Renal failure is defined as the cessation of kidney function with or without changes in urine volume
Anuria – UOP < 0.5 cc/kg/hour
Oliguria – UOP “more than 1 cc/kg/hour”

Acute Renal Failure - Definitions
70% Non-oliguric , 30% Oliguric
Non-oliguric associated with better prognosis and outcome
“Overall, the critical issue is maintenance of adequate urine output and prevention of further renal injury.”
Are we converting non-oliguric to oliguric with our hemofilters?

Pre-renal
Decrease in RBF constriction of afferent arteriole which serves to increase systemic blood pressure by reducing the “shunt” through the kidney, but does so at a cost of decreased RBF
At the same time, efferent arteriole constricts to attempt to maintain GFR
As GFR decreases, amount of filtrate decreases.  Urea is reabsorbed in the distal tubule, leading to increased tubular urea concentration and thus greater re-absorption of urea into the blood.
Creatinine cannot be reabsorbed, thus leading to a BUN/Cr ratio of > 20

Diagnosis
Ultrasound
Structural anomalies – polycystic, obstruction, etc.
ATN –
poor corticomedullary differentiation
Increased Doppler resistive index
(Systolic Peak – Diastolic peak) / systolic peak
Nuclear medicine scans
DMSA – Static - anatomy and scarring
DTPA/MAG3 – Dynamic – renal function, urinary excretion, and upper tract outflow

Overall, renal vasoconstriction is the major cause of the problems in ARF
Suggested ARF be replaced with vasomotor nephropathy
Insult to tubular epithelium causes release of vasoactive agents which cause the constriction
Angiotensin II, endothelin, NO, adenosine, prostaglandins, etc.

Renin Angiotensin Axis
Renin’s role in pathogenesis of ARF
Hyperplasia of JGA with increased renin granules seen in patients and experimental models of ARF
Increased plasma renin activity in ARF patients
Changing intra-renal renin content modifies degree of damage
Feed animals high salt diet (suppress renin production)  renal injury  less renal injury than those fed a low sodium diet..

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