Nephrology Considerations in the Management of Durable and Temporary Mechanical Circulatory Support

Abstract

Durable and temporary mechanical circulatory support (MCS) use is growing for a range of cardiovascular indications. Kidney dysfunction is common in people evaluated for or receiving durable or temporary MCS and portends worse outcomes. This kidney dysfunction can be due to preexisting kidney chronic kidney disease (CKD), acute kidney injury (AKI) related to acute cardiovascular disease necessitating MCS, AKI due to cardiac procedures, and acute and chronic MCS effects and complications. Durable MCS, with implantable continuous flow pumps, is used for long-term support in advanced heart failure refractory to guideline-directed medical and device therapy, either permanently or as a bridge to heart transplantation. Temporary MCS—encompassing in this review intra-aortic balloon pumps (IABP), axial flow pumps, centrifugal flow pumps, and venoarterial ECMO—is used for diverse situations: high-risk percutaneous coronary interventions (PCI), acute decompensated heart failure, cardiogenic shock, and resuscitation after cardiac arrest. The wide adoption of MCS makes it imperative to improve understanding of the effects of MCS on kidney health/function and of kidney health/function on MCS outcomes. The complex structure and functions of the kidney, and the complex health states of individuals receiving MCS, makes investigations in this area challenging, and current knowledge is limited. Fortunately, the increasing nephrology toolbox of noninvasive kidney health/function assessments may enable development and testing of individualized management strategies and therapeutics in the future. We review technology, epidemiology, pathophysiology, clinical considerations, and future directions in MCS and nephrology.

Introduction

Mechanical circulatory support (MCS) encompasses devices and strategies to provide or support circulation over time spans ranging from the duration of a cardiac catheterization to years. Durable MCS is used for long-term support for people with advanced heart failure (HF) refractory to guideline-directed medical and device therapy. Temporary MCS is used to provide hemodynamic support in several clinical situations: prophylactic hemodynamic support during high-risk percutaneous coronary interventions (PCI), acute decompensated HF, cardiogenic shock, and resuscitation after cardiac arrest.

Implantable left ventricular (LV) assist devices (LVADs) are the most commonly used durable MCS device type by far and will be the main focus of the durable MCS portion of this review (Table 1) (1). Currently used devices are small, long-lasting continuous flow devices, and in recent years centrifugal (third generation) pumps have begun to supplant axial flow (second-generation) pumps (1,2). Centrifugal flow pumps were designed to be smaller, more durable, and less thrombogenic and hemolytic than axial flow pumps (3). Although LV support is the most common durable MCS use in advanced HF, a smaller number of individuals—those with severe biventricular failure or predominant right ventricular (RV) disease with substantial LV failure—are treated with biventricular support (1). Durable biventricular support options include a total artificial heart and biventricular implantation of ventricular support devices (4). Finally, isolated durable RV support (RVAD) is used in a small number of individuals with isolated RV dysfunction but preserved LV function (5).

Table 1.

Mechanical circulatory support uses, device types, and considerations

Durable Mechanical Circulatory Support
Use Categories	Uses	Considerations
Left ventricular support	Can be for bridge to transplantation, bridge to candidacy, or as destination therapy	Most common durable MCS category by far
Biventricular support	Used in severe BiV failure
Biventricular replacement device	Used primarily for bridge to transplantation or bridge to candidacy (4)	Replaces the native ventricles and the four valves
Right ventricular support	Used for isolated RV failure
Device types	Considerations
Axial flow devices	The most used devices for many years (1) Mechanical bearings may lead to reduced durability Second-generation devices
Centrifugal flow devices	Designed for improved durability, smaller size, and improved blood flow compared with axial flow pumps Can be implanted within the pericardium Third-generation devices
Pneumatic displacement pump devices	Require larger drivelines than axial or centrifugal flow devices TAH is an example
Temporary Mechanical Circulatory Support
Device types	Uses	Considerations
Intra-aortic balloon pump	High-risk PCI Acute decompensated heart failure Cardiogenic shock	Widely available Easily inserted and maintained Limited hemodynamic support
Axial flow pumps	High-risk PCI Acute decompensated heart failure Cardiogenic shock	Placed percutaneously or surgically Some devices can supply high levels of hemodynamic support
Centrifugal flow pumps	Cardiogenic shock Cardiopulmonary bypass during surgery RV support when LVAD is implanted	Placed percutaneously or surgically Can be used for prolonged periods
Venoarterial ECMO	Cardiogenic shock Cardiac arrest	Placed percutaneously or surgically Can provide respiratory support

