Traumatic bilateral renal infarction.

Published examples of unilateral and bilateral renal artery thrombosis attest to their usual subjection to nephrectomy at diagnosis or soon thereafter, eliminating the opportunity for spontaneous improvement which would enlighten the issue of how often late recovery may occur, and under what circumstances. Seven cases of renal artery thrombosis and five patients with renal artery embolization extracted from the literature have included documentation of patchy histologic viability within otherwise total infarction. Conversely, 47 reports of renal artery thrombosis culminating in nephrectomy or examined post mortem include no reference to any of these histologic features. Presumptions are speculative regarding whether these features were absent, overlooked, or unexamined. Their incidence cannot be estimated--only the possibility of recoverable renal function in an unknown number of involved patients. It may be presumed that the majority of kidneys exposed to sustained arterial interruption will undergo irreversible infarction, with an undefined small subgroup later developing renal hypertension. An unknown number, however, may fortuitously possess arterial collateralization competent to support sufficient numbers of viable nephrons to sustain adequate renal function. It is further speculated that shared pathophysiologic features establish the opportunity for misdiagnosis of renal cortical necrosis, which carries a documented potential for spontaneous recovery. Impulsive bilateral nephrectomy may therefore be unjustified, particularly in consideration of the minimal potential hazards of nonremoval. In the event of convalescent problems of renal origin, delayed nephrectomy remains an option. The requirement for interval hemodialysis is further influenced by the advantages accruing from retention of the native kidneys relative to calcium metabolism and blood product replacement. A final consideration relates to the advisability of secondary revascularization of spontaneously recovered kidneys for the purpose of further improving renal perfusion and renal function. It may be argued that stable renal function at levels compatible with a tolerable or uncompromised lifestyle is best undisturbed, with the intention of avoiding iatrogenic mishap. A more objective consideration relates to the observed late, progressive deleterious influences of hyperfiltration imposed upon the reduced population of surviving nephrons (3); would this process been exaggerated by improved perfusion? Dietary protein restriction has been advocated for patients at risk. Identification of late functional deterioration would initiate a reconsideration of therapeutic revascularization.