Applied Nephrology Master Series

Chapter 15 Nutrition, Protein-Energy Wasting and Metabolic Health in PD

CHAPTER MISSION Build a bedside nutrition system for peritoneal dialysis: detect nutritional decline before serum albumin becomes the only alarm; separate fluid, fat and muscle change; diagnose protein-energy wasting from a multidimensional assessment; account for peritoneal protein losses and dialysate-derived glucose calories; prescribe protein and energy using current KDOQI guidance; remove reversible barriers to eating; escalate from counselling to oral or enteral support when needed; and improve metabolic health without sacrificing lean mass, strength or life participation.

Figure 15.1 — Nutrition in PD is a balance system. Oral intake, absorbed dialysate glucose, peritoneal protein losses, inflammation, physical activity and volume status jointly determine whether body protein and energy reserves are preserved.

MASTER PRINCIPLE Treat the TRAJECTORY, not the ALBUMIN. Nutrition in PD is not a single laboratory value and not a generic “renal diet.” The useful question is whether the person is maintaining adequate intake, lean tissue and function while avoiding excessive metabolic burden from dialysate glucose and unnecessary dietary restriction.

0. One-page chapter map

Table 15.1 — The eight decisions that govern nutrition care in PD.

Decision	Core question	Bedside output
1. Screen	Is there a new risk signal for undernutrition, PEW, sarcopenia or unhealthy weight gain?	Risk status + trigger for full assessment
2. Separate	Is weight change fluid, fat, lean tissue—or mixed?	Named body-composition phenotype
3. Diagnose	Does the patient have PEW, isolated low intake, inflammation-driven hypoalbuminemia or sarcopenia?	Nutritional phenotype
4. Quantify	Are protein and energy needs being met, including calories absorbed from dialysate?	Individual intake prescription
5. Find cause	What reversible factor is suppressing intake or increasing catabolism/losses?	Cause-directed plan
6. Intervene	Can counselling correct the gap, or are oral/enteral/specialized supports needed?	Nutrition support ladder
7. Build muscle	Is resistance/aerobic activity feasible and safe?	Exercise-nutrition plan
8. Verify	Did intake, SGA, muscle/function and patient goals improve without excess glucose burden?	Longitudinal reassessment

Learning outcomes

Define protein-energy wasting (PEW) as a loss of body protein and energy stores rather than a synonym for low serum albumin.
Use the 7-point Subjective Global Assessment (SGA), appetite/intake history, weight trajectory, examination of fat and muscle, functional measures and biochemical context as a multidimensional nutritional assessment.
Apply current KDOQI 2020 recommendations for routine nutrition screening, comprehensive dietitian assessment, protein intake, energy intake and oral nutritional supplementation in adults on PD.
Explain why calories absorbed from glucose-containing dialysate must be included in total energy assessment and why increasing glucose exposure can coexist with loss of lean tissue.
Recognize that PD causes daily protein losses into effluent and that peritonitis/inflammation can amplify losses and catabolism.
Distinguish hypoalbuminemia caused by inflammation, overhydration or protein losses from true inadequate intake/PEW.
Recognize sarcopenia and sarcopenic obesity, where BMI can look reassuring despite low muscle mass or strength.
Use oral nutritional supplements when counselling alone cannot meet requirements and understand when enteral or specialized support should be considered.
Use amino-acid dialysate selectively, recognizing that evidence for patient-important outcomes is limited and product-specific safety rules apply.
Integrate exercise and physical activity with nutrition to preserve strength, function and life participation.
Avoid indiscriminate potassium, phosphorus or calorie restriction that worsens protein-energy intake; individualize according to serum values and food-source bioavailability.
Cross-reference Chapter 8 for sodium/volume balance, Chapter 13 for dysglycemia and hypokalemia, Chapter 14 for EPS-related intestinal failure, and Chapter 16 for frailty/obesity/special-population adaptations.

EVIDENCE POSTURE KDOQI 2020 is the principal current guideline for adult CKD/dialysis nutrition. For metabolically stable adults on PD it recommends 1.0–1.2 g protein/kg ideal body weight/day (opinion) and 25–35 kcal/kg ideal body weight/day, individualized for age, activity, body composition, weight goals, illness and inflammation; PD glucose calories are included in total energy intake. It recommends routine nutrition screening at least biannually and comprehensive dietitian assessment within the first 90 days of dialysis, annually, or when screening/provider referral indicates. A minimum 3-month trial of oral nutritional supplements is suggested when counselling alone cannot meet requirements. ISPD goal-directed PD and exercise recommendations add the patient-centred, life-participation and physical-function framework. Evidence for amino-acid dialysate, specific anabolic therapies and hard-outcome benefits of nutritional supplements remains limited. [1–8]

1. Core concept: nutrition is an outcome of the whole PD system

Nutritional status in PD emerges from the interaction of food intake, calories absorbed from dialysate, daily nutrient losses, inflammation, residual kidney function, acid-base status, comorbidity, gastrointestinal symptoms, physical activity and treatment burden. A patient may therefore gain fat while losing muscle, have a low albumin despite adequate intake, or have a “normal” BMI while becoming functionally sarcopenic. The chapter begins by refusing these false shortcuts. [1,3,9]

Table 15.2 — Four common nutrition phenotypes that look deceptively similar.

Phenotype	Typical pattern	Main danger
True PEW	Low intake + weight/muscle loss ± inflammation	Loss of protein/energy stores and function
Inflammatory hypoalbuminemia	Low albumin with CRP/infection/illness; intake may be adequate	Treating a biomarker instead of the disease
Sarcopenic obesity	High/normal BMI with low muscle strength or lean tissue	Muscle loss hidden by adiposity
Fluid-associated weight change	Rapid “gain” or “loss” with congestion/decongestion	Misclassifying water as tissue

BEDSIDE TRANSLATION Ask “what changed in tissue and function?” before asking “what is the albumin?”

2. Protein-energy wasting: define the syndrome precisely

Figure 15.2 — PEW is sustained by low intake, inflammation/catabolism, dialysis losses and inactivity. Effective treatment usually has to interrupt more than one arm of the loop.

