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Abstract

Background

Nutrition plans are crucial for kidney transplantation, addressing issues like anemia, bone problems, and malnutrition. During surgery and recovery, evaluating malnutrition, reducing risks, and aiding recovery are essential.

Objectives

The purpose of this review is to provide a comprehensive overview of nutritional management during the entire kidney transplantation process. It includes pretransplant challenges, posttransplant issues, acute phase nutrition, and nutritional support during the maintenance phase. Additionally, the study covers the challenges and restrictions associated with nutrition following transplant, such as interactions with immunosuppressive drugs, metabolic problems, and nutrition during graft rejection.

Methodology

With an emphasis on the difficulties and solutions for the best nutrition in each stage of the transplant procedure, a thorough search of numerous internet databases was conducted to find pertinent research and papers and was analyzed and synthesized to give a thorough sketch of the nutritional management of kidney transplant recipients.

Results

Nutrition interventions are crucial for pretransplant, peri- transplant, and long-term maintenance of kidney transplant recipients, controlling graft rejection and improving outcomes through targeted therapies.

Conclusion

The review’s goal is to draw attention to the hitches to good nutrition at each stage and suggested solutions, as well as the interactions between nutrition and other elements such as immunosuppressive drugs and metabolic problems. The analysis identifies many crucial tactics that can enhance outcomes and quality of life of transplant recipients.

Keywords

Kidney transplantation nutritional management peritransplant phase nutrition acute phase nutrition

Introduction

Metabolic disorders associated with dialysis and uremia in end stage renal disease (ESRD) patients are significantly treated through successful transplantation of the kidney.¹ Numerous physiological characteristics of the kidney influence nutrition metabolism, disposal, and the equilibrium of electrolytes, and therefore, its dysfunction causes hindrance in the retention of appropriate nutrition and muscle mass.² After a kidney transplant, pre-existing conditions like diabetes, cardiovascular disease (CVD), low bone mineral density (BMD), obesity, protein-energy wasting (PEW), and inflammation can frequently cause difficulties such as cardiovascular complications, increased risks of bone fracture, infections and poor graft outcome. Kidney transplant recipients face a major impact on their short and long-term health consequences as a result of their pre-existing co-morbidities, new metabolic anomalies developed due to secondary effects of immunosuppressive drugs, and changes in way of day-to-day living after transplantation.³ To improve outcomes following transplantation, one must have a healthy nutritional state. The hormonal shift, discrepancy in energy expenditure, and metabolic derangements related to immunosuppression therapy result in a wide spectrum of metabolic alterations during the transition from ESRD to transplantation.⁴ Additionally, there are alterations between pre- and posttransplant food restrictions. Comorbidities, protein-energy malnutrition, and pretransplant nutritional conditions, all play a role in posttransplant complications. The occurrence of posttransplant complications might result from fasting and restrictions in movement related to surgery, late graft function requiring continued dialysis, gut disorders, injury-related issues, and other events that may arise in the initial days and after a few months following transplantation.^5,6 After transplantation, once the graft kidneys start working, pretransplant uremic milieu subsides, and food restrictions are relaxed, often leading to overeating and weight gain, exacerbated by steroid use. Steroid use also delays wound healing.⁷ Hence complete menu planning is essential after transplantation.

In addition, other associated complications such as graft dysfunction and failure, metabolic disorders like new onset diabetes after transplant (NODAT), hypertension, obesity, bone mineral disorder, cardiovascular disease, and cancer risk rises over time. Hence, an individualized dietary regimen must be followed to prevent posttransplant complications.⁸ Nutrition for transplant patients is divided into four stages: pretransplant, peritransplant, acute phase posttransplant where delayed graft dysfunction, increased infection rate, and high nutritional requirements are major concerns, and chronic or the maintenance phase where long-term complications and graft failure need to be addressed. An individualized strategy is needed for chronic graft malfunction and failing grafts. Management challenges include prompt albumin infusion, glycemic control, and hypophosphatemia.^9,10 Planning nutritional therapy for transplant recipients should therefore consider the patient’s clinical condition, comorbidities, and nutritional needs at each stage of the transplant process, as depicted in Figure 1, which outlines these phases and complications.

