Basic medicine: physiology
Roy Palmer, Diana Wetherill in Medicine for Lawyers, 2020
The prime function of the kidneys is to rid the body of the nitrogenous waste products of metabolism, notably urea and creatinine. The renal reserve is such that about half of one kidney can preserve normal blood levels of these metabolites. By altering the secretion of water and electrolytes into the urine, the kidney plays a crucial role in maintaining the normal physiological balance of these compounds and also in regulating acid-base balance, i.e. the normal pH of the blood (about 7.4). Fluid depletion or dehydration is detected by osmotic receptors in the brain, giving rise to the sensation of thirst. Antidiuretic hormone (ADH or vasopressin) is secreted by the pituitary gland (see p. 13) and acts on the renal tubule to reabsorb water, thereby conserving body fluid and leading to a concentrated urine. After rehydration, any extra water in the bloodstream will switch off ADH secretion and allow the kidney to excrete the excess. This is an example of a process known as feedback inhibition, which helps to maintain a constant internal environment.
Neurological Manifestations of Medical Disorders
John W. Scadding, Nicholas A. Losseff in Clinical Neurology, 2011
The posterior pituitary secretes two peptides, arginine vasopressin (AVP), the antidiuretic hormone (ADH) and oxytocin. Plasma osmolality (normally 285–288 mosmol/kg) is maintained through AVP secretion from the osmoregulation of thirst. AVP causes increased water reabsorption in the renal tubules, thus reducing urine output. In diabetes insipidus, there is commonly thirst with polydipsia and polyuria (urine output of > 3 litres per 24 hours). Diabetes insipidus results from dysfunction of the posterior pituitary. Reduced secretion of arginine vasopressin and antidiuretic hormone cause symptoms of thirst, polyuria and polydipsia. The common causes are trauma, tumours, sarcoidosis and other granulomatous conditions, and infections. If water is restricted, dehydration follows. In diabetes insipidus, the water deprivation test causes the urine osmolality to rise, but the urine volume remains high and the plasma osmolality rises, often to more than 295 mosmol/kg.
Renal system
Pankaj Desai in Pre-eclampsia, 2020
As the renal system is the principal player in the process of pre-eclampsia, it will be useful to review the physiological changes in pregnancy. The GFR increases by about 50%. There is a consequent decrease in serum creatinine, plasma urea and blood uric acid levels in normal pregnancy. The kidneys increase in length but not so much in width. There is an increase in kidney volume. Physiological hydronephrosis during pregnancy occurs in 43%–100% pregnant women, and it is more prevalent with the advancing trimester.1 A rise in serum aldosterone results in a net gain of approximately 1 g of sodium. There is a concomitant rise in progesterone, which protects the pregnant woman from hypokalaemia. The threshold for thirst and antidiuretic hormone secretion are depressed, resulting in lower osmolality and serum sodium levels.2 The rise in GFR in pregnancy leads to a series of changes, including the most obvious increase in urine output. Increase in blood volume and an increase in renal circulation both contribute to increased urine output. There is more blood to be filtered in pregnancy, and therefore, the renal system goes into an unstressed overdrive.
Endogenous markers for kidney function in children: a review
Published in Critical Reviews in Clinical Laboratory Sciences, 2018
Emil den Bakker, Reinoud J. B. J. Gemke, Arend Bökenkamp
Urea is formed in the urea cycle, a series of enzymatic steps to neutralize ammonia, which is released with degradation of amino acids [54]. It is a small nitrogen containing compound, with a molecular weight of 60 Da. Due to its small size, it passes the glomerular barrier freely, making the concentration of urea in the initial filtrate virtually identical to that of serum, which is one of the pre-requisites of a GFR marker. However, the walls of some segments of the renal tubules are also permeable to urea, resulting in complex tubular handling [55]. Urea reabsorption is by a facilitated passive process through urea transporters on the apical membrane. Expression of the urea transporters in the thin descending limb of Henle and the medullary collecting duct is increased by antidiuretic hormone and leads to increased urea reabsorption in anti-diuresis. Therefore, urea clearance is directly related to urine flow and varies by some 300% between anti-diuresis and maximal urine dilution [56]. Other extra renal factors affecting its serum levels include dietary protein intake (+), internal bleeding (+), glucocorticosteroid treatment (+), catabolic state (+), and intestinal excretion (−) [57,58].
Kidney physiology and pathophysiology during heat stress and the modification by exercise, dehydration, heat acclimation and aging
Published in Temperature, 2021
Christopher L. Chapman, Blair D. Johnson, Mark D. Parker, David Hostler, Riana R. Pryor, Zachary Schlader
Dehydration also increases circulating vasopressin (also known as antidiuretic hormone or ADH). Vasopressin acts on type 2 vasopressin receptors (V2) to stimulate NaCl reabsorption by the thick ascending limbs of Henle and promote the localization of the water channel, aquaporin-2, on the apical membrane of the collecting duct to promote water reabsorption [105]. These processes are initiated when the increased plasma osmolality [106] and/or sodium concentration [107] is detected in the brain, and is also stimulated by reductions in blood volume [108]. Ultimately, these processes result in decreased urine output and increased urine concentration [109]. Vasopressin also exhibits vasoconstricting actions in the kidneys by activating V1 receptors in vascular smooth muscle, primarily in efferent arterioles, to reduce renal blood flow [110], which together with angiotensin II is important in maintaining blood pressure during dehydration [111-117] (Table 2).
Pharmacological management of hyponatremia
Published in Expert Opinion on Pharmacotherapy, 2018
Theodosios Filippatos, Moses Elisaf, George Liamis
Restoration of plasma volume either with isotonic saline (154 mEq/L Na+) or balanced crystalloid solution (according to European guidelines) is the treatment of choice in patients with hypovolemic hyponatremia [10,11]. Special attention should be paid in hypovolemic hyponatremic patients to the possibility of an overly rapid increase in serum sodium levels when volume depletion is restored. In this case, an abrupt decrease in antidiuretic hormone (ADH) secretion and subsequently a rapid increase in diuresis is observed [25]. Isotonic saline should be avoided in patients with hyponatremia due to SIAD since it can aggravate hyponatremia if the urine osmolarity is higher than serum osmolarity (especially if urine osmolarity >530 mOsm/kg) [26]. In such cases the administered sodium is excreted in a lower water volume than in which is given leading to net free water retention and further deterioration of hyponatremia.
Related Knowledge Centers
- Animal
- Diuresis
- Diuretic
- Molecule
- Oxytocin
- Urination
- Vasopressin
- Diabetes Insipidus
- Fluid Balance
- Medication