PubMed · 5975941
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G M Davidson, N Harvey. Sustained hydration during surgery.. https://pubmed.ncbi.nlm.nih.gov/5975941/
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Dialysis adequacy indices that are applied for the evaluation of the efficiency of urea removal include fractional water volume cleared from urea during dialysis (KT T/V), fractional solute removal (FSR), and equivalent urea clearance (EKR). Using a constant-volume, one-compartment urea kinetic model for an anuric patient, the FSR and EKR are shown to depend on only three nondimensional parameters: (i) KT/V, where K is the dialyzer clearance for hemodialysis (HD) or peritoneal mass transport coefficient for peritoneal dialysis (PD), T is the time period of dialysis, and V is urea distribution volume; (ii) T/Tc, where Tc is the length of treatment cycle; and (iii) VD/V, where VD is the volume of dialysis fluid applied. In particular, analytical formulas for FSR and EKR, valid for HD as well as for PD, were derived as functions of these three parameters. Numerical simulations, performed using a two-compartment urea kinetic model, showed that the analytical formulas are valid also for the two-compartment model, except for short, highly effective HD, where the overestimation of FSR and EKR using the analytical formulas is however, not higher than 20 and 16%, respectively. KT T/V is equal to KT/V for HD and FSR for PD. Thus, our formulas provide an integrative description of the relationships between dialysis efficiency indices and operational dialysis parameters that is valid for all modalities and schedules of dialysis. They may be applied not only for standard HD and continuous ambulatory PD, but also for HD with circulating dialysis fluid or intermittent forms of PD.
Renal tubular dysgenesis is a clinical disorder that is observed in fetuses and characterized by the absence or poor development of proximal tubules, early onset and persistent oligohydramnios that leads to the Potter sequence, and skull ossification defects. It may be acquired during fetal development or inherited as an autosomal recessive disease. It was shown recently that autosomal recessive renal tubular dysgenesis is genetically heterogeneous and linked to mutations in the genes that encode components of the renin-angiotensin system. This study analyzed the clinical expression of the disease in 29 fetus/neonates from 18 unrelated families and evaluated changes in renal morphology and expression of the renin-angiotensin system. The disease was uniformly severe, with perinatal death in all cases as a result of persistent anuria and hypoxia related to pulmonary hypoplasia. Severe defects in proximal tubules were observed in all fetuses from 18 gestational weeks onward, and lesions also involved other tubular segments. They were associated with thickening of the renal arterial vasculature, from the arcuate to the afferent arteries. Renal renin expression was strikingly increased in 19 of 24 patients studied, from 13 families, whereas no renal renin was detected in four patients from three families. Angiotensinogen and angiotensin-converting enzyme were absent or present in only small amounts in the proximal tubule, in correlation with the severity of tubular abnormalities. No specific changes were detected in angiotensin II receptor expression. The severity and the early onset of the clinical and pathologic expression of the disease underline the major importance of this system in fetal kidney function and development in humans. The identification of the disease on the basis of precise histologic analysis and the research of the genetic defect now allow genetic counseling and early prenatal diagnosis.
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