The International Society of Renal Nutrition and Metabolism defines PEW as a state of decreased body stores of protein and energy fuels. The proposed diagnostic framework uses four domains—serum chemistry, body mass, muscle mass and dietary intake—with evidence from multiple domains rather than one isolated measurement. In contemporary practice, SGA/MIS and longitudinal assessment often operationalize the syndrome more usefully than applying rigid research criteria at a single visit. [2,10]

Table 15.3 — PEW domains: what each contributes.

Domain	Examples	Limitation
Intake	Reduced protein/energy intake, anorexia, meal skipping	Self-report error; short-term intake may not reflect chronic state
Body mass	Unintentional weight/fat loss	Fluid shifts can mimic change
Muscle	Visible wasting, reduced strength/function, low lean mass	Method dependent; obesity can hide loss
Biochemistry	Albumin/prealbumin/cholesterol in context	Inflammation and volume strongly confound
Inflammation/function	CRP, illness burden, frailty, reduced activity	Important mechanism/risk signal but not a stand-alone PEW definition

DEFINITION DISCIPLINE Low albumin is not PEW. Low BMI is not PEW. Low intake alone is not PEW. Diagnose a syndrome of declining protein/energy stores using several converging signals.

3. Why PD creates a distinctive nutrition physiology

PD differs from non-dialysis CKD because dietary protein restriction is no longer the central strategy. Patients lose protein continuously into dialysate, absorb variable amounts of glucose from dextrose solutions, may experience early satiety from intraperitoneal fill, and can develop peritonitis-related catabolism. Contemporary literature reviews report daily PD protein losses commonly in the range of roughly 4–10 g/day, with marked interpatient variation; classic studies and clinical experience show greater loss during peritonitis. These losses are one reason PD protein requirements are higher than in non-dialysis CKD. [9,11,12]

Table 15.4 — PD-specific nutritional forces.

PD feature	Nutrition consequence	Clinical implication
Daily protein loss into effluent	Raises protein replacement requirement	Do not import low-protein CKD diets into PD
Glucose absorption	Adds non-oral calories; may increase fat mass/glycemic burden	Count dialysate energy in total assessment
Intraperitoneal volume	Early satiety/reflux/abdominal fullness in some patients	Adjust meal timing/prescription when relevant
Peritonitis/inflammation	Higher protein losses + catabolic drive + anorexia	Nutrition reassessment after episodes
Continuous home therapy	Meal timing can be flexible but burden can impair eating	Design food plan around real treatment schedule

4. Screening and comprehensive assessment: build a repeatable system

Figure 15.3 — The PD nutrition dashboard. History, weight trajectory, SGA/body examination, biochemical context, dialysis factors and physical function are interpreted together.

KDOQI 2020 states that adults with CKD 3–5D should undergo routine nutrition screening at least biannually. A registered dietitian nutritionist or equivalent should perform comprehensive assessment within the first 90 days of dialysis, annually, or sooner when screening or clinician concern indicates. In CKD 5D, the 7-point SGA is recommended as a valid and reliable nutritional assessment tool. [1]

Table 15.5 — Comprehensive PD nutrition assessment.

Domain	What to document	What changes management
Appetite/intake	Meals, protein sources, dietary recall, ONS use, food insecurity	Identifies actual deficit and barriers
Weight trajectory	Usual weight, target/dry-weight context, unintentional change	Separates tissue loss from fluid
SGA / physical examination	Fat stores, muscle wasting, GI symptoms, intake change	Global PEW phenotype
Function	Handgrip, sit-to-stand/walking capacity, ADL/life participation	Detects clinically meaningful muscle decline
Biochemistry	Albumin, CRP/inflammation, bicarbonate, K, phosphate, glucose/HbA1c	Finds confounders and treatment targets
Dialysis context	Peritonitis, effluent protein loss when relevant, RKF, UF/glucose exposure	Explains losses and metabolic burden
Psychosocial	Depression, cognition, dentition, finances, caregiver burden	Often determines whether a plan can work

SCREENING RULE The scheduled screen is the minimum. New weight loss, poor appetite, hospitalization, peritonitis, functional decline or repeated low intake should trigger assessment immediately rather than waiting for the annual review.

5. Weight and body composition: the scale does not tell you what changed

Body weight in PD is simultaneously affected by extracellular water, dialysate in the abdomen, fat mass and lean tissue. Serial trends are therefore interpreted against a consistent volume state and with attention to whether the abdomen is full or drained. KDOQI recommends considering body composition together with weight/BMI; DEXA is the reference method when feasible, while evidence is insufficient to recommend bioimpedance as a specific body-composition standard in PD. [1]

Table 15.6 — Weight change: four different diagnoses.

Observed change	Possible explanation	How to separate it
Rapid gain + edema/BP rise	Fluid overload	Chapter 8 volume assessment
Slow gain + stable volume + rising waist/fat	Adipose gain	Diet + dialysate glucose + body composition
Weight stable + weaker / visible muscle loss	Sarcopenia masked by fat or fluid	Strength + SGA + lean-mass assessment
Weight loss after decongestion	Water loss, not necessarily malnutrition	Re-establish tissue baseline after euvolemia

NUMERICAL HUMILITY A BMI of 30 kg/m² does not prove good nutrition. A 2-kg fall after correcting edema does not prove PEW. Always identify the compartment that changed.

6. Protein prescription: current KDOQI target for stable PD

For metabolically stable adults with CKD on maintenance PD, KDOQI 2020 recommends prescribing dietary protein intake of 1.0–1.2 g/kg ideal body weight/day to maintain stable nutritional status. The strength of evidence for PD is opinion-level, reflecting the limited direct trial base. The same range is considered reasonable for adults on dialysis who have diabetes, with individualized adjustment when glycemic instability or other clinical circumstances alter requirements. [1]

Table 15.7 — Protein prescription reasoning.

