Next Article in Journal
Examination of an Online Cooking Education Program to Improve Shopping Skills, Attitudes toward Cooking, and Cooking Confidence among WIC Participants
Previous Article in Journal
Ultra-Processed Food as Mediator of the Association between Birthweight and Childhood Body Weight Outcomes: A Retrospective Cohort Study
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:

Nutritional Risk of Candidates for Simultaneous Pancreatic–Kidney Transplantation—A Narrative Review

Agnieszka Mizerska
Marek Durlik
1 and
Karolina Kędzierska-Kapuza
Department of Gastroenterological Surgery and Transplantology, National Medical Institute of the Ministry of Interior Affairs and Administration, Wołoska St. 137, 02-507 Warsaw, Poland
Department of Gastroenterological Surgery and Transplantology, Centre of Postgraduate Medical Education, Marymoncka St. 99/103, 01-813 Warsaw, Poland
Authors to whom correspondence should be addressed.
Nutrients 2023, 15(19), 4179;
Submission received: 4 September 2023 / Revised: 14 September 2023 / Accepted: 21 September 2023 / Published: 27 September 2023
(This article belongs to the Special Issue Nutritional Support for Kidney Transplantation)


Introduction: Not much is known about the significance of nutritional status and support in transplant surgery, least of all in simultaneous pancreatic and kidney transplantation. Malnutrition in the context of simultaneous pancreatic–kidney transplantation seems to be complex and a still poorly investigated problem. Since SPKTX is highly qualified and also has a small volume procedure, it is difficult to obtain data from large cohorts of patients. The aim of this article is to gather existing evidence and information about the subject, as well as to elicit some questions and goals for the future. Methods: We searched through the Pub-Med database using the keywords “pancreas and kidney transplantation” combined with “nutritional risk”, “nutritional status”, “malnutrition”, “nutritional intervention”, and “frailty”, finding a total of 4103 matching results. We then narrowed it down to articles written in English with the full text available. We also researched through the references of articles most accurately matching our researched terms. Results: There are numerous tools that have been investigated for the screening of malnutrition, such as the NRI index, PNI index, NLR, SGA scale, and NRS-2002 scale, each of which proved to be of some use in predicting patient outcomes in different surgical settings. Since all of them differed in components and assessed parameters and, in the absence of more sensitive or infallible indicators, the most reasonable approach seems to evaluate them jointly. Conclusion: It is important to underline the necessity of nutritional screening and the subsequent introduction of adequate therapy while awaiting transplantation in an attempt to improve results. Considering the complexity of surgical procedures and the severity of underlying diseases with their intense metabolic components, the patient’s nutritional status seems to significantly influence results. Consequently, nutritional risk assessments should be a part of the routine care of patients qualified for transplantation.

1. Introduction

Assessing nutritional risk and the subsequent implementation of nutritional support has a well-established place in the peri-operative care of patients undergoing major gastrointestinal surgery [1]. There are also many studies on the nutritional care of patients with cancer diseases, as well as guidelines based on them [2]. Not much has been said, however, about the significance of nutritional status and support in transplant surgery, least of all in simultaneous pancreatic and kidney transplantation (SPKTX). The aim of this article is to gather existing evidence and information about the subject, as well as to elicit some questions and goals for the future.
It has been largely proved that malnutrition is a risk factor for complications in abdominal surgery. It compromises the healing of anastomoses and surgical incisions on the abdominal wall. Malnourished patients are at risk of increased postoperative morbidity and mortality, lengthened hospital stays, and impaired wound healing [3,4].
There is also evidence of malnutrition compromising the outcomes of transplantation of solid organs, such as the liver, lungs, or kidney [5,6,7,8,9].
The prevailing indication for SPKTX is autoimmune diabetes followed by end-stage diabetic nephropathy, with special consideration for brittle diabetes, resulting in hypoglycemia unawareness, frequent severe metabolic complications, or the failure of exogenous therapy to prevent metabolic complications [10,11]. Also, type 2 diabetes might be an indication, alongside other types, such as diabetes correlated with chronic pancreatitis or post-pancreatectomy cases [12].
There is evidence that SPKTX is more beneficial for these patients than a kidney transplant alone, presumably thanks to better metabolic control [13,14,15]. Nevertheless, this complicated surgical procedure still bears a high incidence of postoperative complications, therefore demanding better identification of potential risk factors and ways of reducing them [16,17,18].
The complexity of the procedure itself and the severity of underlying diseases leading to transplantation in the first place require special attention when qualifying for this treatment. A risk assessment and ability to predict outcomes and distinguish groups of patients that could benefit most from the procedure compared to those whose risk profile is too high seems to be of the utmost importance. Patients’ functional impairment, most commonly assessed using the Karnofsky scale, has been described as an important factor when predicting the outcomes of treatment in many medical fields, including simultaneous pancreas–kidney transplantation [19].

2. Aim

Since SPKTX is a highly qualified and small-volume procedure, the aim of this article is to gather existing evidence and information about this subject as well as to elicit some questions and goals for the future.

3. Methods

We searched through the Pub-Med database using the keywords “pancreas and kidney transplantation” combined with “nutritional risk”, “nutritional status”, “malnutrition”, “nutritional intervention”, and “frailty”, finding a total of 4103 matching results. We then narrowed it down to articles written in English with their full text available. We also researched through references of articles most accurately matching our researched terms. The summary of our research, divided into subsections discussing pathophysiology, laboratory markers, risk scales, and nutritional intervention, is as follows.