MCS, mechanical circulatory support; LVAD, left ventricular assist device; BiVAD, biventricular assist device; TAH, total artificial heart; RVAD, right ventricular assist device; RV, right ventricular; BiV, biventricular; PCI, percutaneous coronary intervention; ECMO, extracorporeal membrane oxygenation.

Temporary MCS is used to improve systemic and myocardial perfusion, reduce cardiac filling pressures, and reduce cardiac workload in a less invasive manner than with durable devices (Table 1) (6). Intra-aortic balloon pumps (IABP) and venoarterial extracorporeal membrane oxygenation (ECMO) were the first temporary MCS devices, and IABP remains the most commonly used (7). Newer devices include impeller-driven axial flow pumps, a left atrial-to-femoral artery bypass pump, extracorporeal centrifugal pumps, and new ECMO devices.

The high burden of cardiovascular disease in the United States, along with technological innovations, have led to growing use of durable and temporary MCS (8,9). Kidney dysfunction is common in people receiving MCS due to systemic diseases and the reciprocal relationship between kidney and cardiovascular health, and it is strongly related to adverse outcomes (10,11).

Durable MCS

LVAD utilization has transformed from rare use, primarily for bridge to heart transplantation, to more common use, primarily for destination therapy, with 3198 LVAD implantations in 2019 per the Society of Thoracic Surgeons Intermacs database (9,12). Destination therapy was the goal in 73% of LVAD implantations in 2019 compared with bridge to transplantation in 9% (9). This was a substantial change from 2010, when the goal was destination therapy in 35% of implantations and bridge to transplantation in 29% (9). This evolution of LVAD use occurred with the widespread adoption of continuous flow pumps and Food and Drug Administration approval for destination therapy use (13). We separate nephrology considerations in durable MCS into the preimplantation, early postimplantation, and prolonged MCS periods.

Preimplantation Period

Epidemiology

Kidney dysfunction at the time of LVAD implantation is an important risk factor for mortality and has been incorporated into several prognostic scores. It is challenging in LVAD studies to assess the degree and chronicity of preexisting kidney disease accurately. In part, this is due to limitations in current kidney health assessments, limited largely to endogenous filtration markers and proteinuria. Filtration markers, particularly serum creatinine concentration and derived eGFR, are influenced by muscle mass and fluid balance, resulting in inaccurate estimates in advanced HF (14,15). Chronicity of kidney dysfunction is difficult to determine in large cohort studies and may be challenging to determine even in single-center studies where patient care may be transferred to LVAD implantation centers shortly before implantation. Despite these limitations, and highlighting the importance of kidney function to prognosis, preimplantation creatinine and eGFR-based categorizations correlate with adverse outcomes after LVAD implantation (16,17). One large cohort found that 36% of LVAD recipients had an eGFR <60 ml/min per 1.73 m², and 6% had an eGFR <30 ml/min per 1.73 m² (16). People requiring preimplantation dialysis, particularly those on dialysis classified as having kidney failure with replacement therapy (KFRT), have especially high mortality after LVAD implantation (18–21). The other widely assessed kidney biomarker, proteinuria, also relates strongly with adverse LVAD outcomes (22,23).

