The main pathophysiology of radiocontrast mediated nephropathy is probably a combination of combined hypoxic and toxic renal tubular damage with deranged microcirculation. (7) (8) (9) (10) (11). Studies have showed toxic effects of radiocontrast agents on the proximal tubular cells. (12) The cytotoxic effects were aggravated by tissue hypoxia which is suggestive of interactions between direct cellular mechanisms and vasoconstriction mediated hypoxia. (13)
Post Renal AKI: Most forms of Post Renal causes of AKI are because of obstructive pathology. Severity of the glomerular function derangement …show more content…
Most easily available modality is by serum creatinine. It can be used to estimate the glomerular filtration rate (GFR) (15). The main problems associated with usage of serum creatinine in a setting of AKI are –
(1) It does not reflect accurately the GFR who is an unstable, fluctuant state. In some patients with early AKI, serum creatinine can be even normal. When the serum creatinine is rising, estimates of GFR based on creatinine values will overestimate the true GFR; conversely, estimates of GFR will underestimate the true GFR during recovery of kidney function, when the serum creatinine concentration is declining.
(2) In patients who are initiated on dialysis serum creatinine is of no use. Since it gets removed by dialysis, it cannot be used.
(3) Numerous clinical trials have identified that serum creatinine varies with age/ race/ body mass etc. (15)
Various classifications have been made to quantify the severity of AKI. Several consensuses exist. The most commonly recognised are
(1) RIFLE criteria