Renal Failure
Definition
Classification
Causes
Phases
Complications
Assessment
Investigation
Acute: acute deterioration of renal function resulting in accumulation of nitrogenous wastes, Cr; 13% is acute on
chronic; if Cr <300, a rise >50 = ARF; if CRF >300, a rise >100 = ARF; defined as 50% decr in GFR
AKI: spectrum of functional and structural changes seen in ARF
Chronic: GFR <60 on repeated measurement without reversible cause
ESRF: symptomatic uraemia, GFR <10; GFR <10% normal for age; 25% 2Y to HTN
Acute: Anuric: <50ml/day
Oliguric: <400ml/day
Non-oliguric
Acute: global / regional decr renal blood flow is final common pathyway
Pre-renal: Ur:Cr >20; incr Ur 1st; accounts for 70% in community (most common cause in ED), 20% in hospital;
potentially reversable; if severe, can cause ATN
Caused by decr CO or decr BP with normal / incr CO
Decr preload: serum / plasma losses (eg. Burns, D+V, pancreatitis), blood loss, Oedematous states with
decr effective circulating vol (eg. CCF, nephrotic syndrome)
Pump failure (eg. MI, tamponade)
Incr afterload (eg. AS, PE)
Decr SVR (eg. Sepsis, vasodilators, anaphylaxis)
Vascular  Renal hypoperfusion (eg. RAS, hepatorenal syndrome)
Drugs  decr renal perfusion (eg. ACEi, PG inhibitors, NSAIDs, alpha agonists)
Renal: assoc with release of renal vasoCers; accounts for 20% in community, 70% in hospital
ATN: Ischaemic: similar to pre-renal; most common cause
Toxic: nephrotoxins (eg. Gent, amox, acyclovir, cephs, metals, analgesia, ETOH)
contrast (at risk if incr age, incr baseline Cr, DM, HTN, vol depletion, myeloma, incr dye load,
repeated exposure; risk of ARF in up to 10%; accounts for 10% hospital ARF), pigments (eg. Hb,
myoG)
prolonged pre-renal cause
Rhabdo
GN
tubular obstruction (eg. Urate, oxalate)
venous obstruction (eg. Renal vein thrombosis, IVC)
arterial obstruction (eg. Emboli, dissection, thrombus, trauma; microvascular damage from inflamm;
vasculitis)
severe HTN
Post-renal: accounts for 10% in community, 10% in hospital (ie. Uncommon); must be bilateral, or single kidney
Stones, papilla, tumours (eg. Prostate, uterus, cervix, lymphoma), fibrosis, retroperitoneal haematoma,
neurogenic bladder
Chronic: DM, HTN, reflux nephropathy, GN, PCKD, renovascular, analgesic nephropathy
Acute: oliguric phase: 1st 1-14/7; incr Ur by 0.5/day, Cr by 0.7/day, K by 0.5/day; decr HCO3 by 2/day
Polyuric phase: after if recovery; due to impaired concentrating capacity of nephrons
Acute: CNS: confusion, nausea, seizures
CV: arrhythmia, fluid overload
GI: stress ulcers, ileus
Haem: anaemia, plt dysfunction
Other: infection, poor wound healing, drug accumulation
Chronic: renal bone disease; anaemia (when GFR <30; more severe in DM and analgesic, less severe in PCKD); peri
neuropathy, HTN, incr atherosclerosis, acidosis, hyperCa (3Y hyperPT); metastatic calcification; PID, stress ulcers
Acute: assess vol status; look for signs of CRF, obstruction, infection
Acute:
GFR: less accurate if amputee, v small/large, muscle wasting; can lose 60% GFR and still have normal Cr
Urine: casts (eg. GN), hyaline casts (ATN), crystals; incr specific gravity; Na <20; urine osm > plasma osm; urine Cr :
plasma Cr >40
Bloods: incr K; incr Ur (may be low if severe liver disease, protein malnutrition); incr Cr; metabolic acidosis; incr Mg,
phos; decr Ca (may get incr in recovery stage); Na may be high / low / normal; if nephritic picture present, do ANA,
ANCA, complement, ASOT, hep serology, HIV
ECG: look for hyperK
USS: detect distal obstruction; 98% sens and spec for hydronephrosis; can assess vol status by compressibility of IVC;
always exclude a post-renal cause
Other: CXR, renal biopsy, MRI, renal perfusion scan; post-void bladder vol
Chronic:
Bloods: less severe acidosis; more severe anaemia
USS: kidney <9cm suggests CRF
Acute:
IVF: often vol deplete due to osmotic diuresis and decr PO intake, so often require IVF; renal perfusion dependent on
BP due to loss of autoregulation; may need to use CVP; pass IDC to measure UO; may need fluid restriction if renal /
post-renal
Maintain high UO (if still decr UO after adequate hydration): diuretics (eg. 2mg/kg frusemide in children), mannitol;
clear casts from tubule; may have cellular protective effect; may cause renal vasoD; no convincing evidence it helps,
but may have role in early trt of ATN (24-48hrs)
Mng BP: if >180/120  GTN, nifedipine, hydralazine; may need inotropes
In paeds: urgent trt if >5mmHg higher than 99th percentile for age
Dialysis indicated if: oliguria <5ml/kg/day; fluid XS + hypoxia not responding to diuretics; encephalopathy;
uncontrollable acidosis pH <7.1 resistant to HCO3; uncontrollable HTN; refractory K >6.5; pericarditis; dialysable toxic
cmpd with life threatening poisoning; peritoneal dialysis preferred in children
Also consider if: Cr >1000, Ur >30, Na <100 or >160, uraemic syndrome
Dopamine: only if oliguria despite IVF, BP support and diuretics
Other: relieve obstruction if present (may result in post-obstructive diuresis so monitor UO for 2hrs and admit if
>250ml/hr UO for >2hrs); avoid nephrotoxic drugs; mng K and acidosis; mng electrolytes
Mng
Chronic:
70% receive dialysis, 30% transplant; BP control; protein restriction; phophate binders
Late: salt + K restriction, Ca, vit D, Fe, vit B, folic acid, erythropoietin, renal transplant / dialysis
Acute: Sepsis + ARF = 80% mortality
30-40% mortality if no co-morbities
Chronic: 5yr survival 35%
Of incr Ur: high protein intake, GI bleed, catabolic states (eg. Trauma, infection)
Of incr Cr: high muscle mass, meat intake
Causes: GN, sepsis, HUS, post-op complication; 70% nephrotoxic, 30% ischaemic
Prognosis
DD
In paeds
Notes from: Dunn, TinTin, Cameron
tone tone
WBC
Pre renal
Nil/few
ATN
Nil/few
GN
+++
RBC
Nil/few
Nil/few
+++(note
dysmorphic)
Nil/few
Nil
nil
++
+++
Nil
++
++
+++
TIN
++(note may be
eosinophils)
+
Casts
-
granular
epi
rbc
Urinary chemistry also gives an indication of the cause of ARF
Pre renal
Blood urea/Cr
>100
Urine Na
<10
Urine osmolarity
>500
Urine S.G.
>1.013
renal
<100
>10
<350
<1.013
+
-