Osmolal fraction

Abstract. Isopiestic vapor pressure comparison measurements were performed with aqueous mixtures of sodium chloride (B) with sodium polystyrenesulfonate, NaPSS, (C) and with polyvinylbenzyltri-methyl ammonium chloride, PVR4NCI, (C) to determine molal osmotic coefficients, for typical strong electrolyte-strong polyelectrolyte systems. The McKay-Perring method was applied to compute the stoichiometric mean molal activity coefficients, yn, of NaCl and y c of NaPSS or PVR4NCI, respectively, in the mixtures as a function of the osmolal concentration, m, and of the osmolal fraction of polyelectrolyte, yc. 

While some clinical and laboratory findings assist in the general diagnosis of ARF, others are used to differentiate between prerenal, intrinsic, and postrenal ARF. For example, patients with prerenal ARF typically demonstrate enhanced sodium reabsorption, which is reflected by a low urine sodium concentration and a low fractional excretion of sodium. Urine is typically more concentrated with prerenal ARF and there is a higher urine osmolality and urine plasma creatinine ratio compared to intrinsic and postrenal ARF. 

The new media that are commercially available possess many distinct characteristics some are completely free of animal-derived components, others are serum-free, sometimes requiring addition of some protein fraction or containing a discrete quantity of proteins. Another class is protein-free media, which can include components derived from animals, plants, or yeast hydrolysates. In some cases, the development of novel media is unnecessary, as it is sufficient to supplement basal medium with a few known specific components. It is emphasized that the final osmolality of the formulated medium should be compatible with cellular tolerance, as discussed in Chapter 2. 

In general, the sediment in the urine is normal. Proteinuria or erythrocyturia are not characteristic of hepatorenal syndrome. The excretion of sodium in the urine is lower than 10 mmol/day, with a fractional excretion of sodium of < 1%. For this reason, there is likewise increased renal retention of water. The urine osmolality is greater than the plasma osmolality, which results in a quotient of >1.3. With increasing severity of hepatorenal syndrome and transition of the penultimate phase, the urine becomes iso-osmotic with an osmolality quotient of 1 or < 1. (19, 43,52,53, 60) (s. tab. 17.4)... 

We utihzed the above principle to treat hthium-induced polyuria [26]. This reduction in urine output could not be ascribed to increased proximal fluid reabsorption and decreased dehvery of fluid to the distal nephron as a result of the volume contraction caused by amiloride. Fractional lithium excretion, a marker of proximal sodium reabsorption, did not fall during amiloride treatment, arguing against volume contraction induced by amiloride as possible mechanism [26]. In lithium treated patients, urinary osmolality increased when treated with amiloride. Amiloride attenuates the inhibitory effect of lithium on vasopressin-mediated water reabsorption [26] (Figure 3). 

In persons with normal kidney function, sodium balance is maintained at a sodium intake of 120 to 150 mEq/day. The fractional excretion of sodium (FENa) is approximately 1% to 3%. Water balance is also maintained, with a normal range of urinary osmolality of 50 to 1200 mOsm/L. In patients with severe CKD (Stages 4 and 5), sodium balance is achieved, but results in a volume-expanded state. FENa may increase to as much as 10% to 20%, possibly due to increased concentrations of atrial natriuretic peptide. An osmotic diuresis occurs with an increase in FENa leading to obligatory water losses and impairment in the kidney s ability to dilute or concentrate urine (urinary osmolality is often fixed at that of plasma or approximately 300 mOsm/L). Nocturia is present relatively early in the course of CKD (Stage 3) secondary to the defect in urinary concentrating ability. Total renal sodium excretion decreases despite an increase in sodium excretion by remaining nephrons. Volume overload with pulmonary edema can result, but the most common manifestation of increased intravascular volume is systemic hypertension. ... 

A low sodium concentration is sometimes reported in patients with. severe hyperproteinaemia or hyperlipoprotein-aemia. This is an artefact caused by the method used to measure. sodium concentration by some analytical instruments. These patients have in fact a normal sodium concentration in their plasma water. The increased amounts of protein or lipoprotein occupy a larger fraction of the plasma volutne than usual, and the water a smaller fraction. The analyser measures the amount of sodium in a small volume and assumes that the Witter content of that sample is normal. The result is an apparently reduced sodium concentration (Fig. 4). This so-called pseudohyponatraemia can be detected by measuring the scrum osmolality which will be nomial. 

Distance along the channel, x, is measured from the tight junction (x = 0) to the channel mouth x = L). The cell is at the mucosal bath osmolality, Cq + and the serosal bath is at Q + Cg. The lateral cell membrane has unit water permeabUity RTLp and transports solute into the interspace at rate N(x) (mosm/cm. s). The solute transport rate is written as a function of position because in their model, solute transport was assumed to occur only in an apical segment of the channel. In this apical segment transport, N, is constant. If is the fraction of chaimel length over which solute transport occurs, then... 

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