Renal reabsorption system

Amino acids are precious components of the human organism and therefore urinary losses are small due to an efficient renal tubular reabsorption system. Because of this, and because the analytical approach is aimed at detecting catabolic... 

Reference values for amino acids in the urine show a rather sharp decrease from the neonatal period to adulthood (Table 2.1.6). This is mainly due to the maturation of the renal tubular reabsorption system, but is also the result of increasing muscle mass with age, giving rise to increasing creatinine production. 

Mineralocorticoids are involved in controlling electtolyte and fluid levels.9,44 The primary mineralo-corticoid produced by the adrenal cortex is aldosterone. Aldosterone increases the reabsorption of sodium from the renal tubules. By increasing sodium reabsorption, aldosterone facilitates the reabsorption of water. Aldosterone also inhibits the renal reabsorption of potassium, thus increasing potassium excretion. Mineralocorticoid release is regulated by fluid and electrolyte levels in the body and by other hormones, such as the renin-angiotensin system. 

Much that is known about renal reabsorption mechanisms has been learned from the study of various forms of aminoaciduria. Three types of aminoaciduria have been identified (1) overflow aminoaciduria occurs when the plasma level of one or more amino acids exceeds the renal threshold (tubular capacity for reabsorption) (2) renal aminoaciduria occurs when plasma levels are normal but the renal transport system has a congenital or acquired defect and (3) no-threshold aminoaciduria occurs when excessive amounts of an amino acid, arising from an inherited metabolic block, are present in urine, but plasma levels are essentially normal because ah the amino acid is excreted. The no-threshold aminoacidurias, such as homocystinuria, are not due to congenital or acquired kidney defects but solely to saturation of the normal renal tubular reabsorption mechanisms. 

Since 1,25-(OH)2D3 production responds slowly to parathyroid hormone a more quickly-reacting system is needed to prevent low calcium tetany. Parathyroid hormone secretion and action is very rapid as is the lifetime of the hormone itself Thus parathyroid hormone can, with endogenous 1,25-(0H)2D3, stimulate the mobilization of calcium from bone and renal reabsorption of calcium but not intestinal absorption Nevertheless, plasma calcium rises but... 

In the normal human kidney 98-100% of the filtered urate is reabsorbed. Substrate regulated secretion and postsecretory reabsorption of urate are considered to be the quantitatively most important renal transport systems for the regulation of the urinary excretion of urate (7). 

Monoacetylpolyamines that are reabsorbed by the renal tubular system are converted to free polyamines by acetylpolyamine oxidase (APAO) and subsequently reutilized in the body. Importantly, DiAcSpm is not reabsorbed by this route. It is likely that the total amount of DiAcSpm excreted from cells is recovered in the urine without significant loss, whereas the amount of urinary monoacetylpolyamines decreases by an unknown amount compared to that originally excreted from the cells as a result of renal reabsorption and subsequent reutilization. 

Hyperaldosteronism is a syndrome caused by excessive secretion of aldosterone. It is characterized by renal loss of potassium. Sodium reabsorption in the kidney is increased and accompanied by an increase in extracellular fluid. Clinically, an increased blood pressure (hypertension) is observed. Primary hyperaldosteronism is caused by aldosterone-producing, benign adrenal tumors (Conn s syndrome). Secondary hyperaldosteronism is caused by activation of the renin-angiotensin-aldosterone system. Various dtugs, in particular diuretics, cause or exaggerate secondary peadosteronism. 

Vasopressin (antidiuretic hormone) is a peptide synthesized in the hypothalamus and secreted from the neurohypophysis of the pituitary gland. This substance plays an important role in the long-term regulation of blood pressure through its action on the kidney to increase reabsorption of water. The major stimulus for release of vasopressin is an increase in plasma osmolarity. The resulting reabsorption of water dilutes the plasma toward its normal value of 290 mOsM. This activity is discussed in more detail in Chapter 10 (the endocrine system) and Chapter 19 (the renal system). 

The answers are 370-c, 371-d, 372-c. (Hardman, pp 697, 701, 705.) The loop diuretic ethacrynic acid has its site of action in the ascending limb of the loop of Henle. This drug inhibits the reabsorption of Na and Cl" by interfering with the Na+, K+, 2CL co-transport system. In addition, loop diuretics block the reabsorption of Mg and Ca from the renal tubular fluid into the blood in this segment of the nephron unit. 

Vasopressin is a potent vasoconstrictor that increases blood pressure and systemic vascular resistance. It may have several advantages over epinephrine. First, the metabolic acidosis that frequently accompanies cardiopulmonary arrest can blunt the vasoconstrictive effect of epinephrine this does not occur with vasopressin. Second, stimulation of P receptors by epinephrine can increase myocardial oxygen demand and complicate the postresuscitative phase of CPR. Vasopressin can also have a beneficial effect on renal blood flow in the kidney, causing vasodilation and increased water reabsorption. 

Decreases Ca transport into cells, interferes with Ca -Na active transport system, increases renal tubular reabsorption of Ca and increases serum Ca and parathyroid concentrations ... 

Pregabalin is eliminated from the systemic circulation primarily by renal excretion as unchanged drug, with a mean elimination half-life of 6.3 hours in subjects with normal renal function. Mean renal clearance was estimated to be 67 to 80.9 mL/min in young healthy subjects. Because pregabalin is not bound to plasma proteins, this clearance rate indicates that renal tubular reabsorption is involved. Pregabalin elimination is nearly proportional to Ccr. 

Other actions of kinins include activation of clotting factors simultaneously with the production of bradykinin. In the kidney, bradykinin production results in an increase in renal papillary blood flow, with a secondary inhibition of sodium reabsorption in the distal tubule. In the peripheral nervous system, bradykinin is important for the initiation of pain signals. It is also associated with the edema, erythema, and fever of inflammation. 

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