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Muyinda, Mathew Rogers - Nutrition Therapy in Renal Disease

  1. Mathew Rogers Muyinda BSc. (Hons) Human Nutrition Makerere University
  2. Renal system • Group of organs whose major function is to filter out excess fluid and other substances from the blood stream. • These substances collectively form urine. • The major organs in this system include – the kidneys, – ureter, – bladder, – urethra.
  3. The kidney • The major organ of the renal system • The kidney; – receives 20% of cardiac output, which allows the filtering of approximately 1600L/day of blood. • From this blood, 180L of ultra filtrate fluid is produced and undergoes selective re-absorption and secretion to 1.5L of urine excreted in an average day.
  4. The kidney continued…
  5. Human Kidney Functions • Waste excretion – remove the waste products of metabolism (urea, uric acid, creatinine). • Acid–base balance – eliminate excess hydrogen ions – control composition of the blood • Blood pressure control – regulation of sodium ions in blood – via the Renin-Angiotensin-Aldosterone System (RAAS) • Plasma volume and osmolality control – Under the effect of antidiuretic hormone (ADH)
  6. Human kidney functions continued… • Hormone secretion – Erythropoietin (EPO) – Calcitriol • Carnitine synthesis • Glucose homeostasis – role in gluconeogenesis • Prostaglandin E2 synthesis – impacts renal hemodynamics and salt and water excretion.
  7. Renal Diseases • Ten symptoms of kidney disease – Changes in urination – Confusion – Feeling dizzy – Headache – High blood pressure – Loss of appetite or change in taste – Nausea or vomiting – Severe itching not related to a bite or rash – Shortness of breath – Swelling of face, hands, and/or feet
  8. • Other symptoms – Altered Lipid and Amino Acid Levels – Abnormal BUN:Creatinine Ratio – Anorexia – Bone Pain, Altered Height, or Lean Body Mass – Burning or Difficulty During Urination – Changes in GFR – Chronic Inflammation – Proteinuria, Microalbuminuria – Protein–Energy Malnutrition or Wasting – Puffiness Around Eyes • Other symptoms – Flank Pain – Frequent Weight Shifts – Insomnia – Itching, Dry Skin – Leg Cramps – Polyuria and Nocturia – Pain in Small of Back Just Below Ribs, Not Aggravated by Movement – Hematuria – Serum Creatinine 1.7 mg/dL – Unbalanced Calcium:Phosphorus Ratios – Uremia – Weakness, Pallor, Anemia
  9. Kidney disease diagnosis: overview • The diagnosis of kidney disease is based on the evaluation of signs, symptoms and a series of investigations. • The diagnosis is complicated by the fact that most of the signs and symptoms are non- specific and also appear fairly late in the course of the disease.
  10. Common Renal Diseases • Common renal diseases include; – Glomerular and autoimmune kidney diseases • Glomerulonephritis • Glomerulosclerosis – Acute kidney injury (AKI) – Chronic kidney disease (CKD) – Nephrotic syndrome – Kidney stones (nephrolithiasis) – UTIs
  11. Glomerulonephritis – Glomerulonephritis is a collective term used for diseases with renal inflammation stemming from the glomeruli; immune mechanisms are involved in all of them • The interaction of antigen and antibody activates complement and liberates mediators that attract polymorphonuclear leukocytes. • The actual glomerular injury is caused by destructive lysosomal enzymes that are released from the leukocytes that have accumulated within the glomeruli.
  12. GN continued… • Causes – Bacterial endocarditis. – Lupus – IgA nephropathy. – Polyarteritis • Symptoms and signs – Hermaturia. – High blood pressure. – Frequent night time urination. – Fluid retention. – Foamy urine.