The relationship of preimplantation kidney dysfunction with changes in kidney function after LVAD implantation is variable. Among LVAD recipients, lower preimplantation eGFR is associated with a greater increase in eGFR after implantation (24,25). In an analysis of a national database of LVAD recipients, those with a preimplantation eGFR <60 ml/min per 1.73 m² were more than twice as likely to experience a 50% eGFR rise at 1 month post implantation than those with an eGFR ≥60 ml/min per 1.73 m² (52% versus 22%, P<0.001) (25). However, it is currently unclear to what extent this finding is driven by survival bias (with high short-term mortality in those with lower kidney function), regression to the mean (preimplantation eGFR estimates are often on the basis of single measures with susceptibility to large fluctuations), and by endogenous filtration markers’ confounding by fluid and body composition changes (25).

Severe CKD can be a contraindication to LVAD use, although guidance and clinical practices vary. A recent Centers for Medicare and Medicaid Services Medicare Coverage decision listed “irreversible renal disease” as an absolute contraindication (26). In contrast, the American College of Cardiology’s Heart Failure and Transplant Member Section and Leadership Council recently stated “dialysis-dependent renal failure is no longer an absolute contraindication to LVAD insertion” (27). Some centers use LVADs in advanced CKD for bridge to combined heart/kidney transplantation (28). Individuals with advanced CKD—including KFRT—have received devices (18,19). These individuals have lower survival than those without KFRT, although many achieved >1-year survival (18).

Mechanisms and Pathophysiology

The mechanistic underpinnings of the epidemiologic data are unclear, and discussion is dependent on extrapolation from studies of low cardiac output states, kidney ischemia, non-HF disease states, and conjecture. First, diverse disease processes may be present preimplantation. Chronic kidney parenchymal disease may be driven by type 2 diabetes and atherosclerotic vascular disease in many individuals, and proteinuria or albuminuria measurements provide some information about glomerular aspects of parenchymal kidney health, in addition to reflecting endothelial health (29). Chronic ischemic damage to the kidneys may be an important factor in some patients, with chronic tubular hypoxia caused by low cardiac output leading to inflammation and tubulointerstitial fibrosis (30,31). Elevated central venous pressure (CVP) may cause interstitial fibrosis in the kidneys by causing capillary pericytes to detach from vascular walls and transition to a profibrotic myofibroblast cell type (32). Neurohormonal responses to the failing heart likely play an important role in chronic damage, with activation of the renin-angiotensin-aldosterone system and sympathetic nervous system driving intrarenal inflammation and fibrogenesis (30,33).

AKI in the preimplantation period may be driven by low cardiac output and high renal venous pressures, particularly in patients in cardiogenic shock before LVAD implantation. In addition to causing reduced GFR, these flow disturbances can cause structural ischemia-reperfusion injury to the kidney (34,35). A large portion of LVAD recipients have cardiogenic shock severe enough to be managed with temporary MCS before durable LVAD implantation, presenting additional kidney risks discussed later. A particularly important question for nephrology is to what degree kidney dysfunction and damage drives adverse outcomes in LVAD recipients versus being a marker of severity of cardiac and systemic illness.

Clinical Considerations

Effective methods to improve preimplantation kidney dysfunction currently lie in the years before a patient requires LVAD implantation, when therapies to improve kidney outcomes are available for many disease states. In the short-term preimplantation period, specific measures to improve kidney outcomes are not available beyond systemic hemodynamic optimization. Determination of potential reversibility of kidney dysfunction after LVAD implantation is often desired (26). However, prediction of kidney function improvement currently relies on clinical judgment. Comprehensive evaluation may provide information about the potential for improvement and susceptibility to potentially life-threatening kidney complications (Figure 1). Data about parenchymal kidney health and reserve can be obtained from a detailed history, including long-term eGFR and albuminuria trends, prior AKI episodes, review of any prior kidney procedures (e.g., lithotripsy, partial nephrectomy), urinalysis and sediment examination, and evaluation of the preimplantation period (trends in urine output and endogenous filtration markers, systemic perfusion). Direct information about kidney parenchymal injury in the preimplantation period could be provided by an approved kidney biomarker score calculated from urinary concentrations of the cell-cycle arrest markers insulin-like growth factor-binding protein 7 (IGFBP7) and tissue inhibitor of metalloproteinases-2 (TIMP2), although this biomarker score has not been validated in this setting (36).

