A recent report has suggested that contrast media-induced nephropathy (CMIN) is the third highest cause of hospital-acquired acute renal failure [1]. In nearly half of these patients, CMIN occurred during cardiac diagnostic or interventional procedures such as percutaneous coronary intervention. However, considering the amount of contrast media (CM) used today in extracardiac diagnostic procedures, the incidence of nephropathy still remains relatively low. This low incidence may be attributed to the introduction and use of nonionic, low- or iso-osmolal compounds, to the use of smaller volumes of CM and to an increasing awareness of patients who may be at risk for impairment of renal function. The latter is especially true in patients with pre-existing renal failure, diabetes, or both.

Statins are powerful lipid-lowering drugs that inhibit cholesterol biosynthesis via downregulation of hydroxymethylglutaryl coenzyme-A reductase, which are largely used in patients with or at risk of cardiovascular disease. Available data on thromboembolic disease include primary and secondary prevention as well as bleeding and mortality rates in statin users during anticoagulation for VTE. Experimental studies indicate that statins alter blood clotting at various levels. Statins produce anticoagulant effects via downregulation of tissue factor expression and enhanced endothelial thrombomodulin expression resulting in reduced thrombin generation. Statins impair fibrinogen cleavage and reduce thrombin generation. A reduction of factor V and factor XIII activation has been observed in patients treated with statins. It is postulated that the mechanisms involved are downregulation of factor V and activated factor V, modulation of the protein C pathway and alteration of the tissue factor pathway inhibitor. Clinical and experimental studies have shown that statins exert antiplatelet effects through early and delayed inhibition of platelet activation, adhesion and aggregation. It has been postulated that statin-induced anticoagulant effects can explain, at least partially, a reduction in primary and secondary VTE and death. Evidence supporting the use of statins for prevention of arterial thrombosis-related cardiovascular events is robust, but their role in VTE remains to be further elucidated. In this review, we present biological evidence and experimental data supporting the ability of statins to directly interfere with the clotting system.

The aim of this article is to extract from recent medical literature and nephrologic practice the facts and fallacies concerning the possible prophylaxis of contrast medium-induced nephropathy. A MEDLINE/PubMed search (1985 to January 2006) was conducted, including all relevant articles investigating the pathogenesis and prevention of contrast medium-induced nephropathy from a nephrologic critical point of view. Considerable efforts have been made to develop pharmacologic therapy for the prevention of contrast medium-induced nephropathy, especially in patients at risk, such as elderly subjects and those with preexisting renal impairment, hypovolemia, or dehydration. There is general consensus that hydration protocols implemented before and after imaging with contrast medium may be effective in preventing contrast medium-induced nephropathy. However, definitive and convincing data related to amounts to be infused, infusion timing, and type of solutions (half-isotonic, isotonic saline solution, or bicarbonate) are lacking. Forced diuresis with furosemide or mannitol and use of dopamine, together with concomitant hydration, have been proved to be ineffective or even more risky in the event of inadequate maintenance of euvolemia. Various direct or indirect vasodilators have been investigated (atrial natriuretic peptide, calcium channel blockers, angiotensin-converting enzyme inhibitors, and endothelin receptor antagonists), yet results have been inconsistent and inconclusive. Recent large meta-analyses concerning the protective role of antioxidant action of N-acetylcysteine have led to the conclusion that the statistical significance of the results is borderline. Preventive hemodialysis has not proved to be useful; on the contrary, it might worsen the clinical conditions by inducing hypotension. Hemofiltration, despite some positive studies, is too complex and cannot be used extensively. : It is believed that prevention is actually achieved by correcting hypovolemia, dehydration, or both. Normalization of body fluids is probably the true objective to be achieved by preventive measures in all patients, not only in those at risk. Because limited data have been collected in intensive care units, at present, no firm or specific recommendations can yet be provided for the critically ill.

Antiphospholipid syndrome (APS) is a systemic autoimmune disease characterized by thrombotic or obstetric events occurring in individuals who have persistent antiphospholipid antibodies. Catastrophic antiphospholipid syndrome (CAPS) is a rare and potentially fatal form of APS characterized by severe thrombotic complications occurring in multiple organs over a short period of time or simultaneously. CAPS is associated with a high (50%) death rate. Infections, multi-organ failure, and cerebral and heart thrombosis represent the main complications of this syndrome. Generally, anticoagulants, glucocorticoids, therapeutic plasmapheresis (TPE), and intravenous immunoglobulin (IVIG) are used in combination for treatment. Multidisciplinary care involving different specialists from hematology, rheumatology, nephrology, infectious disease, critical care, and obstetrics is often required due to the complexity of the disease. Recent data emphasize the effectiveness of biologics such as anti-TNF-a monoclonal antibodies (adalimumab, certolizumab), anti-CD38 monoclonal antibody (daratumumab), BAFF/Blys inhibitor (belimumab), and BTK inhibitor (zanubrutinib) against CAPS. In order to understand the underlying causes of CAPS, one future possibility involves investigating and characterizing the hereditary and acquired risk factors associated with CAPS.