4. Results

4.1. Pathophysiology of Malnutrition in Spktx-Transplant Recipients

According to ESPEN (European Society for Clinical Nutrition and Metabolism), malnutrition is “a state resulting from lack of intake or uptake of nutrition that leads to altered body composition (decreased fat-free mass) and body cell mass leading to diminished physical and mental function and impaired clinical outcome from disease” [20].
Different forms of malnutrition can be distinguished according to leading pathophysiological pathways. One of them is disease-related malnutrition with inflammation. Inflammatory response, elicited by disease-specific mechanisms, leads to anorexia, reduced food intake, weight loss, and muscle catabolism [21,22,23,24].
Depending on whether the disease is chronic or acute, the inflammatory response might be milder or stronger. Consecutively, apart from the above-mentioned malnutrition in relation to chronic disease, another form of malnutrition caused by the catabolic state is acute disease- or injury-related ones, and major surgical procedures are considered one of its triggers. Stress metabolic response, consisting of high pro-inflammatory cytokine activity, increased corticosteroid and catecholamine release, and insulin resistance, can lead to fast nutrient storage, which is additionally exacerbated by immobilization and reduced food intake [25].
Therefore, there are many reasons for patients prepared for simultaneous pancreatic–kidney transplantations to have compromised nutritional status.
First of all, chronic kidney disease is proven to induce a state of chronic inflammation through various pathways. The kidneys’ compromised ability to excrete acid leads to excess NH4+ production, resulting in complement activation [26]. Alterations in gut microbiota caused by impaired protein digestion and excess uric acid provoke injury to the intestinal mucosa and, thus, result in the translocation of toxic metabolites and bacterial endotoxins, stimulating pro-inflammatory cytokine production [27,28]. Last but not least, additional sources of inflammation include both hemo- and peritoneal dialysis [29]. Taking into account increased resting energy expenditure in patients with CKD (chronic kidney disease), secondary to a persistent inflammatory state and multiple co-morbidities such as cardiovascular disease, poorly controlled diabetes, and hyperparathyroidism, patients develop a protein–energy wasting syndrome, resulting in the loss of lean body mass [30,31].
Metabolic acidosis that is present in the state of CKD activates proteolysis by activating the ubiquitin–proteasome system and caspase-3, which causes other organ muscle proteins to degrade [32]. Acidosis also contributes to insulin resistance, growth hormone resistance, and glucocorticoid hipersecretion, each of which induces a protein catabolic state [25].
The mode of renal replacement therapy might contribute to malnutrition not only by inducing inflammation but also through other mechanisms. Two main modalities are peritoneal dialysis (PD) and hemodialysis (HD). There is evidence that patients undergoing HD have greater muscle mass and mid-arm circumference [33]. It is estimated that PD might be a risk factor for malnutrition, occurring in 30–50% of patients diagnosed with it [34]. Additional protein loss and higher levels of uremic toxins might also be contributing factors [35,36]. Table 1 summarizes mentioned above causes of malnutrition in SPKTX patients.
The non-inflammatory mechanisms of malnutrition additionally contribute to its development in CKD patients. Patients with insufficient kidney function (CKD 5 stage) but not yet requiring renal replacement therapy have additional risk factors of decreased protein levels due to dietary limitations [37]. Also worth mentioning is possible protein loss due to proteinuria, which occurs in patients with remaining diuresis.
One of the complications of diabetes is gastroparesis, which is delayed gastric emptying that occurs due to neuronal damage caused by chronic hyperglicemia. The result of this might be early satiety, nausea, and vomiting, all of which additionally impair the patient’s nutritional status [38,39]. According to gathered data, approximately 60% of patients suffering from diabetic or idiopathic gastroparesis consume a calorie-deficient diet [40].
Overweight or obese patients are a group requiring special concern. First of all, elevated BMI (body mass index) is a known risk factor in pancreatic transplant surgery [41,42]. Obese patients are also believed to be at a higher risk of complications in other kinds of surgery; however, conflicting data exists [43,44]. Fat tissue has been proven to be metabolically active and can alter the systemic response to surgical injury. In particular, excessive fat tissue in the form of central obesity was proved to be metabolically active, hence inducing and aggravating inflammatory responses. There is evidence that this activity might be particularly strong in patients with CKD [45,46].
As a result of inadequate protein intake and excessive catabolic state, sarcopenia might be present. It is defined as a loss of skeletal muscle mass, strength, and function, leading to increased mortality and worse outcomes in surgical treatment [47]. Diagnostic criteria for sarcopenia are still being discussed [48]. Sarcopenia might be well associated with obesity and, therefore, even more difficult to detect [49,50].
Sarcopenias exacerbate obesity-associated insulin resistance and impair glycemia [51]. The mediators of this are IL-6, which is secreted by muscles, and FGF-21, secreted by muscles in response to insulin [24,52,53]. Muscle also secretes irisin, promoting beta cell survival [54]. Th3 crosstalk between beta cells and myocytes probably has an effect on pancreas graft survival and function [55]. There is evidence of the detrimental impact of sarcopenia on surgical outcomes in pancreas transplant recipients in clinical settings [56,57,58].
Sarcopenia might also be considered as a surrogate of frailty, which has recently been brought to attention as a risk factor for increased mortality and morbidity [59]. The concept of frailty involves a state of vulnerability and non-resilience with limited reserve capacity in major organ systems [60]. Initially described by geriatricians, it made its way into other medical surroundings, investigated as a risk factor for negative outcomes in many non-elderly subpopulations, including solid organ transplant recipients [61,62].
Although the general concept of frailty seems to be widely accepted, tools for its diagnosis are yet to be established. In the literature, there have been numerous scales developed for assessing patients’ frailty in various conditions [63,64]. Some of them have already been proven to predict the outcomes of organ transplantation [65,66,67,68]. The most commonly used is The Physical Frailty Phenotype, which includes weight loss, exhaustion (fatigue), low physical activity, slowness (reduced gait speed), and weakness (low grip strength) [59].
Due to the persistent increased awareness of the prevalence and importance of frailty in transplant settings, the American Society of Transplantation developed a working group designed to discuss the problem of frailty in accordance with different organ transplantation, including the kidney, liver, heart, and lung [69]. Apart from this, there are studies investigating frailty among candidates for simultaneous kidney and pancreas transplantation, estimating its prevalence and assessing it as a potential risk factor. First of all, frailty is associated with a lower chance of being listed for transplantation and higher mortality while being on a waiting list. It is also associated with negative outcomes in transplantations if it finally occurs, such as surgical complications, delayed graft function, postoperative delirium, poor tolerance of immunosuppression, and eventually higher mortality [70].

4.2. Laboratory Markers of Malnutrition

There have been several attempts to establish laboratory markers of malnutrition. One of the first was serum albumin, a protein produced by hepatocytes, with its main function as a carrier molecule for the maintenance of the oncotic pressure of blood. Due to its long half-life time (14–20 days) and its distribution along fluid compartments (with more than half of its total amount being located extravascularly), daily protein intake did not significantly influence its levels [71]. It has been proved that albumin levels remain normal during starvation up until it reaches extreme points with other physical evidence, therefore showing its usefulness as a marker of non-inflammatory malnutrition [72]. However, albumin, as a negative acute-phase protein that has been proven to decrease in multiple serious health conditions, tends to be used as a marker of gravity in illness and correlated inflammation, thus affecting nutritional status at the same time and probably indicating patients with special nutritional risk [73]. There is evidence of hypoalbuminemia being a risk factor for impaired outcomes after a SPKTX transplant [74].
Other possible serum markers of malnutrition might be prealbumin, which is affected by an inflammatory state as well as albumin; however, it acts as a more reliable indicator of decreased protein intake because of its significantly shorter half-life time and its smaller total amount [75,76,77]. However, its estimation might be impaired in CKD patients since it is degraded by the kidneys [78]. Another candidate for a serum marker of malnutrition is transferrin; however, there are similar limitations with regard to the interpretation of its serum level—it is increased in iron-deficiency status and in renal failure [77].
Apart from visceral proteins, total lymphocyte count has also been assessed as a potential malnutrition marker [79]. However, it might be of no use to elderly patients, and due to the administration of immunosuppressive therapy, it is useless as a monitoring tool for patients after transplantation.
Serum lipoproteins might also be a meaningful indicator of nutritional status. Total cholesterol [80] and non-HDL cholesterol have both shown a paradoxical effect on Coronary Artery Disease (CAD) in CKD patients. Low levels of total cholesterol and non-HDL-C have been connected with malnutrition indices and the higher risk of CAD in these patients. It was shown that in elderly malnourished patients, HDL cholesterol was low and that a balanced dietary pattern is positively related to the HDL-C level, while there is also a strong negative association between the thrifty dietary pattern and HDL-C [81].

4.3. Nutritional and Peri-Operative Risk Assessment

There is no clinically established scoring system concerning recipient-related factors that are designed specifically for SPKTX transplantations. Tools designed to predict outcomes, such as P-PASS (Preprocurement Pancreas Suitability Score) and PDRI (Pancreas Donor Risk Index), analyze donor-related factors. However, there are still conflicting results regarding their clinical usefulness [82,83]. There are a few general surgery risk prediction scoring systems that can be used to assess possible outcomes, such as POSSUM (Physiological and Operative Severity Score for the enumeration of Mortality and morbidity), P-POSSUM (Portsmouth modification of POSSUM), MODS (Multiple Organ Dysfunction Score), the Charlson index, ASA (American Society of Anaesthesiologists), and Waterlow score [84]. None of the aforementioned prediction scales involve the assessment of patients’ nutritional status.
The Nutrition Risk Index (NRI) is a diagnostic tool designed to predict surgical outcomes with correlation to malnutrition using the serum albumin level and comparing a patient’s actual weight with the usual one [85]. Among the interesting predictive tools is the Prognostic Nutritional Index (PNI), with its calculation depending on serum albumin levels and lymphocyte count [86]. It has been proven to be a useful prognostic tool in lung transplantation [87]. Consistent with the inflammatory undermining of malnutrition, it is also worth considering the neutrophil-to-lymphocyte ratio (NLR) as an indirect marker of subclinical inflammation [88]. There is some evidence of its ability to predict values in kidney transplantation [89]. Widely used screening scales include the Subjective Global Assessment (SGA) [90,91,92] and Nutrition Risk Screening 2002 (NRS-2002), assessing nutritional status together with disease severity and additionally taking into account patient’s older age [93].
The comparison of parameters assessed in the aforementioned index and scales is presented in the table below (Table 2).