Figure 1.

Kidney considerations throughout the timeline of mechanical circulatory support (MCS). The focus is on durable MCS, but many considerations will apply to temporary MCS as well. CO, cardiac output; CVP, central venous pressure; SBP, systolic blood pressure; DBP, diastolic blood pressure; BUN, blood urea nitrogen; KRT, kidney replacement therapy; RV, right ventricle; MAP, mean arterial pressure; MCS, mechanical circulatory support.

Future Investigations

Syndromic, filtration marker- and albuminuria-dependent AKI and CKD classifications are insufficient to understanding the complexity of kidney disease (37). This is particularly relevant to complex LVAD recipients. Investigations into cellular and molecular processes of kidney pathology are addressing this critical barrier to progress in many disease states, with analysis of kidney tissue and body fluids (37). Obtaining kidney tissue from LVAD recipients would be ideal for understanding kidney pathophysiology in this group, but kidney biopsy is seldom performed in these patients because of their tenuous states. Thus, improved noninvasive assessments of kidney health are crucial to this patient population. Growing availability of urine and blood biomarkers reflecting different aspects of kidney health/function, and growing use of omics-based systems investigations in many areas of medicine, may enable important noninvasive insights into kidney health in MCS (38,39). Pre-LVAD implantation parenchymal biomarkers may enable accurate assessment of kidney damage and differentiation of damage from flow-mediated functional reductions, yielding prognostic information on likelihood of kidney function recovery. Multi-omics studies of blood and urine samples in the preimplantation period have the potential to elucidate further the heterogeneity and mechanistic processes underlying kidney health states in these complex patients. Analysis of exosomes (membrane-derived, 50–200-nm-diameter vesicles) from the urine may provide a noninvasive window into kidney cellular processes (40,41). In addition to accurate diagnosis and prognosis, movement of kidney health understanding from broad syndromes to accurate molecular mechanistic understanding is a crucial step toward therapies (42).

Early Postimplantation Period

Epidemiology

LVAD recipients are at high risk of AKI in the early postoperative period. A recent meta-analysis estimated the incidence of AKI in more than 63,000 LVAD recipients at 37% when AKI was assessed using standardized criteria (21). The incidence of AKI treated with kidney replacement therapy was 13% (21). With AKI, odds of death more than tripled in the first 30 days and more than doubled over 1 year. With AKI treated with kidney replacement therapy, odds of death increased more than seven-fold in the first 30 days and more than five-fold in the first year (21).

Mechanisms and Pathophysiology

AKI in LVAD recipients has many potential contributing factors. LVAD implantation is a major cardiac surgery with prolonged cardiopulmonary bypass (43). Cardiac surgery is thought to damage the kidney through ischemia-reperfusion injury, inflammatory and oxidative injuries, microembolic injury, toxin-mediated injury, and neurohormonal activation (44). Much of this information has come from animal models, although noninvasive data from humans supporting many of these mechanisms is accruing (44–46). LVAD recipients, given their tenuous preimplantation status, may be particularly susceptible to these insults.

Another potential cause of AKI is RV dysfunction through elevated CVP. RV dysfunction is a common complication of LVAD implantation and can occur anytime, although early appearance is most common (43). LVAD support reduces LV volume, which can shift the interventricular septum, distorting RV geometry and reducing function (43). The severity can vary from mild (manageable with inotropes, inhaled nitric oxide, or intravenous vasodilators) to severe (requiring temporary or permanent RV MCS) (47).

Clinical Considerations

Specific interventions to reduce the risk of AKI and improve kidney outcomes in the early postoperative period are not available. Critical care nephrology practices are essential, with review of operative details, close monitoring of urine output and volume status, and frequent measurement of electrolytes and acid-base status to detect impending kidney failure or severe derangements (Figure 1). Diuretic use or ultrafiltration may be required for volume management. Urine microscopy may provide information because the presence of numerous granular casts may suggest severe acute tubular necrosis. Urine cell-cycle arrest biomarker score measurement ([TIMP2]×[IGFBP7]) may provide additional information about parenchymal kidney injury.

