Introduction: Urokinase, which is probably produced in the kidneys, is partly excreted with the urine. Different renal diseases, for example acute renal failure, show low or no excretion of urokinase und many intratubular casts. In postischemic nephropathy of the rat it was investigated whether there is a connection between the excretion of urokinase, the juxtaglomerular complex, and the formation of casts. Furthermore we tried to remove the casts using fibrinolytic agents. Material and Methods: no female Wistar rats were used. The concentration of urokinase in the urine was determined by means of the fibrin plate method ( Astrup and Müllertz, 1952). Temporary ischemia of both kidneys was achieved by clamping the renal pedicles. Quantitative evaluation of the formation of casts was carried out by counting all casts which could be seen in one cross section of the kidney. In addition the percentage of fibrin-positive casts was determined (PTAH-staining of Mallory and Ladewig stain). The granulation index of the juxtaglomerular cells (JGI) was determined according to the method of Hartroft and Hartroft (1953). The excretion of the urokinase, the number of casts and the JGI were investigated after o, ½, 1, 2, 3, and 4 hours and 1, 2, 4, 11, and 30 days in animals having been submitted to a temporary renal ischemia of 15, 30, 45, 60, and 90 min. Frozen sections of the kidney (cryostat) were treated with solutions of urokinase and streptokinase of different concentrations. After temporary ischemia of 45, 60, and 90 min and restoration of blood circulation for 1 to 3 days unilateral nephrectomy was performed; immediately afterwards urokinase solution (1.9 ml, 100 U/ml) was infused into the aorta for 2 hours. Results: The formation of casts and the excretion of urokinase depend on the duration of renal ischemia and the time passed since restoration of blood circulation. After ischemia of 15 min little cast formation can be found after 3 hours at the earliest. A low grade maximum is reached on the first day, afterwards normal values are found. In most cases the concentration of urokinase in the urine is elevated immediately after ischemia of 15 min and remains elevated for 7 days at the longest. More severe alterations of the renal tissue, achieved by ischemia of 30 to 90 min, take less time to cause a formation of even more casts. Here again the maximum is reached after one day. Additionally, a high percentage of fibrin-positive casts and prolonged courses with an occasional increase in the number of casts can be found even after 30 days. Furthermore, the longer durations of ischemia result in an increase in the number of cases with transitorily either diminished or absent urokinase excretion. Subsequently elevated concentrations of urokinase occasionally occur up to 30 days. JGI partially parallels the excretion of urokinase. We were not able to observe an in-vitro elimination of casts by fibrinolytic agents. On the contrary it was possible to induce a considerable reduction of the number of the casts (average 66,5%) by urokinase given in vivo over a period of 2 hours. Discussion: The results presented here support the suggestion that urokinase has a protective function against the formation of intratubular casts. In cases with severe ischemic alteration of the kidney, decrease or absence of urokinase and great numbers of casts combined with a high percentage of fibrin-positive casts suggest a failure of this protective mechanism.