Physiology Flashcards
How do you measure true (most accurate) GFR?
Via nuclear med studies (DTPA or MAG3 studies). MAG3 better for poor renal function and paediatrics. Need to know exact GFR in certain situations e.g. post transplant. MAG3 preferred post transplant.
Features of creatinine and creatinine clearance
- From muscle
- Serum creatinine usually stable throughout the day
- Used for Cr based estimations of GFR via serum Cr formulae or 24 hour urinary Cr clearance
- Freely filtered by glomerulus. Not reabsorbed BUT 15% is secreted by tubules (not exact measure of GFR)… As GFR drops, secreted Cr increases (the worse the renal fn, the less accurate Cr is)
- Plasma Cr only begins to rise substantially when around 50% of renal function is lost (inaccurate) and is dependent on muscle mass
Renal failure blood gas
pH / HCO3 may indicate a metabolic acidosis in renal failure (acute or chronic)
K+ may be elevated (acute or chronic)
Causes of elevated serum creatinine
- Decreased GFR
- Increased skeletal mass
- Extreme vegetarian diet (underestimates kidney injury)
Causes of elevated urea
- Decreased GFR
- Dehydration (ADH also increases urea reabsorption in collecting duct)
- Increased oral protein intake (diet, GI bleeding)
- Increased catabolic rate/protein breakdown (sepsis, steroids, some tetracyclines)
Albumin:cr ratio
Normal, microalbuminaemia and macroalbuminaemia values
mg/mmol
Normal: <2.5 (M), <3.5 (F)
Microalb: 2.5-25 (M), 3.5- 35 (F)
Macroalb: >25 (M), >35 (F)
Haematuria dipstick - false positives and negatives
Usually good correlation
False positives: haemoglobinuria (IV haemolysis), myoglobinuria (rhabdo), iodine contam, oxidising agents in container
False negatives: high urinary nitrate, high urinary vitamin C
Proteinuria on dipstick - false positives and negatives
Normal <150mg/24 hours (higher in pregnancy)
False positives: very alkaline urine, very concentrated urine, reading delay
False negatives: dilute urine, BENCE JONES PROTEIN (not picked up on dipstick)
Bacteruria on dipsticks (nitrites) - what does it mean and when are there false negatives?
- COMMON EXAM Q
Nitrites are +ve when bacteria convert nitrate –> nitrite. Only gram negative bacteria do this (most commonly E coli).
False negatives therefore are from gram positives like STREP FAECALIS*****, staph, acinetobacter and in polyuria.
Urine microscopy
- What can be seen
- Types of casts
- Can help identify source of haematuria. Glomerular haematuria is dysmorphic (squeezed through BM) usually very severe. Non-glomerular are isomorphic (e.g. kidney stones, renal tract ca)
Can also see casts (tiny tube shaped particles seen under microscopy)….
- Cellular casts: red cells, white cells, tubular cells (ATN)
- Acellular casts: hyaline casts (normal), granular casts (cellular injury e.g. ATN), fatty casts (nephrotic syndrome), waxy casts (ESRF - same as the other casts but have been sitting in the tubules so long that they wax to the shape of the tubules)
Can also see pyuria (infection), lipiduria (nephrotic)
Bland vs abnormal vs active urinary sediments?
Bland = nothing in urine to suggest glomerular pathology
Abnormal = something is abnormality, may or may not be GN
Active urinary sediment: includes red cells or glomerular casts that implies GN
Indication for urgent renal biopsy?
Strong, but not urgent, indication for renal biopsy?
Rapid deterioration of renal function with abnormal urinary sediment
Not urgent, but strong indications are:
- Proteinuria + haematuria
- Proteinuria >1g daily (not diabetic)
- Renal impairment with proteinuria or haematuria
Relationship between eGFR and cardiovascular mortality?
An eGFR <60mL/min/1.73m2 = increasing incidence of CV events and mortality
Why is eGFR not a reliable tool in AKI?
Lags behind Cr both during development and resolution of AKI
What classifies an AKI?
- Serum creatinine >1.5 times baseline
OR - Serum creatinine >26.5umol/L increase from baseline
OR - Oliguria <0.5ml/kg/hour for 6-12 hours
Biochemical abnormalities in AKI
- High urea
- High creatinine
- Hyperkalaemia
- Acidosis (low bicarb) in acute and chronic
- Low calcium
- Elevated phosphate in acute and chronic
Prerenal causes of AKI
Hypovolaemia (bleed, CCF, hepatorenal, renovascular stenosis)
Renal causes of AKI
- ATN (ischaemic, toxic e.g. contrasts)
- GN
- Vasculitis
- Tubular obstruction: urate crystals, multiple myeloma
Post renal causes of AKI
Obstruction
What is ATN?
Pre-renal AKI can progress to ATN…
Initially, there is an appropriate response. Reduced renal perfusion due to drop in BP causes renin release –> intrarenal vasoconstriction (preserve the BP at the expense of the kidneys). With a pre-renal AKI, kidney function will improve with adequate replacement of circulating volume.
A prolonged renal response (ongoing intrarenal vasocontriction) causes intrarenal ischaemia –> hypoxia –> ATN..
Why do the tubules die specifically? The tubules are located in the medulla, which is last in line for blood supply in the kidney, and therefore suffer greatest from hypoxia.
How to treat ATN?
Generally reversible, but requires strict monitoring.
First correct the underlying cause of hypovolaemia first (like in a pre-renal AKI)….
BUT afterwards, restrict fluid intake, as patients can easily switch into fluid overload. Monitor electrolytes and support with dialysis if needed.
Classically lasts 10-14 days –> weeks.
In the recovery period, patients may have dilute polyuria which requires fluid replacement.
How to differentiate prerenal hypovolaemia from ATN? What are the caveats of this?
Clinically: replacing with appropriate IV fluids and urine output remains poor, and they are becoming fluid overloaded……
BUT should use biochemical methods
Biochemical methods NOT applicable for patients on diuretics or IV fluids
Pre-renal:
- Urinary Na+: <20 (trying hard to retain sodium)
- Plasma urea:cr ratio: > 80
- Urine osmolality > 500 (trying hard to concentrate urine)
Established renal failure:
- Urinary Na+: >40 (loses concentrating ability and leaks sodium into urine)
- Plasma urea:cr ratio: <80
- Urine osmolality: < 350 (have lost ability to concentrate urine)
Life threatening complications of AKI (5)
- Hyperkalaemia
- Volume overload
- Uraemic pericarditis
- Uraemic encephalopathy
- Metabolic acidosis
Top 6 causes of CKD (in order of prevalence)
- Diabetic nephropathy
- GN
- Vascular disease
- Others (?)
- PCKD/reflux nephropathy
- Analgesic nephropathy