Situation	Direction	Do not do
Stable PD, adequate nutrition	Aim for 1.0–1.2 g/kg IBW/day	Carry forward a pre-dialysis low-protein diet
Poor intake / PEW risk	Identify deficit and increase usable protein-energy intake	Focus on phosphate restriction at the expense of protein
Peritonitis / acute catabolic illness	Reassess intake and losses; individualize with dietitian/clinical team	Assume the stable outpatient target is automatically sufficient
Obesity	Use ideal/appropriate reference weight and body-composition goals	Prescribe from actual weight without considering adiposity
Diabetes	Maintain protein adequacy while coordinating carbohydrate/glucose exposure	Lower protein merely to manage glucose

PROTEIN RULE In PD, “renal diet” must not mean chronic protein restriction. The prescription has changed because the patient is now dialyzed and loses protein through the peritoneum.

7. Energy prescription: include dialysate glucose calories

KDOQI 2020 recommends 25–35 kcal/kg ideal body weight/day for metabolically stable adults with CKD 1–5D, individualized according to age, sex, physical activity, body composition, weight goals, CKD stage, concurrent illness and inflammation. For PD, calories absorbed from glucose-containing dialysate are part of total energy intake; they should not be added on top of the desired energy budget as if metabolically invisible. [1]

Measured glucose absorption varies with membrane transport, dwell duration, glucose concentration and prescription. Observational PD data show that greater glucose absorption is associated with fat-mass gain and may coexist with declining fat-free mass. This is why “enough calories” and “healthy body composition” are different goals. [13]

Table 15.8 — Energy balance in PD.

Problem	Mechanism	Correction direction
Low oral calories + low weight/muscle	Insufficient usable energy	Increase nutrient-dense oral intake/ONS
High dialysate glucose + fat gain	Non-oral caloric load	Reduce unnecessary hypertonic glucose; optimize sodium/volume prescription
High glucose calories + poor oral protein	Calories displace appetite without replacing protein	Protect protein intake; review meal timing and solution strategy
Obesity + low muscle	Energy excess with anabolic deficit/inactivity	Modest energy adjustment + protein adequacy + resistance activity

8. Food quality: stop creating malnutrition with indiscriminate restriction

A PD diet is individualized, not a list of universal prohibitions. KDOQI recommends adjusting dietary phosphorus to maintain serum phosphate in the normal range and considering the bioavailability of phosphorus sources; phosphate additives are more readily absorbed than many plant sources. Potassium intake should be adjusted to maintain serum potassium within the normal range rather than restricted automatically. [1]

Table 15.9 — Restriction discipline.

Issue	Better strategy	Common harmful shortcut
Hyperphosphatemia	Target additives, bioavailable sources, binder timing and total intake	Cut all high-protein foods
Hypokalemia	Increase dietary/supplemental potassium according to need; search causes	Continue a generic low-potassium diet
Sodium/volume	Reduce sodium to support thirst/volume control	Compensate high salt intake with more glucose dialysate
Diabetes/obesity	Reduce refined energy excess and unnecessary dialysate glucose exposure	Protein restriction to reduce calories
Poor appetite	Prioritize nutrient density and achievable meals	Add multiple simultaneous restrictions

DIET QUALITY RULE When nutrition is fragile, remove the least useful restriction first. A technically “renal” diet that the patient cannot eat is not therapeutic.

9. Peritoneal protein losses: important, variable and amplified by inflammation

Peritoneal protein loss is a real component of PD physiology but is highly variable between patients. Recent literature review data report daily protein losses in PD broadly around 4–10 g/day; classic CAPD studies found similar order-of-magnitude losses and demonstrated substantially greater losses during peritonitis. Peritoneal protein clearance also reflects membrane biology and inflammation, so a high loss should not be interpreted only as dietary failure. [9,11,12]

Table 15.10 — When protein loss matters clinically.

Context	Interpretation	Action
Stable patient, good intake/function	Expected PD loss may be compensated	Maintain target protein intake
Recurrent peritonitis	Loss + catabolism + anorexia	Early post-infection nutrition reassessment
Persistent hypoalbuminemia	Loss may contribute but is rarely the only cause	Assess inflammation, volume, liver/urine/GI losses and intake
High transport/inflammatory phenotype	Greater protein permeability may coexist	Treat underlying inflammation/volume and monitor tissue/function

10. Appetite and gastrointestinal symptoms: treat the barrier before prescribing supplements

Poor appetite is often the proximal event that drives PEW. Causes include uremia or underdialysis, constipation, reflux/early satiety from intraperitoneal volume, nausea, gastroparesis, medications, depression, infection, oral/dental disease, food insecurity and overly restrictive diets. EPS-related obstructive symptoms belong to Chapter 14 and should not be managed as routine anorexia. [3,7]

Table 15.11 — Poor appetite: mechanism-based review.

Clue	Likely contributor	First response
Fullness worse with daytime fill	Intraperitoneal volume / meal timing	Review fill/dwell timing and smaller frequent meals
Constipation	GI burden + catheter effects	Treat bowel dysfunction
After peritonitis	Inflammation/catabolism + aversion	Reassess intake, symptoms and losses
Depression/social isolation	Psychosocial anorexia	Screen/treat; engage caregiver/team
Multiple dietary bans	Iatrogenic restriction	Dietitian simplification
Persistent vomiting/obstruction	Not routine nutrition problem	Chapter 14 / urgent GI-surgical pathway

11. Hypoalbuminemia: risk marker, not stand-alone nutrition diagnosis

Serum albumin is strongly associated with outcomes in dialysis populations, but its concentration is influenced by inflammation, hydration/dilution, peritoneal and urinary losses, liver synthesis and acute illness. Studies including PD patients show that inflammation explains a substantial part of the albumin–mortality association. Nutritional assessment should therefore use albumin as a prognostic/context marker rather than as proof that a patient simply needs more protein. [14,15]

Flowchart 15.3 — Low serum albumin in PD. The first task is to identify inflammation, volume expansion and protein losses before interpreting albumin as evidence of inadequate intake.

