Cardiorenal acute kidney injury: Epidemiology, presentation, causes, pathophysiology and treatment

doi:10.1016/j.ijcard.2016.11.156

International Journal of Cardiology

Volume 227, 15 January 2017, Pages 143-150

https://doi.org/10.1016/j.ijcard.2016.11.156 Get rights and content

Highlights

•
Definition and pathophysiology of acute kidney injury (AKI)
•
Risk factors for cardiovascular disease in AKI patients
•
Diagnostic tools (both laboratory and imaging diagnosis)
•
Treatment approaches

Abstract

Cardiovascular disease and major cardiovascular events represent main cause of death in both acute and chronic kidney disease patients.

Kidney and heart failure are common and frequently co-exist; this organ – organ interaction, also called organ cross-talk led to well-known definition of cardiorenal syndrome (CRS). Here we'll describe cardiovascular involvement in patients with acute kidney injury (AKI). Also known as type-3 CRS or acute reno-cardiac CRS, it occurs when AKI contributes and/or precipitates development of acute cardiac injury.

AKI may directly or indirectly produce an acute cardiac event and it can be associated to volume overload, metabolic acidosis and electrolytes disorders such as hyperkalemia and hypocalcemia; coronary artery disease, left ventricular dysfunction and fibrosis have been also described in patients with AKI with consequent direct negative effects on cardiac performance

Introduction

Cardiovascular disease and major cardiovascular events represent main cause of death in both acute and chronic kidney disease patients.

Kidney and heart failure are common and frequently co-exist; this organ – organ interaction, also called organ cross-talk leads to well-known definition of cardiorenal syndrome (CRS). A novel consensus definition and classification about CRS was proposed in 2008 by the Acute Dialysis Quality Initiative workgroup ([1], Table 1) and identified five CRS sub-types according to disease's onset.

Here we'll describe cardiovascular involvement in patients with acute kidney injury (AKI). Also known as type-3 CRS or acute reno-cardiac CRS, it occurs when AKI contributes and/or precipitates development of acute cardiac injury.

AKI may directly or indirectly produce an acute cardiac event and it can be associated to volume overload, metabolic acidosis and electrolytes disorders such as hyperkalemia and hypocalcemia; coronary artery disease, left ventricular dysfunction and fibrosis has been also described in patients with AKI with consequent direct negative effects on cardiac performance [2], [3].

Section snippets

Acute kidney disease

As previously described, type-3 cardiorenal syndrome is characterized by acute worsening of kidney function leading to heart disease. Wide spectrum of cardiac dysfunction includes acute decompensated heart failure (ADHF), acute coronary syndrome (ACS) and arrhythmias as defined by RIFLE (Risk, Injury, Failure, Loss, End-stage kidney disease) and AKIN (Acute Kidney Injury Network) criteria [4], [5].

AKIN criteria contributed to previous RIFLE ones adding serum creatinine increase of 0.3 mg/dl, or

Epidemiology of type-3 CRS

Defining incidence and prevalence of type-3 CRS is quite difficult due to lack of epidemiologic data at present time.

At the same time it's possible to collect data derived from single population studies; among them a 2147 per million population AKI incidence was reported in northern Scotland population-based study [14].

Another prospective, multicenter, community-based study in 748 AKI patients reported common death's causes: infections (48%), hypovolemic shock (45.9%), respiratory distress

Pathophysiology of type-3 CRS

It's clearly established that kidneys play a crucial role in regulating body water and blood volume; at the same time, kidneys are involved in electrolytes balance (such as sodium and potassium levels), help in regulating blood pH and provide to excretion of nitrogen and other toxic molecules.

Kidney holds neuroendocrine functions as underlined by production of erythropoietin and renin to regulate both erythropoiesis and systemic blood pressure.

Therefore kidney is mainly involved in the

Ultrasound diagnosis

Ultrasound evaluation of type-3 CRS patients shows several patterns both on kidney and heart examination.

Kidney size and echogenicity provide primary features to discern between acute and chronic nephropathies always remembering how kidney volume and longitudinal diameters correlate with patient height and body surface [42], [43] and that chronic renal failure does not exclude normal or enlarged kidneys (e.g. early stages of diabetic nephropathy, HIV-related glomerulonephritis or cast

Management approach to type-3 CRS patients

To better provide complete management of type-3 CRS, best treatment strategy is probably to identify various stage of disease (according to RIFLE/AKIN criteria), from patients at high risk of developing AKI to stage 3 AKI patients, those who present a kidney failure requiring renal replacement therapy.

