Prevention of Glomerular Damage with Pharmacologic Agents

Abstract

Histopathologic lesions in the glomerulus may result in increased protein excretion and/or a reduction in glomerular filtration rate, depending on the type and severity of the pattern of injury. In the absence of necrosis and replacement of normal structure with sclerosis it is usually assumed that there is a potential for reversibility. During the past 30 years a variety of pharmacologic agents have been employed clinically in the hope of hastening recovery by inducing resolution of the injury reaction or preventing progressive glomerular sclerosis with further decline in renal function. Since most forms of acquired glomerulopathy are presumably due to immunologic processes, therapeutic modalities have often been employed on the basis of their known or assumed action to alter immunologic responses, or their action to reduce inflammation or inhibit intravascular clotting. Despite this long experience, however, the pharmacologic basis for treating various patterns of glomerular injury remains empirical. Selection of individual pharmacologic agents for their effect on reversing or stabilizing different types of glomerular lesions is usually based on empirical clinical evidence that the cause of changes in renal function of treated patients is or is not more favorable than observed in nontreated patients. In some instances serial renal biopsies have been performed that provide information on changes in the underlying renal histopathologic lesion during the course of treatment.