  13. Interventions Objectives: – Improve renal functioning; prevent systemic complications where possible – Monitor abnormal protein status and serum nitrogen retention – Spare protein for tissue repair. • Prevent further catabolism of protein to lessen production of urea and other protein waste products – Control hypertension and oedema – Manage hyperglycaemia or dyslipidaemia
  14. Interventions continued… – Correct metabolic abnormalities. • Improve nutritional status and appetite – Prevent or correct growth failure in children – Reduce inflammation and attenuate oxidative damage – Reduce workload of circulatory system by decreasing excess weight, where needed
  15. Interventions continued… Food and nutrition strategies: – Modify patient’s diet according to disease progression • maintain sufficient levels of protein as long as kidneys can eliminate waste products of protein metabolism. – Use sufficient energy to spare protein (60% CHOs, 30% fat). • For adults, 30–40 kcal/kg adjusted edema-free BW is needed to spare protein for tissue synthesis and wound healing – In uremia, diet should include 50% high–biologic value proteins, or essential amino acids at 2–3 times the normal should be included. • Limit protein to 0.6–0.8 g/kg
  16. Interventions continued… – In oliguria, restrict fluid intake to 500–700 mL. • Limit protein to 0.6–0.8 g/kg. When urinary output is reduced greatly, restrict phosphorus intakes if needed. – With edema or high blood pressure, restrict sodium intake to 2–3 g/d. – Vegetarian diets, soy products, and use of omega-3 fatty acids may be beneficial for dyslipidemia. • Restrict fat and cholesterol if needed; monitor diet carefully – Control CHO intake with diabetes or hyperglycemia. – If patient is obese, use an energy-controlled diet, but avoid fasting and very low–calorie diets.
  17. Arteriolar nephrosclerosis – a complication of severe hypertension – Extreme elevation of the systemic blood pressure causes degenerative changes characterized by thickening and narrowing of lumens of the small arterioles and arteries – Glomerular filtration is reduced because the arterioles are greatly narrowed. – The renal tubules,also undergo degenerative changes. – Eventually, the kidneys become shrunken and scarred as a result of reduction of their blood supply
  18. Kidney stones (Nephrolithiasis) – These are solid crystals of dissolved minerals in urine, found inside the kidneys. • Calcium oxalate (~75%) • Calcium phosphate (~15%) • Uric acid(~8%) • Struvite (~1%) • Cystine (<1%) – Kidney stones develop when salt and minerals in urine form crystals that coalesce and grow in size. – If large, they cause severe pain in the abdominal and groin region.
  19. Causes of and predisposition to kidney stones
  20. Kidney stones continued… • Dietary risk factors for kidney stones: – Calcium deficient diet leads to upregulation of oxalate absorption – High animal protein intake lowers urine pH favouring crystallisation – High salt intake increases urinary calcium excretion – Oxalate rich foods and vitamin C intake may increase stone formation – Low potassium diet reduces urine citrate excretion and increase calcium excretion
  21. Interventions Objectives: – Determine predominant components and prevent recurrence by normalization of BMI, adequate physical activity balanced nutrition, and sufficient daily fluid intake – To increase excretion of salts, dilute urine by increasing fluid volume to at least 2 L/24 h. – Prevent scarring, recurrence of stones, obstruction, bone demineralization, or kidney damage. – Promote use of a heart-healthy diet.
  22. Food & Nutrition strategies: – Fluid intake should be high, as tolerated (2 L/d). – Limit the use of apple or grapefruit juices. – Consume a diet that is balanced • Fruits and vegetables may reduce the low potassium/high sodium intake. • The DASH diet is a good recommendation. – A heart-healthy weight loss and exercise plan may be needed if the patient is obese – Calcium should not be restricted, except in absorptive hypercalciuria – Include legumes and dried beans for their health- promoting saponins, which are useful in the treatment of hypercalciuria
  23. Nephrotic Syndrome • A group of abnormalities characterized by a severe loss of protein in the urine; – urinary excretion of protein is so great (about 3.5 g/day); – the body is unable to manufacture protein fast enough to keep up with the losses; – the concentration of protein in the blood plasma falls. – This, in turn, causes significant edema owing to the low plasma osmotic pressure.