Renal replacement therapy

Once pharmacological treatment fails in AKI patients and oligo-anuric renal failure is established, renal replacement therapy has to been started and it represents a cornerstone in the management of severe kidney injury although several aspects of RRT remain still controversial.

The timing of RRT initiation is strongly dependent by clear impairment of renal function with electrolytes and acid – base imbalancement, hpercreatininemia and severe fluid overload not responsive to pharmacological

Conflict of interest

The authors report no relationships that could be construed as a conflict of interest.

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Acute kidney injury(AKI) after pancreatic surgery is associated with increased mortality, longer hospital stays and poor prognosis. This study aims to identify the risk factors and establish an easy-to-use prediction calculator by the nomogram to predict the risk of AKI after pancreatic surgery.
From January 2016 to June 2018, 1504 patients who underwent pancreatic surgery in our center were included in this retrospective analysis and randomly assigned to primary (1054 patients) and validation (450 patients) cohorts. The independent risk factors of AKI were identified using univariate and multivariate analyses. A risk-predicted nomogram for AKI was developed through multivariate logistic regression analysis in the primary cohort while the nomogram was evaluated in the validation cohort. Nomogram discrimination and calibration were assessed using C-index and calibration curves in the primary and validation cohorts. The clinical utility of the final nomogram was evaluated using decision curve analysis.
The overall incidence of AKI after pancreatic surgery was 5.3% (79/1504). Independent risk factors including smoking history, cardiovascular disease, ASA score, baseline eGFR, bilirubin＞2 mg/dL, undergoing pancreaticoduodenectomy, and intraoperative blood loss＞400 mL were identified by multivariate analysis. Nomogram revealed moderate discrimination and calibration in estimating the risk of AKI, with an unadjusted C-index of 0.79 (95 %CI, 0.73–0.85). Application of the nomogram in the validation cohort provided moderate discrimination (C-index,0.80 [95% CI, 0.72–0.88]) and good calibration. Besides, the decision curve analysis (DCA) confirmed the clinical usefulness of the nomogram.
An easy-to-use online prediction calculator comprised of preoperative and intraoperative factors was able to individually predict the occurrence risk of AKI among patients with pancreatic surgery, which may help identify reasonable risk judgments and develop proper treatment strategies to a certain extent.
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Acute decompensated heart failure (ADHF) admissions are frequently complicated by different patterns of serum creatinine (SCr) elevation. We aimed to assess the prognostic impact of worsening renal function (WRF) based on the timing of its occurrence.
This was a retrospective cohort of patients admitted for ADHF. Standard WRF was defined as an increase in SCr of ≥0.3 mg/dl during hospitalization. WRF timing was classified as early (within 48 hours of admission) or late (>48 hours). Acute kidney injury (AKI) at admission was defined as a rise in SCr of ≥0.3 mg/dl from outpatient baseline measurement to first measurement at admission. The primary endpoint was a composite of all-cause mortality or hospitalization for cardiovascular events at one-year follow-up.
Overall, 249 patients were included (mean age 77±11 years, 62% with preserved left ventricular ejection fraction). Early WRF occurred in 49 patients (19.7%) and was associated with a higher risk of the primary outcome (HR 2.49; 95% CI 1.66–3.73), whereas late WRF was not (p=0.411). After stratification for the presence of early WRF and/or AKI at admission, only patients with early WRF but no AKI at admission and patients with both AKI at admission and early WRF showed a higher risk of the primary outcome after multivariate Cox regression.
Early WRF was associated with a higher risk of the primary outcome. The timing of WRF seems to be an important factor to take into account when considering the prognostic impact of creatinine variations during hospitalization for ADHF.
Admissões por insuficiência cardíaca aguda (ADHF) são frequentemente complicadas por elevação creatinina sérica (sCr), as quais podem ter padrão variável.
Avaliar o impacto prognóstico do agravamento da função renal (WRF) com base no timing da sua ocorrência.
Estudo retrospetivo de coorte de doentes hospitalizados por ADHF. WRF standard foi definida como um aumento na SCr ≥0,3 mg/dL durante internamento, foi subclassificada consoante o timing da sua ocorrência em precoce (quando ocorreu nas primeiras 48 horas desde a admissão) ou tardia (quando ocorreu após as 48 h). Lesão renal aguda (AKI) à admissão foi definida como um aumento da SCr ≥0,3 mg/dL desde um valor basal ambulatório até a primeira determinação hospitalar. O endpoint primário foi um composto de mortalidade por qualquer causa ou hospitalização por eventos cardiovasculares, com um ano de follow-up.
Foram incluídos 249 doentes (média de 77±11 anos, 62% com fração de ejeção do ventrículo esquerdo preservada). WRF precoce ocorreu em 49 doentes (19,7%) e associou-se a maior risco para o outcome primário (HR 2,49; 95% CI 1,66-3,73), enquanto a WRF tardia não demonstrou essa associação (p=0,411). Após estratificação para a presença de WRF precoce e/ou AKI à admissão, apenas os doentes com WRF precoce mas sem AKI à admissão, bem como os doentes com ambas (WRF precoce e AKI à admissão), demonstraram maior risco para o outcome primário após regressão multivariável de Cox.
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Several pathological alterations in the myocardium have been observed during CRS-3, including oxidative stress, inflammation, mild cardiomyocyte apoptosis, catecholamine accumulation, metabolic reprogramming, intracellular calcium reuptake disorder, mitochondrial dysfunction and endoplasmic reticulum stress [6,7,10,40,41]. Among these pathological inducers, impaired mitochondrial quality seems to drive the other pathological processes that aggravate myocardial damage during CRS-3 [7,42]. The number of mitochondria is higher in cardiomyocytes than in many other types of cells, including skeletal muscle cells, endothelial cells, hepatocytes and renal tubular cells [43].
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ReviewCardiorenal acute kidney injury: Epidemiology, presentation, causes, pathophysiology and treatment

