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Lesson 5 of 6

Renal Diseases (Kidney)

RENAL DISEASES

  • Kidney is part of the urinary system which is composed of organs, tubes muscles and nerves that work together to dispose of waste in the body and to keep the chemicals and water in the body in balance
  • Components of renal system
  • The urinary system includes two kidneys, two ureters
  • Functions of the kidney can be grouped into 2 main categories
  • Excretory
  • Edocrine

Excretory functions

  • The kidney maintains homeostasis balance with respect to fluid and electrolytes. This function is accomplished by continuous filtration of blood and its alternatives (secretion and r-absorption)

Specific functions under this include

  • Water balance- this is achieved through control of excretion of water. It is regulated by ADH excreted by posterior pituitary gland. If there is excess water in the body they will be reduced release of ADH leading to increased water excretion. The kidney has ability to excrete dilute or concentrated urine depending on water status in the body. It can excrete as little as 500ml of concentrated urine or 12litres of dilute urine
  • Excretion of waste products-(renal solute load) this are mainly nitrogenous products which are the end products of protein metabolism-urea, creatinine, ammonia. If waste products are not excreted, they accumulate in abnormal quantities leading to a condition known as azotemia
  • Electrolyte and acid base balance- kidney controls the amounts of electrolytes -Na, K, Cl bicarbonate, phosphorus, Ca, etc. the Ph is controlled by excreting acid or base when there is excess in blood
  • Excretion of foreign substances -e.g medication, food additives

Endocrine functions

  • The kidney secretes hormones and enzymes that regulate mechanisms in the body
  • Rennin-an enzyme that acts in the plasma to form angiotensin 1 which is converted to angiotensin 2 (vasoconstrictor) which when raised, blood protein and Na is also reabsorbed
  • Erythropoietin-a hormone that stimulates maturation of RBCs in the bone marrow
  • Maintenance of calcium, phosphorus homeostasis
  • Involved in the production of active form of vitamin D as well as elimination of calcium and phosphorus. Active form of vitamin D promotes efficient absorption of calcium
  • Creatinine - is used to measure the kidney functioning because there is a constant level and it is not reabsorbed back

Definition of terms in kidney problems

  • Oliguria-low urine output of less than or equal to 500mls/day. Average normal urine output is 1500mls/day
  • Anuria-less than 100mls urine output per day
  • Azotemia-accumalation of toxins (urea,uric acid, creatinines, and other nitrogeneous waste) in the blood in abnormal quantities
  • Uremia-a clinical syndrome of weakness, leathergy, nausea, vomiting, muscle cramps, etc brought about by unacceptable levels of nitrogenous waste in the blood.

Glomerular filtration

  • The quantity of glomelular filtration formed per unit in all nephrons if the kidney is functioning well is 125mls /min.
  • Creatinine clearance is often used as the measure of GFR. In kidney diseases there is decrease in creatinine clearance rate and therefore decrease filtration of waste out of the blood. The normal creatinine clearance is 95-135mls/min

Diseases of the kidney

Nephrosis/nephritic syndrome

  • This is not a diagnosis of a particular renal disease but a distinct cluster of symptoms which include
  • edema (due to low albumin),
  • proteinurea (large loss of protein in the urine>5g/liter in adults
  • hyper albuminaemia (low serum albumin
  • elevated blood lipids (cholesterol and triglycerides)

The symptoms occur due to loss of the glomerular barrier to protein i.e the permeability of the glomerular capillaries increase and plasma protein which are normally retained in the blood escapes. It is characterized by high levels of protein passing from the blood into the urine (proteinuria at least 3.5 grams per day per 1.73m2 body surface area)

Causes

  • The cause is damage to the glomeruli, which can be the cause of the syndrome or caused by it, that alters their capacity to filter the substances transported in the blood
  • Others are:-
  • Damage to the kidney due to infection
  • Blood clots in the renal veins
  • Metabolic disorders such as diabetes mellitus
  • Some drugs and other toxins
  • Nephrosis sometimes is an early stage of kidney failure especially in those with Diabetes. Sometimes treatment of the underlying cause can correct the disorder before renal failure develops

