Studies on changes in parameters of the coagulation and fibrinolysis in association with extracorporeal shock wave lithotripsy.
Tissue damage by extracorporeal shock wave lithotripsy (ESWL) is assumed to be attributable to ischemic changes in the treated region surrounding the particular vessel which is first ruptured by shock waves. Such changes cannot take place without being accompanied by acceleration of coagulation and fibrinolysis. In the literature on renal damage by ESWL, no parameters of the coagulation and fibrinolysis of blood were used. The present study was designed to investigate renal damage by shock waves through the quantification of sequential changes in the following parameters between before and after ESWL: thrombin antithrombin III complex (TAT), alpha 2-plasmin inhibitor-plasmin complex (PIC), fibrin and fibrinogen degradation products (FDP) and D-dimer (D-D). In ESWL for renal stones, a significant acceleration of TAT occurred on the 1st postoperative day, followed by acceleration of PIC on the 3rd postoperative day. A transient acceleration was observed for FDP and D-D after operation. The levels of these parameters, however, returned to normal by the 1st postoperative week. In ESWL for ureteral stones, unlike for renal stones, none of the parameters showed statistically significant acceleration. In the construction of percutaneous nephrostomy (PNS) cases for ureteral stones before ESWL, none of the parameters showed significant acceleration either. Changes in these parameters of coagulation and fibrinolysis due to ESWL for renal stones were greater than those of construction of PNS or ESWL for ureteral stones. The reason for the difference of the alteration in these parameters between renal stones and ureteral stones were more abundant vessels in the kidney than the ureter. All these changes in the parameters, however, disappeared within almost 1 week.
Umekawa
T
T
Department of Urology, Kinki University School of Medicine, Osaka, Japan.
Kohri
K
K
Yamate
T
T
Amasaki
N
N
Ishikawa
Y
Y
Kurita
T
T
D000933:Antifibrinolytic Agents / Q000032:analysis*; D000990:Antithrombin III / Q000032:analysis*; D001777:Blood Coagulation; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis*; D005341:Fibrinolysin / Q000032:analysis*; D005342:Fibrinolysis; D006801:Humans; D007669:Kidney Calculi / Q000097:blood* / Q000503:physiopathology / Q000628:therapy; D008096:Lithotripsy / Q000009:adverse effects*; D010447:Peptide Hydrolases / Q000032:analysis*; D014514:Ureteral Calculi / Q000097:blood* / Q000503:physiopathology / Q000628:therapy; D000979:alpha-2-Antiplasmin
D000933:Antifibrinolytic Agents; D005338:Fibrin Fibrinogen Degradation Products; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; C037742:plasmin-plasmin inhibitor complex; D000990:Antithrombin III; D010447:Peptide Hydrolases; D005341:Fibrinolysin