Hormone renal production

The progenitor cells of the kidney produce 90% of the hormone erythropoietin (EPO), which stimulates red blood cell (RBC) production. Reduction in nephron mass decreases renal production of EPO, which is the primary cause of anemia in patients with CKD. The development of anemia of CKD results in decreased oxygen delivery and utilization, leading to increased cardiac output and left ventricular hypertrophy (LVH), which increase the cardiovascular risk and mortality in patients with CKD. 

PTH and l,25(OH)2D enhance renal retention of calcium, but PTH promotes renal phosphate excretion. FGF23 is a recently discovered hormone that stimulates renal phosphate excretion and inhibits renal production of l,25(OH)2D. Other... 

The concentration of ionized calcium is closely regulated by the interactions of parathyroid hormone (PTH), phosphorus, vitamin D, and calcitonin (Fig. 49-9). Parathyroid hormone increases serum calcium concentrations by stimulating calcium release from bone, reducing renal excretion, and enhancing absorption in the gastrointestinal tract secondary to increased renal production of 1,25-... 

These two hormones, together with the vitamin calcitriol, regulate calciumhomeostasis and thereby indirectly affect phosphate metabolism. Parathyroid hormone (parathormone PTH) is secreted by the parathyroid glands as a polypeptide of 84 amino acid residues, and its action is to increase plasma calcium via parathyroid hormone receptors in bone, kidney, and a few other tissues. PTH secretion is increased in response to hypocalcemia and hyperphosphatemia conversely, increased plasma calcium suppresses PTH secretion. The renal production of 1,25-dihydroxycholecalciferol is also... 

Historically the only melanocortin peptide to be used clinically is the parent hormone from which all these peptides are derived from namely ACTH (see above). It has also been used in the treatment infantile spasms for epilepsy, where it is administered as an intramuscular injection only over a 2-12 weeks period. Obvious side effects include weight gain, puffy face, high blood pressure and an increased risk of infection and should never be administered to patients with diabetics, renal or heart failure. ACTH is also used as a stimulation test to measure adrenal cortex activity, i.e. production of cortisol and is used to ascertain whether someone has Addison s disease. 

Anemia may occur in patients with chronic renal failure as tlie result of the inability of the kidney to produce erythropoietin. Erythropoietin is a glycoprotein hormone synthesized mainly in the kidneys and used to stimulate and regulate the production of erythrocytes or red blood cells (RBCs). Failure to produce the needed erythrocytes results in anemia Two examples of drug used to treat anemia associated with chronic renal failure are epoetin alfa (Epogen) and darbepoetin alfa (Aranesp). 

Although the kidneys are not considered endocrine glands per se, they are involved in hormone production. Erythropoietin is a peptide hormone that stimulates red blood cell production in bone marrow. Its primary source is the kidneys. Erythropoietin is secreted in response to renal hypoxia. Chronic renal disease may impair the secretion of erythropoietin, leading to development of anemia. The kidneys also produce enzymes. The enzyme renin is part of the renin-angiotensin-aldosterone system. As will be discussed, these substances play an important role in the regulation of plasma volume and therefore blood pressure. Other renal enzymes are needed for the conversion of vitamin D into its active form, 1,25-d i hyd ro xyv itamin D3, which is involved with calcium balance. 

The main filtering units of the kidneys are called nephrons-, about one million nephrons are present in each kidney. Each nephron consists of a renal corpuscle and a unit called a tubule. Blood carrying normal metabolic wastes such as urea and creatine moves through a portion of the corpuscle called the glomerulus, where a filtrate forms that contains water, normal metabolic products, and also waste products the filtrate collects in another unit called Bowman s capsule. Glomerular filtrate then moves into a highly convoluted and multifaceted set of tubes - the tubule - where most useful products (water, vitamins, some minerals, glucose, amino acids) are taken back into the blood, and from which waste products are collected as urine. The relative amounts of water and minerals secreted or returned to the blood are under hormonal control. 

Therapy in those with ectopic erythropoietin production depends upon correcting the hormone level by removing whatever tissue is responsible for its production and examples include nephrectomy for renal carcinoma or the classical, albeit rare, cerebellar haemangioblastoma. Where metastases have occurred appropriate cytotoxic chemotherapy is needed and response in haematocrit becomes a rough indicator of the success with which the tumour is responding to therapy. In some individuals venesections are necessary to control the raised haemoglobin. 

Ethanol is a diuretic. This effect may be caused by its ability to inhibit secretion of antidiuretic hormone from the posterior pituitary, which leads to a reduction in renal tubular water reabsorption. The large amount of fluid normally consumed with ethanol also contributes to increased urine production. 

Clinical pharmacology Erythropoietin is instrumental in the production of red cells from the erythroid tissues in the bone marrow. The majority of this hormone is produced in the kidney in response to hypoxia, with an additional 10% to 15% of synthesis occurring in the hver. Erythropoietin functions as a growth factor, stimulating the mitotic activity of the erythroid progenitor cells and early precursor cells. Chronic renal failure patients often manifest the sequelae of renal dysfunction, including anemia. Anemia in cancer patients may be related to the disease itself or the effect of concomitantly administered chemotherapeutic agents. 

See Table 15-6. Potassium-sparing diuretics are most useful in states of mineralocorticoid excess or hyperaldosteronism (also called aldosteronism), due either to primary hypersecretion (Conn s syndrome, ectopic adrenocorticotropic hormone production) or secondary hyperaldosteronism (evoked by heart failure, hepatic cirrhosis, nephrotic syndrome, or other conditions associated with diminished effective intravascular volume). Use of diuretics such as thiazides or loop agents can cause or exacerbate volume contraction and may cause secondary hyperaldosteronism. In the setting of enhanced mineralocorticoid secretion and excessive delivery of Na+ to distal nephron sites, renal K+ wasting occurs. Potassium-sparing diuretics of either type may be used in this setting to blunt the K+ secretory response. 

Diabetes insipidus A disease marked by increased urination (polyuria) and excessive thirst (polydipsia) due to inadequate production of antidiuretic hormone (ADH) and/or a decrease in the renal response to ADH. 

Hyponatremia is caused by an excess of total body water relative to total body sodium and can result from a number of underlying conditions, including the syndrome of inappropriate antidiuretic hormone secretion (SIADH), cirrhosis, and congestive heart failure (CHF). In each of these conditions, inappropriate production of arginine vasopressin (AVP) [also known as vasopressin or antidiuretic hormone (ADH)], a neurohormone that regulates renal electrolyte-free water reabsorption, contributes to enhanced renal water retention, leading to decreased serum sodium concentrations.7 Hyponatremia can be characterized as hypervolemic, euvolemic, or hypovolemic... 

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