Figure 1.

Nutritional and related factors affecting kidney transplant recipients.¹¹

Methods

In the context of kidney transplant recipients, there are significant knowledge gaps in nutritional management. Specifically, personalized dietary strategies for those with pre-existing conditions such as diabetes and cardiovascular disease remain underexplored. The acute post-transplant phase lacks standardized macronutrient and micronutrient guidelines, while long-term nutrition management for preventing chronic complications is also insufficiently studied. Furthermore, there is a shortage of research addressing the unique nutritional needs of special populations, such as pediatric and elderly patients, and the impact of immunosuppressive therapy on nutrient absorption and metabolism is not well understood. These gaps highlight the need for more targeted research to improve dietary guidelines and health outcomes for transplant recipients. This methodology outlines a systematic review aimed at identifying knowledge gaps in the nutritional management of kidney transplant recipients. Recognizing kidney transplantation as the most effective treatment for ESRD, the review focuses on nutritional challenges during the pretransplant, peritransplant, acute, and chronic phases. A comprehensive literature search was conducted across multiple databases (PubMed, Scopus, and Web of Science) using relevant keywords related to nutrition management and transplant complications. The review emphasizes significant gaps in personalized dietary interventions for individuals with pre-existing conditions, standardized nutrition guidelines during the acute post-transplant phase, long-term management strategies, and tailored approaches for special populations, such as pediatric and elderly recipients. By synthesizing current knowledge and pinpointing areas that require further research, this methodology aims to contribute to improved dietary guidelines and better health outcomes for kidney transplant recipients.

To find pertinent papers and articles for this review article, a thorough, methodical search across several internet databases was performed. With an emphasis on the difficulties and solutions for the best nutrition in each stage of the transplant procedure, the included papers and articles were analysed and synthesized to provide a thorough overview of dietary management for renal transplant receivers.

Dietary support before transplantation and after transplantation

ESRD patients awaiting kidney transplants often face metabolic issues, potentially impacting transplant outcomes, despite inconsistent findings on body size and weight relationship and patient survivability.¹² There has been a persistent obesity paradox in dialysis patients. Early research found that obese dialysis patients had worse kidney transplant outcomes,^13–16 mostly due to cardiovascular problems¹⁷ and infectious issues related to surgical wounds.¹⁸ Nevertheless, current research has demonstrated no significant association between pretransplant weight gain, graft loss, and mortality after renal transplantation.¹⁹

All previous studies used Body Mass Index (BMI) as the only indicator of obesity, although BMI does not account for adiposity or muscle mass. Serum creatinine is a proxy for sarcopenia in dialysis patients with limited residual urine and provides a more accurate reflection of muscle mass than BMI.^20–24 The combined mortality or graft failure was found to be higher by 2.2 fold in patients with an average serum creatinine of 4 mg dl⁻¹ in comparison to the serum creatinine of 8 to 10 mg dl⁻¹ during pretransplant phase while 22% improved graft and survivability was reported with an average serum creatinine of 14 mg dl⁻¹ in the pretransplant phase.²⁵ Pretransplant malnutrition, inflammation, atherosclerosis (MIA) syndrome was evaluated in a study with 1348 adult kidney transplant recipients where the patients with MIA scores of 8 to 10 after transplant had the worst outcomes for both fatal and nonfatal coronary syndromes.²⁶

A straightforward scoring system known as the malnutrition inflammatory score (MIS) was established to evaluate the degree of protein energy wasting (PEW) in dialyzed individuals.²⁷ Pretransplant MIS (more than 8) was reported to have an independent association with increased mortality risk, detrimental effects on all-cause mortality, and worse transplant outcomes in a study with 992 renal transplant recipients.²⁸ Molnar et al, studied that pretransplant serum albumin which is an indicator of nutritional status in the dialysis population, is a predictor of mortality, graft failure, and delayed graft function (DGF).²⁹ Malnutrition-inflammation complex can lead to decreased albumin production in the liver, enhanced catabolism, or loss of protein from the intravascular space.³⁰