Future Investigations

Detailed noninvasive assessments of parenchymal health using biomarker panels may enable accurate diagnosis of kidney injury sustained during surgery. In general, cardiac surgery settings the [TIMP2]×[IGFBP7] score has enabled early identification and targeted management of AKI (48–50). Other biomarkers (basic fibroblast growth factor, kidney injury molecule-1, N-terminal pro-B-type natriuretic peptide, and tumor necrosis factor receptor) measured early in the postoperative period are associated with development of CKD after general cardiac surgery (51). Multi-omics approaches hold the promise of more granular insights into kidney health (38). Improved understanding of the molecular mechanisms of kidney dysfunction in the early postoperative period has the potential to inform therapeutic development and to identify individuals who may benefit from specific treatments.

Prolonged MCS Period

Epidemiology

LVADs tend to improve macrocirculatory parameters, increasing cardiac output and decreasing CVP, and disordered macrocirculation may be the primary driver of preimplantation kidney dysfunction in some patients (52,53). Despite these macrocirculatory improvements, LVADs often do not cause substantial sustained kidney function improvement (54–56). Group-average eGFR changes in LVAD recipients shows an early increase in eGFR, a peak eGFR around 1 month after implantation, followed by a decline (25,54). Relationships between changes in kidney function and outcomes are nonlinear (25).

Mechanisms and Pathophysiology

Numerous potential mechanisms have been proposed (Figure 2) for adverse kidney outcomes with prolonged MCS. A long-standing concern is over lack of pulsatility. For a time, continuous flow was thought to induce periarteritis in the kidneys on the basis of an animal study (57); however, this periarteritis has not been found in humans (58). Evidence is stronger for continuous flow causing endothelial dysfunction from reduced endothelial release of nitric oxide, increased secretion of endothelin-1, and other factors (59–62). Continuous flow may activate the sympathetic nervous system and renin-angiotensin system systemically and in the kidneys (63–66). Intravascular hemolysis resulting in free hemoglobin in the plasma can harm the kidneys through vasoconstriction from nitric oxide sequestration, tubular casts, and proximal tubular heme toxicity (67,68). Although hemolysis appears very limited with newer devices, this is a possible mechanism for chronic and acute kidney damage in some cases (69). Chronic RV impairment after LVAD implantation is another potential factor driving long-term kidney dysfunction (70).

Figure 2.

Potential mechanisms for left ventricular assist device effects (beneficial and harmful) on the kidneys. RAS, renin-angiotensin system.

Clinical Considerations

Interventions to improve kidney health with long-term LVAD support are unknown, and limitations of endogenous filtration marker-based kidney function estimates make it difficult to assess kidney health accurately in this setting (71). Nevertheless, large changes in serum creatinine or cystatin C levels or eGFR, or clear trajectories, may allow inferences about health and prognosis. Given the apparent renin-angiotensin system activation with continuous flow, angiotensin-converting enzyme inhibitor or angiotensin receptor blocker use is attractive for kidney preservation; however, the risks and benefits in this setting are uncertain. These medications are often continued after LVAD implantation (72).