ALBUMIN RULE Do not “treat the albumin.” Treat infection/inflammation, volume overload, inadequate intake, protein losses or liver disease—and then follow the albumin trajectory as one part of recovery.

12. Muscle and sarcopenia: function is a nutritional outcome

Muscle loss can occur despite stable weight and can be accelerated by inflammation, inactivity, hospitalization, inadequate protein-energy intake and comorbidity. Sarcopenia and low strength are associated with adverse outcomes across dialysis cohorts. In PD, observational data show low physical activity and declining fitness/strength over time, making muscle function an essential longitudinal outcome rather than an optional research measure. [16,17]

Table 15.12 — Practical muscle surveillance.

Measure	What it adds	Limitation
SGA muscle examination	Low-cost bedside estimate of wasting	Examiner dependent
Handgrip strength	Functional muscle signal; easy serial trend	Affected by arthritis/neurologic disease
Sit-to-stand / gait tests	Life-relevant lower-limb function	Need safe testing environment
DEXA / body composition	Quantifies lean/fat compartments	Volume and access/cost limitations
Activity history	Detects deconditioning and participation loss	Self-report bias

13. Obesity and sarcopenic obesity: metabolic improvement must preserve lean tissue

PD can produce a mixed phenotype in which dialysate glucose and dietary energy promote adipose gain while inactivity and catabolic illness reduce lean tissue. Observational PD data demonstrate that greater glucose absorption can be associated with increasing fat mass and decreasing fat-free mass. Therefore weight-loss strategies that ignore muscle preservation can worsen the clinically important compartment even while BMI improves. [13]

Flowchart 15.4 — Metabolic health without sacrificing muscle. Determine whether weight reflects fluid, fat or lean tissue before changing calories or dialysis glucose exposure.

Table 15.13 — Obesity phenotype → management focus.

Phenotype	Priority	Avoid
Obesity with preserved strength	Metabolic risk reduction + activity	Crash diets / protein inadequacy
Sarcopenic obesity	Resistance exercise + adequate protein + careful energy deficit	Judging success only by scale weight
Fluid + obesity	Treat congestion and metabolic risk separately	Calling all gain adipose
Diabetes + high glucose exposure	Optimize PD osmotic strategy + diabetes treatment + diet quality	Solving volume solely with stronger glucose bags

14. Intervention ladder: fix causes first, then escalate support

Figure 15.4 — Nutrition intervention ladder. Correct reversible causes and individualize the diet before escalating to supplements or artificial nutrition.

KDOQI places medical nutrition therapy and dietary counselling before nutritional supplementation. For adults with CKD 3–5D at risk of or with PEW, a minimum 3-month trial of oral nutritional supplements is suggested when counselling alone does not achieve sufficient protein and energy intake. If chronic intake remains inadequate despite counselling and ONS, enteral tube feeding is a reasonable next consideration when medically appropriate. [1]

Table 15.14 — Nutrition support ladder.

Level	When	What to reassess
1. Cause correction	Any decline	Infection, acidosis, constipation, depression, medications, dialysis delivery, restrictions
2. Dietitian-led food plan	Intake gap or risk	Protein/energy intake, meal pattern, glucose calories, acceptability
3. Oral nutrition supplements	Counselling insufficient; PEW risk/presence	Adherence, GI tolerance, intake, SGA, weight/muscle
4. Enteral feeding	Chronically inadequate intake despite oral strategy and appropriate GI tract	Goals, tolerance, aspiration/volume/electrolytes
5. Specialized support	Selected severe/refractory cases	MDT risk–benefit; underlying disease and route-specific complications

ONS EVIDENCE Meta-analyses of dialysis trials show modest improvements in albumin, BMI, protein intake indices and sometimes handgrip/MIS, but hard-outcome evidence remains limited and most trials are hemodialysis-dominant. PD-specific pilot and small randomized studies support feasibility and nutritional improvement, not a guaranteed survival benefit. [18–20]

15. Amino-acid dialysate and specialized nutrition support: selective tools, not routine escalation

Amino-acid-containing PD solutions can replace part of the dialysate nutrient loss and improve short-term protein kinetics when adequate non-protein calories are available. Small randomized and crossover studies suggest biochemical or nitrogen-balance benefit, but long-term patient-important outcome evidence is weak. Amino-acid dialysate should therefore be viewed as a selective specialist option for patients who cannot meet protein needs orally/enterally, not as a routine substitute for food or treatment of unexplained hypoalbuminemia. [21–23]

Table 15.15 — Amino-acid dialysate: evidence-calibrated use.

Potential role	Important condition	Caution
Supplement protein delivery	Needs adequate concurrent energy intake for anabolism	Does not correct inflammation or obstruction
Glucose-sparing exchange	May reduce one glucose exposure	Not equivalent to eliminating metabolic burden
PEW with poor oral tolerance	Consider only in specialist individualized plan	Product-specific acid-base/urea and formulation issues
Long-term outcome improvement	Not established	Do not promise mortality benefit

16. Exercise–nutrition synergy: feeding muscle without using it is incomplete therapy

The 2021 ISPD/Global Renal Exercise Network practice recommendations support physical activity and individualized aerobic/resistance exercise in people receiving PD, while acknowledging a sparse trial base. A home-based randomized trial showed improvement in exercise capacity and several quality-of-life domains, and observational data show declining fitness and activity during PD. Nutrition and resistance exercise are therefore complementary strategies for preserving muscle, function and life participation. [7,17,24]

Table 15.16 — Exercise–nutrition pairing.

Problem	Nutrition arm	Activity arm
Low muscle strength	Adequate protein/energy intake	Progressive resistance activity when safe
Frailty/deconditioning	Prevent energy/protein deficit	Graded aerobic + strength + balance plan
Obesity with low muscle	Moderate energy strategy preserving protein	Resistance training to protect lean mass
Post-hospitalization decline	Early nutrition reassessment	Rehabilitation/physio-led reconditioning

FUNCTION RULE If the patient is eating more but getting weaker, the nutrition plan is not yet successful. Strength, mobility and life participation belong on the follow-up sheet.

