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The role of hypertension in the pathogenesis of renal damage is a subject of both historical interest and current investigation. Because of the difficulty associated with studying the pathophysiologic role of glomerular injury in systemic hypertension, experimental models have provided much of the data in this field. The mechanisms leading to glomerular injury are complex and not fully elucidated. Mesangial and endothelial cell injury are thought to be important pathophysiologic mechanisms in the renal injury associated with hypertension. One hypothesis suggests that glomerular hypertension (ie, a hemodynamic event) is the primary pathogenetic mechanism, but another supports the notion that glomerular hypertrophy (ie, abnormal growth-related events) contributes to injury. The intrarenal renin-angiotensin system may play an important pathogenetic role in end-stage renal disease. Angiotensin-converting enzyme (ACE) inhibition has been shown to arrest the progression of renal injury in animal models. Although the clinical database is incomplete, the findings of anecdotal reports and short-term studies suggest that ACE inhibition may preserve renal function in patients with scleroderma renal crisis, reduce proteinuria in patients with diabetic nephropathy, and normalize renal hemodynamics in patients with a variety of renal diseases. The beneficial effects of ACE inhibition may be due to both hemodynamic (eg, reduction in glomerular capillary and intraglomerular pressures) and nonhemodynamic (eg, potassium-sparing and reduction in mesangial proliferation) mechanisms. The precise role of ACE inhibitors in the prevention of renal damage awaits the results of ongoing long-term, double-blind clinical studies. Nevertheless, ACE inhibition may be an appropriate therapeutic alternative in the hypertensive patient whose renal injury is progressing despite aggressive antihypertensive therapy.

• During dialysis, it is assumed that the serum electrolyte levels asymptotically approach the concentration in the dialysate. In five patients, we observed an average 20% fall in serum potassium level, although the dialysate contained 42% more potassium than the predialysis serum. One patient had quadriplegia and near respiratory arrest as a complication of hypokalemia. The cause of the hypokalemia was a rapid shift of potassium from the extracellular to the intracellular space secondary to correction of acidosis. All patients entered dialysis with a history suggesting prolonged potassium loss, marked acidosis, and moderate hypokalemia; thus, the dialysate potassium concentration should be higher than normal, and frequent determinations of the serum potassium level should be performed. Therapy resulting in rapid correction of acidosis in uremic patients undergoing hemodialysis may cause large transcompartmental shifts of potassium. Potassium transfer across the dialysis membrane may be inadequate to compensate for such shifts, and life-threatening hypokalemia may occur. (Arch Intern Med 141:167-170, 1981)

Idiopathic membranous nephropathy, also termed "membranous glomerulonephritis," "extramembranous glomerulonephritis," "Ellis type 2 nephritis," and "epimembranous nephropathy,"1,2 is a well-recognized cause of nephrotic syndrome. Its clinical course and pathologic features are thoroughly verified. The presence of immunoglobulin-containing deposits in a subepithelial distribution along glomerular capillary loops and the formation of projections or spikes of basememt membrane between these deposits are commonly accepted pathologic criteria for the diagnosis.3,4 The disease is more common in adults than children and in men than women.2,4-6 Though the clinical course is variable, a certain percentage of patients progress to end-stage renal disease.3,6 Some of these patients will be treated by renal transplantation. The clinical course, however, of such patients after transplantation has yet to be thoroughly documented. This report describes the recurrence of idiopathic membranous nephropathy in a 47-year-old man several months after receiving a cadaver renal allograft. PATIENT SUMMARY This man