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Onconephrology is a rapidly evolving subspecialty that covers all areas of renal involvement in cancer patients. The complexity of the field may benefit from well-defined multidisciplinary management by a dedicated team. Patients with cancer frequently suffer from concurrent chronic kidney disease (CKD), with a prevalence ranging from 12% to 53% at the time of cancer diagnosis. Taking into account the incidence of cancer and the prevalence of CKD in the Italian population, we estimate that about 44,000 patients suffered from both diseases in 2020. Since there is an increasing necessity to address the needs of this population in dedicated outpatient clinics, it is critical to highlight some basic characteristics and to suggest areas of development. Our experience in the nephrological management of cancer patients clearly suggests the need to implement dedicated multidisciplinary teams and to create onconephrology clinics (at least within larger, referral, hospitals). Furthermore, it must be kept in mind that not only is CKD common in cancer patients, but also that the concomitant presence of these two conditions too often excludes cancer patients from clinical trials, thus limiting their access to therapies that could potentially improve their outcomes. Indeed, the Renal Insufficiency and Cancer Medications (IRMA) study found that cancer patients with CKD or on dialysis are often undertreated, or are exposed to either ineffective or toxic anticancer agents. Finally, the aim of this article is to initiate a debate about what an onconephrology outpatient clinic might look like, in order to ensure the highest quality of care for this growing patient population.

Heparin-induced thrombocytopenia (HIT) is an uncommon but severe immunologic adverse effect of heparin therapy, which is associated with an increased thrombotic risk [1]. This syndrome is mediated by platelet-activating antibodies, generally targeting platelet factor 4-heparin (PF4-Hep) complexes, and is characterised by an abrupt onset of thrombocytopenia, and, at the same time, by an abnormal thrombin generation resulting in a hypercoagulable state. A thrombotic complication occurs in over half of the patients affected [1]. The diagnosis of HIT is based both on clinical criteria and laboratory assays, but it is often a difficult diagnosis to make and is frequently delayed [2]. This is a case report of one patient with HIT who developed pulmonary embolism and deep vein thrombosis during haemodialysis. A 83-year-old woman with chronic renal failure started haemodialysis because of worsening of renal function (creatinine = 6.5 mg/dl). During each of the dialysis sessions, lasting 3 h, the patient received unfractionated heparin (UFH), with a bolus of 2,000 U followed by 600 U/h by continuous infusion. To facilitate the dialysis procedures, a venous catheter was inserted in the right common femoral vein. After five sessions of dialysis, 12 days after the first administration of UFH, the patient suddenly developed dyspnea, chest and abdominal pain and right leg swelling. Pulmonary embolism, multiple splenic infarctions and deep vein thrombosis of the right leg (from the popliteal to the external iliac vein) were detected by spiral computer tomography and by color-Doppler ultrasonography. The platelet count dropped to 10,000 platelet/mm. Retrospectively, we observed that a decrease in the platelet counts [50% from baseline was already present after the third session of dialysis (from 236,000 to 44,000/mm). An inferior vena cava filter was placed, and anticoagulant therapy with lepirudin (Refludan, Pharmion Ltd) was started at an initial dose of 0.05 mg/kg/h (i.e. 3.5 mg/h) with the aim of maintaining the aPTT ratio between 1.5 and 2.5. The enzyme-linked immunosorbent assay (EIA, GTIHAT, GTI INC, Brookfield WI) to detect PF4/Hep antibodies showed highly positive results (optical density = 2.77; normal value \0.40). Alternative causes of thrombocytopenia, i.e. disseminated intravascular coagulation and thrombotic thrombocytopenic purpura, were excluded. In the following days, the platelet counts remained low (10–15,000/mm); because of severe renal failure, lepirudin monitoring was extremely difficult, with frequent episodes of overanticoagulation (aPTT ratio [ 3.0), despite a reduced dosage (0.0007 mg/kg/h with average of 1.2 mg/ daily); repeated interruptions of lepirudin administration were necessary. The clinical course of the patient was further complicated by sepsis due to methicillin-resistant Staphylococcus aureus: targeted antibiotic treatment was started. Five days after the beginning of lepirudin therapy, the patient started complaining of left leg pain. A colorDoppler ultrasonography showed a new deep vein thrombosis of the left limb, from the popliteal to the common femoral vein. Therefore, lepirudin was replaced with argatroban (Novastan, Mitsubishi Pharma Europe Ltd). The starting argatroban dose was 2 lg/kg/min (corresponding to 7 ml/h) in order to maintain the aPTT ratio between 1.5 and 3.0. A very quick improvement of the clinical picture A. Alatri (&) O. Paoletti A. Zimmermann S. Testa Haemostasis and Thrombosis Centre, A.O. Istituti Ospitalieri di Cremona, Viale Concordia 1, 26100 Cremona, Italy e-mail: a.alatri@ospedale.cremona.it