4.4. Nutritional Intervention

Thanks to growing knowledge and evidence of the influence of nutritional status on the results of surgery, much has been said regarding nutritional support as a part of prehabilitation protocols. Prehabilitation, considered a way of improving the patient’s overall health status prior to elective surgery in order to induce the best possible systemic response for injury, consists of exercise, nutrition, and psychosocial components [94].
We can hardly call transplantation either elective or emergency surgery. When considering deceased donation, as is almost exclusively the case in pancreatic transplantation, the exact time of the procedure cannot be perceived for obvious reasons [95]. Therefore, there are limitations in the ability to plan processes of prehabilitation. Despite diabetic and often nephrological scrutiny, it may be impossible to always detect changes in patients’ nutritional status or body composition with the potential to affect transplantation results at a time sufficient enough to interfere. Having said that, the need for constant vigilance and perhaps adjusted supplementation must be a part of routine care.
Early enteral nutrition, described as an enteral feed initiated within 24 h of surgery, is one of the main parts of enhanced recovery after surgery (ERAS) protocols in abdominal surgery, regarding, for example, esophageal, gastric, pancreatic, or bowel surgery [96,97,98,99]. Some protocols for liver and renal transplantation also exist [100,101]. ERAS protocols in post-pancreatic transplantation surgery are yet to be established [102].
The main concern about introducing early enteral nutrition in pancreas transplant patients concerns the presence of high small bowel anastomosis. However, there have not been RCTs evaluating early enteral nutrition in these patients. Retrospective studies indicate the safety of these modes of nutrition, as well as demonstrating better nutritional support and increasing postoperative albumin levels; however, it has to be underlined that there is no clear evidence of benefits in these exact groups of patients [103]. ESPEN guidelines based on existing evidence suggest early enteral nutrition in pancreatic transplant patients [1].
Apart from concerns about the influence of enteral input on the healing of anastomoses, there is also the possibility of limited tolerance toward early enteral nutrition due to intestinal dysfunction and gastroparesis, especially in the early postoperative phase, as pancreatic transplantation consists of severe surgical injury to the abdominal cavity. As already mentioned, diabetic patients are at risk of delayed gastric emptying. Altogether, the decreased motility of the small intestine due to an autonomic nervous system might be present [104]. If limited tolerance occurs, the patient is at risk of inadequate energy and protein intake. Such a situation might require the additional use of parenteral nutrition [93].
It is important to notice that enteral nutrition does not compromise tacrolimus absorption or blood levels [105]. Enteral nutrition has also been proven to decrease the rate of viral infections after liver transplantations [106]. High-fiber diets enriched with Lactobacillus plantarum have also been proven to decrease the rate of infections [107]. However, it has to be underlined that these studies concern liver transplant recipients, and the extrapolation of the results on pancreas transplant recipients requires further investigations.
There are some data concerning immuno-modulatory substrates available, although they are limited, and there are no recommendations regarding this subject [108]. In the literature, there is some evidence of the beneficial impact of parenteral glutamine supplementation on immune function after surgery as it decreases systemic IL-6 production, therefore improving nitrogen balance; however, data are limited and do not concern transplant recipients in particular [109]. There is also interesting evidence from animal experiments on small bowel transplantations indicating that glutamine supplementation might decrease intestinal mucosa permeability, thus diminishing the rate of bacterial translocation [110].

5. Conclusions

Malnutrition in the context of simultaneous pancreatic–kidney transplantation seems to be complex and still a poorly investigated problem. Since SPKTX is highly qualified and also has a small volume procedure, it is difficult to obtain data from large cohorts of patients. Considering the complexity of this surgical procedure and the severity of underlying diseases with their intense metabolic component, the patient’s nutritional status seems to significantly influence results. Consequently, nutritional risk assessments should be a part of routine care in patients who qualify for transplantation. There are numerous tools calculating malnutrition, differing in their components and assessed parameters; therefore, the most reasonable approach seems to be joint evaluation. Its usefulness and predictive value in patients undergoing simultaneous pancreas–kidney transplantation requires further investigation.


This research received no external funding.

Institutional Review Board Statement

Not applicable.

Informed Consent Statement

Not applicable.

Data Availability Statement

Not applicable.

Conflicts of Interest

The authors declare no conflict of interest.


