Choice and management of anticoagulation during CRRT

Abstract

Continuous renal replacement therapies (CRRT) are widely used in the treatment of acute kidney injury. Several causes, related to the treatment itself or to the patient’s condition, determine the coagulation of the extracorporeal circuit. These interruptions (or down-time) have a negative impact on the effectiveness of the treatment in terms of solute clearance and fluid balance. Historically, the choice of anticoagulant has fallen on unfractionated heparin because it is cheap and easy to use. Today, the use of citrate is recommended in most instances because of its high efficacy and safety. Several studies demonstrate the superiority of citrate in terms of filter survival. The reduction of down-time results in a reduction of the delta between the prescribed dialysis dose and the dose that is actually administered (ml/Kg/hour of collected effluent). The literature also agrees that there is a reduction in the incidence of major bleeding events when citrate is used instead of heparin, although there is no impact on mortality rates.

Some technical and clinical complexities, secondary to citrate action both as anticoagulant and buffer, still exist in the use of regional citrate anticoagulation. However, complications due to citrate use, such as acid-base balance disorders and hypocalcaemia, are rare and easily reversible.

There is not much data about the costs and benefits of using citrate instead of heparin; according to the experience within our own Unit, we have observed a reduction in costs when the data is normalized for 35 ml of effluent administered. Appropriate protocols, accurate surveillance and the automated management of regional citrate anticoagulation thanks to dedicated software make this technique safe and effective.

Keywords: anticoagulation, citrate, acute kidney injury, CRRT

Sorry, this entry is only available in Italian.

Extracorporeal therapy in sepsis

Abstract

Acute renal injury (AKI) occurs in 19% of patients with sepsis, 23% of those with severe sepsis and up to 50% of patients with septic shock. AKI represents an independent prognostic factor of mortality (about 45%); epidemiological studies have pointed out that the onset of AKI in sepsis (S-AKI) correlates with an unfavourable outcome, reaching a mortality of 75%.

Over the years, efforts have been made to prevent and treat “low flow” hemodynamic damage resulting from shock by increasing renal blood flow, improving cardiac output and perfusion pressure. New experimental studies in S-AKI have shown that renal blood flow is maintained, and indeed increases, in the course of septic shock. Recently, a “single theory” has been proposed that defines acute renal injury as the final result of the interaction between inflammation, oxidative stress, apoptosis, microcirculatory dysfunction and the adaptive response of tubular epithelial cells to the septic insult.

The type of treatment, the dose and the starting time of RRT are of strategic importance in the recovery of AKI in septic patients.

The use of new anticoagulation strategies in critically ill patients with S-AKI has allowed treatments to be carried out for enough time to reach the correct dose of purification prescribed, minimizing down-time and bleeding risk.

The availability of new technologies allows to customize treatments more and more; the collaboration between nephrologists and intensivists must always increase in order to implement modern precision medicine in critical care.

Keywords: S-AKI, septic shock, CRRT, citrate, CPFA, adsorption

Sorry, this entry is only available in Italian.

Use of citrate in patients with nephrolithiasis

Abstract

Citrate is a tricarboxylic acid and an intermediate metabolite of Krebs cycle. It contributes to oxidative metabolism of both kidney and liver. Alkaline sodium or potassium salts have the potential to increase alkaline reserve. In the kidney citrate is completely filtered at the glomerulus, undergoing to 10-40% tubular resorption. Renal insufficiency, even early, metabolic acidosis, potassium depletion induce hypocitraturia. Its importance in nephrolithiasis stems from its ability to form soluble complexes with calcium and to interfere with crystal formation, thus exerting a dual inhibition, thermodynamic and kinetic. Moreover, its alkalizing property has shown benefits of bone mineralization. The alkalizing effect is also useful in uric acid and cystine stone disease. Hypocitraturia has a significant incidence in the course of calcium nephrolithiasis, either secondary to aforementioned causes, or in idiopathic and/or familial forms. Citrate is used in the prevention of stone recurrences and given as tripotassic or potassium-magnesium salt, 0.1 mmol/kg/day in 2-3 dosages. In uric acid disease, in addition to prevention, it can induce dissolution of renal stones, provided urine pH is maintained at higher than 6.5 values. As concerns its effects on bone, it was shown to induce both decreases in marker of bone resorption and increases in bone mineral density.

Key words: citrate, potassium citrate, hypocitraturia, calcium nephrolithiasis

Sorry, this entry is only available in Italian.