Special management is necessary for maintenance dialysis in people with LVADs. Earlier devices were quite sensitive to reductions in preload, complicating ultrafiltration (73). Modern devices, however, have limited preload sensitivity, facilitating volume removal (74). Several case series of outpatient hemodialysis and case reports of outpatient peritoneal dialysis have been published (75–77). A theme of these reports is close cooperation between the dialysis providers and MCS teams, including initial education about interpreting LVAD device information (pump speed, flow rate, and pulsatility index) and availability of immediate communication. Blood pressure measurement is important and depends on whether the aortic valve continues to open during the cardiac cycle, causing a detectable pulse pressure. Aortic valve opening is influenced by native heart contractility and pump flow. If the aortic valve opens, systolic and diastolic blood pressure may be measurable with the usual techniques (78). If the aortic valve does not open, blood pressure can be measured using a Doppler ultrasound device and manual sphygmomanometer, and the mean arterial pressure (MAP) is obtained from the pressure at which flow is detected. The goal MAP is generally 70–80 mm Hg; MAP >90 mm Hg is avoided, given the increased risk of stroke (79–81). Vascular access for maintenance hemodialysis is an important consideration. Arteriovenous access placement, and avoidance of long-term tunneled catheter use, is desirable given the elevated risk of bloodstream infections with dialysis catheters (82). Several cases of successful arteriovenous fistula placement, maturation, and use have been reported (83,84). Concerns remain, however, about arteriovenous fistula maturation in the setting of low pulsatile blood flow, and others have advocated for arteriovenous grafts as the preferred access (85). Peritoneal dialysis is an option because modern LVADs do not compromise the peritoneal space (43,77). Both KFRT treated with dialysis and LVAD use alone have high complication rates related to underlying disease factors and treatment factors. Patients presenting with both are therefore at very high risk (86).

Future Investigations

The growing availability of techniques discussed in prior sections may enable important insights into the effects of prolonged MCS on kidney health. Longitudinal assessments of biomarker panels and multi-omics data and accurate, comprehensive assessments of clinical characteristics in large cohorts would be needed to assess the multiple dimensions of kidney health in LVAD recipients accurately and to draw inferences about mechanistic effects of durable LVAD support on the kidneys. It seems clear now that the idea of a single, predominant salutary effect on kidney function with macrocirculatory parameter improvement with LVAD support does not capture most patients’ experiences, and that molecular mechanisms rather than macrocirculatory mechanisms underlie much of cardiac-LVAD-kidney interactions.

Temporary MCS

Several temporary MCS devices are available for use in high-risk PCI, acute decompensated HF, cardiogenic shock, and cardiac arrest resuscitation (Table 1). The evidence basis to guide usage decisions is limited, and decisions rely on expert opinion and experience, pathophysiological considerations, and observational studies. A recent analysis of administrative data found an increase in the use of temporary MCS for postcardiac surgery cardiogenic shock (87). Temporary MCS use before durable MCS has also increased (88). ST-elevation myocardial infarction was complicated by cardiogenic shock in 9% of cases in an analysis of data from 2003 to 2012, and temporary MCS was used in more than half of these cases (89).

Nephrology Considerations and Kidney Pathophysiology

Temporary MCS devices improve macrocirculatory parameters that affect kidney function, and clinical experience of marked kidney function improvement in some individuals is clear. However, there are limited published data on kidney outcomes. A case series of five patients who underwent placement of a left atrial-to-femoral artery bypass pump found no change in serum creatinine, although urine output more than doubled after device placement (90). Observational studies suggest that impeller-driven axial flow pumps are associated with a lower risk of AKI during high-risk PCI (11). A small study of 15 patients with cardiogenic shock found that increasing axial flow pump rate decreased renal resistive index without changing blood pressure, suggesting kidney perfusion may have increased (91). The effects of venoarterial ECMO on kidney function are challenging to assess, given it is reserved for situations involving respiratory failure or cardiac arrest where numerous processes affecting kidney health/function are at play (92,93). Studies of long-term kidney outcomes are not available.

There are several explanations for why kidney function improvement is often not observed with temporary MCS. The limits of routine kidney assessments mean that preexisting subclinical kidney damage with loss of reserve capacity and sensitivity to insults may be underestimated. This, combined with the perturbations of the acute process necessitating temporary MCS, puts these patients at high risk for damage regardless of macrocirculatory improvement, and assessment of kidney microcirculation and parenchymal markers may improve understanding.