  24. Causes • NS is caused by renal diseases that increase the permeability across the glomerular filtration barrier, such as: – Diabetes mellitus (diabetic nephropathy) – Systemic lupus erythematosus (SLE) – Amyloidosis – Kidney diseases; • membranous nephropathy • focal glomerulosclerosis • membranoproliferative glomerulonephritis
  25. Diagnosis of nephrotic syndrome • It is classically characterised by four clinical features, but the last two may not be seen in all patients: – nephrotic range proteinuria • urinary protein excretion greater than 50 mg/kg per day or urine protein-to-creatinine ratio >2 – hypoalbuminaemia • serum albumin concentration <3 g/dL (30 g/L) – oedema – hyperlipidaemia
  26. Interventions Objectives: – Treat the underlying condition and take appropriate medications – Prevent thrombotic episodes and manage infectious complications – Ensure efficient utilization of fed proteins, spared by use of adequate calories. Prevent muscle catabolism – Correct anorexia and prevent malnutrition – Reduce edema, control sodium intake, prevent or control renal failure – Manage hyperlipidemia and elevated triglycerides – Monitor for potassium deficits with certain diuretics. – Replace any other nutrients, especially those at risk (e.g., calcium, vitamin D)
  27. Interventions continued… Food & Nutrition strategies: – Use a diet of modest protein restriction – Diet should provide 35–40 kcal/kg/d. • CHO intake should be high to spare protein for lean body mass; use high–complex CHO and high-fiber foods. – Limit saturated fats and cholesterol; decrease intake of concentrated sugars and alcohol. – Encourage use of linoleic acid and omega-3 fatty acids. A vegetarian, soy-based diet with amino acid replacements may be beneficial.
  28. Interventions continued… – If patient has edema, restrict sodium intake to 2–3 g. – Provide adequate sources of potassium, vitamin D, and calcium. • Replace zinc, vitamin C, folacin, and other nutrients. – Monitor the need for iron but do not use excesses, especially with infections. – Fluid restrictions may be necessary if edema is refractory to diuretic therapy. – Offer appetizing meals to increase intake.
  29. Acute Kidney Injury (AKI) • AKI involves abrupt decline in renal function with waste retention. • AKI is characterized by; – a sudden reduction in GFR – altered ability of the kidney to excrete the daily production of metabolic waste. • Causes – causes are generally classified into three categories: • inadequate renal perfusion (prerenal) • diseases within the renal parenchyma (intrinsic) • urinary tract obstruction (postrenal).
  30. Classification of the major causes of AKI
  31. AKI continued… • The phases of ARF include the following: – Prodromal phase — varies in duration depending on cause — urine output may be normal – Oliguric (average 10–14 days)—output typically between 50 and 400 mL/d – Postoliguric phase (average 10 days)—urine output gradually returns to normal – Recovery (from 1 month or up to 1 year).
  32. Diagnosis criteria for AKI • The Acute Kidney Injury Network definition includes the following elements as diagnostic criteria: – an abrupt (within 48 hours) absolute increase in the serum creatinine concentration of >0.3 mg/dL from baseline, – a percentage increase in the serum creatinine concentration of >50% – oliguria of less than 0.5 mL/kg per hour for more than 6 hours.
  33. Complications for AKI
  34. Clinical and laboratory evaluation of AKI
  35. Summary of MNT for acute kidney injury
  36. Chronic Kidney Disease (CKD) • CKD is a syndrome that results from progressive and irreversible destruction of nephrons resulting from a number of causes. – CKD is characterized by the inability of kidney function to return to normal after acute kidney failure or progressive renal decline from disease. • Excess urea and nitrogenous wastes accumulate in the bloodstream (azotemia). • CKD causes permanent reduction in kidney function
  37. CKD continued… • Common causes of CKD: – Diabetic nephropathy – Glomerulonephritis – Hypertension-associated CKD – Autosomal dominant polycystic kidney disease – Other cystic and tubulointerstitial nephropathy
  38. Diagnosis of CKD • CKD is defined as kidney damage for >3 months, as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifested by either: – pathological abnormalities or the presence of markers of kidney damage, including abnormalities in the composition of the blood or urine, or abnormalities in imaging studies or – GFR <60 mL/min/1.73m2 for 3 months, with or without kidney damage.