17. Longitudinal monitoring: success is a stable or improving phenotype

The aim is not to normalize every biomarker. A useful nutrition follow-up asks whether appetite and intake are adequate, tissue weight and muscle function are stable or improving, fluid status is controlled, inflammatory drivers have resolved, metabolic burden is acceptable and the plan is sustainable for the person. Serial change in SGA is prognostically meaningful in dialysis cohorts. [15]

Table 15.17 — Nutrition follow-up dashboard.

Domain	Success looks like	Escalation trigger
Intake/appetite	Requirements met with tolerable meal plan	Persistent deficit or anorexia
Weight/body composition	Stable desired tissue trajectory	Unintentional loss or rapid fat gain
Muscle/function	Stable/improving strength and activity	New weakness/falls/functional decline
SGA	Stable or improving score/phenotype	Deteriorating SGA
Inflammation/albumin	Cause addressed; trajectory consistent with recovery	Persistent CRP/infection or unexplained albumin decline
Metabolic health	Acceptable glycemia/lipids/weight goals without high glucose burden	Escalating hypertonic glucose + worsening metabolic phenotype
Patient burden	Plan affordable, culturally acceptable and feasible	Nonadherence caused by complexity or restrictions

18. Major clinical algorithms

Flowchart 15.1 — Nutrition screening and assessment. Routine screening is only the entry point; any risk signal triggers multidimensional assessment and a named phenotype.

Flowchart 15.2 — Weight loss or poor appetite. First separate fluid change from tissue loss, then identify reversible medical, dietary and functional drivers before escalating nutritional support.

Flowchart 15.3 — Low serum albumin. Inflammation, volume and protein loss are assessed before albumin is interpreted as nutritional failure.

Flowchart 15.4 — Metabolic health. Weight gain is decomposed into fluid, adipose and muscle compartments so that glucose/energy reduction does not unintentionally worsen sarcopenia.

19. Retention tables: pattern recognition

Table 15.18 — If you see this, think this first.

Finding	First hypothesis	Immediate action
Falling weight + edema improving	Could be decongestion, not tissue loss	Re-establish euvolemic baseline
Stable BMI + weaker grip/legs	Sarcopenia may be hidden	SGA + strength/body composition assessment
Low albumin + high CRP	Inflammation-driven hypoalbuminemia likely contributes	Find/treat inflammatory source
Low albumin + edema	Dilution/volume contributes	Volume pathway + nutrition assessment
Poor appetite + many food bans	Iatrogenic dietary restriction	Dietitian simplification
Hyperphosphatemia + PEW risk	Protein cannot simply be cut	Target additives/binders/bioavailability
Obesity + high dialysate glucose	Metabolic burden may be prescription-linked	Optimize sodium/UF and glucose-sparing strategy
After peritonitis + weight/muscle loss	Catabolism + increased losses	Early nutrition recovery plan

Table 15.19 — What not to confuse.

Do not confuse	With	Correction
Serum albumin	Direct measurement of protein intake	Inflammation/volume/losses strongly affect it
Body weight	Lean mass	Fluid and fat can move in opposite directions
Obesity	Good nutrition	Sarcopenic obesity exists
Dialysate glucose calories	Nutritionally balanced energy	Adds calories without protein/micronutrients
Protein restriction	Phosphate treatment	Use source/bioavailability/binders while preserving protein
ONS prescription	Treatment success	Verify intake, SGA, muscle/function and cause correction
Amino-acid dialysate	Evidence-based routine PEW cure	Selective low-certainty adjunct
Higher Kt/V alone	Nutrition treatment	Adequacy may help appetite but PEW is multifactorial

20. Clinical pearls

1. Nutrition screening is scheduled; nutrition assessment is triggered by change.

2. In PD, always ask what proportion of apparent weight change is water, fat and muscle.

3. The 7-point SGA is more useful than albumin alone for nutritional phenotype.

4. KDOQI 2020 protein target for metabolically stable PD is 1.0–1.2 g/kg ideal body weight/day.

5. KDOQI energy target is 25–35 kcal/kg ideal body weight/day—and PD glucose calories count.

6. Peritoneal protein loss is real but does not explain every low albumin.

7. Peritonitis is both an infection event and a nutrition event.

8. A high BMI can conceal clinically important muscle wasting.

9. Hyperphosphatemia should not be solved by starving a patient of protein.

10. Potassium restriction should be individualized; PD patients frequently develop hypokalemia.

11. ONS is an escalation step after individualized food counselling—not a replacement for cause-finding.

12. Muscle strength and mobility are nutrition outcomes.

13. Reducing unnecessary glucose exposure can improve metabolic health, but never at the expense of safe volume control.

14. Food plans must be culturally and financially feasible or they will not be delivered.

15. Persistent vomiting or obstructive symptoms in long-vintage PD belongs to the EPS pathway, not routine nutrition counselling.

21. Common pitfalls — and the correction

Table 15.20 — High-frequency errors in PD nutrition care.

Pitfall	Why it fails	Correction
Calling low albumin “malnutrition”	Inflammation/volume/losses confound	Use multidimensional assessment
Using actual obese body weight blindly for protein/energy targets	Can overprescribe substantially	Use guideline reference/ideal weight and individual goals
Ignoring dialysate glucose calories	Underestimates energy exposure	Include absorbed PD calories
Keeping a pre-dialysis low-protein diet	Worsens protein deficit in PD	Use dialysis protein targets
Restricting all potassium routinely	PD often has low potassium	Individualize to serum level and causes
Cutting protein to control phosphate	May worsen PEW	Target phosphate additives/source + binders
ONS without investigating poor appetite	Does not fix constipation, depression, infection or obstruction	Treat cause + supplement if still needed
Judging obesity treatment by kilograms alone	May lose muscle while weight falls	Track strength/body composition
Assuming exercise is unsafe in all PD patients	Promotes deconditioning	Use ISPD/GREX individualized activity guidance
Treating PEW with higher dialysis dose alone	PEW is not simply underdialysis	Review adequacy but address intake/inflammation/function

22. Mini-cases: decisions, not trivia

Case 1 — Low albumin after peritonitis

A stable PD patient had albumin 36 g/L before peritonitis. Two weeks after treatment it is 27 g/L; CRP remains elevated, appetite is only mildly reduced and weight is unchanged.

