🍓Medical Nutrition Therapy II Unit 3 – Renal Disease: Nutrition & Pathophysiology
Renal disease impacts kidney function, disrupting the body's ability to filter waste and maintain balance. From chronic kidney disease to acute kidney injury, these conditions require careful management of protein, sodium, potassium, phosphorus, and fluid intake. Understanding the kidneys' role is crucial for effective treatment.
Nutritional strategies play a vital role in managing renal diseases. Tailoring diets to restrict certain nutrients while ensuring adequate nutrition is key. Medical interventions, including medications and renal replacement therapies, complement dietary approaches to support kidney function and improve patient outcomes in various stages of renal disease.
Renal disease encompasses a range of conditions that impair kidney function and disrupt homeostasis
Kidneys play a vital role in filtering waste products, regulating fluid and electrolyte balance, and producing hormones (erythropoietin, renin, calcitriol)
Chronic kidney disease (CKD) is characterized by a progressive decline in kidney function over time
Classified into five stages based on glomerular filtration rate (GFR) and albuminuria
Leading causes include diabetes, hypertension, and glomerulonephritis
Acute kidney injury (AKI) is a rapid deterioration of kidney function, often resulting from ischemia, nephrotoxins, or obstruction
Nutritional management is crucial in preventing and managing renal diseases, focusing on protein, sodium, potassium, phosphorus, and fluid intake
Renal replacement therapies, such as hemodialysis, peritoneal dialysis, and kidney transplantation, are used to support kidney function in advanced stages of renal disease
Anatomy and Physiology Review
Kidneys are bean-shaped organs located in the retroperitoneal space, with each kidney containing approximately one million nephrons
Nephrons are the functional units of the kidney, consisting of the renal corpuscle (glomerulus and Bowman's capsule) and renal tubule (proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting duct)
Glomerular filtration is the first step in urine formation, where blood is filtered through the glomerular capillaries into Bowman's capsule
Filtration is driven by Starling forces (hydrostatic and oncotic pressures)
Glomerular filtration rate (GFR) is a measure of kidney function, normally around 125 mL/min
Tubular reabsorption and secretion modify the filtrate as it passes through the renal tubule, reclaiming essential nutrients and electrolytes while secreting waste products and excess ions
Juxtaglomerular apparatus (JGA) regulates glomerular filtration and systemic blood pressure through the renin-angiotensin-aldosterone system (RAAS)
Kidneys maintain acid-base balance by reabsorbing bicarbonate and secreting hydrogen ions
Pathophysiology of Renal Diseases
Chronic kidney disease (CKD) is characterized by a progressive loss of nephrons and decline in GFR over months to years
Risk factors include diabetes, hypertension, obesity, age, and family history
Pathophysiological mechanisms involve glomerular hyperfiltration, inflammation, fibrosis, and oxidative stress
Diabetic nephropathy is a leading cause of CKD, resulting from hyperglycemia-induced damage to glomerular and tubular structures
Characterized by albuminuria, hypertension, and progressive decline in GFR
Hypertensive nephrosclerosis is another common cause of CKD, where chronic hypertension leads to glomerular and vascular damage
Glomerulonephritis encompasses a group of diseases characterized by inflammation and damage to the glomeruli
Can be caused by immune-mediated mechanisms (lupus nephritis, IgA nephropathy) or infections (post-streptococcal glomerulonephritis)
Acute kidney injury (AKI) is a rapid decline in kidney function, often resulting from ischemia, nephrotoxins, or obstruction
Prerenal AKI is caused by decreased renal perfusion (hypovolemia, heart failure, sepsis)
Intrinsic AKI involves direct damage to kidney structures (acute tubular necrosis, acute interstitial nephritis)
Postrenal AKI is caused by obstruction of the urinary tract (kidney stones, prostate enlargement, tumors)
Nutritional Implications
Protein intake must be carefully managed in renal disease to prevent further kidney damage and uremic toxicity
In CKD, protein intake is typically restricted to 0.6-0.8 g/kg/day to reduce glomerular hyperfiltration and proteinuria