  39. Common reversible factors in CKD
  40. Pathophysiology of CKD • In response to a decreasing GFR, the kidney undergoes a series of adaptations to prevent decline. • As nephrons die, the surviving nephrons are forced to ―work harder‖ in order to accomplish the functions previously performed by a full complement of nephrons. • Each of the remaining nephrons receives a larger volume of blood to process at a higher than normal pressure.
  41. CKD pathophysiology continued… • The high blood volumes and pressures damage the arterioles and glomerular capillaries, which leads to; – Arteriolosclerosis, along with glomerular capillary injury; and – scarring (glomerulosclerosis). • The tubules are also damaged because the blood vessels that supply the glomeruli also supply the tubules.
  42. CKD pathophysiology continued… • As more nephrons are lost, an additional burden is placed on those that still survive, which eventually causes many of them to fail. • As this process continues, progressively more nephrons are lost at an increasing rate, until eventually renal function deteriorates to the point where the kidneys are no longer able to perform their regulatory and excretory functions.
  43. Stages of CKD Description Stage eGFR in ml/min Kidney damage, but normal to increased kidney function 1 90 – 130 Mild decrease in kidney function 2 60-89 Moderate decrease in kidney function 3 30-59 Severe decrease in kidney function 4 15-29 Kidney failure 5 <15 or dialysis.
  44. CKD continued… • Factors influencing CKD progression: – Poor glycemic control – Smoking. – Underlying diseases. – Uncontrolled metabolic acidosis. – Dyslipidaemia – Race - higher in blacks – Levels of proteinuria
  45. Population at risk of CKD
  46. Nutrition recommendations
  47. Complications in CKD • Anemia – due to lack of erythropoietin • Renal Bone disease – Reduction of bone density and demineralization – due to lack of calcitriol and increased plasma phosphate levels.
  48. Complications associated with CKD • Fluid, electrolyte and acid-base disorders: – ECFV expansion, hyponatremia,  TB sodium, hyperkalemia, metabolic acidosis • Disorders of Ca and PO43- metabolism: – Bone demineralisation • Cardiovascular abnormalities – Ischaemic vascular disease; Heart failure; Hypertension & left ventricular hypertrophy; Pericardial disease • Haematological disorders – Anemia; abnormal haemostasis; • PEM/malnutrition (occurs in in >50% of the people with CKD)
  49. Complications of CKD continued… • Factors that lead to malnutrition in CKD: – Decreased intake – Poor appetite – Uremia – Endocrine disorders like insulin resistance. – Acidosis – Diet restrictions – Increased leptin – Loss of nutrients in the dialysate
  50. Differentiating CKD from AKI
  51. Urinary Tract Infections (UTI) • UTI may be defined as a condition in which bacteria enter, persist and multiply within the urinary tract. • The infection is mostly caused by: – Gram-negative bacteria such as Escherichia coli, Klebsiella, Enterobacter, Pseudomonas and Proteus. – Fastidious organisms – anaerobic bacteria – fungi like Candida
  52. Host factors predisposing to UTIs
  53. Diagnosis of UTIs • Microscopic examination of urine is the crucial first step in confirming UTI. • The gold standard for diagnosis of UTI is urine culture. – Growth of 105 colony forming units (CFU) of a single bacterial strain signifies a positive culture.
