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The most common cause of iatrogenic injuries to the ureter (75%) is a gynecological or surgical pelvic procedure. The diagnosis of ureteral injuries is delayed in 66% (after days or weeks). Lack of hematuria is an unreliable sign to exclude injury, since 30% of all ureteral injuries do not even demonstrate microscopic hematuria or classic clinical symptoms and signs. In view of this, the diagnosis must be one of suspicion and further evaluations are mandatory in all cases of penetrating or blunt abdominal injuries. The most accurate diagnostic tools are CT scan with delayed excretory images and retrograde ureterography, which can also be used to guide stent placement. Low-grade injuries can be sufficiently treated with urinary diversion by PCN drainage or endoscopic ureteric stenting. The treatment of high-grade injuries depends on the localization and extent of the damage. The principles of repair include débridement, spatulation, lack of tension, stenting, postoperative drainage, and a watertight anastomosis with fine nonreactive absorbable suture. A delay in diagnosis is the most important factor contributing to the morbidity of ureteric injuries, and early treatment can reduce the complication rate to below 5%.

In order to clarify the pathogenesis of gross hematuria in mild forms of mesangioproliferative glomerulonephritis without crescents, systematic light microscopic, immunohistologic, electron microscopic, and some scanning electron microscopic investigations were carried out on 17 cases of this disease, in part on serial sections. The investigations produced the following results: In gross hematuria, erythrocytes pass into Bowman's space in the area of basement membrane ruptures. The basement membrane ruptures occur at sites where the basement membrane is infiltrated in its entire width by aggregated immune complexes. This occurs when these immune complexes are detached from the basement membrane by lysosomal digestion. As a working hypothesis, it is furthermore considered possible that in diseases accompanied by increased IgA production, circulating IgA is deposited at a higher rate in the glomerular filtration barrier and it is there degraded by an excessive reaction of local cells before morphologically identifiable immune complexes appear. In this process the basement membrane undergoes local destruction. It is also assumed that in gross hematuria, immune complexes other than IgA or hitherto unknown substances enter the basement membrane during the filtration process and trigger frustrane phagocytosis at the basement membrane by their presence, with consecutive basement membrane destruction. It is pointed out that gross hematuria occurs most often in mild forms of mesangioproliferative glomerulonephritis with IgA and C3 deposits in the mesangium and sometimes also in the capillary periphery. It could be shown that in mild forms of mesangioproliferative glomerulonephritis, hematuria occurs more often in the male sex.(ABSTRACT TRUNCATED AT 250 WORDS)

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