In dialysis patients, protein requirements are increased to 1.2-1.4 g/kg/day to compensate for losses during dialysis and maintain nitrogen balance
Sodium restriction is important in managing hypertension and fluid overload in renal disease
Typically limited to 2-3 g/day in CKD and dialysis patients
Potassium intake may need to be restricted in advanced CKD and dialysis patients to prevent hyperkalemia
Dietary sources of potassium include fruits, vegetables, nuts, and legumes
Phosphorus restriction is necessary to prevent hyperphosphatemia and secondary hyperparathyroidism in CKD
Dietary sources of phosphorus include dairy products, meat, poultry, fish, and processed foods
Phosphate binders (calcium carbonate, sevelamer) are often used to reduce intestinal absorption of phosphorus
Fluid intake may need to be restricted in advanced CKD and dialysis patients to prevent fluid overload and hypertension
Typically limited to 1-1.5 L/day plus urine output in dialysis patients
Renal vitamin and mineral supplementation may be necessary to address deficiencies and prevent complications
Vitamin D supplementation is often required to manage hypocalcemia and secondary hyperparathyroidism
Iron supplementation may be needed to treat anemia, as erythropoietin production is impaired in CKD
Assessment and Diagnosis
Glomerular filtration rate (GFR) is the gold standard for assessing kidney function
Estimated using serum creatinine-based equations (Cockcroft-Gault, MDRD, CKD-EPI)
Staging of CKD is based on GFR categories (G1-G5) and albuminuria categories (A1-A3)
Urinalysis is used to detect proteinuria, hematuria, and other abnormalities suggestive of renal disease
Albumin-to-creatinine ratio (ACR) is a sensitive marker of kidney damage
Renal imaging studies (ultrasound, CT, MRI) are used to assess kidney size, structure, and obstruction
Renal biopsy may be performed to establish a definitive diagnosis and guide treatment in certain cases
Nutritional assessment includes evaluation of dietary intake, anthropometric measurements, and biochemical markers
Dietary recall, food frequency questionnaires, and food diaries are used to assess nutrient intake
Serum albumin, prealbumin, and transferrin are markers of nutritional status and inflammation
Biochemical monitoring of electrolytes, minerals, and acid-base balance is crucial in managing renal disease
Serum potassium, phosphorus, calcium, and bicarbonate levels are routinely monitored
Parathyroid hormone (PTH) and vitamin D levels are assessed to monitor bone and mineral metabolism
Dietary Management Strategies
Protein restriction is a key strategy in managing CKD to reduce glomerular hyperfiltration and uremic toxicity
Low-protein diets (0.6-0.8 g/kg/day) are recommended in non-dialysis CKD patients
High-quality, bioavailable protein sources (eggs, lean meats, fish) are preferred to minimize uremic toxin production
Sodium restriction is important in managing hypertension and fluid balance in renal disease
Typically limited to 2-3 g/day, with an emphasis on reducing processed and high-sodium foods
Flavor enhancement techniques (herbs, spices, lemon juice) can improve palatability of low-sodium diets
Potassium restriction may be necessary in advanced CKD and dialysis patients to prevent hyperkalemia
Low-potassium food choices include apples, berries, carrots, green beans, and rice
Leaching techniques (soaking, boiling) can reduce potassium content of high-potassium vegetables
Phosphorus restriction is crucial in preventing hyperphosphatemia and secondary hyperparathyroidism in CKD
Avoiding processed foods and limiting intake of dairy products, meat, and poultry can help control phosphorus intake
Phosphate binders taken with meals can reduce intestinal absorption of dietary phosphorus
Fluid management is important in advanced CKD and dialysis patients to prevent fluid overload and hypertension
Fluid intake is typically limited to 1-1.5 L/day plus urine output in dialysis patients
Strategies to manage thirst include chewing gum, sucking on ice chips, and using lemon wedges
Renal-specific oral nutritional supplements may be used to address malnutrition and micronutrient deficiencies in CKD patients
Supplements are typically high in calories, protein, and essential vitamins and minerals, while being low in potassium and phosphorus
Medical Treatments and Interventions
