver and pancreatic cysts, intracranial berry anerusm, cardiac abnormalities.
PKD diagnosis
ultrasound scan
genetic testing
autosominal dominant
PKD-1 chromosome 16
PKD-2 chromosome 4
autosominal resessive
chromosome 6
presents early in pregnancy with oligohydraminos as the fetus does not produce enough urine
*this leads to underdeveloped lungs= respiratory failure shortly after birth. dialysis in first few days of life. dysmorphic features- underdeveloped ears, low set ears, flat nasal bridge. end-stage renal failure before adulthood.
PKD complications
Chronic loin pain
Hypertension
Cardiovascular disease
Gross haematuria can occur with cyst rupture (this usually resolves within a few days
Renal stones are more common in patients with PKD
End-stage renal failure occurs at a mean age of 50 years
PKD management
tolvaptan (vasopressin receptor antagonist)
this slows cyst development
support complications:
Antihypertensives for hypertension.
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 PKD mx:
Genetic counselling
Avoid contact sports due to the risk of cyst rupture
Avoid anti-inflammatory medications and anticoagulants
Regular ultrasound to monitor the cysts
Regular bloods to monitor renal function
Regular blood pressure to monitor for hypertension
MR angiogram can be used to diagnose intracranial aneurysms in symptomatic patients or those with a family history
HUS- haemolytic uraemic syndrome
destruction of RBC and declining function of the kidneys from blood clots in the blood vessels.
triggered by bloody diarrhoea (D+ HUS). E.Coli is usually the cause (enterohaemorrhagic 0157:H7) attaches to the intestinal wall and secretes shiga-like toxin. absorbed by blood vessels and picked up by immune cells into the site of filtration (glomeruli) forming lots of tiny blood clots.]
can get atypical HUS (D-) and familial/genetic causes.
antibiotics and anti motility drugs (loperamide) can increase risk of developing HUS
HUS classic triad
- microangiopathic haemolytic anaemia (endothelial damage in the small blood vessels) *jaundice
- Low platelet count (thrombocytopenia) (all used up in clot formation) (easy bruising, purpura)
- Acute kidney injury (urea in the blood)
the excessive formation of blood clots leads to thrombocytopenia. clots break up the RBC= haemolysis = anaemia
blood flow is affected = AKI
HUS presentation
E.coli= brief gastroenteritis, bloody diarhrhoea
5 days after diarrhoea: Reduced urine output Haematuria or dark brown urine Abdominal pain Lethargy and irritability Confusion Hypertension Bruising
HUS management
diagnosis: proteinuria, haematuria. elevated urea and creatinine in blood.
blood smear: schistocytes and helmet cells.
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
antibiotics could potentially cause more release of toxins