BEST NEXT STEP Do not diagnose dietary protein failure from albumin alone. Reassess inflammation, volume, intake and recovery trajectory; post-peritonitis protein loss/catabolism likely contribute.

Case 2 — “Healthy BMI” but weaker

A patient with BMI 28 kg/m² has stable weight but reports difficulty rising from a chair. Examination shows reduced quadriceps bulk.

BEST NEXT STEP Suspect sarcopenia/sarcopenic obesity. Add SGA, strength/function assessment and dietary review rather than reassuring from BMI.

Case 3 — Hyperphosphatemia and poor appetite

A frail patient eats little but phosphate remains high. The family has removed meat, dairy, legumes and nuts.

BEST NEXT STEP Do not intensify global protein restriction. Review phosphate additives, binder timing, source bioavailability and preserve adequate protein-energy intake.

Case 4 — Weight gain after starting PD

Over 12 months a patient gains 7 kg, edema is absent, waist increases and glucose-containing dialysate exposure is high.

BEST NEXT STEP Separate metabolic gain from volume. Review total energy including PD glucose, dietary quality, sodium/UF strategy and physical activity while preserving muscle.

Case 5 — Intake remains low after counselling

A patient with SGA deterioration continues to reach only a fraction of prescribed protein/energy despite tailored food advice.

BEST NEXT STEP KDOQI supports a minimum 3-month ONS trial when counselling alone is insufficient. Define reassessment endpoints.

Case 6 — Persistent vomiting in long-vintage PD

A 9-year PD patient is losing weight and repeatedly vomits after meals.

BEST NEXT STEP Do not manage as simple PEW. Enter Chapter 14 EPS/obstruction pathway urgently while providing nutrition/intestinal-failure support.

Case 7 — Hypokalemia and “renal diet”

A PD patient with poor appetite has K 3.2 mmol/L and avoids nearly all fruits and vegetables because of prior CKD advice.

BEST NEXT STEP Individualize potassium intake; do not maintain reflex restriction. Search GI losses, medications and intake causes and manage Chapter 13 hypokalemia pathway.

Case 8 — Obesity with falling function

An obese diabetic patient wants rapid calorie restriction. Grip strength and walking capacity are already low.

BEST NEXT STEP Prioritize lean-mass preservation: adequate protein, modest individualized energy strategy, glucose-exposure review and resistance/aerobic activity rather than aggressive caloric restriction.

23. Active recall

MUST MEMORIZE

Table 15.21 — Core facts.

Prompt	Answer
Routine nutrition screening in CKD 3–5D?	At least biannually (KDOQI opinion).
Comprehensive dietitian assessment?	Within first 90 days of dialysis, annually, or when screening/referral indicates.
Validated CKD 5D assessment tool?	7-point SGA (KDOQI 1B).
Stable PD protein target?	1.0–1.2 g/kg ideal body weight/day.
Stable CKD 1–5D energy target?	25–35 kcal/kg ideal body weight/day, individualized.
Do PD glucose calories count?	Yes—include absorbed dialysate calories in total energy assessment.
PEW definition?	Loss of body protein and energy stores; multidimensional syndrome.
Does albumin diagnose PEW?	No.
What can lower albumin besides low intake?	Inflammation, overhydration/dilution, peritoneal/urinary/GI losses, liver disease.
ONS when counselling fails?	KDOQI suggests minimum 3-month trial in PEW risk/presence.
If oral strategy remains chronically inadequate?	Consider enteral feeding when medically appropriate.
Phosphate restriction principle?	Preserve protein; consider source bioavailability/additives and binders.
Potassium restriction?	Individualize to serum potassium and clinical need.
Obesity protects from sarcopenia?	No.
Peritonitis nutrition effect?	Anorexia/catabolism and increased peritoneal protein loss.
Amino-acid dialysate outcome evidence?	Limited; selective adjunct, no proven hard-outcome benefit.
Exercise role?	Individualized aerobic/resistance activity supports function and muscle.
Final mental model?	Screen → separate fluid/fat/muscle → diagnose phenotype → quantify intake → remove drivers → support → exercise → verify.

USE AS REFERENCE

Exact oral supplement formulation and electrolyte content.
Enteral formula choice and route-specific feeding protocols.
Amino-acid dialysate product labelling, dose/exchange schedule and contraindications.
Diabetes medication/insulin adjustment for PD glucose exposure.
Phosphate binder selection and timing.
Potassium replacement dose and monitoring.
Individual calorie deficit strategies in severe obesity.
Disease-specific nutrition for cirrhosis, cancer, critical illness or pregnancy.

24. Flashcards: spaced repetition

1. Q: What is PEW? A: Loss of body protein and energy stores in kidney disease.

2. Q: Best single lab test for PEW? A: There is none.

3. Q: KDOQI PD protein range? A: 1.0–1.2 g/kg ideal body weight/day if metabolically stable.

4. Q: KDOQI energy range? A: 25–35 kcal/kg ideal body weight/day, individualized.

5. Q: Dialysate glucose calories? A: Count them in total energy intake.

6. Q: Routine screening frequency? A: At least biannually.

7. Q: Comprehensive assessment timing? A: Within 90 days, annually, or earlier if indicated.

8. Q: Recommended assessment tool in CKD 5D? A: 7-point SGA.

9. Q: Low albumin + high CRP means? A: Inflammation likely contributes; do not diagnose malnutrition from albumin alone.

10. Q: Stable BMI + weak muscles? A: Think sarcopenia or sarcopenic obesity.

11. Q: Peritoneal protein loss magnitude? A: Variable; modern literature commonly reports roughly 4–10 g/day.

12. Q: Peritonitis effect on protein loss? A: Increases losses and catabolism.

13. Q: ONS indication? A: PEW risk/presence when counselling cannot meet protein/energy needs.

14. Q: ONS trial duration? A: Minimum 3 months per KDOQI.

15. Q: Persistent inadequate oral intake? A: Consider enteral feeding if medically appropriate.

16. Q: Amino-acid dialysate? A: Selective adjunct; limited outcome evidence.

17. Q: High phosphate + PEW? A: Do not cut protein indiscriminately; target additives/bioavailability/binders.

18. Q: Low potassium + low intake? A: Individualize potassium upward as appropriate; no automatic restriction.

19. Q: Exercise type for muscle? A: Progressive resistance activity, with aerobic activity as tolerated.

20. Q: Success endpoint? A: Intake, SGA, tissue/muscle/function and patient goals improve—not just albumin.

25. Rapid differential / troubleshooting

Table 15.22 — PD nutrition troubleshooting from problem to action.

