NUTRITION AND KIDNEY/RENAL DISEASE
The important function of the kidneys i.e. nephrons, is to maintain the normal composition and volume of blood. This is done by excretion of nitrogenous and other metabolic wastes, by regulation of electrolytes and fluid excretion in order to maintain fluid balance, by maintaining acid base balance and by synthesis of other enzymes and other substances that influence metabolic activities. The nephrons filter most constituents of the blood other than red blood cells and protein, reabsorb needed substances, secrete hydrogen ions to maintain acid-base balance, and excrete unneeded materials in concentrated urine.
The kidneys may be affected by many different diseases but the ways in which renal function may be impaired and require dietetic treatment are relatively few. These are glomerulonephritis, nephrosis / nephrotic syndrome, acute renal failure and chronic renal failure.
GN is specific form of renal inflammation particularly involving the glomeruli as a result of reaction between circulating streptococcal toxins and antibodies present in cells of the glomeruli.
Type I cases: have an abrupt onset, usually one or two weeks after an acute streptococcal infection.
Symptoms: Blood and protein may be found in the urine along some nitrogen retention. Urine output decreases or in some cases there may be no urine output. Swelling around the ankles, puffiness around the eyes, headache, nausea and vomiting are very common symptoms.
Fluid balance: The input should match the output. If it is seen that the urine is diminished, then the intake of fluids should be between 500-700 ml/day.
Protein: Unless renal failure develops or there is diminished urine output protein is not is not restricted. An adequate protein intake can be given. However, if protein restriction is necessary, a diet not exceeding 40g protein is used. If there is loss of albumin in urine, then the protein intake may be increased in proportion to the protein lost in it. Protein of high biological value is preferred.
Energy: Caloric value of the diet is according to the requirements of the person’s height, age and sex. When protein intake is lowered then calorie intake is met by using sources which yield calories but no protein.
Symptoms include proteinuria, haematuria, hypertension and vascular changes in the retina. Frequent urination and nocturia are seen. In some persons, nephrotic syndrome characterized by massive oedema and severe protein losses through urine may develop.
Protein: when protein loss through the urine is found, the protein intake may be increased to compensate for the losses. But, if retention of urea nitrogen in blood is seen then the protein in diet must be decreased to 40 g or les per day.
Carbohydrates and fat: the energy needs from these sources should be met as per the requirements so that there is no breakdown of protein for energy.
Sodium restriction: this may be done to supply 500-1000 mg sodium in the diet if oedema is present. Mild sodium restriction may be advised even if there is no oedema.
It is the inflammation of the nephron. It is characterized by group of symptoms resulting from kidney damage and impaired nephron function. In nephrotic syndrome, an injury to the glomerular basement membrane causes an increased glomerular permeability, resulting in the loss of albumin and other plasma proteins in the urine. Urinary protein losses greater than 3-3.5 grams per day usually indicate nephrotic syndrome. Although, albumin synthesis in the liver is increased in nephrotic syndrome, it is not enough to compensate for losses in the urine. The loss of albumin leads to edema.
Low albumin levels also trigger cholesterol and lipoprotein synthesis in the liver, resulting in hyperlipidemia. At the same time, hepatic catabolism of serum lipoproteins is reduced and urinary excretion of HDL is increased. It is the clinical state of hypoproteinemic oedema associated with marked proteinuria irrespective of its etiology. Cases of nephrosis may occur from infancy to extreme old age. It is most common in young children with 80% of the cases occurring under 15 years of age.
A good diet plan can replace lost protein and ensure efficient utilization of ingested proteins through provision of adequate calories. Dietary changes can also help control hypertension, oedema, malnutrition, massive loss of protein and hyperlipidemia, and slow the progression of renal disease.
Energy: Calorie intake should be adequate to achieve and maintain ideal body weight and maintain protein stores. Foods rich in complex carbohydrates should provide the majority of calories. The food must be appetizing and easily tolerated.
Protein: replacement of the prolonged protein loss is a most immediate and fundamental need. A high protein intake is associated with a positive nitrogen balance and so a high protein diet is recommended for these patients.
Lipids: A diet low in saturated fat and cholesterol, combined with loss of excess weight, is recommended to reduce the risk of cardiovascular disease.