  1. Weimann, A.; Braga, M.; Carli, F.; Higashiguchi, T.; Hübner, M.; Klek, S.; Laviano, A.; Ljungqvist, O.; Lobo, D.N.; Martindale, R.G.; et al. ESPEN practical guideline: Clinical nutrition in surgery. Clin. Nutr. 2021, 40, 4745–4761. [Google Scholar] [CrossRef] [PubMed]
  2. Muscaritoli, M.; Arends, J.; Bachmann, P.; Baracos, V.; Barthelemy, N.; Bertz, H.; Bozzetti, F.; Hütterer, E.; Isenring, E.; Kaasa, S.; et al. ESPEN practical guideline: Clinical Nutrition in cancer. Clin. Nutr. 2021, 40, 2898–2913. [Google Scholar] [CrossRef] [PubMed]
  3. Barker, L.A.; Gout, B.S.; Crowe, T.C. Hospital Malnutrition: Prevalence, Identification and Impact on Patients and the Healthcare System. Int. J. Environ. Res. Public Health 2011, 8, 514–527. [Google Scholar] [CrossRef]
  4. Zhang, B.; Najarali, Z.; Ruo, L.; Alhusaini, A.; Solis, N.; Valencia, M.; Sanchez, M.I.P.; Serrano, P.E. Effect of Perioperative Nutritional Supplementation on Postoperative Complications-Systematic Review and Meta-Analysis. J. Gastrointest. Surg. 2019, 23, 1682–1693. [Google Scholar] [CrossRef]
  5. Pikul, J.; Sharpe, M.D.; Lowndes, R.; Ghent, C.N. Degree of preoperative malnutrition is predictive of postoperative morbidity and mortality in liver transplant recipients. Transplantation 1994, 57, 469–472. [Google Scholar] [CrossRef]
  6. Selberg, O.; Bottcher, J.; Tusch, G.; Pichlmayr, R.; Henkel, E.; Muller, M.J. Identification of high- and low-risk patients before liver transplantation: A prospective cohort study of nutritional and metabolic parameters in 150 patients. Hepatology 1997, 25, 652–657. [Google Scholar] [CrossRef]
  7. Schwebel, C.; Pin, I.; Barnoud, D.; Devouassoux, G.; Brichon, P.; Chaffanjon, P.; Chavanon, O.; Sessa, C.; Blin, D.; Guignier, M.; et al. Prevalence and consequences of nutritional depletion in lung transplant candidates. Eur. Respir. J. 2000, 16, 1050–1055. [Google Scholar] [CrossRef]
  8. Stephenson, G.R.; Moretti, E.W.; El-Moalem, H.; Clavien, P.A.; Tuttle-Newhall, J.E. Malnutrition in liver transplant patients: Preopera-tive subjective global assessment is predictive of outcome after liver transplantation. Transplantation 2001, 72, 666–670. [Google Scholar] [CrossRef]
  9. Sabbatini, M.; Ferreri, L.; Pisani, A.; Capuano, I.; Morgillo, M.; Memoli, A.; Riccio, E.; Guida, B. Nutritional management in renal transplant recipients: A transplant team opportunity to improve graft survival. Nutr. Metab. Cardiovasc. Dis. 2019, 29, 319–324. [Google Scholar] [CrossRef]
  10. Boggi, U.; Vistoli, F.; Andres, A.; Arbogast, H.P.; Badet, L.; Baronti, W.; Bartlett, S.T.; Benedetti, E.; Branchereau, J.; Burke, G.W., 3rd; et al. First World Consensus Conference on pancreas transplantation: Part II—Recommendations. Am. J. Transplant. 2021, 21 (Suppl. S3), 17–59. [Google Scholar] [CrossRef]
  11. Samoylova, M.L.; Borle, D.; Ravindra, K.V. Pancreas Transplantation: Indications, Techniques, and Outcomes. Surg. Clin. N. Am. 2019, 99, 87–101. [Google Scholar] [CrossRef] [PubMed]
  12. Durlik, M.; Baumgart-Gryn, K. Almost 200 Pancreas Transplantations: A Single-Center Experience. Transplant. Proc. 2018, 50, 2124–2127. [Google Scholar] [CrossRef] [PubMed]
  13. Mohan, P.; Safi, K.; Little, D.M.; Donohoe, J.; Conlon, P.; Walshe, J.J.; O’Kelly, P.; Thompson, C.J.; Hickey, D.P. Improved patient survival in recipients of simultaneous pancreas-kidney transplant compared with kidney transplant alone in patients with type 1 diabe-tes mellitus and end-stage renal disease. Br. J. Surg. 2003, 90, 1137–1141. [Google Scholar] [CrossRef] [PubMed]
  14. Sung, R.S.; Zhang, M.; Schaubel, D.E.; Shu, X.; Magee, J.C. A Reassessment of the Survival Advantage of Simultaneous Kid-ney-Pancreas Versus Kidney-Alone Transplantation. Transplantation 2015, 99, 1900–1906. [Google Scholar] [CrossRef] [PubMed]
  15. Rajkumar, T.; Mazid, S.; Vucak-Dzumhur, M.; Sykes, T.M.; Elder, G.J. Health-related quality of life following kidney and simultaneous pancreas kidney transplantation. Nephrology 2019, 24, 975–982. [Google Scholar] [CrossRef]
  16. Humar, A.; Kandaswamy, R.; Granger, D.; Gruessner, R.W.; Gruessner, A.C.; Sutherland, D.E.R. Decreased Surgical Risks of Pancreas Transplantation in the Modern Era. Ann. Surg. 2000, 231, 269–275. [Google Scholar] [CrossRef]
  17. Troppmann, C.; Gruessner, A.C.; Dunn, D.L.; Sutherland, D.E.; Gruessner, R.W. Surgical complications requiring early relaparotomy after pancreas transplantation: A multivariate risk factor and economic impact analysis of the cyclosporine era. Ann. Surg. 1998, 227, 255–268. [Google Scholar] [CrossRef]
  18. Fellmer, P.T.; Pascher, A.; Kahl, A.; Ulrich, F.; Lanzenberger, K.; Schnell, K.; Jonas, S.; Tullius, S.G.; Neuhaus, P.; Pratschke, J. Influence of donor- and recipient-specific factors on the postoperative course after combined pancreas–kidney transplantation. Langenbeck’s Arch. Surg. 2010, 395, 19–25. [Google Scholar] [CrossRef]
  19. Lentine, K.L.; Alhamad, T.; Cheungpasitporn, W.; Tan, J.C.; Chang, S.-H.; Cooper, M.; Dadhania, D.M.; Axelrod, D.A.M.; Schnitzler, M.A.; Ouseph, R.; et al. Impact of Functional Status on Outcomes of Simultaneous Pancreas-kidney Transplantation: Risks and Opportunities for Patient Benefit. Transplant. Direct 2020, 6, e599. [Google Scholar] [CrossRef]
  20. Cederholm, T.; Barazzoni, R.; Austin, P.; Ballmer, P.; Biolo, G.; Bischoff, S.C.; Compher, C.; Correia, I.; Higashiguchi, T.; Holst, M.; et al. ESPEN guidelines on definitions and terminology of clinical nutrition. Clin. Nutr. 2017, 36, 49–64. [Google Scholar] [CrossRef]
  21. McCarthy, D.O.; Kluger, M.J.; Vander, A.J. Suppression of food intake during infection: Is interleukin-1 involved? Am. J. Clin. Nutr. 1985, 42, 1179–1182. [Google Scholar] [CrossRef] [PubMed]
  22. Schuetz, P.; Bally, M.; Stanga, Z.; Keller, U. Loss of appetite in acutely ill medical inpatients: Physiological response or therapeu-tic target? Swiss Med. Wkly. 2014, 144, w13957. [Google Scholar] [CrossRef] [PubMed]
  23. Morley, J.E.; Thomas, D.R.; Wilson, M.-M.G. Cachexia: Pathophysiology and clinical relevance. Am. J. Clin. Nutr. 2006, 83, 735–743. [Google Scholar] [CrossRef] [PubMed]
  24. Ellingsgaard, H.; Hauselmann, I.; Schuler, B.; Habib, A.M.; Baggio, L.L.; Meier, D.T.; Eppler, E.; Bouzakri, K.; Wueest, S.; Muller, Y.D.; et al. Interleukin-6 enhances insulin secretion by increasing glucagon-like peptide-1 secretion from L cells and alpha cells. Nat. Med. 2011, 17, 1481–1489. [Google Scholar] [CrossRef]