Patients with a serum albumin less than 3.5 g dl⁻¹ experienced the maximum rates of acute and chronic rejection as well as DGF and suffered from more posttransplant infections like fungus and Cytomegalovirus (CMV) infections.³¹ The risk of DGF in earlier studies^32,33 was also found to be 25% and 15% higher with blood haemoglobin 10.00–10.99 g dl⁻¹, and 13 g dl⁻¹ levels respectively compared to 12.00–12.99 g dl⁻¹ pretransplant haemoglobin. The pretransplant erythropoietin hyporesponsive population was unable to even reach the target of more than 11 g dl⁻¹ haemoglobin with erythropoietin, iron, and other haematites and have a higher mortality rate and greater frequency of graft dysfunction at 5 years.³³

Mineral bone disease which includes the metabolic disorders of vitamin D, calcium, phosphorus, and parathyroid hormone, is a well-known consequence of chronic kidney disease (CKD). Deranged mineral metabolism before transplantation has significant effects on kidney transplantation. The risks of functional graft failure, all causes and cardiovascular mortality are higher in the patients with pretransplant phosphorus level ranges between 7.5 and 9.5 mg dl⁻¹ in comparison to those with 3.5 to 5.5 mg dl⁻¹ pretransplant phosphorus level.³⁴ It is debatable whether serum calcium levels affect the results of kidney transplantation, however, Kruger et al.³⁵ did not find any impact of pretransplant calcium levels on DGF, acute rejection episode, the incidence of cardiovascular events, graft functioning, or on survivability. Vitamin D levels in renal recipients frequently low several months succeeding transplantation, but the connection between vitamin D and kidney adverse effects is not well understood.³⁶

In a prospective cohort consisting of 634 renal recipients, a low concentration of 25-hydroxyvitamin D was found to be an independent risk factor for the advancement of interstitial fibrosis and was linked to a decreased glomerular filtration rate (GFR) after 1 year of transplantation.³⁶ The dysregulation of the parathyroid (PTH) hormone was discovered to be linked to severe skeletal abnormalities like osteitis fibrosa cystica, adynamic bone disease and the risk of graft failure was found to be two times higher at a pretransplant parathyroid level of 90 pmol l⁻¹.³⁷ Pretransplant nutritional therapy should increase calorie and protein intake, prevent muscle and fat loss, and address fluid retention, anemia, osteoporosis, and other conditions (Table 1). This can enhance quality of life and reduce posttransplant complications when combined with other medications. Depending on each patient’s demands, further therapies such as intradialytic oral nutritional supplements, megestrol acetate, prokinetic agents, and anabolic steroids should be employed. Figure 1 lists the nutritional objectives prior to transplant.

Table 1.

Nutrient requirement during pre -transplant at end stage renal disease, immediately after transplantation, during maintenance phase and for conservative patients according to kidney disease outcomes quality initiative (KDOQI) guideline.

Nutrient	Pretransplant phase/haemodialysis phase	Posttransplant phase	Daily recommended intake for maintenance phase	CKD patients
Protein	1.2–1.4 g/kg IBW	1.0–1.1 g/kg IBW	0.8–0.85 g/kg IBW	0.5–0.6 g/kg IBW (low protein diet) (non-diabetic metabolically stable)
				0.4–0.5 g/kg with keto acid analogue for very low protein diet
Calorie	25–30 kcal/kg IBW	20-25 kcal/kg IBW	20–25 kcal/kg IBW	20–25 kcal/kg (based on age, sex, BMI)
Carbohydrate	50–60% of total calorie	50% total energy (high fiber, low GI, complex carbs)	<30% total energy (high fiber, low GI, complex carbs)	55–60 g/day (non-diabetic); <55 g/day (diabetic)
Fat	25–30% of total calorie	<30% total energy; 8–10% n-6 PUFA, 20% MUFA, >10% saturated fat	<30% total energy; 8–10% n-6 PUFA, 20% MUFA, >10% saturated fat	25–30% of total calorie
Cholesterol	<200 mg/day	<200 mg/day	<200 mg/day	<200 mg/day
Saturated fat	<7% of total energy	>10% of total energy	>10% of total energy	<7% of total energy
Crude fiber	20–30 g/day	25–30 g/day	25–30 g/day	35 g/day
Sodium (Na)	<5g (<217 mmol/day)	80–100 mmol/day	80–100 mmol/day (no added salt)	<5 g/day
Potassium (K)	2 g/day (60 mmol/day)	As per requirement	Normal intake; restrict if hyperkalemia	2 g/day (60 mmol/day)
Phosphorus (P)	0.8–1.0 g/day (26–32 mmol/day)	1000–1500 mg/day	1200–1500 mg/day	1000 mg/day
Calcium (Ca)	600 mg/day	1000–1300 mg/day	800-1000 mg/day; supplement if required	600 mg
Zinc (Zn)	Not specified	To promote wound healing	As per RDI recommendations	Not specified
Iron	10–15 mg/day	10–15 mg/day	10 mg/day	10–15 mg/day
Vitamin D (vit D)	Not specified	5–15 mcg/day	Supplementation necessary if required	Not specified
Fluid	Within 1 lit	Depending on fluid status	Free fluid	Depending on fluid status