Sodium and Fluid: A limit on sodium of 500mg per day is usually recommended to control edema and hypertension. Diuretics may also be used. A fluid restriction is not warranted unless renal failure occurs.
Calcium and potassium: potassium restriction is not necessary as the symptoms of oliguria and anuria are not present. In some patients with severe and prolonged proteinuria, deficiency of calcium and potassium may occur resulting in bone rarefaction and hypokalemia.
ACUTE RENAL FAILURE
Acute renal failure, manifested by oliguria or anuria, usually occurs suddenly and is often reversible. It is marked by a reduction in the glomerular filtration rate and a modification in the kidneys ability to excrete metabolic wastes.
The disturbed renal function is exhibited in two phases:
An oliguric phase – it immediately follows the precipitating event and may last for few days to several weeks. The excretion of water, sodium, potassium, and nitrogenous wastes are all reduced as there is increased breakdown of damaged tissue leading to increased release of intracellular potassium, there is danger of hyperkalemia which is life threatening. The BUN rises alarmingly. The blood creatinine, phosphate and sulphate also increase. The blood levels of sodium, calcium and bicarbonate are decreased.
The diuretic phase – after passing little or no urine for two weeks or more, the patient may start passing moderate amount of urine proceeding to larger volumes. But the urine contains too little urea and too much sodium and potassium at this time. When diuresis is established, the urine volume gradually increases between 3-5 litres /day and the excretion of sodium, potassium, urea and other solutes also increase.
Protein: A low-protein diet is recommended initially. During the acute phase, no protein should be given. As the condition improves, only 20g protein daily should be given which is the minimum amount required to compensate for endogenous losses.
Calories: As protein is usually quite restricted, calorie needs may be met by providing greater amounts of carbohydrate and fat in the diet. A daily intake of 100-200g or more of sugar has a marked protein sparing effect, helps to reduce the weight loss, also prevent keto-acidosis.
Sodium and Fluid: Sodium is restricted depending on urinary excretion, edema, serum sodium levels, and dialysis needs. During the oliguric phase, sodium may be restricted to 500-1000 milligrams per day, and fluid requirements are based on replacing losses via urine, vomitus, and diarrhea, plus approximately 500 ml/day.
CHRONIC RENAL FAILURE - URAEMIA
It is the final common pathway of many different diseases. The common causes are:
Metabolic diseases with renal involvement like diabetes.
Exposure to toxic substances or prolonged use of certain drugs.
Infections causing obstruction to the urinary tract
Renal tubular disease
There are progressive degenerative changes in renal tissue markedly affecting all renal functions. Many complex biochemical changes occur. These include elevation of BUN, disturbances in hydrogen ion concentration and abnormalities in water and electrolyte balance.
Protein – Its intake should be sufficient to prevent tissue protein catabolism at the same time not too excess so as to lead to uremia.
Energy – Sufficient non-protein calories in the form of carbohydrate and fat is essential to spare protein for tissue protein synthesis as well as to meet energy needs.
Water - There is a danger of both water intoxication from overloading as well as dehydration due too little water intake as the capacity of failing kidneys to handle water is limited. Therefore the fluid intake has to be monitored carefully.
Sodium – Since sodium is chief ion determining the ECF osmolarity, its dietary need is closely related to the handing of water by the patient’s body. The need for sodium varies and both severe restriction and excess are to be avoided.
Potassium – The potassium has to be adjusted to maintain normal levels in blood. In severe vomiting and diarrhea, significant losses of potassium can occur, and potassium supplementation may be needed. However the failing kidney can’t clear potassium adequately and therefore the dietary potassium is kept at about 1500 mg/day.
Kidney stones may be found in the kidney itself, ureter, bladder or the urethra. Different types of calculi occur under different circumstances.
Stones usually result from the crystallization of calcium (which are originally present in some in foods or supplements) and oxalate, a part of many plant foods, when diet is mainly derived from fruits and vegetables. Kidney stones can also form from uric acid, which is a breakdown product of protein, or from struvite (ammonio-magnesium phosphate) or cystine.
Nutritional steps are important in preventing stones and can also help prevent recurrences.
Fluid intake - It should be increased depending on the tolerance of the patient, since it helps dilute the urine which discourages the constituents of the stone.
Diet – It may involve restriction of the mineral which is the main constituent of the stone. For E.g. Calcium and oxalates are restricted when these are the main constituent of the stones.
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