Formation Of Concentrated Urine

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Presentation transcript:

Formation Of Concentrated Urine Dr .imrana ehsan

OBLIGATORY URINE VOLUME: The minimum amount of urine that must be excreted.(to excrete 600 mosm of solute each day. 600mosm/day/1200mosm /L=0.5L/day Human kidneys have limited ability to concentrateurine-1200mosm/L Dehydration develops if drinking sea water

Mechanism of urine dilution and concentration CONDITIONS IN WHICH DILUTE URINE IS FORMED Dilute urine is called hypotonic urine, in which urine osmolality is less than blood osmolality. It is produced under the following conditions: 1. Low levels of ADH ,central diabetes insipidus 2. ADH is ineffective The principal factors governing formation of dilute and concentrated urine are hyperosmolality medullary gradient and the presence or absence of ADH.

Production of concentrated urine: Concentrated urine is also called hyperosmotic urine, osmolality is greater than that of blood. Hyper osmolality of medullary interstitium :50 to 60 %of hyperosmolality is contributed by counter current multiplier and exchange system Role of urea: 40 to 50% It is produced when circulating ADH levels are high e.g Water deprivation,Haemorrahage, Syndrome of inappropriate antidiuretic hormone (SIADH)

Principal factors governing formation of concentrated urine The high level of ADH is the main factor for governing the formation of concentrated urine; because it increases the size of hyperosmolarity medullary gradient Augments the urea cycling from the inner medullary collecting ducts into the medullary interstitial fluid.

Segmental changes in the tubular fluid during formation of concentrated urine. From proximal tubule to ascending thick limb and even early distal tubule, the changes occurring in the tubular fluid is same as during formation of dilute urine. Only change is that the ADH stimulates NaCl reabsorption in the thick ascending limb and increases the size of medullary gradient by counter current multiplier, which is important for the formation of conc urine. Tubular fluid entering the late distal tubule is hypo-osmolar (osmolality about 150mOsm/L) In the presence of ADH, H20 permeability of the principal cells is increased and consequently H20 is reabsorbed until the osmolality of distal tubular fluid equals that of the surrounding cortical interstitium (300m0sm/L) Hence osmotic equilibrium occurs in the presence of ADH.

The initial portion of the collecting duct is impermeable to urea, hence it remains the tubular fluid, its conc in the tubular fluid inceases. In the presence of ADH, urea permeability of the last portion of the medullary collecting duct is increased. Hence urea diffuses out into the medullary interstitium. The final osmolalityof urine is about 1200m0sm/L and high conc of urea and other non reabsorbed solutes.

Collecting ducts: As the tubular fluid flows through the collecting ducts, it passes through the corticopapillary gradient( regions of increasingly higher osmolality, from 300m0sm/L to 1200m0sm/L) that is previously established by counter current multiplier and urea cycling. Consequently H20 is reabsorbed from the collecting ducts until the osmolality of tubular fluid equals that of the surrounding interstitial fluid. Osmolality may reach upto 1400m0smol/L, almost five times that of plasma, with a total of 95.7% or more of the filtered water being reabsorbed. Urine under this condition can be as low as 0.5L/day.

Other systems of counter current mechanism Heat exchange taking place between arteries & veins of limbs. Human intestinal villi – diaadvantageous Brain – for regulation of brain temperature. Testes – for maintaning high levels of testoterone.

Assessment of renal diluting and concentrating ability: Measurement of urine osmolality, Measurement of urine specific gravity, The urine concentration test, The urine dilution test and Estimation of free water clearance test.

Applied aspect: Clinical Serum ADH Ser Osm/ Ser Na+ Urine osmolality Urine flow rate Free water clearence Primary polydypsia decreased hyposmotic high positive Central diabetes insipidus increased Nephrogenic DI Water deprivation High/nomal hyperosmo low negative SIADH Markedly increased

Thank you