IBW, Ideal body weight.

Nutritional objectives for transplant patients during surgery

During the perioperative period, the primary nutritional objectives include assessing patients for pre-existing malnutrition through several important aspects, as illustrated in Figure 2. These include laboratory investigation, determining protein stores and body composition, physical examination for nutrient deficiencies. The figure outlines the key components of a nutritional assessment, which begins with taking a detailed medical history and progresses to identifying risks for malnutrition. Proper malnutrition diagnosis is crucial to determine necessary interventions that will improve the surgical outcome. Additionally, identifying risk factors helps in supporting anabolism for quicker recovery.

Figure 2.

Schematic diagram representing the key components of nutritional assessment during the perioperative period.

Understanding the surgical stress response is crucial for effective recovery. It’s categorized by hormonal, metabolic, hematological, and immunological variations. A thorough medical history is essential for evaluating nutritional status. Monitoring body composition, including fat-free mass, muscle mass, fat quantity, waist-to-hip ratio, and MIS score, is essential for malnutrition prevention. Biochemical indicators like serum albumin, pre-albumin, total cholesterol, pre-dialysis creatinine, and haemoglobin are also used (Table 2). The protein catabolic rate (PCR), or the protein equivalent of nitrogen appearance (nPNA), can also be calculated by using kinetic modeling to predict dietary protein consumption only when the patient has a neutral nitrogen balance.³⁸ A screening marker for protein-energy nutritional status is serum cholesterol. Posttransplant mortality is higher in those with low-normal nonfasting blood cholesterol (less than 150 to 180 mg dL⁻¹) than in people with higher cholesterol levels.³⁹ The persistent deficiency in protein-energy nutrition is clinically assessed through reliable markers such as serum creatinine and creatinine index.⁴⁰ Individuals with low pre-dialysis serum creatinine levels are at risk for protein energy metabolism and skeletal muscle wasting, which can increase mortality rates after transplant. Assessing potential dietary deficiencies using tools like Subjective Global Assessment and Malnutrition Inflammation Score is crucial.⁴¹ Nutritional assessment is crucial for identifying and stratifying risks of bone fracture, hypoalbuminemia, new-onset diabetes after transplant (NODAT), and wound healing. Obesity and malnutrition increase delayed wound healing, and zinc can speed up healing. Risk factors include older age, type 2 diabetes, race, ethnicity, and infections.⁴² NODAT is also induced by risk factors such as impaired pretransplant elevated fasting glucose, increased visceral fat, obesity, increased carbohydrate intake, and a sedentary lifestyle. Each transplant recipient should undergo screening for the possibility of developing NODAT, and they should be instructed to take about 50% of their calories from foods high in dietary fibre and with a low glycemic index, like grains and whole grain cereals. Serum albumin level should not be less than 4.0 g dl⁻¹ during the pretransplant phase for successful survival of the graft³⁰ and its low value (less than 3.5 g dl⁻¹) was thought to be associated with subpar longstanding graft functioning and increasing posttransplant complications.²⁹ A previous study⁴³ found that the risk of mortality due to any cause, cardiovascular events and delayed graft function has been shown to decrease by 13%, 17%, and 4%, respectively, with every 0.2 g dl⁻¹ increase in blood albumin concentration in pretransplant phase. Due to a number of factors, including altered bone and mineral metabolism resulting from renal bone disease and the administered glucocorticoids after transplantation, kidney transplant receivers had a greater fracture risk than the general population.⁴⁴ Patients with pretransplant metabolic bone disorders should have their bone mineral profiles, including calcium, phosphate, vitamin D, and parathyroid levels, evaluated and maintained at normal serum levels. Low bone mineral density (BMD), which has been reported to increase rates of fracture and vascular calcification in posttransplant patients,^45,46 has been linked to calcium shortage, low body weight, low BMI, and low vitamin D levels.⁴⁷

