ACUTE RENAL INSUFFICIENCY



Acute or subacute declines in the glomerular filtration rate and/or in tubular function (acute renal insufficiency) can occur in a variety of clin­ical settings and as a consequence of different types of insults to the kidney (Table 32-1). De­creases in the effective circulating blood volume or renal blood flow may result in a decline in the glomerular filtration rate with relatively intact tu­bular function. Such conditions are termed pre­renal azotemia. Obstruction to urine flow results in an acute decrease in renal function and the de­velopment of obstructive nephropathy. Renal pa­renchymal inflammatory diseases such as glo­merulonephritis and interstitial nephritis can also result in acute changes in kidney function. The term acute tubular necrosis (ATN] is generally taken to describe a clinical syndrome in which there is a simultaneous and progressive deterio­ration of both glomerular and tubular function in the absence of documented glomerular or inter­stitial nephritis, vascular disease, or obstruction of the collecting system. It is to be noted that the term acute tubular necrosis is not a valid histo­logical description of this syndrome (see page 215). Nonetheless, this terminology is widely used and will be employed in this chapter. Synonyms for acute tubular necrosis include vasomotor ne­phropathy, toxic nephropathy, and the acute renal failure syndrome. Acute tubular necrosis usually refers to rapid changes in renal function conse­quent to a severe reduction in the effective cir­culating extracellular fluid volume and/or the ingestion, administration, or generation of sub­stances that are directly toxic to the renal tubular cells. In the clinical setting, the diagnosis of ATN is often suggested from the history and physical examination of the patient but is, in fact, a diag­nosis of exclusion. Said in another way, it is nec­essary to carefully exclude the other defined renal syndromes before concluding that ATN is present. In the first part of the present chapter, the general approach to a patient with an acute decline in renal function is considered. The second part of this chapter deals more specifically with the ATN syndrome.