Major consequences of the condition

  • Protein energy malnutrition
  • Increased risk of infection
  • Blood coagulation disorders
  • Accelerated atherosclerosis

Treatment

  • Involves both diet and drugs. Drugs include diuretics to reduce oedema, antibiotics and antinflammatory drugs

Diet

  • Central in preventing protein energy malnutrition, alleviating oedema and hyperlipidemia
  • Protein- give 0.8-1g/kgBWT (ideal). Use 75% of high biological value proteins for maximum utilization
  • CHO-give adequate CHO to spare protein and for maintenance of desirable weight. For malnourished patients give 35-50kcal/kg BWT, for obese patients give 25kcl/kg/BWT to help in losing weight. Restricted energy helps in control of lipids.
  • Fats -< 30% of the total energy. Low in saturated fatty acids to control the elevated blood lipid
  • Sodium-restrict due to oedema and sodium retention. Early treatment use low sodium level (250mg,/day) then progress to moderate restriction as the condition improves (300mg/day)
  • Adjust fluid intake to fluid output, which occurs through urine, vomiting and diarrhea. Volume of fluid intake is calculated from volume of urine passed in previous 24hrs. If urine out put is above 1000ml in 24 hours do not restrict, if out put is below 1000ml in 24 hours restrict by giving output equivalent plus 500ml, if no urine output give 500ml to 700ml

2. Glomerulonephritis

  • This is the inflammation of the glomerular capillaries loops. It can either be acute or chronic

Causes

  • Streptococcal infection
  • Shock (hypovolemia)
  • Drugs
  • Surgery in other parts of the body(related to shock)
  • This results to damage of the glomerular barrier, allowing large molecules of Red blood cells and proteins to be filtered out of the blood. It occurs mostly in children and young adults

Symptoms

  • Nausea and vomiting
  • Hematuria (blood in the urine)
  • Protenuria especially albumin
  • Odema (due to loss of protein
  • Oliguria (low urine output about 500mls)
  • Elevetaed blood nitrogen (BUN). It is also used as a measure of kidney functioning
  • Hypertension due to reduced blood flow

Chronic glomerunephritis

  • Occurs after repeated episodes of the acute phase leading to increased loss of nephrons. It is characterized by high loss of proteins and accumulation of metabolic waste

Management

Dietary

  • Na and fluids-restrictions depend on the level of fluid retention and presence of hypertension. In oliguria restrict fluids to 500mls plus previous days urine output
  • Salt should be 80-100ml/mols
  • Protein- restrict in uraemic patients to 0.6g/kg BWT in increased BUN

Renal failure

  • This is a condition in which the kidneys are no longer able to maintain the normal composition of the blood. Inability to excrete the daily load of waste (renal solute load)
  • Renal failure is both acute and chronic

Acute renal failure

  • A condition where nephrones suddenly lose function and are unable to maintain body homeostasis. The degree varies from mild to severe, with prompt treatment the condition can be reversed while in some cases the damage is permanent. The condition is characterized by a sudden decrease in glomerular filtration rate and inability to excrete metabolic wastes.

Causes

  • Fluid loses leading to dehydration as a result of diarrhea, vomiting, burns and excessive dieresis
  • Blood loss due to GIT bleeding, surgery or accidents
  • Due to hypotension or low blood pressure like in cardiogenic shock, heart failure or sepsis
  • Impaired vascular supply (renal artery thrombosis)
  • Drugs and poisons
  • Intrinsic renal disease
  • Obstruction like in prostate gland enlargement or renal stone

Consequences

  • Sudden reduction in GFR and urine output
  • Accumulation of waste products in the blood
  • Hyperkalemia-elevated blood potassium
  • Blood volume changes. In early stages the kidneys fails to excrete fluids and this can lead to pulmonary edema especially among the elderly
  • Clinical symptoms like uraemic syndrome due to toxic waste products acidosis may occur since hydrogen is not being excreted