Highlights

Abstract

Introduction

Section snippets

Acute kidney disease

Epidemiology of type-3 CRS

Pathophysiology of type-3 CRS

Ultrasound diagnosis

Management approach to type-3 CRS patients

Renal replacement therapy

Conflict of interest

J. Card. Fail.

Semin. Nephrol.

J. Mol. Cell. Cardiol.

Am. J. Pathol.

Kidney Int.

J. Mol. Cell. Cardiol.

J. Mol. Cell. Cardiol.

Am. J. Pathol.

Kidney Int.

Am. J. Cardiol.

Atherosclerosis

Lancet

Kidney Int.

Kidney Int.

Am. J. Kidney Dis.

Am. J. Surg.

Cardio-renal syndromes: report from the consensus conference of the acute dialysis quality initiative

Eur. Heart J.

Cytokine-induced modulation of cardiac function

Circ. Res.

Influence of acute renal failure on coronary vasoregulation in dogs

J. Am. Soc. Nephrol.

Epidemiology of cardio-renal syndrome: workgroup statements from the 7th ADQI Consensus Conference

Nephrol. Dial. Transplant.

Acute renal failure—definition, outcome measures, animal models, fluid therapy and information technology needs. The Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group

Crit. Care

Acute kidney injury network (AKIN): report of an initiative to improve outcomes in acute kidney injury

Crit. Care

Renal Association Clinical Practice Guidelines on acute kidney injury

Nephron Clin. Pract.

Beginning and Ending Supportive Therapy for the Kidney (BEST Kidney) investigators. Acute renal failure in critically ill patients: a multinational, multicenter study

JAMA

ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM)

Eur. J. Heart Fail.

ACCF/AHA guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation

Circulation

Failure syndromes: current state and framework for future research

Circulation

Characteristics, outcomes, and predictors of 1 year mortality in patients hospitalized for acute heart failure

Eur. Heart J.

Incidence and outcomes in acute kidney injury: a comprehensive population-based study

J. Am. Soc. Nephrol.

Acute kidney injury after trauma: prevalence, clinical characteristics and RIFLE classification

Indian J. Crit. Care Med.

Report on management of renal failure in Europe. XXII

Nephrol. Dial. Transplant.

Epidemiology of acute renal failure and outcome of haemodiafiltration in intensive care

Intensive Care Med.

Renal cell therapy and beyond

Semin. Dial.

Pathophysiology of acute kidney injury: a new perspective

Contrib. Nephrol.

The severe cardiorenal syndrome: ‘Guyton revisited’

Eur. Heart J.

Coronary endothelial and cardiac protective effects of a monoclonal antibody to intercellular adhesion molecule-1 in myocardial ischemia and reperfusion

Circulation

Review
Cardiorenal acute kidney injury: Epidemiology, presentation, causes, pathophysiology and treatment