Acute Renal Failure - Kidney Disease

Acute Renal Failure

·        =Abrupt reduction in glomerular filtration rate ® ­plasma urea & creatinine and (usually) ¯urine volume (oliguria < 400 ml/day, auria < 100 ml/day). If ­­urea but only ­Cr then ?dehydration or catabolic state

·        Assess severity using Cockcroft-Gault equation .  Normal clearance >= ~ 100 ml/min 

·        Due to acute damage to any part of the kidney or renal tract. Usually Acute Tubular Necrosis but always consider differentials

Pre-renal Acute Renal Failure

·        =¯ in glomerular perfusion in absence of structural kidney damage

·        Kidney usually autoregulates – but can‟t cope with extremes

·        Can‟t interpret results if patient has had recent diuretics 

·        If prolonged ® ischaemic damage ® loss of medullary gradient and reabsorbing capacity ® dilute urine 

·        Causes:

o  Volume depletion: Usually GI loss, but also renal loss, burns, haemorrhage 

o  Cardiac failure ® ¯renal perfusion

o  Systemic vasodilation: sepsis or antihypertensives

o  Also:

§  Reno-vascular disease: renal artery stenosis 

§  Vasoconstriction in kidneys, e.g. due to NSAIDs (® ¯vasodilating PGs), ACE inhibitors (® ¯efferent arteriolar tone® ¯intraglomerular pressure)

·        Intense reabsorption of salt and water leads to:

o  Low volume of urine, high osmolality (> plasma), but low urine Na (usually < 20 mmol/l)

o  ­ Urine to plasma ratio of creatinine and urea 

o  Urea is re-absorbed preferentially to creatinine at low urine flows Þ plasma urea to creatinine is increased 

o  Hyaline casts: aggregations of urine protein if low urine flow

·        Kidneys try to compensate by: 

o  Vasodilating afferent arterioles (via ­PGs)

o  Activation of renin-angiotensin ® ­BP and vasoconstricts efferent arterioles

·        Management:

o  Rapid fluid resuscitation

o  Correct underlying disorder (eg inotropes)

o  Monitor intravascular volume and watch for ATN

Intrinsic Acute Renal Failure

·        Possible presentations:

o   Oliguria (rather than auria)

o   Nephritic syndrome: haematuria, hypertension, oliguria +/- oedema

o   Proteinuria: excludes pre and post-renal 

o   Hypertension: intrinsic renal disease ® ­BP, pre-renal ® ¯BP 

o   Systemic features of disorders causing intrinsic failure (eg fever, arthralgia, skin rash, vasculitis etc)

·        Due to:

o   Acute Tubular Necrosis (most common cause)

o   Acute Interstitial Nephritis 

o   RPGN: Urine chemistry midway between pre-renal acute renal failure and acute tubular necrosis - ­urine to plasma ratios for osmolality and creatinine, and Na between 20 – 40 mmol/L. 

o   Nephrotoxins

o   Other tubular diseases (eg myeloma)

·        Investigations:

o   Urinalysis: cells, casts, protein 

o   US: ­echogenicity

o   Renal biopsy

o   Also blood tests to exclude specific causes: ANA, ANCA, Complement, CK, etc

Post-renal Acute Renal Failure

·        Presentation: 

o   Complete auria: most pre-renal and intra-renal failure is oliguric. But partial obstruction may give moderate tubular dysfunction ® osmotic diuresis ® polyuria 

o   Normal urinalysis: no proteinuria or casts, any blood (eg from stones, cancer) will be normal not dysmorphic 

o   Specific diseases pre-dispose: eg diabetes and analgesic use ® papillary necrosis ® bits fall off and cause obstruction.  

·        Due to obstruction:

o   Usually in urethra: bladder stones or tumours.  Prostate usually chronic 

o   If at ureteric level must be bilateral to lead to severe kidney failure or obstruction on one side and a poor functioning kidney on the other

o   Extrinsic obstruction due to eg retroperitoneal fibrosis following radiotherapy, etc 

·        ® ­tubular pressure ® ¯glomerula filtration

·        Usually obvious from history, confirm with:

o   Ultrasound of kidneys for hydronephrosis

o   CT to determine the level of the blockage

o   IVU only if the kidney is functioning (ie Cr < 200)

Investigations in Acute Renal Failure

·        Renal biopsy is rarely needed to differentiate causes of renal failure, mainly in RPGN

Management

·        Treat cause

·        Resuscitate if hypovolaemia 

·        Monitor for ­K

·        Treat pulmonary oedema, ?dialysis

·        Monitor fluid balance carefully

·        Avoid nephrotoxic drugs