Effects of chondroitin sulphate, human serum albumin and Tamm-Horsfall mucoprotein on calcium oxalate crystallization in undiluted human urine.

The effects of physiological concentrations of chondroitin sulphate, human serum albumin and Tamm-Horsfall mucoprotein on the crystallization of calcium oxalate in undiluted, ultrafiltered human urine were investigated using particle size analysis and scanning electron microscopy. Neither the amount of oxalate required to induce detectable calcium oxalate crystal nucleation nor crystal morphology was affected by the presence of any of these macromolecules. Chondroitin sulphate had no effect on the amount of crystalline material deposited or on the size of the particles precipitated in response to a standard oxalate load. Human serum albumin slightly reduced the size of the crystal aggregates and caused a small increase in the amount of crystal matter precipitated. By contrast, Tamm-Horsfall mucoprotein significantly inhibited crystal aggregation and markedly increased the volume of matter deposited, although this could not be attributed to a promotion of solute precipitation. It was concluded that chondroitin sulphate, human serum albumin and Tamm-Horsfall mucoprotein cannot account for the inhibitory effects of macromolecules with a relative mass greater than 10 kDa in spun and filtered urine. Nonetheless, Tamm-Horsfall mucoprotein is likely to inhibit crystal aggregation in whole urine in vivo and may therefore be instrumental in preventing calcium oxalate stone formation.

Urinary risk factors in calcium oxalate stone disease: comparison of men and women.

The daily excretion of calcium, oxalate, uric acid and glycosaminoglycans, the 24-h urinary pH and volume, and the inhibitory effects of the urines on calcium oxalate crystal growth and aggregation, were measured in 44 normal women, 41 normal men, 32 female stone formers and 63 male stone formers. No significant differences could be found between the normal men and women, the male and female stone formers, or between the patients and their normal controls with regard to the excretion of oxalate and glycosaminoglycans, and the urinary pH. The normal women exhibited significantly lower urinary volumes and excreted less calcium per day than did the other subject groups. The excretion of calcium by the female stone formers was indistinguishable from that of both groups of men. The male and female stone formers did not differ from their corresponding control groups with regard to the excretion of urate, but both groups of male subjects had significantly higher daily urate excretions than did either female category. This was attributed to the greater body weights of the men. There were no discernible differences between any of the subject groups with regard to the inhibitory effects of their urines on calcium oxalate crystal growth, but urines from both groups of female subjects demonstrated a significantly greater inhibitory influence on crystal aggregation than did those of the men. It would appear that the relatively low incidence of uninfected calcium oxalate urolithiasis in women compared with men may be attributable to (a) a lower daily calcium excretion and (b) a higher inhibitory activity of their urines towards crystal aggregation.

Macromolecules inhibit calcium oxalate crystal growth and aggregation in whole human urine.

Removal of macromolecules with Mr greater than 10,000 had no discernible effect on the detectable nucleation of calcium oxalate crystals from undiluted human urine, but promoted the deposition of crystalline material and markedly increased the degree of aggregation of the precipitated crystals. Calcium oxalate crystals and crystal aggregates precipitated from ultrafiltered urine were, on average, 68% larger than those deposited from whole urine. These findings suggest that urinary macromolecules play a key role in preventing calcium oxalate kidney stone disease by inhibiting the formation of large crystal aggregates and thereby reducing the probability of particle retention in the kidney tubules.

The effect of monosodium urate on the capacity of urine, chondroitin sulphate and heparin to inhibit calcium oxalate crystal growth and aggregation.

In order to investigate the possibility of interaction between urinary glycosaminoglycans and particulate monosodium urate, growth and aggregation rates of calcium oxalate seed crystals were measured in the presence of heparin, chondroitin sulphate and normal urine after preincubation with and without monosodium urate (0.5 mg./ml.). Rates of crystal aggregation in the presence of heparin and chondroitin sulphate were significantly (p less than 0.0005) increased after pretreatment with sodium urate, indicating a reduction in the inhibitory potency of heparin and chondroitin sulphate by this salt. A similar effect was observed with the rate of crystal growth in the presence of heparin (p less than 0.01). In contrast, the rate of growth in the presence of chondroitin sulphate was unaffected. Pretreatment with sodium urate had an inconsistent effect on the rate of crystal growth in the presence of 10 normal human urine samples, but significantly (p less than 0.001) raised the rate of crystal aggregation. It was concluded that the influence of urate on crystal aggregation in the presence of urine may be a result of its binding to endogenous chondroitin sulphate, but may not be of practical consequence in the pathogenesis of calcium oxalate renal stones.

A review of the literature concerning resuscitation from hypothermia: Part II--Selected rewarming protocols.

In Part I of this paper, a description of the problems confronted in resuscitation from immersion hypothermia was presented and the debate between passive and active rewarming approaches was summarized. In this paper, a review of the literature concerning selected specific rewarming protocols is given. The protocols considered are: peritoneal irrigation, gastrointestinal rewarming, extracorporeal blood rewarming, airway rewarming, and diathermy.

The effect of urine, pyrophosphate, citrate, magnesium and glycosaminoglycans on the growth and aggregation of calcium oxalate crystals in vitro.

The effects of pyrophosphate, citrate, magnesium, heparin and chondroitin sulphate on the growth and aggregation of calcium oxalate crystals were measured at concentrations likely to be found in 1% urine. The degrees of inhibition of growth and of aggregation caused by these compounds were related to the effects of normal 1% urine on these processes. It was concluded that chondroitin sulphate is responsible for the major portion of the inhibitory effect of urine on crystal aggregation, but that the effect on crystal growth is probably due to the additive or synergistic effects of a number of urinary constituents.

Initial treatment of profound accidental hypothermia.

The performance of inhalation, heating pads, plumbed garment, inhalation + heating pads, inhalation + plumbed garment, and body-to-body heat exchange rewarming were compared to trunk immersion and spontaneous rewarming under laboratory conditions with mildly cooled volunteers. The experiment included 72 rewarmings. Trunk immersion exhibited the smallest afterdrop, shortest recovery period, and most rapid rewarming. Of the therapies suitable for use in the field, small afterdrops were seen with inhalation, inhalation + plumbed garment, inhalation + heating pads, and spontaneous rewarming. The largest afterdrops were seen with the heating pads and plumbed garment. Body-to-body heat exchange was seen to produce somewhat larger afterdrops than spontaneous rewarming. It is concluded that heating pads and plumbed garment should not be used in treatment of profound hypothermia. It is further concluded that, because of the depression in respiratory minute volume accompanying profound hypothermia, the heating pads and plumbed garment in combination with inhalation therapy should not be used. This leaves inhalation therapy alone as the recommended treatment for profound hypothermia in the field.