An introduction to nutrition in selected renal diseases

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.

8. 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

9. • 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

10. 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.

11. 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

12. 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.

13. GN continued…
• Causes
– Bacterial endocarditis.
– Lupus
– IgA nephropathy.
– Polyarteritis
• Symptoms and signs
– Hermaturia.
– High blood pressure.
– Frequent night time urination.
– Fluid retention.
– Foamy urine.

14. 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

15. 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

16. 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

17. 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.

18. 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

20. 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.

22. Causes of and predisposition to kidney stones

23. 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

24. 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.

25. 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

26. 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.

27. 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

28. 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

29. 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)

30. 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.

31. 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.

32. 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).

33. Classification of the major causes
of AKI

34. 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).

35. 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.

36. Complications for AKI

37. Clinical and laboratory evaluation
of AKI

38. Summary of MNT for acute kidney injury

39. 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

40. CKD continued…
• Common causes of CKD:
– Diabetic nephropathy
– Glomerulonephritis
– Hypertension-associated CKD
– Autosomal dominant polycystic kidney disease
– Other cystic and tubulointerstitial nephropathy

41. 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.

42. Common reversible factors in CKD

43. 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.

45. 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.

46. 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.

47. 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.

48. CKD continued…
• Factors influencing CKD progression:
– Poor glycemic control
– Smoking.
– Underlying diseases.
– Uncontrolled metabolic acidosis.
– Dyslipidaemia
– Race - higher in blacks
– Levels of proteinuria

49. Population at risk of CKD

50. Nutrition recommendations

51. 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.

52. 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)

53. 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

54. Differentiating CKD from AKI

55. 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

56. Host factors predisposing to UTIs

57. 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.

58. Interventions
• Objectives:
– Preserve kidney function
– Control blood pressure
– Acidify urine to decrease additional bacterial
growth
– Prevent bacteremia
– Force fluids unless contraindicated

59. 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

60. 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

61. Renal Replacement Therapy
• Used for medical treatment of patients
with ESRD.
• Forms of dialysis
– Hemodialysis
– Peritoneal dialysis
• Transplantation

63. 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

64. 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

67. 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.

68. – 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.

69. 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.

72. • 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.

73. 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.

74. Conclusion
• Nephrology is a very wide field and should
be carefully understood.
• Nephrologists should work very closely
with nutritionists in management of renal
diseases.

75. 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.