I think it means that elevated serum creatinine and blood urea nitrogen occur subsequent to the start of toxicity. These are markers of advanced kidney damage. The toxicity would have begun well before these markers became apparent. Recently, markers have been established for kidney toxicity that can be detected when the damage is less advanced.

Hi Tauqeer, this refers to the time period between the patient commencing a known or suspected nephrotoxic drug and the onset of renal dysfunction.  For example if that time period is such that it would be plausible to suggest that the commencement of the drug is related to the renal dysfunction then there is a temporal (i.e. time) relationship.  Commonly this refers to the diagnosis of interstitial nephritis e.g. a patient presents with acute kidney injury, on biopsy there is evidence of interstitial nephritis; according to the history the patient started taking a proton pump inhibitor for example 2-3 weeks prior to the onset of acute kidney injury - this all implies a temporal relationship.  Hope this helps.

@Adam and @Dimitrios Thank you so much for you valuable suggestions. I got point here.

You raise a very good point as when we prepare our cases we define the temporal relationship to abnormal renal (or hepatic function test) based on the date these were first detected. Of course, we do not often know the exact time pathologically when renal function started to deteriorate unless there was sequential measurement (as can happen in intensive care) and certainly difficult if no previous baseline values to compare with.

Increased levels of creatinine and urea in the blood (azotemia Retention) is fully reliable screening method for detecting renal dysfunction toxic origin in acute and subacute periods. Retention azotemia develops as a result of reduction of glomerular filtration rate. However, its decline is secondary to damage to the epithelium of the proximal segments of the nephron. Have expressed nephrotoxic antimicrobials (gentamicin) and cytostatics.