Treatment

  • The goal is to treat the underlying disorders e.g rehydration incase of dehydration by use of IV fluids
  • Blood transfusion to restore blood volume
  • Dialysis (renal replacement therapy for restoring fluids and electrolyte balnce through removal of waste products
  • Diet therapy

Dietary management

  • In early stages patient are unable to eat since they are very sick, there may also be vomiting and diarrhea. TPN and Dialysis is normally used.
  • The patients are normally divided into three groups
  • Non catabolic patients
  • Moderate catabolic
  • Highly catabolic
  • Energy-initially due to diarrhea TPN are usually used to reduce protein catabolism, glucose and essential amino acids reduce catabolism more than glucose alone.
  • When oral intake is permitted a high energy diet should be provided, ranging between 35-50kcals/kgBWT (35 kals for non catabolic and 50 kcals for catabolic patients)

Proteins-requirements depend on renal function, metabolic rate and nutrition status. Those not on dialysis are given 0.6g/kg bwt to reduce nitrogenous waste. Majority (70-75% should be high biological value protein) those on dialysis, a more liberal intake is allowed as some proteins are lost in the process. Give 1.1-2.5g/kg BWT

Fluids-it is regulated according to urine output and any additional loss from vomiting, diarrhea, fever. In the oliguric phase little fluids are require about 500mls/day while in diuretic (recovery phase urine output increase therefore more fluid is allowed

Electrolytes

  • Sodium-restrict to 500-1000mg in oliguric phase and increase in diuretic phase

Potassium-requirements depend on serum levels and whether one is on dialysis or not. Normally restrict to <2gms/day in oliguric and do supplementation in diuretic phase. There is need for monitoring weight, fluids and electrolyte balance

Chronic renal failure

  • It is unirriversable destruction of kidney tissue by disease leading to insufficiency of renal excretory and regulatory functions. It is gradual in progression.

Causes

  • Nephritis or inflammation of the kidney
  • Hypertension
  • Diabetic nephropathy
  • Obstruction due to stones or prostate enlargement
  • Atherosclerosis

Stages of CRF

  • Stage 1-reduces renal reserve where about 50% of the renal function is lost. There may be no symptoms (creatinines may be normal)
  • Stage 2-renal insufficiency-over 25% of the kidney damaged. Creatinine clearance is 40mls,min. and the levels in the blood are 120-250mmols/liter
  • Stage 3-renal failure-creatine clearance is 20mls/min and creatine levels in the blood is above 300mmols/litre
  • Stage 4-end stage renal failure- over 90% of the renal tissue is damaged. GFR is 10-12mmol/min while normal is 95-155mmols/min. usually in this stage uraemic syndrome is present, some symptoms observed include;-shortness of breath, lethargy, tiredness, GIT irritability with diarrhea and vomiting, nausea, anorexia, thirst in some pple, weight loss, bad or metallic taste, low mental alertness, oliguria

Consequences

Bone disease or renal osteodystrophy

The kidney is unable to excrete phosphorus. Its level in the blood rises. Phosphorus forms salt with calcium which are deposited in the soft tissue like the lungs, heart, blood vessels and eyes and thus the level in the blood falls

The kidney is unable to effectively activate vitamin D which increases calcium absorption from the GIT. Thus all the above leads to renal osteodystrophy (oesteomalacia, oesteoporosis) all this are bone problems.

  • Hypocalcaemia-low blood levels of calcium
  • Hyperphosphotaemia-eleveted phosphorus levels
  • Hyperkaelemia-eveleted potassium levels
  • Sodium and fluids retention
  • Elevated lipids
  • Anaemia
  • Nitrogen retention
  • Increases BUN
  • Growth failure in children and wasting in adults

Management

  • Conservative management-diet and surgery alone
  • Replacement management -dialysis or use of artificial kidney
  • Transplant of kidney

Conservative management-diet and surgery alone

  • This is done prior to needing replacement therapy
  • Aims of dietary management
  • To retard progression of renal failure
  • To reduce and control the amount of waste products which accumulate in the body
  • To prevent or improve symptoms of uraemia
  • To maintain optimal nutrition status
  • To provide dietary freedom to lead a near normal life