  25. Preiser, J.-C.; Ichai, C.; Orban, J.-C.; Groeneveld, A.B.J. Metabolic response to the stress of critical illness. Br. J. Anaesth. 2014, 113, 945–954. [Google Scholar] [CrossRef]
  26. Zha, Y.; Qian, Q. Protein Nutrition and Malnutrition in CKD and ESRD. Nutrients 2017, 9, 208. [Google Scholar] [CrossRef]
  27. Ondrussek-Sekac, M.; Navas-Carrillo, D.; Orenes-Piñero, E. Intestinal microbiota alterations in chronic kidney disease and the influence of dietary components. Crit. Rev. Food Sci. Nutr. 2021, 61, 1490–1502. [Google Scholar] [CrossRef]
  28. Bammens, B.; Verbeke, K.; Vanrenterghem, Y.; Evenepoel, P. Evidence for impaired assimilation of protein in chronic renal failure. Kidney Int. 2003, 64, 2196–2203. [Google Scholar] [CrossRef]
  29. Snaedal, S.; Qureshi, A.R.; Lund, S.H.; Germanis, G.; Hylander, B.; Heimbürger, O.; Carrero, J.J.; Stenvinkel, P.; Bárány, P. Dialysis modality and nutritional status are associated with variability of inflammatory markers. Nephrol. Dial. Transplant. 2016, 31, 1320–1327. [Google Scholar] [CrossRef]
  30. Fouque, D.; Kalantar-Zadeh, K.; Kopple, J.; Cano, N.; Chauveau, P.; Cuppari, L.; Franch, H.; Guarnieri, G.; Ikizler, T.A.; Kaysen, G.; et al. A proposed nomenclature and diagnostic criteria for protein–energy wasting in acute and chronic kidney disease. Kidney Int. 2008, 73, 391–398. [Google Scholar] [CrossRef]
  31. Kovesdy, C.P.; Kopple, J.D.; Kalantar-Zadeh, K. Management of protein-energy wasting in non-dialysis-dependent chronic kidney disease: Reconciling low protein intake with nutritional therapy. Am. J. Clin. Nutr. 2013, 97, 1163–1177. [Google Scholar] [CrossRef] [PubMed]
  32. Pickering, W.P.; Price, S.R.; Bircher, G.; Marinovic, A.C.; Mitch, W.E.; Walls, J. Nutrition in CAPD: Serum bicarbonate and the ubiq-uitin-proteasome system in muscle. Kidney Int. 2002, 61, 1286–1292. [Google Scholar] [CrossRef] [PubMed]
  33. Pontón-Vázquez, C.; Vásquez-Garibay, E.M.; Hurtado-López, E.F.; Serrano, A.d.l.T.; García, G.P.; Romero-Velarde, E. Dietary Intake, Nutritional Status, and Body Composition in Children With End-Stage Kidney Disease on Hemodialysis or Peritoneal Dialysis. J. Ren. Nutr. 2017, 27, 207–215. [Google Scholar] [CrossRef] [PubMed]
  34. Satirapoj, B.; Limwannata, P.; Kleebchaiyaphum, C.; Prapakorn, J.; Yatinan, U.; Chotsriluecha, S.; Supasyndh, O. Nutritional status among peritoneal dialysis patients after oral supplement with ONCE dialyze formula. Int. J. Nephrol. Renov. Dis. 2017, 10, 145–151. [Google Scholar] [CrossRef] [PubMed]
  35. Vanholder, R.; Glorieux, G.; Lameire, N. The other side of the coin: Impact of toxin generation and nutrition on the uremic syn-drome. In Seminars in Dialysis; Blackwell Science Inc.: Malden, MA, USA, 2002; Volume 15, pp. 311–314. [Google Scholar]
  36. Kiebalo, T.; Holotka, J.; Habura, I.; Pawlaczyk, K. Nutritional Status in Peritoneal Dialysis: Nutritional Guidelines, Adequacy and the Management of Malnutrition. Nutrients 2020, 12, 1715. [Google Scholar] [CrossRef]
  37. Ikizler, T.A.; Burrowes, J.D.; Byham-Gray, L.D.; Campbell, K.L.; Carrero, J.-J.; Chan, W.; Fouque, D.; Friedman, A.N.; Ghaddar, S.; Goldstein-Fuchs, D.J.; et al. KDOQI Clinical Practice Guideline for Nutrition in CKD: 2020 Update. Am. J. Kidney Dis. 2020, 76 (Suppl. S1), S1–S107. [Google Scholar] [CrossRef]
  38. Bharucha, A.E.; Kudva, Y.C.; Prichard, D.O. Diabetic Gastroparesis. Endocr. Rev. 2019, 40, 1318–1352. [Google Scholar] [CrossRef]
  39. Camilleri, M.; Bharucha, A.E.; Farrugia, G. Epidemiology, Mechanisms, and Management of Diabetic Gastroparesis. Clin. Gastroenterol. Hepatol. 2011, 9, 5–12. [Google Scholar] [CrossRef]
  40. Parkman, H.P.; Yates, K.P.; Hasler, W.L.; Nguyan, L.; Pasricha, P.J.; Snape, W.J.; Farrugia, G.; Calles, J.; Koch, K.L.; Abell, T.L.; et al. Dietary Intake and Nutritional Deficiencies in Patients With Diabetic or Idiopathic Gastroparesis. Gastroenterology 2011, 141, 486–498.e7. [Google Scholar] [CrossRef]
  41. Sampaio, M.S.; Kuo, H.T.; Bunnapradist, S. Outcomes of simultaneous pancreas-kidney transplantation in type 2 diabetic recipi-ents. Clin. J. Am. Soc. Nephrol. 2011, 6, 1198–1206. [Google Scholar] [CrossRef]
  42. Bédat, B.; Niclauss, N.; Jannot, A.-S.; Andres, A.; Toso, C.; Morel, P.; Berney, T. Impact of Recipient Body Mass Index on Short-Term and Long-Term Survival of Pancreatic Grafts. Transplantation 2015, 99, 94–99. [Google Scholar] [CrossRef] [PubMed]
  43. Drake, T.M.; Nepogodiev, D.; Chapman, S.J.; Glasbey, J.C.; Khatri, C.; Kong, C.Y.; Claireaux, H.A.; Bath, M.F.; Mohan, M.; McNamee, L.; et al. Multicentre prospective cohort study of body mass index and postoperative complications following gastrointestinal surgery. Br. J. Surg. 2016, 103, 1157–1172. [Google Scholar] [CrossRef]
  44. Mullen, J.T.; Moorman, D.W.; Davenport, D.L. The obesity paradox: Body mass index and outcomes in patients undergoing non-bariatric general surgery. Ann. Surg. 2009, 250, 166–172. [Google Scholar] [CrossRef] [PubMed]
  45. Witasp, A.; Carrero, J.J.; Heimbürger, O.; Lindholm, B.; Hammarqvist, F.; Stenvinkel, P.; Nordfors, L. Increased expression of pro-inflammatory genes in abdominal subcutaneous fat in advanced chronic kidney disease patients. J. Intern. Med. 2011, 269, 410–419. [Google Scholar] [CrossRef]
  46. Axelsson, J.; Qureshi, A.R.; Suliman, M.E.; Honda, H.; Pecoits-Filho, R.; Heimbürger, O.; Lindholm, B.; Cederholm, T.; Stenvinkel, P. Truncal fat mass as a contributor to inflammation in end-stage renal disease. Am. J. Clin. Nutr. 2004, 80, 1222–1229. [Google Scholar] [CrossRef]
  47. Friedman, J.; Lussiez, A.; Sullivan, J.; Wang, S.; Englesbe, M. Implications of Sarcopenia in Major Surgery. Nutr. Clin. Pract. 2015, 30, 175–179. [Google Scholar] [CrossRef]
  48. Santilli, V.; Bernetti, A.; Mangone, M.; Paoloni, M. Clinical definition of sarcopenia. Clin. Cases Miner. Bone Metab. 2014, 11, 177–180. [Google Scholar] [CrossRef]
  49. Isıklar, A.; Safer, U.; Safer, V.B.; Yiyit, N. Impact of sarcopenic obesity on outcomes in patients undergoing living donor liver transplantation. Clin. Nutr. 2019, 38, 964–965. [Google Scholar] [CrossRef]
  50. Bosy-Westphal, A.; Müller, M.J. Identification of skeletal muscle mass depletion across age and BMI groups in health and dis-ease--there is need for a unified definition. Int. J. Obes. 2015, 39, 379–386. [Google Scholar] [CrossRef]
  51. Srikanthan, P.; Hevener, A.L.; Karlamangla, A.S. Sarcopenia Exacerbates Obesity-Associated Insulin Resistance and Dysglycemia: Findings from the National Health and Nutrition Examination Survey III. PLoS ONE 2010, 5, e10805. [Google Scholar] [CrossRef]