Problem	Differential	First actions
Unintentional weight loss	Decongestion vs PEW, depression, GI disease, infection, malignancy, EPS	Confirm volume state; SGA/intake; symptom-directed evaluation
Low albumin	Inflammation, volume, losses, liver disease, low intake	CRP/infection + volume + losses + SGA/intake
Poor appetite	Constipation, nausea, intraperitoneal fullness, drugs, depression, underdialysis, EPS	Treat reversible cause; simplify diet; dietitian plan
Weight gain	Fluid vs fat vs mixed; dialysate glucose	Volume assessment + waist/body composition + glucose exposure
Weakness with normal BMI	Sarcopenia, inactivity, neuropathy, anemia	Strength/function + nutrition + exercise review
High phosphate + low intake	Additives/binder timing vs protein source	Protect protein; target high-bioavailability phosphate
Hypokalemia	Low intake, GI loss, insulin, residual diuretics, dialysate losses	Individualized dietary/supplemental replacement + cause search
ONS not working	Poor adherence/tolerance, unresolved inflammation, wrong diagnosis	Reassess cause and route; consider enteral/specialist support
Persistent vomiting/obstruction	EPS or surgical disease	Chapter 14 urgent pathway

26. Final revision sheet

CORE CONCEPT PD nutrition is a longitudinal balance of oral intake, dialysate-derived glucose calories, protein losses, inflammation, body composition and physical function. PEW is a multidimensional loss of protein and energy reserves—not a low albumin result.

Table 15.23 — One-minute revision.

Domain	Must remember
Screen	At least biannually; assess sooner with any risk signal.
Assess	7-point SGA + intake + weight/body composition + function + biochemical/inflammatory context.
Protein	1.0–1.2 g/kg IBW/day in metabolically stable PD.
Energy	25–35 kcal/kg IBW/day; include absorbed PD glucose calories.
Albumin	Risk marker; inflammation, volume and losses confound.
PEW	Loss of protein/energy stores across multiple domains.
Muscle	Track strength/function; BMI can hide sarcopenia.
Food quality	Individualize K/P restrictions; preserve protein and nutrient density.
ONS	Minimum 3-month trial when counselling alone is insufficient.
Enteral	Consider if chronic needs cannot be met orally.
AA dialysate	Selective adjunct; limited hard-outcome evidence.
Exercise	Pair nutrition with individualized resistance/aerobic activity.
Cross-references	Chapter 8 volume; 13 metabolic/K; 14 EPS; 16 special populations.

Table 15.24 — One-minute bedside synthesis.

If you see…	Think…	Do now…
Low albumin + CRP	Inflammation	Find/treat cause; assess nutrition separately
Stable weight + low strength	Hidden sarcopenia	SGA + functional assessment
Weight gain + no edema	Fat/metabolic gain	Count PD glucose + diet/activity review
PEW + high phosphate	Competing priorities	Protect protein; target phosphate source/binders
Poor intake after counselling	Need support escalation	3-month ONS trial
Persistent oral failure	Enteral/specialized support	MDT route decision
After peritonitis	Catabolic recovery need	Early nutrition reassessment
Long-vintage PD + vomiting	Possible EPS	Chapter 14 urgent evaluation

FINAL MENTAL MODEL SCREEN → separate WATER / FAT / MUSCLE → identify PEW or metabolic phenotype → quantify PROTEIN + ENERGY including PD glucose → remove reversible DRIVERS → escalate FOOD → ONS → ENTERAL/specialized support → pair with EXERCISE → verify INTAKE + SGA + FUNCTION + metabolic burden.

Rapid oral viva

Explain why serum albumin cannot diagnose malnutrition in PD.
Give the KDOQI 2020 protein and energy targets for metabolically stable PD and explain the weight basis.
Explain how dialysate glucose changes energy assessment.
Walk through the nutritional assessment of a patient losing weight after peritonitis.
Differentiate PEW, sarcopenia and sarcopenic obesity.
Explain why hyperphosphatemia should not automatically trigger protein restriction.
Describe the escalation from dietitian counselling to ONS and enteral feeding.
Explain the evidence limitations of amino-acid dialysate.
Build a combined nutrition–exercise plan for a frail PD patient.

SAFETY BOUNDARY This chapter teaches assessment and management architecture. Exact supplement composition, tube-feeding formulas/rates, amino-acid dialysate prescriptions, insulin adjustment, potassium replacement, phosphate binder dosing and nutrition in pregnancy, cirrhosis, cancer, critical illness or severe intestinal failure require current product information, renal dietitian/pharmacy input and disease-specific protocols.

27. Selected authoritative references

1. Ikizler TA, Burrowes JD, Byham-Gray LD, et al. KDOQI Clinical Practice Guideline for Nutrition in CKD: 2020 Update. Am J Kidney Dis. 2020;76(3 Suppl 1):S1–S107. https://doi.org/10.1053/j.ajkd.2020.05.006. PMID: 32829751.

2. Fouque D, Kalantar-Zadeh K, Kopple J, et al. A proposed nomenclature and diagnostic criteria for protein-energy wasting in acute and chronic kidney disease. Kidney Int. 2008;73(4):391–398. https://doi.org/10.1038/sj.ki.5002585. PMID: 18094682.