Antihypertensive medications are used to control blood pressure and slow the progression of renal disease
ACE inhibitors and ARBs are preferred agents due to their renoprotective effects
Diuretics may be used to manage fluid overload and hypertension
Erythropoiesis-stimulating agents (ESAs) are used to treat anemia in CKD patients
Recombinant human erythropoietin (epoetin alfa) and darbepoetin alfa stimulate red blood cell production
Iron supplementation is often necessary to ensure adequate iron stores for erythropoiesis
Phosphate binders are used to reduce intestinal absorption of dietary phosphorus and manage hyperphosphatemia
Calcium-based binders (calcium carbonate, calcium acetate) are commonly used
Non-calcium-based binders (sevelamer, lanthanum carbonate) are used in patients with hypercalcemia or vascular calcification
Vitamin D analogs (calcitriol, paricalcitol) are used to manage secondary hyperparathyroidism and bone mineral disorders in CKD
Renal replacement therapies are used to support kidney function in advanced stages of renal disease
Hemodialysis involves the use of an artificial kidney (dialyzer) to filter blood and remove waste products and excess fluid
Peritoneal dialysis uses the patient's peritoneal membrane as a natural filter, with dialysate solution exchanged through a catheter in the abdomen
Kidney transplantation is the preferred treatment for end-stage renal disease, offering improved quality of life and survival compared to dialysis
Case Studies and Clinical Applications
Case 1: A 55-year-old male with type 2 diabetes and hypertension presents with a GFR of 45 mL/min/1.73m² and an ACR of 200 mg/g
Diagnosis: Stage 3b CKD with moderately increased albuminuria (A2)
Nutritional management: Protein restriction to 0.6-0.8 g/kg/day, sodium restriction to 2-3 g/day, and phosphorus restriction to 800-1000 mg/day
Medical management: ACE inhibitor for blood pressure control and renoprotection, statin for lipid management, and regular monitoring of GFR and albuminuria
Case 2: A 70-year-old female with a history of chronic hypertension presents with a GFR of 20 mL/min/1.73m², serum potassium of 5.8 mmol/L, and signs of fluid overload
Diagnosis: Stage 4 CKD with hyperkalemia and fluid overload
Nutritional management: Protein intake of 0.6-0.8 g/kg/day, potassium restriction to 2000-2500 mg/day, fluid restriction to 1.5-2 L/day, and phosphorus restriction to 800-1000 mg/day
Medical management: Loop diuretic for fluid management, potassium binder (patiromer or sodium zirconium cyclosilicate) for hyperkalemia, and preparation for renal replacement therapy
Case 3: A 30-year-old female with lupus nephritis presents with a GFR of 25 mL/min/1.73m², serum albumin of 3.0 g/dL, and a history of poor appetite and weight loss
Diagnosis: Stage 4 CKD with protein-energy wasting
Nutritional management: Protein intake of 0.8-1.0 g/kg/day, with high-quality, bioavailable protein sources, and renal-specific oral nutritional supplements to address malnutrition
Medical management: Immunosuppressive therapy (corticosteroids, mycophenolate mofetil) for lupus nephritis, and regular monitoring of nutritional status and inflammation markers
Case 4: A 60-year-old male with end-stage renal disease on hemodialysis presents with a serum phosphorus of 7.5 mg/dL and a PTH level of 600 pg/mL
Diagnosis: Hyperphosphatemia and secondary hyperparathyroidism in ESRD
Nutritional management: Protein intake of 1.2-1.4 g/kg/day, phosphorus restriction to 800-1000 mg/day, and use of phosphate binders with meals
Medical management: Adjustment of dialysis prescription to improve phosphorus removal, use of a non-calcium-based phosphate binder (sevelamer), and vitamin D analog (paricalcitol) for PTH suppression
Case 5: A 50-year-old female with a history of recurrent urinary tract infections and kidney stones presents with acute flank pain, fever, and a GFR of 30 mL/min/1.73m²
Diagnosis: Acute kidney injury secondary to obstructive pyelonephritis
Nutritional management: Adequate hydration to maintain urine output, temporary protein restriction to 0.6-0.8 g/kg/day, and avoidance of high-oxalate foods to prevent further stone formation
Medical management: Intravenous antibiotics for pyelonephritis, ureteral stenting or nephrostomy tube placement to relieve obstruction, and monitoring of kidney function and electrolytes during recovery