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Impact of calcium, phoshporus and magnesium on renal diet

Diet plays a significant role in the management of kidney disease. Diet prescribed is based on the level of kidney function, body size, food tolerance, and any other medical condition. These changes may include limiting fluids, …

Diet plays a significant role in the management of kidney disease. Diet prescribed is based on the level of kidney function, body size, food tolerance, and any other medical condition. These changes may include limiting fluids, eating moderate /high protein diet, limiting salt, potassium, phosphorus and other electrolytes with getting enough nutrition (A.S.P.E.N). There is no single renal diet, it varies from patient to patient
Calcium, phosphorus and magnesium are vital for many biological and cellular functions. Kidneys to play a central role in homeostasis of these ions and gastrointestinal absorption is balanced by renal excretion.When stores of these ions decline significantly in the body, gastrointestinal absorption, bone reabsorption, and renal reabsorption increase to normalize their levels. Renal regulation of these ions occurs through glomerular filtration, tubular reabsorption and secretion.

It is difficult during hemodialysis to filter phosphorus from blood, therefore it is essential to limit foods that contain this mineral. Phosphorus can build to high levels in the bloodstream and cause weak bones, heart problems, joint pains, or skin ulcers. Doctors may prescribe a medicine called phosphorus binders to keep levels normal. Hyperphosphatemia usually becomes a problem in later stages of renal failures (stage 4 and 5 CKD or less than 20% kidney function) In healthy adults, the normal range is 0.80-1.45 mmol/l (Berndt and Kumar 2007)

In both CKD and dialysis patients the aim is to keep phosphate levels below 1.8 mmol /l It is same for patients with impaired kidney function until the glomerular filtration rate (GFR  falls below 30 ml per minute /1.73 m2- representing stage 4 CKD). At this point, serum phosphorus levels start rising and continue so as these patients reach ESRD- stage 5. Removal of phosphate during one hemodialysis session amounts to only 800 mg to1000 mg.It is extremely tough to limit phosphorus intake while attempting to meet the recommended daily protein requirement for patients on regular hemodialysis Administration of high doses of calcitriol  its analogues are also know to enhance active phosphate absorption from small intestine. These two main factors impede the patient’s efforts to control their phosphate burden. The 2003 K/DOQI guidelines proposed maintaining serum phosphorus levels in CKD-(non-dialysis) between 2.7mg/dL and 4.6mg/dL and between 3.5 and 5.5mg/dL in dialysis CKD(dialysis )  patients (Guideline 3, Evidence) Additional phosphorus additives found in food include

• Di-Calcium phosphate
• Disodium phosphate
• Monosodium phosphate,
• Phosphoric acid
• Sodium hexametaphosphate
• Trisodium phosphate

Bioavailability of vegetarian souses of phosphorus is less than non-vegetarian sources 

Managing hyperphosphatemia 
• Diet—restricting dietary phosphate intake
• Elimination – removing phosphate with dialysis
• Minimizing phosphate absorption, by using phosphate binders 

 Chicken. Seafood
 Nuts and seeds
 Whole grains, Amaranth quinoa
 Beans, soy, colas, baked   foods
 Milk and  milk products 

Adequate calcium intake in CKD patients is needed to prevent negative calcium balance.  Chronic kidney disease causes an imbalance in bone metabolism and increases the risk of bone renal osteodystrophy These imbalances can cause calcium to deposit in the blood vessels. If calcium levels are low, supplements may be prescribed. Sometimes calcium-basedd phosphorus binders are given to treat both low calcium and high phosphorus levels (The international journal of Reno vascular diseases)
Patients with serum level of corrected total calcium below the lower limit (less than 8.4mg/dl.)2.10mmol/l) should receive therapy to increase serum level calcium. The renal capacity of handling calcium varies in different staged of CKD and sometimes calcium excretion is diminished rather than enhanced. Positive calcium balance arises easily as intestinal absorption of calcium is greater than kidney’s capacity of excretion. It is important to emphasize that calcium from phosphorus binder is also absorbed and needs to be considered while calculating total calcium intake in patients (KDOQI clinical practice guidelines)RDA for calcium is 1gm/d which is sufficient to prevent a negative calcium balance however for CKD patients the precise dose has not been accurately determined .This aspect is more fundamental in patients with ESRD here calcium balance is effected by influx or efflux  from the dialysate. High calcium intake should be avoided  since patient with CKD may encounter difficulties in buffering increased calcium loads and may result in hypercalacemia {NKF guidelines (KDOQI)}If calcium levels are high ,high calcium foods ,supplements and calcium based phosphorus binders may be limited or avoided .
The KDOQI goal range for calcium is between 8.4 to 10.2mg/dl .Calcium levels above 10.2 are considered high and may require an adjustment in diet and decrease in vitamin D therapy 
An impaired gastrointestinal absorption related to low 1,25 dihydroxy Vit D3 levels and decrease renal excretory capacity may render kidney failure patients at risk of either negative or positive calcium balance .Total calcium intake should be between 800-1200mg/dl to prevent hypo or hypercalacemia 

While calculating one has to calculate corrected calcium level and which should be within the normal range. 