Table 2.

Biochemical goal during peri-transplant phase.

Parameter	Target value
Hemoglobin	>11 g dl⁻¹
Albumin	4 – 4.5 g dl⁻¹
Phosphate	4.5 – 5.0 mg dl⁻¹
Intact parathyroid hormone (iPTH)	Within normal range
Body mass index (BMI)	22 – 25 kg m⁻²
Alkaline phosphatase	<120 U L⁻¹

Nutrition during the acute phase (posttransplant phase)

The acute phase (initial 4 to 6 weeks after transplant) is when nutritional needs are at their peak because of the high immunosuppressant doses, surgical stress, and wound healing. Occurrences of rejection, infection, and surgical complications during the acute phase can make recovery more difficult. Figure 3 provides a description of the nutritional challenges encountered during the acute phase of the transplant. During this time, it is essential to give the body the nutrition it needs to manage catabolism, promote healing, monitor and treat electrolyte imbalances, boost the immune system, prevent muscle loss, and maintain stable blood sugar levels. High doses of glucocorticoids are necessary for kidney transplant recipients in the initial posttransplant phase which in turn results in an enhanced rate of protein catabolism and a higher likelihood of a nitrogen balance disorder. Consuming food containing at least 1.4 g of protein per kilogram of body weight has been shown to rectify nitrogen imbalance and enhance muscle mass within the initial 4 weeks after a kidney transplant.⁴⁸ Since these individuals may expend more energy owing to surgical stress followed by high doses of immunosuppressive drugs immediately after transplantation, an energy intake of 30 to 35 kcal per kg ideal body weight is recommended to resist negative nitrogen balance.⁴⁹ Limiting carbohydrates (to 50% of total calories) and engaging in regular exercise is beneficial for people who have glucose intolerance and Cushingoid effects from corticosteroids (Table 1).

Figure 3.

Nutritional challenges in the acute phase.

In the early posttransplant phase, the fluid and electrolyte requirements are influenced by the kidney function and the presence of necrosis in the tubular cells of the kidney. During this time, a modest salt restriction of 2 to 3 g per day reduces fluid retention and aids in blood pressure management. Individual’s recommended sodium intakes depend on their blood pressure and fluid retention.⁴⁹ If serum potassium is on the high side, potassium intake should be limited. The diet should include enough cholecalciferol (vitamin D3, 2000 IU daily), calcium, and phosphorous (1200 mg each day).⁴⁹ Fluid and electrolyte needs should be assessed daily. Additionally, after transplantation, hydration needs to be carefully managed.⁴⁹ From the second surgical day onward, oral food should be promoted. Enteral feeding should be encouraged if oral nutritional support is unable to meet the nutritional demand.⁵⁰ However, if patients are suffering from severe acute pancreatitis, acute mesenteric ischemia, short bowel syndrome, and small bowel obstruction, parenteral feeding is advised. Figure 1 details the nutritional requirements for the acute phase.

