Fluid and electrolyte changes when creatinine decreases, where the ability to concentrate or dilute urine is impaired. Limitation of water intake can result in volume contraction and fluid hypernatremia, on the other hand, if salt and water intake is excessive, hyponatremia, edema or both can occur. Body fluids and substances or electrolytes / ions dissolved in them always tend to change due to metabolic processes. On the other hand, so that it remains constant, the kidneys help maintain the amount of electrolytes or ions within certain limits, so that there is no disturbance in the body and this is one of the functions of the kidneys. The process of hemostasis is by concentrating or diluting the urine, through a counter current process in the kidneys.4) In chronic renal failure, hyperkalemia, hyperkalemia, hyperphosphatemia, hypocalcemia and bicarbonate deficiency (metabolic acidosis) often occur.
Potassium is a cation with the highest number of cells in the cell. Maintaining the proper distribution of potassium across cell membranes is essential for normal cell function. Transfer of potassium between extracellular and intracellular is influenced by various endogenous and exogenous factors. The state of acidosis and alkalosis affects potassium, as it can compensate the protons movement (Hydrogen ions). In acidosis, the H + ions move to the cells, and to maintain the electrical balance, potassium is moved outside the cell. In alkalosis the opposite occurs.5)
The level of potassium of less than 3.5 mEq/L indicated hypokalemia and the level of potassium which is more than 5.3 mEq/L indicated hyperkalemia. One of the causes of hypercalemia is reduced renal excretion of potassium which occurs in hyperaldosteronism, renal failure, use of cyclosporine or due to excessive potassium ion correction and in cases receiving angiotensin-converting enzyme inhibitor therapy, and potassium sparing diuretic.5)
Potassium is passively handled in the kidneys by being reabsorbed at the proximal tubule end. Then, it is supplemented to tubular fluid at the henle arch’s descending limbs. The thick ascending of the henle arch is the major spot of the active potassium to be reabsorbed. The filtered potassium remain in the tubular lumen is only 10% to 15% at the end of the distal convoluted tubule. Potassium is primarily excreted by cortical collecting duct main cells and collecting duct outer medullary. The reabsorption of potassium takes place through intercalated cells in the medullary collecting duct. As the total potassium of the body is depleted, it reabsorption is increased. It reabsorption firstly moves in the medullary interstitium; however, it is secreted into the pars recta from the henle arch’s descending limb. The recycle of the medullary potassium, as part of its physiological role, can reduce “backleak” exit from the collecting tubule lumen or to increase renal secretion of potassium when potassium is overloaded.5)
The CKD patients with LFG less than 10-20% of normal can still maintain serum potassium concentrations. If the LFG is less than 25%, the activity of Na +, K +, ATPase will increase in the liver and muscle, so there will be an increase in the transport of potassium ions from extracellular to intracellular.6)
Hans et al, concluded that the occurrence of hyperkalemia in CKD can predict the occurrence of complications in the heart and mortality.7) This study contradicts the previous ones that a reduced LFG value can result in a significantly high serum sodium level. Serum and urine potassium concentrations can be independently associated with impaired renal function.8.9, 10)