HMO education - kidney function Flashcards
Creatinine as a measure of renal function - in what way is it subpar?
Freely filtered by glomerulus, not reabsorbed, but 15% actively secreted by the tubules
In advanced renal failure the % tubular secretion increases…
It also varies with muscle mass and diet (small amount)
- Strict vegans, less cr intake, underestimates Cr therefore overestimates eGFR
- More muscle mass, more Cr released, overestimates Cr, underestimates eGFR
Serum Cr also only starts to increase substantially when approx 50% renal function is lost
If you really need to know the exact GFR - nuclear medicine studies (DTPA/MAG3). This is better than eGFR from Cr clearance and than 24 hour collections
Indications for 24 hour urine collection
Higher quality egFR for chemo dosing
24 hour bence jones protein, light chains in MM
BPT EXAM QUESTIONS: which drug increases serum Cr without impacting on eGFR
cotrimoxazole!!!
Everything goes back to normal once the drug is stopped
Factors that increase plasma Cr
Decreased GFR
Increased muscle mass
Cotrimoxazole effect
Factors that increase plasma urea
Decrease GFR
Dehydration (ADH response to dehydration)
Increased oral protein intake (diet/GI bleeding)
Increased catabolic rate and protein breakdown (sepsis, steroids, some tetracyclines)
Haematuria on dipsticks - false positives and negatives
…. compared to when you actually look under the microscope and see RBCs
False positives:
- haemoglobinuria
- myoglobinuria
- iodine contamination
- oxidising agents in container
false negatives:
- high urinary nitrate
- high urinary vit c
Proteinuria on dipstick… false positives and negatives
Normal <150mg / 24 hours or double in pregnancy
False positives: very alkaline urine, very concentrated urine, reading delay
false negatives
dilute urine
bence jones protein (need to specifically test)
Which organisms will not show up with nitrites on urine dipstick?
strep faecalis!!!!
others may be: staph, acinetobacter
Urine casts types
ACELLULAR
Hyaline - normal
Granular - cellular injury (e.g. ATN), immunoglobulin light chains, plasma proteins (e.g. albumin)
Fatty casts - hyaline casts with fat deposits (e.g. nephrotic syndrome)
waxy casts - ESRF
CELLULAR
- red, white
- tubular cells (ATN)
What is a bland vs abnormal vs active urinary sediment?
Bland: Nothing in urine to imply glomerular pathology
Abnormal: either casts of abnormal degree of protein - ddx may include GN
Active sediment: - includes red cell/glomerular casts –> implies glomerulonephritis!
Urgent indications for renal biopsy
Rapid deterioration of renal function with abnormal urinary sediment
Strong indications for renal biopsy
Proteinuria+ haematuria
Proteinuria >1g/day (not diabetic)
Renal impairment with either proteinuria or haematuria
What is microalbuminaemia an independent risk factor for?
Cardiac disease!!!!
Prerenal causes of AKI
Hypovolaemia
- bleeding
- low cardiac output
- hepatorenal
- renovascular stenosis
Renal causes of AKI
- ATN (ischaemic or toxic)
- GN
- Small/medium vessel - disease (vasculitis)
- Tubular obstruction (urate crystals, MM)
What is ATN?
Tubules are quite sensitive to ischaemia (blood supply is last in the line in the medulla)
Most risk of necrosis and cell death
Generally reversible. but once hypovol corrected you need to restrict fluid intake and correct electrolyte imbalances. May need dialysis to support.
Lasts 10-14 days classically
Polyuria with dilute urine may occur in recovery period
Hypovol vs progression to ATN - labs to differentiate
Urinary Na+
Pre-renal <20, ATN >40 (lost function of tubules, can’t retain Na)
Plasma urea/creatinine ratio
Pre-renal > 80
ATN < 80
Urine osmolality
Pre-renal > 500
ATN > 350
Ix for every AKI + initial clinical steps
- Bloods: VBG, UEC, LFT, FBE, CK, CMP, coags, CRP
- Urine: dipstick, MCS, protein:cr
- Imaging: USS or CT
Initial clinical steps:
- fluid balance / IDC insertion if required
- bladder scan
Criteria for post-obstructive diuresis
UO 200mls/hour for 2 hours
OR
>3L in 24 hours
Can cause severe dehydration and electrolyte imbalances
Management of post-obstructive diuresis
- N saline at 50-80% urine output / hour (depending on PO intake) –> slightly less than match to avoid continuing to drive polyuria
- 12 hourly UECs/CMP
- Replace electrolytes
- Accurate fluid balance
- Investigate the underlying cause of obstruction: constipation, tumour, stone, clot, etc.
Mechanism of triple whammy
NSAIDs: inhibit PGs at the afferent arteriole (constricts aff. art)
ACEi: reduce angiotensin II production at efferent arteriole (dilates eff art.)
Mechanisms of renal protection of ACEI in CKD
In a well patient…. ACEi protect the nephrons:
- Anti-proteinuric
- Reduced intraglomerular stress
- Delays progression of CKD
- Good antihypertensive
PPIs and AKI?
Can be associated with interstitial nephritis
Indications for dialysis
A - acidosis E - electrolytes (hyperK) I - intoxication O - overload (refractory to diuretics - can't make them pee despite large amounts of diuretics) U - uraemic pericarditis (right now!)
