CLINICAL MANIFESTATIONS OF ENDSTAGE RENAL DISEASE



The clinical manifestations of ESRD are pro­tean. The initial clinical presentation is also extremely varied. Clinical signs and symptoms may arise as a direct consequence of organ dysfunction secondary to the “uremic state” or as an indirect consequence of primary dysfunction of another system. There is not one single compound or path­ophysiological event that explains the multiple organ and systems abnormalities in uremia. Urea, monitored as the blood urea nitrogen concentra­tion fBUN), is not, in and of itself, the “uremic toxin.” Much discussion has focused on the pos­sible role of the so-called middle molecules, mol­ecules of molecular weight of 500 to 2000 (Na­varro et al., 1982). These middle molecules are retained in patients with renal disease, but their exact pathophysiological role remains to be de­fined. It has also been proposed that PTH may be an important factor in the genesis of some of the clinical manifestations of ESRD.

Table 33-2 lists the major clinical manifesta­tion of ESRD and divides them into those that are lifethreatening, those that are common but not an immediate threat to existence, and those that occur with variable clinical frequency and expres­sion. This division, however, is arbitrary and in any given patient, one organ system dysfunction may be the major threat to life or rehabilitation. The major causes of death in patients with ESRD are cardiovascular catastrophes and infections. The major morbid complications are the devel­opment of uremic bone disease (uremic osteo­dystrophy) and neuropathy.