Nephrotoxicity clinical presentations

There are four potential clinical presentations for acute CSA nephrotoxicity asymptomatic increases in serum creatinine (SCr) without overt renal dysfunction, acute kidney injury, delayed graft function after renal transplantation and recurrent or de novo hemolytic uremic syndrome (Table 2). 

Table 2. Clinical presentations of acute cyclosporine A nephrotoxicity.

Theoretically, any of the protective interventions mentioned in the previous section may be applicable to a clinical setting, but few have actually been studied, in some instances, because there are practical limitations to their use. For example, the duration of protection conferred by furosemide is brief, being confined to the time furosemide is present in the renal tubule. Furosemide would exacerbate electrolyte imbalance by causing sodium and potassium depletion, which, if not adequately monitored and replaced, would be expected to potentiate AmB-induced nephrotoxicity. Furthermore, none of the advocated drug interventions are itmocuous. Of all the alternatives, manipulation of sodium status or of the method of administration offer simple interventions that can be readily and usually... 

Diuretics have been shown to have variable effects in relationship to urinary calcium excretion and supersaturation, most notably including loop diuretic induced hypercalciuria and attenuation of urinary calcium excretion by thiazide diuretics. The factors contributing to nephrotoxicity are most commonly associated with multiple factors that favor calcium salt or uric acid deposition at the tubulo-interstitial level. Management of renal stone formation and nephrocalcinosis therefore presents a unique clinical challenge, balancing factors that increase risk for abnormal calcium salt deposition or crystallization, and factors that reduce this risk. 

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