3. Brown EA, Blake PG, Boudville N, et al. International Society for Peritoneal Dialysis practice recommendations: Prescribing high-quality goal-directed peritoneal dialysis. Perit Dial Int. 2020;40(3):244–253. https://doi.org/10.1177/0896860819895364. PMID: 32063219.

4. KDOQI US Commentary on the 2020 ISPD Practice Recommendations for Prescribing High-Quality Goal-Directed Peritoneal Dialysis. Am J Kidney Dis. 2021. PMID: 33341315.

5. National Kidney Foundation. Pocket Guide to Nutrition Assessment of the Patient with Kidney Disease. Updated to align with KDOQI 2020 Nutrition Guideline.

6. Guedes AM. Peritoneal Protein Loss, Leakage or Clearance In Peritoneal Dialysis, Where Do We Stand? Perit Dial Int. 2019;39(3):201–209. https://doi.org/10.3747/pdi.2018.00138. PMID: 31088933.

7. Bennett PN, Bohm C, Harasemiw O, et al. Physical activity and exercise in peritoneal dialysis: ISPD and Global Renal Exercise Network practice recommendations. Perit Dial Int. 2022;42(1):8–24. https://doi.org/10.1177/08968608211055290. PMID: 34743628.

8. de Mutsert R, Grootendorst DC, Boeschoten EW, et al. Subjective global assessment of nutritional status is strongly associated with mortality in chronic dialysis patients. Am J Clin Nutr. 2009;89(3):787–793. https://doi.org/10.3945/ajcn.2008.26970. PMID: 19144733.

9. Mafrici B, Viramontes-Hörner D, Gardner DS, Smith K, Taal MW, Selby NM, et al. Amino acid and protein losses in adult patients receiving maintenance dialysis: a literature review. J Ren Nutr. 2026;36(1):30–48. https://doi.org/10.1053/j.jrn.2025.07.012. PMID: 40759352.

10. Law S, Davenport A. Glucose absorption from peritoneal dialysate is associated with a gain in fat mass and a reduction in lean body mass in prevalent peritoneal dialysis patients. Br J Nutr. 2020;123(11):1269–1276. https://doi.org/10.1017/S0007114520000306. PMID: 31992383.

11. Blumenkrantz MJ, Gahl GM, Kopple JD, et al. Protein losses during peritoneal dialysis. Kidney Int. 1981;19(4):593–602. https://doi.org/10.1038/ki.1981.57. PMID: 7241892.

12. Rubin J, McFarland S, Hellems EW, Bower JD. Peritoneal dialysis during peritonitis. Kidney Int. 1981;19(3):460–464. https://doi.org/10.1038/ki.1981.40. PMID: 7241884.

13. de Mutsert R, Grootendorst DC, Indemans F, et al. Association between serum albumin and mortality in dialysis patients is partly explained by inflammation, and not by malnutrition. J Ren Nutr. 2009. PMID: 19218039.

14. CANUSA Peritoneal Dialysis Study Group. Adequacy of dialysis and nutrition in continuous peritoneal dialysis: association with clinical outcomes. J Am Soc Nephrol. 1996. PMID: 8785388.

15. Kwon YE, Kee YK, Yoon CY, et al. Change of Nutritional Status Assessed Using Subjective Global Assessment Is Associated With All-Cause Mortality in Incident Dialysis Patients. Medicine (Baltimore). 2016;95(7):e2714. https://doi.org/10.1097/MD.0000000000002714. PMID: 26886609.

16. Modifiable Physical Factors That Influence Physical Function for People Receiving Peritoneal Dialysis. Kidney Int Rep. 2024. PMID: 38707811.

17. Uchiyama K, Washida N, Morimoto K, et al. Home-based Aerobic Exercise and Resistance Training in Peritoneal Dialysis Patients: A Randomized Controlled Trial. Sci Rep. 2019. PMID: 30796338.

18. Liu et al. Oral nutritional supplement helps to improve nutritional status of dialysis dependent patients: a systematic review and meta-analysis of randomized controlled trials. 2023. PMID: 38075233.

19. Salamon KM, Lambert K. Oral nutritional supplementation in patients undergoing peritoneal dialysis: a randomised, crossover pilot study. J Ren Care. 2018;44(2):73–81. https://doi.org/10.1111/jorc.12224. PMID: 29151280.

20. González-Espinoza L, Gutiérrez-Chávez J, del Campo FM, Martínez-Ramírez HR, Cortés-Sanabria L, Rojas-Campos E, et al. Randomized, open label, controlled clinical trial of oral administration of an egg albumin-based protein supplement to patients on continuous ambulatory peritoneal dialysis. Perit Dial Int. 2005;25(2):173–80. PMID: 15796146.

21. Li FK, Chan LYY, Woo J, et al. A 3-year, prospective, randomized, controlled study on amino acid dialysate in patients on CAPD. Am J Kidney Dis. 2003. PMID: 12830470.

22. Tjiong HL, van den Berg JWB, Wattimena JLD, et al. Dialysate as food: combined amino acid and glucose dialysate improves protein anabolism in renal failure patients on automated peritoneal dialysis. J Am Soc Nephrol. 2005. PMID: 15800130.

23. Tjiong HL, Rietveld T, Wattimena JLD, et al. Peritoneal dialysis with solutions containing amino acids plus glucose promotes protein synthesis during oral feeding. Clin J Am Soc Nephrol. 2007. PMID: 17699390.

24. Cheng et al. Sarcopenia and Its Individual Traits Independently Predict Mortality in Patients on Dialysis: A Systematic Review and Meta-Analysis. 2025. PMID: 41069070.

SOURCE NOTE Guideline status and contemporary evidence were checked 3 September 2026. KDOQI 2020 remains the principal comprehensive adult CKD/dialysis nutrition guideline, while the ISPD repository continues to list 2020 goal-directed PD and 2021/2022 exercise guidance as relevant current standards. Exact food plans, supplements, amino-acid solutions, glucose exposure, body-weight reference method and electrolyte replacement must be individualized by the renal dietitian and PD team.