Important nutrients in CRF

  • Proteins- it is important for repair and maintenance of tissue and for growth in children. The level of restriction should be sufficient to maintain vital body processes. Generally protein should be restricted to 0.6g/kg BWT and should be adjusted to the level the kidney can cope. Provide high biological value protein.
  • Energy-adequate amount are necessary to spare proteins and to ensure positive nitrogen balance. Too much energy is undesirable as it will be stored in the fatty tissue and can cause a problem during dialysis or transplant. Give 35-40kcals/kg BWT for people of normal weight. For obese people give 20-30 kcals/kgBWT. For malnourished or catabolic patients give 45-50kcals/kgBWT.
  • CHO-50% of energy should come from CHO
  • Fat -give 40% of the total energy. Due to dietary protein restriction
  • NB-hyperlipidemia is a common feature in CRF and it is thought not to be associated with refined CHO or fat but with kidney disease. There is no conclusive evidence that reducing fat or CHO will alter hyperlipidemia but however it is good to restrict saturated fats
  • Na and fluids-individual needs depend on blood electrolyte levels, blood pressure, urine output and edema. Restrict sodium in presence of edema and hypertension to a level of 2-3g per day.
  • For fluids give previous days output plus 500mls
  • Potassium-generally not restricted in non oliguric patients or urine output of >1000mls per day and a serum potassium of <5.5mmmols/litre. When serum potassium is >5.5mmols and urine <100mls, restrict urine output to upto 50-60mmols/day
  • Phosphorus-it is retained in renal failure. It should be restricted to 600-800mg/day. Doctors mostly prescribe phosphate binders with meals
  • Vitamins-water soluble vitamins such as B vitamins and folate and vitamin D may need supplementation as deficiency may occur due to poor appetite, altered metabolism and restricted diet. Vitamin D should be given under strict medical observation.
  • Calcium-oral supplementation of 100-1500mgs elemental calcium per day is recommended due to reduced intake and absorption. NB serum phosphate levels should be under control before calcium supplementation.

Dietary challenges

  • There may be challenges in achieving adequate energy because of protein restriction. Glucose polymers may be used plus other refined CHO, sweets, and soft drinks.
  • A lot of restrictions e.g K,Na, P, fluids it may difficult comply with the diet

Ways of boosting energy intake

  • Use of thick spread e.g jam and margarine
  • Add margarine to vegetables, mashed potatoes, and rice
  • Adding sugar to cereals
  • Drink soft drinks instead of water

Replacement therapy

  • This is normally done in end stage renal failure for sustaining life. GFR is normally <5mls /min.

Dialysis

  • This is removal of waste products from the blood using the principals of simple diffusion and osmosis through semi permeable membrane of artificial kidney.

Dialysate- is the fluid used in dialysis to remove waste products and excess fluids from blood. It is similar to plasma but with no waste products. Through osmosis and diffusion it clears the waste products in someone's blood

Main types of dialysis

Haemodialysis

The blood rich in nitrogenous waste is circulated from the body into a dialyser machine. The blood passes through a semipermiable membrane that is bathed in a dialysate fluid. The dialyser is made of sheets of memebranes to separate the blood or dialysate. As the blood circulates in the dialyser, waste products, electrolytes and water are exchanges by osmosis and diffusion. The purified blood is returned into the vein. The process takes 4-6hrs 3 times a week.

Disadvantages

  • Loss of proteins amino acids about 9-12 gms /6 hrs treatment
  • It is very costly
  • Risk of infection
  • Altered taste, anorexia, fatigue and nausea after haemodialysis

Perinoneal dialysis

It utilizes the semipermiable memebrane of the peritoneum which covers most of the abdominal cavity organs. A catheter or a tube is surgically inserted into the abdomen, then into the peritoneum cavity. Dialysate fluid is infused into the peritonila cavity via tubes. Waste nitrogenous products, excess fluids and electrolytes are exchanged from the blood through the pritonium by osmosis into dialysate fluid. The fluid is drained out and fresh dialysate instilled. The treatment takes 10-12 hrs 3 times per week. There is greater loss of proteins.