  54. Interventions • Objectives: – Preserve kidney function – Control blood pressure – Acidify urine to decrease additional bacterial growth – Prevent bacteremia – Force fluids unless contraindicated
  55. Interventions continued… • Food & nutrition – Restrict protein intake only if renal function is decreased. – Otherwise, use sufficient amounts of high BV proteins, including foods such as meat, fish, poultry, eggs, and cheese – Increase intake of urine acidifiers; • Cranberries, plums, and prunes produce hippuric acid • Corn, lentils, breads/starches, peanuts, and walnuts
  56. Interventions continued… – Increase vitamin C to stimulate the anti-infective process – Avoid an excess of caffeine because of its diuretic effect • Stimulants such as caffeine rapidly leave the bladder, a vulnerable site where additional infections may begin. – Vitamin A may be low; encourage improved intake, especially from beta-carotene–rich foods – Offer probiotic choices, such as yogurt to replenish good intestinal bacteria
  57. Renal Replacement Therapy • Used for medical treatment of patients with ESRD. • Forms of dialysis – Hemodialysis – Peritoneal dialysis • Transplantation
  58. Dialysis • Absolute Indication to Start Dialysis – Fluid overload or pulmonary oedema refractory to diuretics – Uraemia: • Pericarditis, persistent nausea, vomiting, bleeding due to platelet dysfunction, progressive uraemic encephalopathy or neuropathy with signs of confusion, asterixis, myoclonus or seizures – Accelerated hypertension poorly responsive to anti- hypertensive medication – BUN >100 mg/mL and serum creatinine above 10 mg/dL
  59. Dialysis continued… • 2005 European Best Practice Guidelines: – Dialysis should be initiated: • when GFR is <15 mL/min and there are one or more symptoms or signs of uraemia • in all, before GFR has fallen to 6 mL/min/1.73 m2 irrespective of symptoms
  60. Dialysis continued… • Hemodialysis – Here, blood is exposed to dialysate through a semipermeable membrane (dialyser) – Pores in the membrane enable small molecules and electrolytes to pass through.
  61. – Concentration differences allow molecules to diffuse down the concentration gradients, thereby expelling waste products and replacing desirable molecules or ions. – Water can be driven through the membrane by ultrafiltration. – There is need for an anticoagulant.
  62. Dialysis continued… • Peritoneal hemodialysis – The semipermeable membrane of the peritoneum is used as the dialyzer membrane. – It is dependent on diffusion across the concentration gradient across the peritoneum. – Fluid removal depends on the presence of a high intraperitoneal osmotic gradient.
  63. • Renal transplantation – Requires compatibility in terms of blood group, tissue typing, antibodies, donor-recipient characteristics. – Its beneficial because of the decreased cardiovascular risk, normalization of anemia, bone disease and electrolyte imbalances.
  64. Summary • The renal system is very vital in the body. • It is affected by many diseases • These diseases are on a rise and continue to increase with the increase of NCDs. • They can be managed through diet management and modifications and appropriate treatment.
  65. Conclusion • Nephrology is a very wide field and should be carefully understood. • Nephrologists should work very closely with nutritionists in management of renal diseases.
  66. References Crowley, L. V. (2013). An Introduction to Human Disease: Pathology and Pathophysiology Correlates (9th ed.). Jones & Bartlett Learning. Escott-Stump, S. (2012). Nutrition and Diagnosis-Related Care (7th ed.). Lippincot Williams & Wilkins. Mahan, L. K., & Raymond, J. L. (2017). Krause’s Food & The Nutrition Care Process (14th ed). Elsevier Academic Press. Sakhuja, V. (2012). Nephrology. In A. K. Agarwal, R. K. Singal, P. Gupta, S. Sundar, S. A. Kamath, S. Varma, & M. Y. Nadkar (Eds.), API Textbook of Medicine (9th ed.). The Association of Physicians of India. Waikar, S. S., Bonventre, J. V., Bargman, J. M., Skorecki, K., & Curhan, G. C. (2015). Disorders of the Kidney and Urinary Tract. In D. L. Kasper, A. S. Fauci, S. L. Hauser, D. L. Longo, J. L. Jameson, & J. Loscalzo (Eds.), Harrison’s Principles of Internal Medicine (19th ed.). McGraw-Hill Education.