Few caveats in nutritional management

There are a few restrictions to nutritional management during the peritransplant and acute phases of nutrition, including the need for albumin infusion during the peritransplant phase, rigorous glycemic control, and the treatment of hypophosphatemia following transplantation. DGF, due to ischemic/reperfusion injury during renal transplantation, is known to be harmful to both early and late allograft survival. To promote ideal graft perfusion and early graft function after renal transplantation, intravascular volume maintenance is essential. Crystalloids, colloids, or both, along with mannitol or loop diuretics, have been tested in numerous trials to increase intravascular volume and enhance diuresis in renal transplant patients. Various recommendations for the ideal fluid therapy, at best, are based solely on observational studies and scant evidence. The best volume expander during the peri-transplant phase has long been human albumin with the fewest negative effects. However, studies have demonstrated that the administration of 20% human albumin intra-operatively as a volume expander should be used selectively instead of routine practice as it does not enhance the early functioning of graft in renal transplantation from a living donor.⁵¹ Albumin ought to be used sparingly rather than as part of standard procedure.

During transplantation, strict glycemic control is not preferred.⁵² To prevent negative effects, hyperglycemia must be managed as best as possible in patients undergoing kidney transplants who have diabetes or reduced glucose tolerance. A randomized control trial with blood glucose lower than 180 mg dl⁻¹ resulted in a lower occurrence of renal rejection in comparison to blood glucose of 70-110 mg dl⁻¹.⁵³ Therefore, it is not advised to practice strict glycemic control during kidney transplantation.

Hypophosphatemia is common after transplant due to less absorption of phosphate from the intestine and increased loss of urinary phosphate due to less tubular absorption, as a result of immunosuppressive medications. A longitudinal cohort analysis study with 957 renal transplant recipients revealed that individuals with low serum phosphate levels have a lower risk of graft failure and cardiovascular death in comparison to those who have not experienced hypophosphatemia after transplant.⁵⁴ Instead of treating individuals with low serum phosphate levels, it’s critical to monitor patients who do not develop hypophosphatemia.

Chronic posttransplant phase (maintenance phase)

Six months after transplantation, patients enter the chronic posttransplant phase, which can lead to hyperglycemia, obesity, hypertension, cardiovascular events, hypercalcemia, and vitamin D metabolism changes. Proper nutritional support during the maintenance phase can minimize death risks. Protein intake, combined with energy, can stabilize kidney function immediately after transplantation, especially when high doses of prednisone are essential.^55–57 In order to maintain normal graft function and to reduce work load of newly implanted kidney, the consumption of protein should be decreased (0.75 g – 0.85 g kg⁻¹ day⁻¹) along with the necessary consumption of energy^55,58 (Table 1).

Special nutritional issues

Obesity and weight gain

Weight gain after transplantation happens frequently and affects more than 40% of those who have had a kidney transplant. Obesity and high BMI in association with the complications related to surgery, metabolism, and cardiovascular events also cause long-term chronic allograft nephropathy (CAN) and reduce the overall survivability of patients as well as graft.^15,59,60 Weight gain is caused by lack of exercise, fluid imbalance, and steroid-induced hunger. Preventing weight gain involves consuming complex carbohydrates, low-glycemic foods, and fat, adjusting immunosuppressive medications, and encouraging physical exercise.

New onset diabetes after transplant (NODAT)

The occurrence of NODAT is 10–40% during the first year of transplant (14) and is a robust sovereign predictor of all-cause mortality, cardiovascular events, graft dysfunction, and death.^61,62 NODAT is a condition characterized by obesity, glucose intolerance, insulin insufficiency, and insulin resistance, with modifiable causes including diet, obesity, and immunosuppressive agents^63–66 and consequently increase the incidence of NODAT after transplantation. Pharmacotherapy, dietary changes, lifestyle adjustments, and immunosuppression optimization are all part of managing NODAT. Patients with NODAT should have a meal with 50% carbohydrate content including whole grain cereals and grain products that are high in dietary fibre (more than 25 g) and with a low glycemic index.⁵² Patients should also be encouraged to eat at least two servings of fish per week, less than 2400 mg of sodium per day, less than 7% calories from saturated fat, and 2 to 3% calories from trans-fat.

