Kidney sodium homeostasis

Bonventre JV, Leaf A. Sodium homeostasis Steady states without a setpoint. Kidney Int 1982 21 880-883. 

Inasmuch as sodium intake may vary considerably, the maintenance of sodium homeostasis requires a broadly adjustable mechanism of renal sodium excretion and reabsorption. Regulatory mechanisms for sodium reabsorption in the kidney include (1) rapid adjustment of the levels of tubular reabsorption through the glomerular filtration rate (2) secretion of aldosterone, which stimulates sodium reabsorption (3) the possible elaboration of a natriuretic hormone that stimulates secretion. 

Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP) are members of a family of so-called natriuretic peptides, synthesized predominantly in the cardiac atrium, ventricle, and vascular endothelial cells, respectively (G13, Y2). ANP is a 28-amino-acid polypeptide hormone released into the circulation in response to atrial stretch (L3). ANP acts (Fig. 8) on the kidney to increase sodium excretion and glomerular filtration rate (GFR), to antagonize renal vasoconstriction, and to inhibit renin secretion (Ml). In the cardiovascular system, ANP antagonizes vasoconstriction and shifts fluid from the intravascular to the interstitial compartment (G14). In the adrenal cortex, ANP is a powerful inhibitor of aldosterone synthesis (E6, N3). At the hypothalamic level, ANP inhibits vasopressin secretion (S3). It has been shown that some of the effects of ANP are mediated via a newly discovered hormone, called adreno-medullin, controlling fluid and electrolyte homeostasis (S8). The diuretic and blood pressure-lowering effect of ANP may be partially due to adrenomedullin (V5). 

Chronic renal failure is a common consequence of diabetes but this case is complicated by the loss of fluid and electrolytes (sodium and potassium) due to diarrhoea and vomiting. Normally, the kidneys would respond to such a challenge and maintain homeostasis but Mrs Amin s kidneys were unable to do so. Mrs Amin was put on haemodialysis and treated to control the diabetes. 

A variety of renal diseases may interfere with the kidney s critical role in volume homeostasis. Although renal disorders will occasionally cause salt wasting, most kidney diseases cause retention of salt and water. When loss of renal function is severe, diuretic agents are of little benefit, because there is insufficient glomerular filtration to sustain a natriuretic response. However, a large number of patients with milder degrees of renal insufficiency can be treated with diuretics when they retain sodium. 

The primary organ for the regulation of sodium, potassium, calcium, and magnesium is the kidney. An intricate series of physiological sensing elements and hormonal response mechanisms maintains homeostasis. A variety of diuretic drugs can be used to enhance urinary output of various soluble salts, primarily sodium and potassium chloride. Profuse sweating is also a pathway of excretion for soluble salts and occasionally zinc. ... 

In addition to vasodilatory responses, PGs have a number of other effects in the kidney. For example, PGs stimulate adenylate cyclase in juxtaglomerular cells, resulting in an increase in cAMP production this, in turn, increases renin release. Renin stimulates the release of aldosterone, which increases renal tubular secretion of potassium (Stillman Schlesinger 1990). PGs also enhance tubular excretion of sodium and water (Patrono Dunn 1987). By causing these effects in the kidneys, PGs can alter electrolyte homeostasis. Therefore, other renal side-effects of NSAID therapy can include hyperkalemia, hypernatremia and edema. Often these metabolic changes are not observed in individuals with normal renal function, but in the presence of pre-existing disease they can become clinically significant. 

Under normal conditions each of the two million nephrons of the kidney work in an organized approach to filter, reabsorb, and excrete various solutes and water. The kidney is a primary regulator of sodium and water as well as acid-base homeostasis. The kidney also produces hormones necessary for red blood cell synthesis and calcium homeostasis. Impairment of normal kidney function is often referred to as renal insufficiency. Based on the time course of development, renal insufficiency has historically been divided into two broad categories. Acute renal failure (ARF) refers to the rapid loss of renal function over days to weeks. Chronic kidney disease (CKD)", also called chronic renal insufficiency (CRI) by some, is defined as a progressive loss of function occurring over several months to years, and is characterized by the gradual replacement of normal kidney architecture with interstitial fibrosis. Progressive kidney disease or nephropathy is... 

Maintenance of fluid volume, osmolarity, electrolyte balance, and acid-base status are aU regulated in large part by the kidney. Homeostasis of sodium, potassium, chloride, calcium, magnesium, and phosphorus is altered due to changes in urinary excretion that occur in patients with impaired kidney function. A comprehensive discussion... 

Kidney dysfunction can lead to edema formation as a result of decreased formation of urine and the subsequent imbalance of water and electrolyte (e.g., sodium ion) homeostasis. Retention of salt and water results in an expansion of the extracellular fluid volume and, thus, edema formation. Thus, when salt intake exceeds salt excretion, edema can form. Edema formation also is associated with deceased protein levels in blood, as seen in nephrotic syndrome and liver disease. Cirrhosis of the liver leads to increased lymph in the space of Disse. Eventually, the increased lymph volume results in movement of fluid into the peritoneal cavity and ascites develops. 

The role of arachidonate metabolites in tubular function [41,42] is more complex although the PGE compounds were shown early on to block the effect of the antidiuretic hormone (ADH) on transporting epithelia. The reason for the complexity is the effect of PGE compounds on sodium and water transport on the one hand and their effect in changing renal blood flow and intrarenal distribution on the other. It is now generally believed that the role of the vasodilator metabolites is to preserve renal homeostasis and that their effect becomes apparent when the kidney function is compromised [43]. The problem with which one is faced is to fit into this scheme the ADH-like effects of thromboxane [44] and the effects of the leukotrienes, when they are properly defined. It is possible that thromboxane and leukotrienes only become prominent in the pathological situation but this remains to be documented. 

Urea and electrolytes Urea (Creatinine) Sodium Potassium (hydrogen carbonate) (chloride) Serum or plasma mmoll pmol I mmoll mmoll mmoll mmoll Yes Kidney function Kidney function Fluid and electrolyte balance Potassium homeostasis Acid-base status Acid-base status... 

The kidneys are two fist-sized organs whose primary function is to generate urine for excretion of water and metabolic waste products. The kidneys not only remove accumulated nitrogen products (urea, creatinine, uric acid, and others) but also maintain homeostasis of water and electrolytes (sodium, potassium, chloride, calcium, phosphate, magnesium) and regulate acid-base balance. In addition, human kidneys perform a few endocrine and metabolic functions, such as production of the hormone erythropoietin (a hormone that stimulates blood cell production) and conversion of vitamin D to its active form. Because of the tremendous overcapacity of normal kidney function, a person can live with only a fraction of normal kidney capacity, and the 0.1% of the population who are bom with a single kidney often are not even aware of the missing kidney. 

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