  52. Hojman, P.; Pedersen, M.; Nielsen, A.R.; Krogh-Madsen, R.; Yfanti, C.; Akerstrom, T.; Nielsen, S.; Pedersen, B.K. Fibroblast growth fac-tor-21 is induced in human skeletal muscles by hyperinsulinemia. Diabetes 2009, 58, 2797–2801. [Google Scholar] [CrossRef] [PubMed]
  53. Barlow, J.; Carter, S.; Solomon, T.P.J. Probing the Effect of Physiological Concentrations of IL-6 on Insulin Secretion by INS-1 832/3 Insulinoma Cells under Diabetic-Like Conditions. Int. J. Mol. Sci. 2018, 19, 1924. [Google Scholar] [CrossRef] [PubMed]
  54. Natalicchio, A.; Marrano, N.; Biondi, G.; Spagnuolo, R.; Labarbuta, R.; Porreca, I.; Cignarelli, A.; Bugliani, M.; Marchetti, P.; Perrini, S.; et al. The Myokine Irisin Is Released in Response to Saturated Fatty Acids and Promotes Pancreatic β-Cell Sur-vival and Insulin Secretion. Diabetes 2017, 66, 2849–2856. [Google Scholar] [CrossRef] [PubMed]
  55. Christensen, C.S.; Christensen, D.P.; Lundh, M.; Dahllöf, M.S.; Haase, T.N.; Velasquez, J.M.; Laye, M.J.; Mandrup-Poulsen, T.; Solomon, T.P.J. Skeletal Muscle to Pancreatic β-Cell Cross-talk: The Effect of Humoral Mediators Liberated by Muscle Contraction and Acute Exercise on β-Cell Apoptosis. J. Clin. Endocrinol. Metab. 2015, 100, E1289–E1298. [Google Scholar] [CrossRef] [PubMed]
  56. Meier, R.P.H.; Noguchi, H.; Kelly, Y.M.; Sarwal, M.; Conti, G.; Ward, C.; Halleluyan, R.; Tavakol, M.; Stock, P.G.; Freise, C.E. Impact of Sarcope-nia on Simultaneous Pancreas and Kidney Transplantation Outcomes: A Retrospective Observational Cohort Study. Transplant. Direct 2020, 6, e610. [Google Scholar] [CrossRef]
  57. Fukuda, Y.; Asaoka, T.; Eguchi, H.; Sasaki, K.; Iwagami, Y.; Yamada, D.; Noda, T.; Kawamoto, K.; Gotoh, K.; Kobayashi, S.; et al. Clinical Impact of Preoperative Sarcopenia on the Postoperative Outcomes After Pancreas Transplantation. World J. Surg. 2018, 42, 3364–3371. [Google Scholar] [CrossRef]
  58. Noguchi, H.; Miyasaka, Y.; Kaku, K.; Kurihara, K.; Nakamura, U.; Okabe, Y.; Ohtsuka, T.; Ishigami, K.; Nakamura, M. Preoperative Muscle Vol-ume Predicts Graft Survival After Pancreas Transplantation: A Retrospective Observational Cohort Study. Transplant. Proc. 2018, 50, 1482–1488. [Google Scholar] [CrossRef]
  59. Calvani, R.; Marini, F.; Cesari, M.; Tosato, M.; Anker, S.D.; Von Haehling, S.; Miller, R.R.; Bernabei, R.; Landi, F.; Marzetti, E.; et al. Biomarkers for physical frailty and sarcopenia: State of the science and future developments. J. Cachexia Sarcopenia Muscle 2015, 6, 278–286. [Google Scholar] [CrossRef]
  60. Fried, L.P.; Tangen, C.M.; Walston, J.; Newman, A.B.; Hirsch, C.; Gottdiener, J.; Seeman, T.; Tracy, R.; Kop, W.J.; Burke, G.; et al. Car-diovascular Health Study Collaborative Research Group. Frailty in older adults: Evidence for a phenotype. J. Gerontol. A Biol. Sci. Med. Sci. 2001, 56, M146–M156. [Google Scholar] [CrossRef]
  61. Kao, J.; Reid, N.; Hubbard, R.E.; Homes, R.; Hanjani, L.S.; Pearson, E.; Logan, B.; King, S.; Fox, S.; Gordon, E.H. Frailty and solid-organ trans-plant candidates: A scoping review. BMC Geriatr. 2022, 22, 864. [Google Scholar] [CrossRef]
  62. Exterkate, L.; Slegtenhorst, B.R.; Kelm, M.; Seyda, M.; Schuitenmaker, J.M.; Quante, M.; Uehara, H.; El Khal, A.; Tullius, S.G. Frailty and Transplantation. Transplantation 2016, 100, 727–733. [Google Scholar] [CrossRef] [PubMed]
  63. Harhay, M.N.; Rao, M.K.; Woodside, K.J.; Johansen, K.L.; Lentine, K.L.; Tullius, S.G.; Parsons, R.F.; Alhamad, T.; Berger, J.; Cheng, X.S.; et al. An overview of frailty in kidney transplantation: Measurement, management and future considerations. Nephrol. Dial. Transplant. 2020, 35, 1099–1112. [Google Scholar] [CrossRef] [PubMed]
  64. Haugen, C.E.; Gross, A.; Chu, N.M.; Norman, S.P.; Brennan, D.C.; Xue, Q.L.; Walston, J.; Segev, D.L.; McAdams-DeMarco, M. Development and Validation of an Inflammatory-Frailty Index for Kidney Transplantation. J. Gerontol. Ser. A 2021, 76, 470–477. [Google Scholar] [CrossRef] [PubMed]
  65. Varughese, R.A.; Theou, O.; Li, Y.M.; Huang, X.R.-M.; Chowdhury, N.; Famure, O.M.; Selzner, N.; MacIver, J.R.-N.; Mathur, S.; Kim, S.J.; et al. Cumulative Deficits Frailty Index Predicts Outcomes for Solid Organ Transplant Candidates. Transplant. Direct 2021, 7, e677. [Google Scholar] [CrossRef]
  66. Pérez-Sáez, M.J.; Redondo-Pachón, D.; Arias-Cabrales, C.E.; Faura, A.; Bach, A.; Buxeda, A.; Burballa, C.; Junyent, E.; Crespo, M.; Marco, E.; et al. Outcomes of Frail Patients While Waiting for Kidney Transplantation: Differences between Physical Frailty Phenotype and FRAIL Scale. J. Clin. Med. 2022, 11, 672. [Google Scholar] [CrossRef]
  67. dos Santos Mantovani, M.; Coelho de Carvalho, N.; Archangelo, T.E.; Modelli de Andrade, L.G.; Pires Ferreira Filho, S.; de Souza Cavalcante, R.; Kawano, P.R.; Papini, S.J.; Costa, N.A.; Monteiro de Barros Almeida, R.A. Frailty predicts surgical complications after kidney transplantation. A propensity score matched study. PLoS ONE 2020, 15, e0229531. [Google Scholar] [CrossRef]
  68. Schaenman, J.; Castellon, L.; Liang, E.C.; Nanayakkara, D.; Abdalla, B.; Sarkisian, C.; Goldwater, D. The Frailty Risk Score predicts length of stay and need for rehospitalization after kidney transplantation in a retrospective cohort: A pilot study. Pilot Feasibility Stud. 2019, 5, 144. [Google Scholar] [CrossRef]
  69. Kobashigawa, J.; Dadhania, D.; Bhorade, S.; Adey, D.; Berger, J.; Bhat, G.; Budev, M.; Duarte-Rojo, A.; Dunn, M.; Hall, S.; et al. Report from the American Society of Transplantation on frailty in solid organ transplantation. Am. J. Transplant. 2019, 19, 984–994. [Google Scholar] [CrossRef]
  70. Parsons, R.F.; Tantisattamo, E.; Cheungpasitporn, W.; Basu, A.; Lu, Y.; Lentine, K.L.; Woodside, K.J.; Singh, N.; Scalea, J.; Alhamad, T.; et al. Comprehensive review: Frailty in pancreas transplant candidates and recip-ients. Clin. Transplant. 2023, 37, e14899. [Google Scholar] [CrossRef]
  71. Doweiko, J.P.; Nompleggi, D.J. The role of albumin in human physiology and pathophysiology, Part III: Albumin and disease states. JPEN J. Parenter. Enter. Nutr. 1991, 15, 476–483. [Google Scholar] [CrossRef]
  72. Lee, J.L.; Oh, E.S.; Lee, R.W.; Finucane, T.E. Serum Albumin and Prealbumin in Calorically Restricted, Nondiseased Individuals: A Systematic Review. Am. J. Med. 2015, 128, 1023.e1–1023.e22. [Google Scholar] [CrossRef] [PubMed]
