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
diabetic nephropathy
DM - common cause of glomeular pathology. chronic hyperglycaemia lads to glomerulosclerosis (hardening of the glomeruli) which leads to reduced function
routine screening
optomise co-morbidities
diabetic nephropathy pathophysiology
‘glomerulosclerosis’
- increased viscocity of blood due to hyperglycaemia
- reduced blood flow within small capillaries
- this leads to small infarcts
- this damages the tissue through hypoxia and inflammation from capillary leak resopnse to injury
diabetic nephropathy clinical presentation
lethargy
polyruia
polydipsia
retinopathy
neuropathy
peripheral vascular disease
diabetic foot disease
*proteinuria is a key feature
albumin:creatinine ratio
U&E’s
management: ACE inhibitors
chronic reflux nephropathy
history of UTI as a child
scarring of kidney
raised creatinine
Diagnosis: renal tract CT
voiding cystourethrogram
Faconi syndrome
disturbance of the proximal convoluted tube function. generalised impairment of reabsorption of amino acids, K+, HCO3, phosphate and glucse
idiopathic, inherited (Wilson’s, inborn errors), acquired (tubule damage)
polyuria, hypophosphoateaemia, acidosis, hypokalaemi
Kidney surface anatomy
lie retroperitoneal
either side of the vertebral column
extend from T12 to L3
Renal blood supply
renal arter 5 segmental arteries interlobal arteries arcuate arteries afferent arterioles efferent arterioles peritubular capillaries
drained b the renal vein > IVC
lymph into para aortic nodes
what do the kidneys do?
electrolyte regulation endocrine role erythropoietin production renin and BP vitamin D activation fluid balance gluconeogenesis drug excretion acid base balance
filter 150L of blood per day
get 1/4 of the cardiac output
ANP
Atrial natriuretic peptide
released by the atria in the heart
in response to an incresase in blood volume
causes a decrease in sodium reabsorption which helps decrease fluid volume and BP
vasodilated the blood vessels int eh afferent arteriole
inhbitis RAAS
inhbitis aldosterone secretion
loop diuretics
inhbiti the Na/K/2Cl transporter on the ascending loop of Henle
- furosemide
- bumetanide
1st line for acute pulmonary oedema and fluid overload / HF.
can cause hypovolemia, hypokalaemia, hyponatraemia, ototoxicity
kidney stones
chronically dehydrated, poor diet (high salt / protein intake)
obsese
acute, severe flank pain (loin to groin)
can be calcium oxalate ar uric acid
tx: pain relief, hyration, US to break stones.
