PubMed · 14924995
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H HARRIS, I R McDONALD, W WILLIAMS. 1952. The electrolyte pattern in experimental anuria.. https://doi.org/10.1038/icb.1952.4
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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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BACKGROUND: The risk of intravascular radiocontrast to residual renal function (RRF) in patients on peritoneal dialysis (PD) remains largely unknown. HYPOTHESIS: This study sought to estimate the effect of coronary angiography on RRF in patients on PD. METHODS: All patients at the VA Pittsburgh Healthcare System and University of Pittsburgh who underwent coronary angiography between 1993 and 2005 while on PD and who had RRF measured prior to angiography were identified retrospectively. For patients without a postprocedure RRF recorded, medical records were reviewed to determine whether anuria had developed. The longer-term rate of loss of RRF among cases was compared with a composite rate of decline in RRF among cases before angiography and matched controls. RESULTS: Twenty-nine patients with a mean preprocedure RRF of 4.4+/-3.2 ml/min/1.73m(2) were evaluated. Of these patients, 23 (79%) had postangiography RRF assessments (mean clearance 3.4+/-3.0 ml/min/1.73m(2)). One of the remaining six patients definitely became permanently anuric following angiography, one was lost to follow-up, and there was no postprocedure RRF assessment in four others. The rate of decline in RRF in the cases was similar to the composite rate (0.07 ml/min/1.73m(2)/month vs. 0.09 ml/min/1.73m(2)/month, p=0.53) CONCLUSION: The risk for permanent anuria in patients on PD undergoing coronary angiography appears to be quite small. Patients who do not develop anuria following coronary angiography have the same gradual rate of loss of RRF as other patients on PD. Providers should be vigilant in protecting RRF in patients on PD undergoing coronary angiography.