Potassium ions renal secretion

Figure 3j5. A. The movements of hydrogen and potassium ions between intra- and extracellular fluid compartments produced by a fall in hydrogen ion concentration of the extracellular fluid. B. Similarly for a fall in potassium ion concentration of the extracellular fluid. C. Movements of ions between the renal tubular fluid and the renal interstitial fluid sodium, chloride and bicarbonate are reabsorbed, hydrogen and potassium ions are secreted.

Triamterene is a pyrazine derivative that inhibits reabsorption of sodium ions without increasing excretion of potassium ions. It exhibits the same approximate effect as spironolactone however, it does not competitively bind with aldosterone receptors. Its action does not have an effect on secretion of aldosterone or its antagonists, which are a result of direct action on renal tubules. 

Major functions of the distal nephron include the regeneration of bicarbonate, the excretion of acid (hydrogen ion), the secretion of potassium, and the reabsorption of water. Damage to this portion of the nephron may present as significant acidemia and either hypo-or hyperkalemia, depending on the mechanism of injury. For example, amphotericin B produces small pores in the luminal membrane of distal tubular cells. These pores allow small molecules such as potassium to leak out the molecules are then wasted in the urine. Consequently, amphotericin B nephrotoxicity is characterized by hypokalemia secondary to renal potassium wasting. ATN is associated with urinary sediment characterized by the presence of tubular cells, coarse granular casts, and rarely, RBC casts. 

In type II renal tubular acidosis there is a defect in the secretion of hydrogen ions by the proximal tubule. Because the proximal tubule is the major site of bicarbonate reabsorption (4000 mEq of bicarbonate per day as compared to 70 mEq in the distal tubule), the defect in secretion of hydrogen ions in this condition leads to the flooding of the distal tubule with bicarbonate. The capacity of hydrogen ions secreted by the distal tubule to buffer this massive efflux of bicarbonate is soon overwhelmed and, as a result, large quantities of bicarbonate are excreted in the urine. Much more bicarbonate needs to be administered in this condition to correct the acidosis than is necessary in type I renal tubular acidosis. In general, in renal tubular acidosis the impairment in hydrogen ion secretion leads to excretion of potassium ions in urine. 

These observations on the effect of body fluid volumes and electrolyte concentrations on aldosterone secretion may have some bearing on the pathogenesis of classical clinical changes. For example, in renal tubular acidosis there is an obligatory sodium loss. The plasma potassium levels are decreased, and aldosterone secretion is stimulated. The administration of bicarbonate, a procedure which usually leads to potassium diuresis, induces potassium retention in these cases. To explain such intricate interactions between hormonal secretion, body fluid volume, and ion concentration, one could assume that the sodium loss, which is obligatory in renal acidosis, leads to reduction in the body fluid volume followed by a loss of potassium. The administration of bicarbonate, which prevents sodium loss and thereby influences the body fluid volume, reduces aldosterone secretion and prevents the loss of potassium ions. 

Additional epithelial aqueous pathways of significantly smaller radius (<3 A) have also been documented utilizing both equivalent pore and circuit theory [25], These pathways may correspond to specific channels through lipid membranes as opposed to paracellular pathways. Osmotically activated ion channels [35] and even specific water channels [36] have been characterized in renal epithelia. In intestinal epithelia, mucosal chloride channels have been studied in secreting crypt cells, and basolateral potassium channels in colonic epithelia serve cellular ion and volume homeostatic functions. 

Tubular secretion is the transfer of substances from the peritubular capillaries into the renal tubule for excretion in urine. This process is particularly important for the regulation of potassium and hydrogen ions in the body it is also responsible for removal of many organic compounds from the body. These may include metabolic wastes as well as foreign compounds, including drugs such as penicillin. Most substances are secreted by secondary active transport. 

Selective Aldosterone Deficiency (Type IV RTA). In type IV RTA, there is failure of distal potassium and hydrogen ion secretion because of aldosterone deficiency or resistance. This may occur because of a range of steroid or steroid receptor synthetic defects or because of hyporeninemic hypoaldosteronism (e.g., due to diabetic nephropathy, tubulointerstitial disease, urinary obstruction, renal transplantation, or SLE). Hyperkalemia, although mild, is a usual manifestation. 

Henle (e.g., furosemide, bumetanide, and torsemide) and distal convoluted tubule (thiazides), have most commonly been associated with the generation of metabolic alkalosis. These agents promote the excretion of sodium and potassium almost exclusively in association with chloride, without a proportionate increase in bicarbonate excretion. Collecting duct hydrogen ion secretion is stimulated directly by the increased luminal flow rate and sodium delivery, and indirectly by intravascular volume contraction, which results in secondary hyperaldosteronism. Renal ammoniagenesis may also be stimulated by concomitant hypokalemia, further augmenting net acid excretion. 

Alternative explanations have been considered to determine whether lead can induce hypertension in the absence of chronic renal disease [47, 51]. One postulated mechanism involves an alteration in intracellular calcium concentration by lead so as to cause an increased tonic contraction of arterioles leading to hypertension. Others have suggested a direct effect of lead on juxtaglomerular cells leading to an increase in renin secretion. Others have suggested alterations in renal ion transport, particularly relating to an effect of lead on sodium potassium ATPase. 

Potassium depletion has been reported in hyperparathyroidism (B9). This would be expected if there was impaired hydrogen ion secretion into the renal tubule such impairment may be associated with a compensatory increase in potassium secretion in exchange for sodium. Magnesium depletion has also been described, and parathyroidectomy is followed by magnesium retention (Bl). It is thought that these effects may be the result of the action of the hormone on bone (F6). 

From the point of view of potassium balance, there is increased renal excretion of potassium, loss of potassium in the vomitus and no potassium being delivered for absorption in the alimentary tract. All these factors contribute to a severe depletion of the body s total potassium content. Yet another factor contributes to potassium loss. A drop in volume of the circulating blood leads to aldosterone secretion via the renin-angiotensin mechanism which, in turn, promotes sodium reabsorption in the renal tubule this contributes further to excessive renal loss of potassium and hydrogen ions. The acidity of the urine is inappropriate as a response to metabolic alkalosis, but the preservation of electrolyte and fluid volume takes precedence over the acid-base disturbance. These various efiects all combine to yield a positive feedback system driving the metabolic alkalosis which, if not treated, reaches lethal levels in a few days. 

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