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.

Differential diagnosis of acute kidney injury in critically ill patients: the nephrologist’s role in identifying the different causes of parenchymal damage

Abstract

The management of acute kidney injury in the critical area is complex and necessarily multidisciplinary, but the nephrologist should maintain a pivotal role, both in terms of diagnosis and of indication, prescription and management of extracorporeal replacement therapy.

The most frequent causes of AKI in the critically ill patients are correlated to sepsis and major surgery, but the incidence of different causes, of strict nephrological relevance, is probably higher than the estimate.

Nephrologists have the competence to evaluate data relating to renal functions, urinary electrolytes, urinary sediment, and to identify which specific examinations can be useful to define the cause of AKI. A nephrological consultation will therefore improve the clinical management of AKI by guiding and integrating the diagnostic path with traditional or more advanced assessments, useful for the identification of the different causes of acute kidney damage and consequently of the most appropriate therapy.

The etiological diagnosis of AKI will also be crucial in defining the renal prognosis and therefore an appropriate nephrological follow up.

Keywords: Acute kidney injury, differential diagnosis, critical care nephrology

Sorry, this entry is only available in Italian.

Acute kidney injury and rhabdomyolysis after cocaine overdose: case report and literature review

Abstract

Cocaine, a natural alkaloid derived from the coca plant, is one of the most commonly used illicit drugs.
Cocaine abuse causes systemic adverse effects like stroke, myocardic infarction, arterial dissection, vascular thrombosis and rhabdomyolysis.
Cocaine use is, also, associated with renal complications such as acute kidney injury, vasculitis, acute interstitial nephritis, chronic kidney disease, malignant hypertension with thrombotic microangiopathy.
Acute kidney injury may or may be not associated to rhabdomyolysis.
Rhabdomyolysis caused by cocaine abuse is multifactorial, involving tissue ischemia secondary to vasoconstriction and cellular damage caused by the drug.
We report a 50-year-old man with history of chronic hepatitis C and substance abuse admitted to our unit with severe rhabdomyolysis and acute kidney failure after nasal insufflation of cocaine overdose. Renal function recovered after several treatments of dialysis.
We conclude that cocaine adversely impacts kidney function; in addition cocaine and rhabdomyolysis are the double danger for acute kidney injury. Medical management of cocaine toxicity requires a multisystem approach, with close monitoring cardiac, neurological and renal function.

Keywords: Acute kidney injury, rhabdomyolysis, cocaine

Sorry, this entry is only available in Italian.

Nephrologist and ICU: the need of new expertise

Abstract

Episodes of dialytic Acute Kidney Injury (AKI stage III KDIGO) can lead to chronic kidney disease (CKD), even after a long time. Prelimary data indicate that the relationship between AKI and CKD is affected by dialysis technical modalities and factors in part modifiable, such as an early dialysis timing, dose adeguacy, continuous treatment, use of biocompatible membranes and regional citrate anticoagulation. However, in most ICUs involvement of nephrologist consultant is marginal. Of more, nephrological follow-up after discharge, which allows to slow down the progression rate of CKD even just by a correct pharmacological and dietetic approach (sartans, ACEis), is an uncommon practice. Indeed, a better organ survival could lead to a delay of the dialytic treatment, reducing the costs sustained by the National Health Service.  To face such challenges locally, in Piedmont and Aosta Valley the Dialysis Units were required to put themselves at disposal for ICU needs both in terms of dedicated staff and resources. Additionally, since many years consultant nephrologists have established the “Acuti” work-group, which has been able to provide an high level of professional expertise, while incentivizing innovation and training in ICU environment. In order to cope with these new requirements a redefinition of the nephrologist’s role in ICU through a constant exchange with the intensive care background is needed.

Key words: Acute kidney injury., Critical Care nephrology, Organization, Work group

Sorry, this entry is only available in Italian.

Complement factor B mutation in atypical hemolytic uremic syndrome. Rare cause of rare disease

Abstract

Hemolytic uremic syndrome (HUS) is a rare disease characterized by microangiopathic hemolysis, platelet consumption and multiple organ failure with predominant renal involvement. In the most of cases (85-90%), it is associated with enteric infection due to Shiga-toxin or verocytotoxin (STEC-VTEC)-producer Escherichia coli. Rarely, in about 10-15% of cases, HUS develops in the presence of a disorder of alternative complement pathway regulation and it is defined atypical (aHUS).

We describe the case of a 65-year-old man who came to our attention with a clinical presentation of aHUS and a clinical course characterized by rapidly progressive acute renal failure (ARF), which required renal replacement treatments, and by a stable clinical picture of hematological impairment as a marker of a non-severe and self-limiting form. The clinical and laboratory course allowed us not to perform specific therapies such as plasma exchange and/or block of the complement with eculizumab. Less than two weeks after hospital admission, there was a gradual recovery of renal function with spontaneous diuresis and hematological remission.

Genetic screening has revealed a heterozygous mutation in the complement factor B (CFB) that is not described in the literature and therefore not yet characterized in the genotype/phenotype correlation, also for the extreme rarity of the forms associated with CFB alteration. In conclusion, the presence of a new mutation in the CFB, such as the one described in our case, is probably associated with the development of aHUS but has not led to a poor prognosis, as generally reported in the literature for known variants of the CFB.

Key words: Acute kidney injury., Atypical hemolytic uremic syndrome, Complement factor B mutations, Thrombotic microangiopathy

Sorry, this entry is only available in Italian.