True about free water clearance is:
A i.e. Regulated by ADH- 100 mOsm/ kg H20. It does not mean that urine osmolality is greater than that of plasma. It only means that the urine is less than maximally diluted. And urine osmolality is not necessarily elevated inappropriately at all levels of plasma osmolality. 4. Elevated urinary sodium excretion (Turinary Na*) on a normal salt & water intake. It is present in most patients but is neither 100% diagnostic nor its absence rules out the diagnosis. " align="left" height="278" width="339">Concentration and dilution of urine i.e. free water and osmolar clearances are regulated by antidiuretic hormone (ADH) or vasopressinQ.SIADH is characterized by relatively excessive ADH levels, euvolemia, hypoosmolality (decreased osmolality) of serum, hyponatremia (.1seim Na*), inappropriately high urine osmolality and elevated urinary Na* excretionQSyndrome of Inappropriate ADH Secretion (SIADH)- Syndrome of inappropriate ADH secretion (SIADH) is characterized by relatively excessive ADH levels or plasma ADH levels that are elevated above what would be expected on the basis of body fluid osmolality, blood volume andblood pressure - hence named inappropriate ADH secretion. Patients with SIADH retain water and their body fluids (eg serum) becomes progressively hypoosmotic. In other words, decreased excretion of excess water results in reduced (low)plasma osmolality (ie hypoosmotic body fluids), hyponatremia (reduced plasma Na*) but the urine is hyper-osmotic (more concentrated) and contain increased urinaryNa* than would be expected on the basis of low body fluid osmolality.- SIADH is characterized by low plasma osmolality,hyponatremia (decreased plasma / serum Na*), inappropriately high urine osmolality and significant amounts of sodium in urine (Turinary Na*)In SIADH, restricted Ovate intake is necessary to prevent cellular overhydration. Declomycin , an agent causing reversible nephrogenic diabetes insipidus (ie ADH deficiency 1/t dehydration, polyduria & polydipsia), may also be useful.- Bater & Schwaz clinical criteria for diagnosis of SIADH includeSIADH is most common cause of euvolemic-hypoosmolality. Euvolemia is defined clinically on the basis of absence of signs of hypovolemia (ie tachycardia, ohostatic or postural hypotension decreased skin turgor & dry mucous membranes ) or hypervolemia (generalized edema, ascites etc). Other causes of euvolemic hypoosmolality such as hypothyroidism, hypocoisolism (pituitary ACTH deficiency or Addison's disease) and diuretics must be excluded.Hypoosmolality (decreased effective osmolality) of ECF or serum (20) and hyponatremia (reduced plasma Na*); however, pseudo hyponatremia or hyper glycemia must be excluded.Inappropriately high urine osmolality (concentration) ie > 100 mOsm/ kg H20. It does not mean that urine osmolality is greater than that of plasma. It only means that the urine is less than maximally diluted. And urine osmolality is not necessarily elevated inappropriately at all levels of plasma osmolality.Elevated urinary sodium excretion (Turinary Na*) on a normal salt & water intake. It is present in most patients but is neither 100% diagnostic nor its absence rules out the diagnosis.Nephrogenic Syndrome of Inappropriate AntidiuresisNephrogenic syndrome of inappropriate antidiuresis (NSIA) occurs d/t gain of function (activating) mutations is V, receptor gene resulting in its constitutive activation even in the absence of ADH. It present with same laboratory findings as those of SIADH including hypoosmolar serum, hyponatremia (4,serum Na*), hyperosmolar urine and Turine Nat But unlike SIADH (where high ADH levels are responsible for water retention by kidneys) patients with NSIA have underevels levels of ADH in their plasma.
Regulated by ADH
Regulated by aldosterone
Increased by furosemide
None of the above