Figure 412

Relationship between nephron with long loops and those with short loops of Henle. In the normal human kidney, approximately 85% of the nephrons have short loops of Henle restricted to the outer medullary zone. These nephrons may be largely responsible for achieving the interstitial osmolality of about 450 mOsm/kg H2O that exists at the transition of the outer and inner medulla. The remaining 15% of human nephrons are juxtamedullary nephrons with long loops of Henle, extending into the inner medullary zone and renal papillae. Together with the parallel hairpin vasa recta, these units are responsible for further increasing interstitial osmolality during antidiuresis to about 1200 mOsm/kg H2O at the tip of the papillae. In experiments with rats, selectively removing the papillae destroys only nephrons originating in the juxtamedullary cortex. In such animal preparations, a severe loss of concentrating capacity during fluid deprivation has been observed. Thus, juxtamedullary nephrons are necessary for achieving a maximal urine osmolality. These pathophysiologic mechanisms help clarify the abnormal findings in sickle cell nephropathy. On the basis of these mechanisms, the concentrating defect in sickle cell disease can be explained as a consequence of the sickling process per se and the resultant ischemic changes in the medullary microcirculation [5]. It has been demonstrated that Hb SS erythrocytes form sickle erythrocytes within seconds when placed in surroundings as hyperosmotic as is the renal medulla during hydropenia [8]. Sickling of renal blood cells causes a significant increase in blood viscosity that could interfere with the normal circulation through the vasa recta, preventing both active and passive accumulation of solute in the papillae necessary to achieve maximally concentrated urine. Increased viscosity of blood and intravascular aggregations of Hb SS erythrocytes could also produce local hypoxia and eventually infarction of the renal papillae.

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