Annual Update in Intensive Care and Emergency Medicine 2011

266 C.Y. Goh and C. Ronco
VII
from patient to patient. The mechanisms that have been identified as being
involved include: Hemodynamic mechanisms in which a reduced cardiac output,
together with an increased renal venous congestion may affect intra-renal circulation
and glomerular filtration rate (GFR); neurohormonal biofeedback mechanisms
including activation of the renin-angiotensin-aldosterone system (RAAS).
A non-osmotic secretion of vasopressin and a parallel sympathetic nervous system-mediated
vasoconstriction may lead to perpetuation and extension of the
primary insult. We may also suggest immune-mediated damage in which the activationofmonocytesandthedirecteffectofpro-inflammatorymediatorsmay
play an important role in renal tissue apoptosis and damage [10]. Finally, exogenous
nephrotoxic agents such as contrast media, aminoglycosides, diuretics or
angiotensin converting enzyme (ACE) inhibitors may represent another important
source of kidney insult in patients with acute heart failure or acute decompensated
heart failure.
Cardio-renal Syndrome Type 2 or Chronic Cardio-renal Syndrome
Patients with chronic heart failure with secondary worsening renal failure have
significantly increased adverse cardiovascular mortality and prolonged hospitalization.
However, chronic heart disease and CKD frequently coexist in the same
patient, and often the clinical scenario does not allow one to distinguish which
disease came first. Notably, about 45 to 64 % of patients with chronic heart failure
have evidence of CKD with estimated GFR (eGFR) < 60 ml/min/1.73m2 [11, 12].
The mechanisms causing secondary worsening renal failure in these patients
likely differ from those in cardio-renal syndrome type 1. Concomitant hemodynamic
alterations with poor cardiac contractility, and neurohormonal abnormalities
with excessive production of vasoconstrictive mediators (epinephrine, angiotensin,
endothelin) as well as altered sensitivity and/or release of endogenous
vasodilatory factors (natriuretic peptides, nitric oxide [NO]) are commonly present
in patients with chronic heart failure. Hence, kidneys that are chronically
hypoperfused will be highly susceptible to any minor or major insults. Genetic
and acquired micro- or macrovascular risk factors, such as diabetic mellitus,
hypertension,dyslipidemia,maycontributetoinitiateandperpetuatethekidney
damage. Moreover, subclinical inflammation, endothelial dysfunction and accelerated
atherosclerosis, determine progressive sclerosis and fibrosis in the kidney
tissue with a progressive loss of nephrons. These processes result in an initial
phase of CKD that contributes to pathological conditions such as anemia, calcium-phosphate
abnormalities, reduction in vitamin D receptor activation, hyperparathyroidism
and hypertension. A vicious cycle is activated and a combined
worsening of heart and kidney function inevitably occurs.
Cardio-renal Syndrome Type 3 or Acute Reno-cardiac Syndrome
The development of AKI as a primary event subsequently leading to cardiac
injury and/or dysfunction has been recently observed with high prevalence. Type
3 cardio-renal syndrome is associated with poor short- and long-term outcomes.
Unfortunately, it has not been systematically evaluated or studied because of the
heterogeneity in the etiology of AKI, variability in the definition of AKI, and the
failure of many clinical studies of AKI to report the occurrence of acute cardiac
dysfunction as an outcome. AKI can affect the heart through several pathways.