The inflammatory environment in temporary MCS may be damaging to the kidneys. Systemic inflammation is well documented in settings that can lead to temporary MCS use—such as acute myocardial infarction or acute HF decompensation—in clinical and experimental settings (94). Although systemic and cardiac inflammatory environments have been most studied, it is likely that the kidneys are affected by systemic and intrarenal inflammation as well (30,94). Temporary MCS may exacerbate inflammation through procedural factors and exposure of the blood to artificial material. This has been most noticeable with ECMO, where a systemic inflammatory response syndrome often develops, attributed to activation of the innate immune system with extensive blood exposure to artificial material, in addition to a pro-inflammatory effect of nonpulsatile blood flow (95,96). Experimental studies have demonstrated that ECMO in healthy animals causes systemic inflammatory response syndrome with mobilization of cellular stores of inflammatory cytokines (97). In contrast to ECMO, IABP use has been reported to reduce inflammation in some settings, perhaps due to pulsatility (98,99).

Nephrology Clinical Management Considerations

Nephrology evaluation of acutely ill people on temporary MCS includes assessing their pre-episode kidney health/function, their recent exposures to kidney insults, and their current status, with particular attention to urine output, electrolytes, and likely trajectory (Figure 1). Routine nephrology critical care assessments, including consideration of a wide differential diagnosis for causes and contributors to kidney injury, in addition to clinical judgment on how the acute cardiac process is affecting the presentation, are appropriate. Frequent monitoring of urine output, electrolytes, and acid-base status is crucial as well to enable optimal supportive care and assess the need for dialysis, with close communication with the cardiovascular and intensivist teams.

Patients requiring temporary MCS who develop severe AKI may require dialysis. Given the hemodynamic instability and risk for severe acid-base, electrolyte, and volume disturbances, continuous renal replacement therapy is usually the modality of choice. Management considerations are similar to other situations, with volume management paramount. Catheter placement location may be influenced by the temporary MCS method if venous access is used for MCS, such as with venoarterial ECMO or percutaneous RV support devices. With venoarterial ECMO, attachment of the continuous renal replacement therapy machine to the ECMO circuit is often possible, making an additional catheter unnecessary. In all forms of temporary MCS, systemic anticoagulation is used, and thus regional or systemic anticoagulation specifically for dialysis is not necessary.

Future Investigations

To understand the effects of temporary MCS on the kidneys, the improved noninvasive assessments of kidney function discussed in the context of durable MCS will be crucial. Temporary MCS devices differ greatly in function, uses, and potential risks, leading to great heterogeneity in potential kidney effects—heterogeneity that will require detailed noninvasive molecular techniques to understand and characterize. This will enable individualized diagnosis and prognosis and development of targeted therapeutic and management strategies to improve kidney and overall outcomes.

Conclusions

The high burden of cardiovascular disease in the United States, improving MCS technologies, and changing use patterns, combined with the common coexistence of kidney and cardiovascular disease, mean that the need for nephrology care for patients receiving MCS will continue to increase. Nephrologists play an important role in ensuring patient safety and improving outcomes in this setting. Although current kidney-related management strategies in MCS are mostly opinion and experience based, the rapid development of tools and techniques for granular, individualized kidney assessment hold the promise of improved diagnostic tools and development of targeted management strategies and therapies in the future.

Disclosures

A.B. Civitello reports consultancy agreements with Medtronic; honoraria from Abbott and Medtronic; and being a scientific advisor for Medtronic Titan Medical Advisory Board. S.D. Navaneethan reports consultancy agreements with Bayer, Boehringer Ingelheim, Tricida, and Vifor; research funding from Keryx; honoraria from Bayer, Boehringer Ingelheim, Tricida, and Vifor; and being a scientific advisor for AJKD, CJASN, CardioRenal Medicine, Current Opinion in Nephrology and Hypertension, American Journal of Nephrology, and KDIGO (guideline writing committee member). The remaining authors have nothing to disclose.

Funding

C.P. Walther is supported by the National Institute of Diabetes and Digestive and Kidney Diseases (grant/award number: K23DK122131).

Author Contributions

S.D. Navaneethan and C.P. Walther conceptualized the study; S.D. Navaneethan was responsible for supervision; C.P. Walther was responsible for visualization and wrote the original draft of the manuscript; and all authors reviewed and edited the manuscript.