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A 21-year-old male presented with a one day history of right flank pain and signs of severe sepsis. The recorded vital signs included a temperature of 39. Celsius, blood pressure of 95/65 mmHg and heart rate of 165. The laboratory investigations confirmed a raised C-reactive protein (CRP) of 485 mg/l but it was interesting to note thatthe white cell count and creatinine were respectively normal (5.85 x 109/l; 77 mol/l). Microbiological investigations confirmed Klebsiella pneumoniae (>106 cfu/mL) on urine culture whilst two blood cultures were negative. Intravenous fluid resuscitation was successful in restoring hemodynamic stability. Amoxicillin/clavulanic acid (1200mg) was administered and continued for seven days after confirmation on antibiotic sensitivity testing. After ultrasonography confirmed severe right hydronephrosis, a contrasted computed tomography (CT) scan confirmed a horseshoe kidney (A, B, C, D) with an obstructed right-sided renalmoiety secondary to right pelvi-ureteric junction (PUJ) obstruction (B) and urothelial enhancement suggestive of an infected collecting system. Horseshoe kidneys are the most common congenital renal abnormality with an incidence of 1:400-600. It is commonly asyptomatic and rarely require interventionunless treating complications such as ureteral obstruction (PUJ), urinary tract infections, urolithiasis andWilms Tumour. It is associated with Trisomy 18 and females with Turner syndrome. Our patient underwent a right percutaneous nephrostomy (PCN) and 500 millilitres of infected urine were aspirated. He made a complete recovery at discharge. An interval MAG3 renogram confirmed that both moeities had good and excretion. A pelvi-ureteric junction repair will be performed after 6 weeks.

Strong circumstantial evidence suggests that the activation of the hemostatic system is involved in the growth and spread of malignant tumors. Nevertheless, the considerable experimental and clinical data presently available cannot be interpreted in one specific direction. The presence of a fibrin and/or a platelet thrombus in the environment of tumor cells only represents the visible end product of a complex biochemical and biophysical process during which other phenomena like haemodynamic changes and the generation of many biologically active enzymes occur. In the interpretation of experimental studies and clinical trials of anticoagulants in cancer disease, a wider concept of the hemostatic process and its multiple interactions with other biological systems is needed. The complement system, adhesive glycoproteins of the cell surface, chemotaxis, growth factors and prostaglandins are some examples of factors which interact with the hemostatic system as well as with the pathology of cancer. The definite pathogenic connection between the clinically observed hypercoagulability of patients with malignant disease and the biology of tumor growth and tumor dissemination remains unclear. Agents which modify hemostatic reactions must be evaluated in specific tumor categories using carefully controlled prospective trials. The results of such studies on tumor regression and also on longevity will permit to assess the efficacy of these agents as adjuvant therapy in the treatment of cancer.

Strong circumstantial evidence suggests that the activation of the hemostatic system is involved in the growth and spread of malignant tumors. Nevertheless, the considerable experimental and clinical data presently available cannot be interpreted in one specific direction. The presence of a fibrin and/or a platelet thrombus in the environment of tumor cells only represents the visible end product of a complex biochemical and biophysical process during which other phenomena like haemodynamic changes and the generation of many biologically active enzymes occur. In the interpretation of experimental studies and clinical trials of anticoagulants in cancer disease, a wider concept of the hemostatic process and its multiple interactions with other biological systems is needed. The complement system, adhesive glycoproteins of the cell surface, chemotaxis, growth factors and prostaglandins are some examples of factors which interact with the hemostatic system as well as with the pathology of cancer. The definite pathogenic connection between the clinically observed hypercoagulability of patients with malignant disease and the biology of tumor growth and tumor dissemination remains unclear. Agents which modify hemostatic reactions must be evaluated in specific tumor categories using carefully controlled prospective trials. The results of such studies on tumor regression and also on longevity will permit to assess the efficacy of these agents as adjuvant therapy in the treatment of cancer.