To our knowledge these are the first documented cases of TMA associated with HES. We propose that products released from degranulated eosinophils caused endothelial injury and microvascular thrombosis. Recognition of this serious renal complication associated with blood eosinophilia should prompt early diagnosis and treatment.

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The etiological factors responsible for the hypertensive phenotype are complex and several experimental and clinical observations point to a major role of the kidney as being responsible. Genetic studies of uncommon diseases which express monogenetic inheritance all have in common a dysregulation of Na⁺ balance and volume expansion. Furthermore, epidemiological data suggest an increased incidence of hypertension in communities with high excretory rates of Na⁺. Experimental data also suggest that low birth weight is associated with an increase in the frequency of hypertension later in life and raises the possibility that intrauterine imprinting may contribute to the expression of the phenotype. Upregulation of the Na⁺/K⁺/2Cl^– and thiazide-sensitive transporters in low birth weight animals may provide the physiological basis for these observations. In addition, low birth weight is associated with a decrease in nephron number. Therefore, low nephron number may induce adaptive changes in utero which influence volume homeostasis later in life and subtle gain of function mutations in one or more of these transporters may unmask defects in volume homeostasis with increasing salt intake. Finally, the high prevalence of hypertension in functionally anephric patience seems to respond to sustained maintenance of ‘dry weight’ through ultrafiltration.

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