  73. Zhang, Z.; Pereira, S.L.; Luo, M.; Matheson, E.M. Evaluation of Blood Biomarkers Associated with Risk of Malnutrition in Older Adults: A Systematic Review and Meta-Analysis. Nutrients 2017, 9, 829. [Google Scholar] [CrossRef] [PubMed]
  74. Becker, B.N.; Becker, Y.T.; Heisey, D.M.; Leverson, G.E.; Collins, B.H.; Odorico, J.S.; D’Alessandro, A.M.; Knechtle, S.J.; Pirsch, J.D.; Sollinger, H.W. The impact of hypoalbuminemia in kidney-pancreas transplant recipients. Transplantation 1999, 68, 72–75. [Google Scholar] [CrossRef] [PubMed]
  75. Robinson, M.; Trujillo, E.; Mogensen, K.; Rounds, J.; McManus, K.; Jacobs, D. Improving nutritional screening of hos-pitalized patients: The role of prealbumin. J. Parenter. Enter. Nutr. 2003, 27, 389–395. [Google Scholar] [CrossRef]
  76. Dellière, S.; Cynober, L. Is transthyretin a good marker of nutritional status? Clin. Nutr. 2017, 36, 364–370. [Google Scholar] [CrossRef]
  77. Dellière, S.; Neveux, N.; De Bandt, J.-P.; Cynober, L. Transthyretin for the routine assessment of malnutrition: A clinical dilemma highlighted by an international survey of experts in the field. Clin. Nutr. 2018, 37, 2226–2229. [Google Scholar] [CrossRef]
  78. Keller, U. Nutritional Laboratory Markers in Malnutrition. J. Clin. Med. 2019, 8, 775. [Google Scholar] [CrossRef]
  79. González Madroño, A.; Mancha, A.; Rodríguez, F.J.; de Ulibarri, J.I.; Culebras, J. The use of biochemical and immunological parame-ters in nutritional screening and assessment. Nutr. Hosp. 2011, 26, 594–601. [Google Scholar]
  80. Contreras, G.; Hu, B.; Astor, B.C.; Greene, T.; Erlinger, T.; Kusek, J.W.; Lipkowitz, M.; Lewis, J.A.; Randall, O.S.; Hebert, L.; et al. Malnutrition-Inflammation Modifies the Relationship of Cholesterol with Cardiovascular Disease. J. Am. Soc. Nephrol. 2010, 21, 2131–2142. [Google Scholar] [CrossRef]
  81. Song, P.; Man, Q.; Li, Y.; Jia, S.; Yu, D.; Zhang, J.; Ding, G. Association between Dietary Patterns and Low HDL-C among Community-Dwelling Elders in North China. Nutrients 2021, 13, 3308. [Google Scholar] [CrossRef]
  82. Franz, C.; Görtz, M.; Wührl, M.; Kulu, Y.; Hoffmann, K.; Hackert, T.; Morath, C.; Zeier, M.; Büchler, M.W.; Mehrabi, A. The Role of Pre-Procurement Pancreas Suitability Score (P-PASS) and Pancreas Donor Risk Index (PDRI) in the Outcome of Simultaneous Pancreas and Kidney or Pancreas After Kidney Transplantation. Ann. Transplant. 2019, 24, 439–445. [Google Scholar] [CrossRef] [PubMed]
  83. Śmigielska, K.; Skrzypek, P.; Czerwiński, J.; Michalak, G.; Durlik, M.; Grochowiecki, T.; Nazarewski, S.; Szmidt, J.; Ziaja, J.; Król, R.; et al. Usefulness of Pancreas Donor Risk Index and Pre-Procurement Pancreas Allocation Suitability Score: Results of the Polish National Study. Ann. Transplant. 2018, 23, 360–363. [Google Scholar] [CrossRef] [PubMed]
  84. Khambalia, H.; Moinuddin, Z.; Summers, A.; Tavakoli, A.; Pararajasingam, R.; Campbell, T.; Dhanda, R.; Forgacs, B.; Augustine, T.; van Dellen, D. A prospective cohort study of risk prediction in simultaneous pancreas and kidney transplantation. Ind. Mark. Manag. 2015, 97, 445–450. [Google Scholar] [CrossRef] [PubMed]
  85. Buzby, G.P.; Williford, W.O.; Peterson, O.L.; Crosby, L.O.; Page, C.P.; Reinhardt, G.F.; Mullen, J.L. A randomized clinical trial of total parenteral nutrition in malnourished surgical patients: The rationale and impact of previous clinical trials and pilot study on protocol design. Am. J. Clin. Nutr. 1988, 47, 357–365. [Google Scholar] [CrossRef]
  86. Onodera, T.; Goseki, N.; Kosaki, G. Prognostic nutritional index in gastrointestinal surgery of malnourished cancer patients. Nihon Geka Gakkai Zasshi 1984, 85, 1001–1005. [Google Scholar] [PubMed]
  87. Kim, C.Y.; Kim, S.Y.; Song, J.H.; Kim, Y.S.; Jeong, S.J.; Lee, J.G.; Paik, H.C.; Park, M.S. Usefulness of the preoperative prognostic nutritional index score as a predictor of the outcomes of lung transplantation: A single-institution experience. Clin. Nutr. 2019, 38, 2423–2429. [Google Scholar] [CrossRef]
  88. Drăgoescu, A.N.; Pădureanu, V.; Stănculescu, A.D.; Chiuțu, L.C.; Tomescu, P.; Geormăneanu, C.; Pădureanu, R.; Iovănescu, V.F.; Ungureanu, B.S.; Pănuș, A.; et al. Neutrophil to Lymphocyte Ratio (NLR)—A Useful Tool for the Prognosis of Sepsis in the ICU. Biomedicines 2021, 10, 75. [Google Scholar] [CrossRef]
  89. Hogendorf, P.; Suska, A.; Skulimowski, A.; Rut, J.; Grochowska, M.; Wencel, A.; Dziwisz, F.; Nowicki, M.; Szymański, D.; Poznańska, G.; et al. Neutrophil-lymphocyte ratio and creatinine reduction ratio predict good early graft function among adult cadaveric donor renal transplant recipients. Single institution series. Ann. Surg. 2018, 90, 28–33. [Google Scholar] [CrossRef]
  90. Baker, J.P.; Detsky, A.S.; Wesson, D.E.; Wolman, S.L.; Stewart, S.; Whitewell, J.; Langer, B.; Jeejeebhoy, K.N. A Comparison of Clinical Judgment and Objective Measurements. N. Engl. J. Med. 1982, 306, 969–972. [Google Scholar] [CrossRef]
  91. da Silva Fink, J.; Daniel de Mello, P.; Daniel de Mello, E. Subjective global assessment of nutritional status—A systematic review of the literature. Clin. Nutr. 2015, 34, 785–792. [Google Scholar] [CrossRef]
  92. Bharadwaj, S.; Ginoya, S.; Tandon, P.; Gohel, T.D.; Guirguis, J.; Vallabh, H.; Jevenn, A.; Hanouneh, I. Malnutrition: Laboratory markers vs nutritional assessment. Gastroenterol. Rep. 2016, 4, gow013. [Google Scholar] [CrossRef] [PubMed]
  93. Kondrup, J.; Allison, S.P.; Elia, M.; Vellas, B.; Plauth, M. ESPEN guidelines for nutrition screening 2002. Clin. Nutr. 2003, 22, 415–421. [Google Scholar] [CrossRef] [PubMed]
  94. Gillis, C.; Ljungqvist, O.; Carli, F. Prehabilitation, enhanced recovery after surgery, or both? A narrative review. Br. J. Anaesth. 2022, 128, 434–448. [Google Scholar] [CrossRef]
  95. Boggi, U.; Amorese, G.; Marchetti, P.; Mosca, F. Segmental live donor pancreas transplantation: Review and critique of rationale, outcomes, and current recommendations. Clin. Transplant. 2011, 25, 4–12. [Google Scholar] [CrossRef]
  96. Gustafsson, U.O.; Scott, M.J.; Hubner, M.; Nygren, J.; Demartines, N.; Francis, N.; Rockall, T.A.; Young-Fadok, T.M.; Hill, A.G.; Soop, M.; et al. Guidelines for Perioperative Care in Elective Colorectal Surgery: Enhanced Recovery After Surgery (ERAS®) Society Recommendations: 2018. World J. Surg. 2019, 43, 659–695. [Google Scholar] [CrossRef]
