AKI/Rhabdo/Renal replacment therapy Flashcards
Define AKI
abrupt decline in renal function manifested by increased plasma creatinine and increased BUN and a declining urine output
Small concentration of more than 0.3mg/dl over one to several days is clinically significant
Discuss RIFLE criteria
RISK: increased creatine x1.5, <0.5mg/kg/hour urine out for 6 hours
Injury: creatinine x2: <0.5mg/kg/hour urine out for 12 hours
Failure: creatanine x3: <0.3mg/kg/hour for 24 hours or anuria for 12 horus
Loss: Persistant ARF: complete loss of renal function for greater than 4 weeks
End stage
Discuss Mortality of AKI patient
high mortality rate: 25% in non olgiuric and 50% in oligouric
Discuss classification of AKI
Pre-renal: decreased renal perfusion Post-renal: obstruction to flow Renal: -Acute tubular necrosis -Glomerular, vascular
Discuss physiological mechanism to maintain GFR in states with reduced renal perfusion
Moderate decrease in renal perfusion stimulates both neuronal and hormonal factors to maintain GFR including
-RAS
-Aldosterone
-prostraglandins
-chatecholamines
-vasopressin
This causes selective constriction of efferent arterioles leading to increased GFR and renal NA re-absorption
With prolonged or more severe perfusion reduction GFR is not maintained and waste products accumulate
Discuss causes of pre-renal failure
True intravscular depletion or states depleting effective arteolar volume can lead to pre renal AKI
Volume depletion
- Decreased effectvie arterial volume (CCF, cirrhosis, nephrotic syndrome)
- true intravascular depletion (bleeding, dehydration)
renal vasocontriction
- cyclosporine
- hepatorenal
- hypercalcaemia
- NSAIDS
- tacrolimus
Discuss the use of ACE and NSAIDs in pre-renal AKI
This medications blunt physiological response to reducing perfusion and may worsen AKI
Discuss hepatorenal syndrome
The kidney failure in hepatorenal syndrome is believed to arise from abnormalities in blood vessel tone in the kidneys
The predominant theory is that vaso-active substance NO and PGs are produced by the cirrhotic liver (more common in alcholic cirrhosis) which causes splanchnic vasodilation. This reduces the perfusion pressure arriveing at the JG apparatus which leads to acitvation of RAS and efferent constriction. This is leads to persistent underfilling of renal vasculature with increase post glomerular constriction leading to reduced flow and failure
Discuss criteria of hepatorenal syndrome
- cirrhotic liver
- Creatanine >1.5mg/dl
- nil improvement for 48 hours despite withdrawal of diuretics
- absence of shock
- nil renal parenchymal disease as indicated by proteinuria less than 500, microhematuria >50 or abnormal renal ultrasound
Discuss post renal failure
Can be lower or upper. To produce AKI upper obstruction must be bilateral or patient must have a sole kidney
Lower:
- BPH
- Bladder cancer
- bladder stone
- blood clot
- neurogenic bladder
- prostate cancer
- urethral stricture
upper:
- AAA
- Blood clot
- renal calculi
- pelvic malignancy
- renal papilary necrosis
- retropertineal firbosis
- TCC
Discuss intrinsic renal failure
This can be broken down into 5 categories
1) ATN most common
2) AIN(acute intersitial nephritis)
3) acute glomerulanephritis
4) intratubular obstruction
5) acute vasuclar syndomes
Discuss ATN
characterised pathologically by injury and death of tubular epithelial cells, intratubular obstruction by exfoliated nectrotic cells back leakage of glomerular filtrate through the damaged tubular epithelium and a decreased GFR from reactive vasco-constriction
Can be split almost equally between ishcaemic and nephrotoxic.
There is a variable response to the kidney from ischaemia – some patient require on trasnient reduction in perfusion to produce ATN where as others may have prolonged hypoprofusion leading only to pre-renal azotemia. Any cause of pre-renal AKI can progress to ATN
Depending on the severity of parenchymal injury ATN may be either oliguric or nonoliguric. Loss of tubular integrity destroys both diluting and concentrating ability so urine osmolality is approx 300mOsm/kg, similarly Na reabsorption is impaired leading to urinary sodium of greater the 40
List causes of ATN
Ischemic
- Cardiopulmonary arrest
- hypotension
- hypovolaemic shock
- sepsis
Nephrotoxic
- Acetaminophen, aminoglycosides, amphotericin B, IV contrast
- pigment nephropathy
Discuss acute interstitial nephritis
is characterised by inflammation of the renal interstitium and tubules with a lymphocytic and eosinophlic infiltrate seen in biopsy. The clinical triad of fever, rash and eosinophilia is classic but one is often missing.
Most cases of AIN are secondary to drug hypersensitivy from penicillin, cephalosporins, PPI, sulfa Abs, diuretics, anticonvulasnats, NSAIDs, H2 antagonists.
Can more rarely be an immune reaction to an infection
Nephrotic range proteinuria may be present with NSAID induced but not with other
Discuss intratubular obstruction
intralobular obstruction by crystal deposition or paraproteins may produce AKI
1) acute uric acid nephropathy most commonly occurs in tumor lysis syndrome after chemo of sensitive tumors. is usually associated with hyperkalaemia, hyperphosphataemia and severe hyperuricemia
2) ethylene glycol ingestion can produce acute oxalate nephropathy characterised by heavy oxalate crystalluria
3) MM can cause via hypercalcaemia, hyperuricemia and direct nephrotoxcity from immunoglobin light chanins
