Renal disease Flashcards
Pre-renal disease
Clinical markers?
Reduced blood supply.
Very common cause of AKI
Leads to reduction in GFR
Creatinine and Urea increase in concentration
Doesn’t cause kidney damage unless iscahemia is severe
Causes of pre-renal disease
Shock: hypovolaemic, cardiogenic, distributive
Renovascular: embolus, aortic dissection, renal artery stenosis and thrombosis, or ACE-Is given in bilateral RAS
post-renal disease?
Normal blood supply, but increased intratubular pressure and decreased GFR.
=hydronephrosis
Affects medulla: LoH and CT
causes of post-renal disease?
catheterisation, stones, strictures, clots, external/internal malignancy
Bladder outlet obstruction can also cause post-renal AKI, e.g. prostatic enlargement, urethral strictures or phimosis / paraphimosis.
bladder extension a strong indicator
Intrinsic kidney disease
normal blood supply
disease of
1.glomerulus (glomerulitis) (5%)
2. tubules (acute tubular necrosis caused by ischaemia, or nephrotoxicity) (85%)
3. interstitial area (inflammatory reactions)/ interstitial nephritis (10%)
How can pre-renal lead to renal disease?
prolonged interruption of blood supply could cause ischaemia and Acute Tubular Necrosis, where cells lining tubules necrose, leading to porous/leaky tubule membranes and blockage due to necrosed cells.
Most common cause of AKI?
pre-renal disease
How could Acute Tubular Necrosis be identified with U&E analysis?
In initial pre-renal AKI, urine osmolality is high {>S00mosmol/kg), and urine sodium is low, as concentrating powers are retained.
If ATN develops, urine is isotonic with plasma {<400mosmol/kg) and has high sodium, as concentrating powers are lost.
Drugs causing ATN? Toxins?
aminoglycosides, nephalosporins, radiological contrast
mediums, NSAIDs
Toxins: heavy metal poisoning, myoglobinuria or haemolytic uraemic syndrome {HUS).
What is myoglobinuria?
rhabdomyolysis: when in excess, myoglobin is released
but too much to be efficiently filtered, and some precipitates into tubules to cause damage
What is haemolytic uraemic syndrome?
Occurs in children following a diarrhoeal illness caused by verotoxin- producing E.coli 0157, or following an URTI in adults.
It leads to thrombocytopenia (can cause purpura), haemolysis and ATN. Children usually recover within a few weeks, but prognosis is poor in adults. Treatment is supportive, including dialysis.
What is interstitial nephritis?
Most commonly caused by drugs, however the damage is not limited to tubular cells (such as in ATN), and bypasses the basement membrane to cause damage to the interstitium.
Antibiotics are the most common cause of interstitial nephritis, with other agents including diuretics, allopurinol and proton pump inhibitors.
It normally responds to withdrawal of the drugs and a short course of oral steroids.
What are normal protein levels?
What about in proteinuria?
Normally 150mg day-1 max
30mg-300mg day-1
Are urine dipsticks sensitive to all protein?
Just albumin, less so for globulin, haem, or light chain
Risk factors for diabetic nepropathy?
Men T1DM before 20 years South Asian or Afro-Carribean Diabetic retinopathy HT Genetic: FMX
Stage 1 DN?
hyperfiltration stage:
GFR increases
there is increased circulating volume
-glucose cotransport means sodium absorption in proximal tubule, but low delivery to distal, where more is taken in!
-glucose also inhibits the renin-angiotensinogen system: afferent vasodilation and loss of auto-regulation
no protein in urine
Stage 2 DN
Latent phase:
GFR normalises
sub-clinical amounts of protein in the urine
podocyte failure or loss: glomerular hypertrophy leading to leakage of protein, and podocyte apoptosis because more ROS from heightened glucose metabolism
Stage 3 DN?
Microalbuminaemia: stage II progresses to stage III if there is poor diabetic control, hypertension (loss of nocturnal BP dip), smoking, increased protein intake or obesity.
Stage 4 DN?
Proteinuria
Leads to renal damage, because high protein not tolerated by kidney and causes scarring and damage
How do you treat stage II DN?
identify risk factors and address them if possible ACEI-I for HT glucose control cholesterol smoking diet and exercise
Treating stage III and IV DN?
manage HT with ACE-I or ARBs
diuretics
beta blockers to address sympathetic hyperactivity in DM
SDLT2
glucose control won’t help renal pathology much any longer, but there is likely to be other complications where this would be important, so should be parrt of the overall treatment strategy
How might Uss identify DN?
Would show increased size of kidney
Describe the assessment o f CKD using estimated glomerular filtration rate and the 5 stages of CKD
What is eGFR?
CKD is diagnosed when any two tests three months apart show reduced eGFR, and can be staged 1-5 depending on the level of reduction. Stage 1 has no reduction in eGFR, yet there is other long-term evidence of kidney disease, e.g. proteinuria/haematuria, a genetic diagnosis of kidney disease, or evidence of structuraly abnormal kidneys Stage 2: evidence of structural damage GFR 60-89 Stage 3: GFR 30-59 Stage 4: 15-29 Stage 5: ESRF <15
eGFRis just an estimate of GFR based on a plasma level of creatinine. This can be inaccurate in certain situations, so a 24hour urinary creatinine may be collected to calculate true creatinine clearance.
Aetiology of CKD
Diabetes Mellitus (20-40%). Hypertension. Chronic Glomerulonephritis . Chronic pyelonephritis. Obstructive uropathy. Renovascular disease. Drugs (long-term NSAIDs). Polycystic kidney disease.
