Acute Renal Failure/Acute Renal Injury Flashcards
Define acute kidney injury/renal failure
Abrupt decrease in renal function as
measured by increased creatinine + increased BUN = azotaemia
often with oliguria = decreased during production
What is the normal BUN/creatinine ratio?
Tell me about the filtration + absorption of BUN + creatnine
Ratio = 15
BUN: urea = filtered + partly reabsorbed
Creatinine: filtered + not reabsorbed + secreted
What is prerenal azotaemia due to?
Explain Prerenal azotaemia
Decreased renal blood flow- eg hypotension
Decreased RBF – >decreased GFR = decreased blood filtered – >
(Sodium/water + BUN = retained by kidney to conservevolume – >oliguria + azotaemia +
increase BUN flow into blood -> bun/creatinine >15)
+
(Increased RAAS = aldosterone from adrenals release – >resorb sodium therefore H2O follows)
What is the tubular function like in prerenal azotaemia? And what effect does this have on urine osmolality and sodium, fraction of excreted sodium, and serum BUN/creatinine ratio
Tubular function = fine
Urine osmolality >500 i.e. tubules can conc. urine
Urine Na+ < 20
FENa 20
What is post renal azotaemia due to?
Obstruction to outflow from kidney e.g.
BPH, stones, neoplasia, congenital anomaly
Explain postrenal azotaemia
Obstruction outflow from kidney – >backpressure
– >decrease GFR – >
– Azotaemia due to nitrogen products building up + blood
- Oliguria
Explain early-stage postrenal azotaemia
What’s the tubular function like at at this stage?
Increased tubular pressure – >force BUN into blood – >increased BUN/creatinine ratio
FENa 500
Explain long-standing Obstruction @Postrenal azotaemia
Tubular damage – >decreased BUN reabsorption As reabsorption depends on in tact tubule– >Sarum BUN/creatinine ratio less than 15 as epithelium of tubular = damaged
Tubular damage – >
decrease sodium reabsorption ability -> FENa >2% +
Urine osmolality <500
What is the most common cause of ARF/AKI?
Explain the injury leads to intrarenal azotemia.
Due to ATN what is the FENa + urine osm?
What is ischaemic ATN often preceded by?
Explain ischaemic ATN.
Acute tubular necrosis = injury + necrosis @tubular epithelial cells
Injury – >necrotic cells – >plug tubules – >
decrease GFR – >intrarenal azotaemia
FENa > 2% – Decreased sodium resorption
Urine osm prerenal azotaemia – >
decreased RBF for ages – >ischaemic ATN
Decreased blood supply – >
necrotic tubules = PT + medullary segment of thick asc. limb = susceptible
What toxic agents cause nephrotic ATN ?
- Heavy metals e.g. Pb
- Aminoglycosides
- Radiocontrast dye
- Ethylene glycol = antifreeze = oxalate crystals
- Myoglobinuria = crush injury release myoglobin into blood
- Urate: tumour lysis syndrome =
CHEMO – >kill cells @ blood – >
rapid breakdown of nuclear material – >
increasing uric acid level – >damage tubules by ATN
To Resolve: hydrate = increase bloodflow
Allopurinol: decrease uric acid level
Clinically what do you see in intrarenal azotaemia ?
Brown granular casts @ urine
Oliguria due to plugging of tubules = decreased GFR
BUN+creatinine increase = cos can’t filter from blood
Decreased excretion of K+ – > hyperkalaemia
Decreased excretion of organic acids – >
met. acidosis + increased anion gap
What introduces acute interstitial nephritis?
What effect does drug cessation have on AIN?
Explain pathogenesis of AIN
Drug induced HS are interstitium + tubules =
NSAIDs, penicillin, diuretics – >
Inflam. infiltrate @connective-tissue/interstitium – > Acute renal failure – >
fever rash oliguria eosinophilia
Drug stop = AIN stop
Explain what causes renal papillary necrosis
How does the patient present?
Sickle-cell disease/trait
Acute pyelonephritis
Analgesic Chronic abuse = Phenacetin/aspirin
Diabetes
Haematuria + flank pain
What are the consequences of renal failure?
Explain renal osteodystrophy
Can’t make urine
Can’t x-rayed nitrogenous wastes
Metabolic acidosis = Buffer against bone = calcium leak out overtime = osteoporosis
Dyslipidaemia – increased TG
Hyperkalaemia
Uraemia = increased BUN =
asterixis, pericarditis, plated dysfunction, nausea, encephalopathy
Na/H2O retention
Growth retardation
EPO failure
Renal osteodystrophy:
(Vitamin dehydroxylation failure, hypocalcaemia, hyperphosphataemia) – >Secondary hypoparathyroidism
Vitamin dehydroxylation Failure – >
decreased 1,25 dihydroxyvitamin D3 – >
Decreased intestinal calcium absorption – >
Subperiosteal bone thinning =Osteitis fibrosis cystica
Can’t mineralise osteoid = osteomalacia
Hyperphosphataemia –> Cause tissue calcifications – >decreased serum calcium
What are the three stages of acute tubular necrosis
1.inciting event
2.maintenance phase = oliguric: 1 to 3 weeks
Hyperkalaemia, uremia, metabolic acidosis
3.recovery phase = Polyuric =
BUN + creatinine decrease + hypokalaemia
