4.3 MNT: Renal & Hepatic Disease

Chronic Kidney Disease (CKD) Staging

Chronic kidney disease (CKD) is classified by glomerular filtration rate (GFR), which estimates filtering capacity per 1.73 m² of body surface area. Memorize the five-stage table — items frequently give a GFR and ask for the stage or the matching diet.

The goals of MNT in CKD are to slow progression, manage uremia and electrolyte derangements, prevent metabolic bone disease, and avoid protein-energy malnutrition. Energy is kept generous (about 25-35 kcal/kg/day) so dietary protein is spared for tissue maintenance rather than burned for fuel. Nutrient targets shift dramatically once a client begins dialysis, which is the single most important distinction the exam tests.

Protein: Non-Dialysis vs. Dialysis

The protein guidance reverses across the dialysis line, which is counterintuitive and therefore high-yield:

• Non-dialysis CKD (stages 3-5, not yet on dialysis): restrict protein to ~0.6-0.8 g/kg/day to reduce nitrogenous waste, uremic symptoms, and the rate of progression
• Maintenance hemodialysis or peritoneal dialysis: increase protein to ~1.0-1.2 g/kg/day (peritoneal dialysis often slightly higher because of protein losses into the dialysate)

Why the reversal? Before dialysis, excess protein floods failing kidneys with urea and other nitrogenous waste, accelerating decline. Once dialysis begins, the treatment clears that waste but simultaneously removes amino acids and raises catabolism, so intake must rise to prevent muscle wasting, hypoalbuminemia, and a high normalized protein catabolic rate. A scenario item that places a stage-4 client and a dialysis client side by side is testing exactly this flip — restrict for the pre-dialysis client, liberalize for the dialysis client.

Electrolyte and Fluid Management on Dialysis

Dialysis clients usually require restriction of potassium, phosphorus, sodium, and fluid because these accumulate between treatments (the kidneys no longer excrete them and dialysis is intermittent).

Phosphorus is the hardest to control by diet alone, so phosphate binders are taken with meals to bind dietary phosphorus in the gut. Counsel clients to avoid inorganic phosphate additives (highly bioavailable) in processed foods, colas, and processed cheeses, plus high-phosphorus dairy and organ meats. High-potassium foods to limit include bananas, oranges, potatoes (leaching/double-boiling lowers content), tomatoes, avocados, dried fruit, and salt substitutes (potassium chloride). For anemia of CKD, support erythropoiesis-stimulating agent therapy with adequate iron.

The exam often pairs a high serum potassium with a menu and asks which food to remove — the answer targets the highest-potassium item, such as the baked potato or orange juice.

Nephrotic Syndrome

Nephrotic syndrome is a glomerular disorder defined by heavy proteinuria (> 3.5 g/day), hypoalbuminemia, edema, and hyperlipidemia.

MNT Goals

• Protein: provide adequate protein (~0.8-1.0 g/kg/day). High-protein diets do not replace urinary losses and may actually increase proteinuria and glomerular pressure.
• Sodium: restrict (often ~2,000 mg/day) to control edema and ascites
• Lipids: manage the secondary hyperlipidemia with a heart-healthy, low-saturated-fat pattern
• Fluid: individualized based on edema and serum sodium

The key teaching point and frequent distractor: do not overfeed protein to chase urinary losses. That strategy is outdated and harmful.

Cirrhosis and Hepatic Encephalopathy

Cirrhosis is end-stage liver fibrosis causing impaired protein synthesis, portal hypertension (ascites, varices), and progressive malnutrition. These clients are catabolic, deplete glycogen quickly, and are at high risk of sarcopenia — making protein adequacy, not restriction, the priority.

Modern Protein Guidance (Critical Update)

Protein should NOT be routinely restricted in cirrhosis. Current guidance (ESPEN/AASLD) provides 1.2-1.5 g/kg/day of protein to preserve lean mass. Energy needs are high (~30-35 kcal/kg/day). Because hepatic glycogen stores are tiny, recommend frequent small meals and especially a late-evening carbohydrate-protein snack to shorten the overnight fast and prevent the body from catabolizing muscle for gluconeogenesis. Branched-chain amino acid supplements may help selected protein-intolerant clients.

Hepatic Encephalopathy (HE)

Hepatic encephalopathy (HE) is neurocognitive impairment (confusion, asterixis, coma) from accumulated ammonia and other gut-derived toxins the failing liver cannot clear. First-line therapy is lactulose — a nonabsorbable disaccharide that acidifies the colon and traps ammonia for excretion — often with rifaximin, plus treating precipitants (GI bleeding, infection, constipation, electrolyte imbalance, excess diuretics). Long-term protein restriction is obsolete; it worsens malnutrition and survival, and is reserved only for rare, truly refractory cases.

For ascites and edema, restrict sodium to ~2,000 mg/day and individualize fluid. The exam scenario that pairs new HE with a tempting "eliminate dietary protein" option is testing whether you know the modern standard: keep protein adequate and manage ammonia pharmacologically.