Despite the great importance of calcium in heath, its administration may not always be healthy .Calcium should be regarded as a therapeutic agent in CKD  and it requires careful scrutiny of its risk and benefits before being prescribed . The 2003k/DOQI guidelines advice maintaining   serum levels of total calcium, corrected for albumin levels within normal range for laboratory (Guidelines 6, opinion )

Factors that alter renal regulation of calcium 
Increase calcium absorption decrease calcium absorption
Hyperparathyroidism Hyporparathyroidism
Calcitrol Low calcitrol levels
Hypocalcemia Hypercalcemia
Volume contraction Extracellular fluid expansion 
Metabolic alkalosis Metabolic acidosis
Thiazides diuretics Loop diuretics 

Food sources of calcium 
• Seeds and nuts, figs 
• Milk and milk products
• Leafy vegetables, amaranth , ragi 
• Tofu, soybean, 

Ten to fifteen % of hemodialysis patients have been reported to have hyper serum magnesium(Mg) Hypermagnesemia is  when Mg levels are >2.6mg/dl(1.05mmols )Concentration is linked generally to dietary magnesium however adherence to dietary recommendation in hemodialysis patient is low . In case of CKD renal regulating mechanism may be insufficient to balance intestinal Mg absorption. Usually, Mg remains normal however when glomerular filtration rate(GFR) declines changes in serum Mg are observed .Patients with ESRD  are largely dependent on dialysate Mg concentration for maintain Mg levels although it has been suggested to be beneficial in these patients assuming a normal GFR kidney filters approximately 2000-2400mg of Mg/day. This takes into account that only 70% of Mg is available for filtration other 30% is protein bound .Under normal condition 96% of filtered Mg is reabsorbed in renal tubules by several transport processes Intake and increased intestinal absorption of Epsom salts and Mg containing cathartics, antacids laxatives use, long term parental nutrition and enemas lead to hypermagnecemia .Serum Mg levels are also increased when GFR falls below 20-30ml/min. Sometimes in more advanced CKD (as creatinine clearance falls <30 mL/min), this compensatory mechanism becomes inadequate such that overt hypermagnesaemia develops frequently in patients with creatinine clearances <10 mL/min.(Clinical kidney journal) Loop diuretics and long term administration of thiazides can induce hypomagnesaemia generally. 

Intestinal absorption of Mg can also be influenced by calcium and vice versa (for review see Hardwick et al.)high doses of 1.25 dihdryoxy Vit D3 increases the absorption of Mg. 

Whole body balance of calcium phosphate and Mg is maintained by fine adjustment of urinary excretion to equal the net intake .

Sources of Mg rich foods 
• Green leafy vegetables
• Banana, raspberries ,figs , avocados
• Seeds and nuts
• Kidney beans, chickpeas, black beans
• Peas, broccoli, Green beans, asparagus, Brussels sprouts
• Salmon fish, tuna, mackerel
• Dark chocolate, Tofu, whole grains

Magnesium rich foods are also rich in potassium


The importance of kidney in maintain normal calcium ,phosphorus and Mg homeostasis can be seen in renal failure and in these  patients .The abnormalities of above minerals is very common.  It is directly related to levels of   GFR, creatinine clearance and stages of kidney diseases 

1) A.S.P.E.N Clinical guidelines :nutrition support in Adult Acute and Chronic Renal Failure 
2) Articles from International Journal of Nephrology and Reno vascular  disease Dis Sakaguchi, Y.,                   fuji  N., Shoji, T. et al. Hypomagnesaemia as a significant predictor of cardiovascular and non-cardiovascular mortality in patients undergoing hemodialysis. Kidney Int. 2013; 85: 174–181
3) Factors associated with magnesia in patients with chronic kidney disease Division of Nephrology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Kaohsiung, Taiwan
4) Reduced Mortality in Maintenance Hemodialysis Patients on High versus Low Dialysate Magnesium: A Pilot Study Christopher Schmaderer, Matthias C Braunisch , YanaSuttmann , Georg Lorenz , Dang Pham , Bernhard Haller , Susanne Anger Mann, Julia Matschkal , Lutz Renders , Marcus Baumann , Jürgen R. Braun , Uwe Heemann and Claudius Küchle
5) Chiu Y.W., Teitelbaum I., Misra M., de Leon E.M., Adzize T., Mehrotra R. Pill burden, adherence, hyperphosphatemia, and quality of li
fe in maintenance dialysis patients. Clin. J. Am. Soc. Nephrol. 2009;4:1089–1096
6) K/DOQI clinical practice guidelines for bone metabolism and disease in chronic kidney disease. Am J Kidney Dis. 2003;42:S1–201
7) Magnesium in chronic kidney disease Stages 3 and 4 and in dialysis patients John Cunningham,1 Mariano Rodríguez,2 and Pier Giorgio Messa

Guljeet kaur 
(Head Clinical Nutrition dep’t Fortis Escorts Hospital Amritsar)

Dr. Hilal.A.Malla
(Head Nephrology Fortis Escorts Hospital, Amritsar)

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