Mineral bone disease

As a result of the early stage of chronic renal failure, multiple interrelated variables affect the metabolism of calcium, phosphorus, and vitamin D (Figure 4) posttransplant. This figure illustrates the complex interplay between these essential nutrients and their metabolic pathways in renal transplant patients. High turnover bone disease is often linked to conditions such as hyperparathyroidism and CAN, which can lead to osteomalacia characterized by vitamin D deficiency and hypophosphatemia. Conversely, adynamic bone disease can arise from various factors, including the use of bisphosphonates and steroid therapy, leading to low bone turnover. The diagram also highlights potential complications of these conditions, such as osteoporosis, osteitis, and osteonecrosis, which can significantly impact the patient’s quality of life. Dietary calcium intake should range from 800 to 1500 mg per day. When dietary calcium is insufficient, calcium supplements may be necessary.⁶⁷ Individual daily phosphorus intake should be determined by the patient’s serum phosphate levels. As most of the transplant recipients suffer persistently from hypophosphatemia, the daily intake of phosphorus should be ranged from 1200 to 1500 mg per day (Table 1) whereas, some individuals may additionally need to take supplements of vitamin D and phosphorus (1 to 2 g) daily.⁶⁸

Figure 4.

Impact of CKD MBD.

Dyslipidemia

De novo dyslipidemia, a serious, frequently occurring complication following transplantation, is stimulated by a number of variables, including immunosuppressive medications (calcineurin inhibitors, mTOR inhibitors, and corticosteroids), a sedentary lifestyle, and increasing body weight.⁶⁹ Dyslipidemia has a significant correlation with both posttransplant patient cardiovascular death and atherosclerotic cardiovascular disease.^70,71 Diets consisting of whole grains, plant foods (vegetables, fruits, and phytosterol-rich legumes),⁵⁶ food with a low glycemic index, high dietary fibre, vitamin E-rich sources, and monosaturated fats are advised for people with posttransplant dyslipidemia in addition to adequate exercises.

Hypertension

Between 50% and 80% of individuals with kidney transplants usually have hypertension. CAN, early graft dysfunction, DGF, and cardiovascular disease are all risk factors for hypertension.⁷² In addition to these, the age and sex of the recipient and the donor, diabetes, obesity, and immunosuppressant medications, also influence the development of hypertension in the posttransplant period.⁷³ Based on the few limited studies and sparse data currently available, kidney transplant recipients with hypertension should be urged to limit their sodium intake to 80-100 mmol per day with no added salt. A balanced, healthy diet comprised of whole grains, fruits and vegetables, foods rich in calcium, dairy products with low-fat content, and regular exercise is always encouraged by posttransplant patients.

Nutrition and immunosuppressants

Food has an impact on how well immunosuppressants are absorbed. The rate of nutrient absorption is slowed down by plant proteins that contain phytates. The intestinal cytochrome P450 system, which is in charge of many drugs’ first-pass metabolism, including cyclosporine and tacrolimus, is inhibited by grapefruit juice.⁷⁴ Grapefruit juice affects the metabolism of immunosuppressants by inhibiting this enzyme system, which raises their serum concentrations.⁷⁵ Therefore, each transplant recipient should receive advice regarding any foods that may interfere with the pharmacokinetics of immunosuppressive medications (Figure 1). Cranberry juice administration has been reported to lower the prevalence of urinary tract infections⁷⁶ in general however no such studies are available for the population having renal transplantation. If a receiver is susceptible to infection after transplantation, cranberry juice can be an option.

Graft rejection and dietary strategy

Acute, hyperacute and chronic are different types of rejections. Nutritional needs vary, and there is no clear treatment recommendation. A daily protein intake of 1.3–1.5 g per kg body weight is recommended. Diets should maximize nutritional status, address imbalances, reduce side effects, and restore kidney function. Chronic rejection is the most common cause of graft failure.⁷⁷ In several short-term comparative studies where the calorie intakes were fixed, the plasma renin activity and proteinuria were significantly reduced for the low protein diet (0.55 g kg⁻¹day⁻¹) in comparison to the high protein diet (2 g kg⁻¹day⁻¹) by the transplant recipients with chronic allograft dysfunction without affecting their blood pressure, GFR, or renal blood flow.^78,79 Studies have demonstrated that a diet low in protein (0.6 g kg⁻¹d⁻¹) and high in calories (>25 kcal kg⁻¹day⁻¹) can keep the nitrogen balance in check⁷⁹ (Table 1). Intake of 0.8 g protein per kg body weight per day can preserve the functions of the kidney and maintain the nutritional profile in most renal transplant individuals suffering from chronic rejection.⁸⁰ Researchers suggested that protein consumption may enhance the course of chronic rejection and protein restriction may be a beneficial tactic for reducing the advancement of renal failure in chronic rejection.⁵⁶