  97. Melloul, E.; Lassen, K.; Roulin, D.; Grass, F.; Perinel, J.; Adham, M.; Wellge, E.B.; Kunzler, F.; Besselink, M.G.; Asbun, H.; et al. Guidelines for Perioperative Care for Pancreatoduodenectomy: Enhanced Recovery After Surgery (ERAS) Recommendations 2019. Mol. Med. 2020, 44, 2056–2084. [Google Scholar] [CrossRef]
  98. Low, D.E.; Allum, W.; De Manzoni, G.; Ferri, L.; Immanuel, A.; Kuppusamy, M.; Law, S.; Lindblad, M.; Maynard, N.; Neal, J.; et al. Guidelines for Perioperative Care in Esophagectomy: Enhanced Recovery After Surgery (ERAS®) Society Recommendations. Mol. Med. 2019, 43, 299–330. [Google Scholar] [CrossRef]
  99. Mortensen, K.; Nilsson, M.; Slim, K.; Schäfer, M.; Mariette, C.; Braga, M.; Carli, F.; Demartines, N.; Griffin, S.M.; Lassen, K.; et al. Consensus guidelines for enhanced recovery after gastrectomy: Enhanced Recovery Af-ter Surgery (ERAS®) Society recommendations. Br. J. Surg. 2014, 101, 1209–1229. [Google Scholar] [CrossRef]
  100. Tan, J.H.S.; Bhatia, K.; Sharma, V.; Swamy, M.; van Dellen, D.; Dhanda, R.; Khambalia, H. Enhanced recovery after surgery recommenda-tions for renal transplantation: Guidelines. Br. J. Surg. 2022, 110, 57–59. [Google Scholar] [CrossRef]
  101. Brustia, R.; Monsel, A.; Skurzak, S.; Schiffer, E.; Carrier, F.M.; Patrono, D.; Kaba, A.; Detry, O.; Malbouisson, L.; Andraus, W.; et al. Guidelines for Perioperative Care for Liver Transplantation: Enhanced Recovery After Surgery (ERAS) Recommendations. Transplantation 2022, 106, 552–561. [Google Scholar] [CrossRef]
  102. Elango, M.; Papalois, V. Working towards an ERAS Protocol for Pancreatic Transplantation: A Narrative Review. J. Clin. Med. 2021, 10, 1418. [Google Scholar] [CrossRef] [PubMed]
  103. Finlay, S.; Asderakis, A.; Ilham, A.; Elker, D.; Chapman, D.; Ablorsu, E. The role of nutritional assessment and early enteral nutrition for combined pancreas and kidney transplant candidates. Clin. Nutr. ESPEN 2017, 17, 22–27. [Google Scholar] [CrossRef] [PubMed]
  104. Du, Y.T.; Rayner, C.K.; Jones, K.L.; Talley, N.J.; Horowitz, M. Gastrointestinal Symptoms in Diabetes: Prevalence, Assessment, Pathogenesis, and Management. Diabetes Care 2018, 41, 627–637. [Google Scholar] [CrossRef] [PubMed]
  105. Murray, M.; Grogan, T.A.; Lever, J.; Warty, V.S.; Fung, J.; Venkataramanan, R. Comparison of tacrolimus absorption in transplant pa-tients receiving continuous versus interrupted enteral nutritional feeding. Ann. Pharmacother. 1998, 32, 633–636. [Google Scholar] [CrossRef] [PubMed]
  106. Kim, J.M.; Joh, J.W.; Kim, H.J.; Kim, S.H.; Rha, M.; Sinn, D.H.; Choi, G.S.; Kwon, C.H.; Cho, Y.Y.; Suh, J.M.; et al. Early Enteral Feeding After Living Donor Liver Transplantation Prevents Infectious Complications: A Prospective Pilot Study. Medicine 2015, 94, e1771. [Google Scholar] [CrossRef]
  107. Rayes, N.; Seehofer, D.; Hansen, S.; Boucsein, K.; Müller, A.R.; Serke, S.; Bengmark, S.; Neuhaus, P. Early enteral supply of lactobacillus and fiber versus selec-tive bowel decontamination: A controlled trial in liver transplant recipients. Transplantation 2002, 74, 123–127. [Google Scholar] [CrossRef]
  108. Plank, L.D.; McCall, J.L.; Gane, E.J.; Rafique, M.; Gillanders, L.K.; McIlroy, K.; Munn, S.R. Pre- and postoperative immunonutrition in patients undergoing liver transplantation: A pilot study of safety and efficacy. Clin. Nutr. 2005, 24, 288–296. [Google Scholar] [CrossRef]
  109. Lin, M.-T.; Kung, S.-P.; Yeh, S.-L.; Liaw, K.-Y.; Wang, M.-Y.; Kuo, M.-L.; Lee, P.-H.; Chen, W.-J. Glutamine-supplemented total parenteral nutrition attenuates plasma interleukin-6 in surgical patients with lower disease severity. World J. Gastroenterol. 2005, 11, 6197–6201. [Google Scholar] [CrossRef]
  110. Li, Y.-S.; Li, J.-S.; Jiang, J.-W.; Liu, F.-N.; Li, N.; Qin, W.-S.; Zhu, H. Glycyl-Glutamine-Enriched Long-Term Total Paren-teral Nutrition Attenuates Bacterial Translocation Following Small Bowel Transplantation in the Pig. J. Surg. Res. 1999, 82, 106–111. [Google Scholar] [CrossRef]
Table 1. Table summarizing causes of malnutrition in SPKTX patients.
Table 1. Table summarizing causes of malnutrition in SPKTX patients.
Inflammatory responseanorexia, reduced food intake, weight loss and muscle catabolism[21,22,23,24]
Acute disease- or injury-related onehigh pro-inflammatory cytokine activity, increased corticosteroid and catecholamine release and insulin resistance[25]
Chronic kidney diseaseexcess NH4+ production resulting in complement activation[26]
metabolic acidosis[32]
Alterations in gut microbiotainjury to intestinal mucosa translocation of toxic metabolites and bacterial endotoxins[27,28]
Jatrogenic–hemodialysis or peritoneal dialysis complicationsinflammation[29]
additional protein loss and higher levels of uremic toxins[33,34,35,36]
Co-morbidity (cardiovascular disease, poorly controlled diabetes, and hyperparathyroidism)protein-energy wasting syndrome, loss of lean body mass[30,31]
Dietary limitationsdecreased protein level[37]
Gastroparesisearly satiety, nausea and vomiting[38,39,40]
Table 2. Comparison between anthropometric parameters and biomarkers in various nutritional assessment and screening tools investigated in transplant surgery (adapted from [77]).
Table 2. Comparison between anthropometric parameters and biomarkers in various nutritional assessment and screening tools investigated in transplant surgery (adapted from [77]).
Prognostic Nutritional IndexNutritional Risk Index Subjective Global Assessment (SGA)Nutritional Risk Screening (NRS) 2002
Anthropometric parametersweight loss++
present weight+
usual body weight+
History and symptomsfood intake/diet history++
gastrointestinal function/symptoms+
stress level (severity of diagnosis)++
primary diagnosis+
physical symptoms+
functional capacity+
total lymphocyte count+
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

Mizerska, A.; Durlik, M.; Kędzierska-Kapuza, K. Nutritional Risk of Candidates for Simultaneous Pancreatic–Kidney Transplantation—A Narrative Review. Nutrients 2023, 15, 4179.

AMA Style

Mizerska A, Durlik M, Kędzierska-Kapuza K. Nutritional Risk of Candidates for Simultaneous Pancreatic–Kidney Transplantation—A Narrative Review. Nutrients. 2023; 15(19):4179.

Chicago/Turabian Style

Mizerska, Agnieszka, Marek Durlik, and Karolina Kędzierska-Kapuza. 2023. "Nutritional Risk of Candidates for Simultaneous Pancreatic–Kidney Transplantation—A Narrative Review" Nutrients 15, no. 19: 4179.

Note that from the first issue of 2016, this journal uses article numbers instead of page numbers. See further details here.

Article Metrics

Back to TopTop