1. Waste excretion in urine
1.1. The kidney functions as the body's main excretory organ, eliminating the body's metabolic waste products . The major waste product of protein metabolism is urea, of which about 2- to 30 g are produced and excreted daily. All of this urea must be excreted in the urine, otherwise it accumulates in body tissues.
1.2. Metabolic wastes- urea, creatinine, uric acid, nitrogenous waste.
1.3. Drug metabolites-most pharmacological agents are detoxified in liver and then excreted through the kidney.
1.4. Excess ions - sodium, potassium, magnesium,
2. Regulation of Acid-base balance
2.1. Normal pH of body fluids is maintained by buffer systems of body fluids, the lungs and the kidneys. pH scale is a logarithmic scale (range 1-14) that measures the concentration of free hydrogen ions in a fluid. The scale is reciprocal, when pH is low, hydrogen ions is high. Normal pH is between 7.35-7.45.
2.1.1. Kidney controls the acid base balance by controlling the bicarbonate ions concentration in the body. An acid urine is formed if the pH of body fluids is in the acid range and the kidneys excrete more hydrogen ion than bicarbonate. An alkaline urine is formed if the pH of the body fluids in the alkaline range and the kidneys excrete more bicarbonate than hydrogen.
2.1.1.1. When the body is in acidosis, the kidney responds by increasing bicarbonate reabsorption and excess hydrogen ions are excreted.
2.1.1.2. When the plasma bicarbonate concentration is higher than normal, the bicarbonate reabsorption decreases, so the kidney increases bicarbonate excretion. Active secretion of hydrogen decreases and is retained in the body fluids.
2.2. The kidney's mechanism for regulating acid-base balance are bicarbonate reabsorption and hydrogen secretion, excretion of hydrogen by synthesis of ammonia and excretion of ammonium chloride. The processes primarily occur in the proximal tubule, distal tubule and collecting duct.
3. Erythropoietin production
3.1. When the kidneys sense a decrease in the oxygen tension in the renal blood flow, they release erythropoietin. Erythropoeitin stimulates the bone marrow to produce red blood cells, thereby increasing the amount of hemoglobin available to carry oxygen.
3.1.1. Erythropoeitin production is regulated by renal erythropoietin. With chronic kidney disease, anemia occurs, and hematocrit, hemoglobin and ethrocyte count are decreased.
4. Fluid volume balance
4.1. ADH- is secreted by the posterior pituitary gland and ADH receptors are found in collecting ducts of kidney tubules.
4.1.1. When there is rise in plasma osmolality, water is reabsorbed into the blood, diluting the plasma and reducing osmolality to normal.
4.1.2. A fall in plasma osmolality leads to decrease in ADH secretion by negative feedback. ADH receptors are found in collecting ducts of kidney tubules.
4.2. Aldosterone- is a steroid hormone secreted from the adrenal cortex of the kidney and effects the distal tubule of the nephron. Secretion of aldosterone is regulated by peptide, angiotensin II.
4.2.1. When more aldosterone is secreted, the more sodium is reabsorbed and therefore water is reabsorbed.
4.3. Atrial natriuretic peptide (ANP)- is released from cardiac atrial cells in response to stretch in atrium from fluid overload.
4.3.1. ANP inhibits aldosterone secretion by adrenal cortex, reduce renin release by kidney and reduction of ADH from the posterior pituitary to reduce the fluid volume by excreting sodium and water.
5. Electrolytes balance
5.1. Sodium is freely filtered through the glomerular capillaries of the kidneys, and although much of the filtered sodium is reabsorbed in the proximal convoluted tubule, some remains in the filtrate and urine, and is normally excreted.
5.1.1. Hyponatremia is a lower-than-normal concentration of sodium, usually associated with excess water accumulation in the body, which dilutes the sodium. AnAn abnormal loss of sodium from the body can result from several conditions, including excessive sweating, vomiting, or diarrhea; the use of diuretics..
5.1.1.1. Hypernatremia is an abnormal increase of blood sodium. It can result from water loss from the blood, resulting in the hemoconcentration of all blood constituents. Hormonal imbalances involving ADH and aldosterone may also result in higher-than-normal sodium values.
5.2. Potassium is excreted, both actively and passively, through the renal tubules, especially the distal convoluted tubule and collecting ducts. Potassium participates in the exchange with sodium in the renal tubules under the influence of aldosterone, which also relies on basolateral sodium-potassium pumps.
5.2.1. Hypokalemia is an abnormally low potassium blood level. An absolute loss of potassium can arise from decreased intake, frequently related to starvation. It can also come about from vomiting, diarrhea, or alkalosis.
5.3. Phosphate-is important in buffer systems to maintain the plasma pH and exists in equilibrium with calcium.
5.3.1. When plasma phosphate level is low, the filtered phosphate is reabsorbed in the early proximal tubule and if it is high, it is excreted in the urine.
5.3.2. Hyperkalemia, an elevated potassium blood level, also can impair the function of skeletal muscles, the nervous system, and the heart. Hyperkalemia can result from increased dietary intake of potassium.
5.4. Magnesium-also an important intracellular cation involved in energy storage and production.
5.4.1. Similar to calcium, increase in PTH, increase tubular reabsorption of magnesium.
6. Blood pressure regulation
6.1. A decrease in renal blood flow decreases sodium in chloride concentration in the area of macula dense. The macula densa, in turn, causes afferent arteriole dilatation. This increases glomerular blood flow and capillary hydrostatic pressure, thus maintaining the glomerular capillary pressure and GFR.
6.1.1. The opposite occurs if the GFR increases and there is an increased concentration of sodium and chloride int he macula dense. The macula densa dilates the afferent arteriole, resulting in relative vasoconstriction. Renin is secreted in response to decreased afferent arteriole pressure and in response to SNS stimulation.
6.1.1.1. Regulation of blood pressure is secondary to the regulation of glomerular blood flow. As blood flow to the glomerular capillaries increases or decreases, blood flow through the arteries and arterioles leading up to the glomerulus increases or decreases accordingly.
6.2. In cases where there is dehydration, sodium deficiency, or haemorrhage, there will be decrease in blood flow to the kidney.
6.2.1. Release of angiotensin II stimulates adrenal cortex to produce aldosterone which reabsorbed more sodium and water and eliminates potassium which increase blood volume and hypertension. If the level of circulating angiotensin II is extremely high, the resulting vasoconstriction can lead to hypertension.
6.2.2. This will stimulate kidney to renin, which in turn, converts angiotensinogen to angiotensin I. Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II, causing vasoconstriction. Efferent arteriole vasoconstriction impedes blood flow from the glomerular capillaries and helps maintain glomerular hydrostatic pressure and a normal GFR.