The fish oil was reported to be essential in the diet of renal transplant receivers as the high level of eicosapentaenoic (EPA) and docosahexaenoic acids (DHA) in the erythrocytes and ornithine in blood plasma reduce the incidence of rejection and other complications after transplantation.⁸¹ Although previous studies⁸² showed that a very low protein diet (VLPD) added with keto analogues (0.3–0.4 g kg⁻¹day⁻¹) slows the progression of chronic renal failure in conservative patients, no clinical evidence is available on the impact of VLPD with keto analogues on patients with chronic graft rejection. Keto analogues can be an effective treatment for people who have chronic posttransplant rejection, and more study needs to be done on this treatment.

An approach to failing grafts through diet

Dialysis restarting in transplant patients with failing grafts can lead to severe clinical and social consequences, including decreased kidney function, inadequate blood circulation, anxiety, and socioeconomic costs. Factors like nutritional conditions and acidosis can influence re-initiation. Nondiabetic patients should consume 0.55–0.66 g protein daily whereas, diabetic patients can have 0.6–0.8 g protein per kg body weight per day according to KDOQI guideline⁸³ (Table 3). Other metabolic anomalies, such as fluid balance, electrolyte levels, and the existence of metabolic acidosis, should be closely evaluated and improved according to the situation (Figure 5).

Table 3.

Nutritional side effects of immunosuppressive medications and proposed nutrition therapy.

Drug	Possible side effects	Proposed nutrition therapy
Cyclosporine	Hyperlipidemia	Limit fat and simple carbohydrate
	Hyperglycemia	Limit simple carbohydrate
	Hypomagnesemia	Magnesium supplements
	Hyperkalemia	Decrease potassium intake
Glucocorticoids	Catabolism/impaired wound healing	Increase protein intake
	Hyperlipidemia	Limit fat and simple carbohydrate
	Hyperglycemia	Limit simple carbohydrate
	Sodium retention	Reduce sodium intake
	Hyperphagia	Avoid overeating
	Increased calciuria	Increase calcium intake or take supplements
Azathioprine	Nausea, vomiting, sore throat, anorexia	Adjust food/meals as needed, monitor intake
Azathioprine	Altered taste acuity	Offer variety of foods, flavours
OKT3	Nausea, vomiting, diarrhea, anorexia	Adjust food/meals as needed, monitor intake
Tacrolimus	Hyperglycemia	Limit simple carbohydrate
	Hyperkalemia	Decrease potassium intake
	Nausea and vomiting	Adjust food/meals as needed, monitor intake
Mycophenolate mofetil	Diarrhea	Replace lost fluid

Figure 5.

Infographics showing the nutritional management during renal transplantation.

Conclusion

Posttransplant nutrition significantly impacts organ transplantation effectiveness and recipient well-being. Optimizing nutritional status during pretransplant can improve outcomes, immune system function, and posttransplant recovery. During the perioperative period, individualized dietary adjustments, adequate energy, and food intake are crucial for wound healing, infection prevention, and postoperative problem reduction. Customized nutritional treatments, including protein, energy, vitamins, and minerals, are essential for quicker recovery. To effectively manage transplant patients’ nutritional needs, individualized care, monitoring of vitamin deficiency, and potential drug-nutrient interactions are essential. Nutritional management plans should address specific issues like obesity, bone disease, dyslipidemia, hypertension, NODAT, and immunosuppressant medication effects. Emphasizing immune regulation and graft function is crucial. Post-transplant nutrition is crucial for long-term health and transplantation success. A multidisciplinary approach with nephrologists, renal dieticians, and transplant care teams can optimize nutrition, improve patient outcomes, and reduce complications.

Footnotes

Author contributions

All Authors contributed for writing and editing of this manuscript.

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iD

Kavita Rathore

Data availability statement

Data sharing is not applicable to this article as no datasets were generated or analysed during the current study.

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