Continuous ambulatory peritoneal dialysis

This is similar or PD except that the dialysate is left in the peritoneum and exchanged manually so that no machine is required. A disposable bag with dialysate is connected permanent catheter in the peritoneum. The diaysate stays in the peritoneum for about 20-30 mins to allow for soln exchange. The bad is the lowered to allow the waste to flow or drain into the bag by force of gravity. Exchange of dialysate fluid is done 4-5 times daily and it is 24 hr treatment on continuous basis. Protein losses are higher than for the regular PD

  • Advantages
  • Avoidance of large fluctuations in blood chemistry
  • The patient can achieve a more normal lifestyle because they are mobile
  • With CAPD there is more liberal allowance for fluids, sodium and K since the therapy is continuous.

Disadvantages of peritoneal dialysis

  • More risk of infection than HD (inflammation of peritoneal cavity)
  • Weight gain- the dialysate contains glucose or dextrose.
  • There is greater loss of protein than in HD

Dietary management in dialysis

Kidney stone

  • They are formed when the concentration of components in the urine reaches a level in which crystallization is possible or when certain combinations of ions which are sparingly soluble in urine precipitate and become lodged in a section of urinary tract forming a nucleus around which a stone may grow.

Types of stones

  • They are classified according to chemical constituents. There are 4 main types.
  • Calcium- about 95%
  • Uric acid -3%
  • Cystinine 1%
  • Struvite-remaining %. it is combination of mg , ammonium phosphate and caPo4 , it is referred to as infection stones

Calcium stones

  • Calcium oxalate or calcium phosphate, caoxalate is caused by excess oxalate hyperoxaluria. (Elevated blood levels of oxalate) due to over production of oxalate)

Treatment

  • Reducing dietary intake of e.g tubers, spinach, strawberry and chocolate, wheat burns, nuts and tea.

Hypercalcuria

  • Over 200mg of Ca in 24hrs

Cause

  • Due to increased calcium absorption in GUT
  • Impaired renal calcium reabsorption
  • Excessive resorption of calcium from the bone due to hyperthyroidism

Treatment

  • A high protein diet increase calcium excretion. Give the RDA
  • Increase fluid intake to dilute concentration of calcium in the urine
  • Use thiazide diuretics which decrease urinary calcium
  • NB mild salt restriction) 4-5g/day improves thiazide effectiveness

Hyperuricosuria

Elevated uric acid in urine. This leads to formation of calcium oxalate stones rather than uric acid stones. Uric acid encourages formation of calcium oxalate stones by binding calcium inhibitors. Dietary animal proteins increase excretion of uric acid and calcium and decreases urinary citrate excretion which is a risk for stone formation.

Treatment

  • Protein intake should be as RDA
  • Potassium supplementation decreases calcium excretion and therefore reduces the incidence of stones.

Uric acid stones

  • This are associated with gout, malignant disease. Drugs such as asprin also increase uric acid excretion. The important factor in uric acid stones seems to be production of acidic urine.
  • Foods that will lead to acidic urine include, meat, fish, eggs, cheese, peanut butter, whole grain cereals, lentils,

Treatment

  • Increase fluid intake to increase urine Ph to 6-6.5 using alkalis such as sodium or potassium bicarbonate or citrate
  • A reduction of animal protein may be useful

Cystinine stones

  • It is a hereditary disorder of amino acid transport leading to high concentration of cystinine in the urine

Treatment

  • Dilution of urine through fluid intake of over 4 liters a day including drinking at night to form 3 liters of urine a day
  • Alkalinization of urine using sodium bicarbonate to increase urine PH to 7-7.4

Struvite stones

They are composed of ammonia, mg and phosphate. They are more common in women. They are formed when the urinary tract is infected by urea splitting organism. Urea is broken to ammonia leading to alkaline urine. The stones are completely insoluble in alkaline condition and will crystallize immediately.

Treatment

  • Surgery to remove the stone
  • Use of antibiotics
  • Acidification of urine by use of ascorbic acid and ammonia chloride
  • Diet has very little role in the stone