Renal hemodynamic studies in adults with sickle cell anemia

Etteldorf, James N.; Smith, J. Douglas; Tuttle, A. H.; Diggs, L. W.

doi:10.1016/0002-9343(55)90239-4

Cited by 93 publications

(34 citation statements)

References 2 publications

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“…The mechanism leading to an increased GFR was previously shown to be associated with enhanced renal blood flow (9,13,18,19), a pathologic feature also detected in early diabetic nephropathy at the stage of hyperfiltration (20). Interestingly, mean mGFR values obtained from microalbuminuric non-insulin-dependent diabetic patients are in about the same order of magnitude (9,21).…”

Section: Discussionmentioning

confidence: 85%

Glomerular Hyperfiltration in Adult Sickle Cell Anemia

Haymann¹,

Stankovic²,

Lévy³

et al. 2010

Clinical Journal of the American Society of Nephrology

145

144

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Background and objectives: Sickle cell anemia-associated nephropathy is a growing matter of concern because renal failure affects most aging sickle cell anemia patients. Glomerular damage is a common feature revealed by a microalbuminuria or a macroalbuminuria. Although glomerular hyperfiltration has been described for decades in this population, its prevalence in young adults is unknown.Design, setting, participants, & measurements: To address this issue, as well as the clinical and biologic correlates of hyperfiltration, a single-center, cross-sectional study of 280 homozygous SS disease patients was performed.Results: The prevalence of hyperfiltration assessed by Modification of Diet in Renal Disease estimated GFR was 51%. Among patients with hyperfiltration, 49% had hyperfiltration alone, whereas 36% and 15% had an associated microalbuminuria or macroalbuminuria, respectively. Estimated GFR sensitivity and specificity for hyperfiltration were 94% and 63%, respectively, in a selected subgroup of 48 patients (measured GFR was assessed by urinary 51 Cr EDTA clearance). In patients with no albuminuria, hyperfiltration status was significantly associated with a young age (years), the absence of alpha thalassemia, a lower hemoglobin level (g/dl), and a lower fetal hemoglobin. The role of chronic hemolysis was further strengthened by multivariate analysis showing a correlation between estimated GFR and a low plasma fetal hemoglobin level, a young age, and a high reticulocyte count (r 2 ‫؍‬ 0.54). Conclusions: Together, the data suggest that the pathophysiology of hyperfiltration would rather be attributable to the hemolysis-associated vasculopathy rather than a viscosity-vaso-occlusive process.

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Section: Discussionmentioning

confidence: 85%

Glomerular Hyperfiltration in Adult Sickle Cell Anemia

Haymann¹,

Stankovic²,

Lévy³

et al. 2010

Clinical Journal of the American Society of Nephrology

145

144

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“…It obviously is not due to extensive renal disease since the GFR, PAH clearance (12)(13), water diuresis and other renal functions (18) are often normal or supernormal. The finding that sickle cell trait subjects also exhibit the urine concentration defect indicates that the defect is not primarily due to anemia, if one assumes that the etiology of the concentration defect in these subjects is the same as in the sickle cell anemia patients.…”

Section: Discussionmentioning

confidence: 99%

“…A frequent finding in children with sickle cell anemia is an increase in the glomerular filtration rate (GFR) (12). However, adults with sickle cell anemia usually have a normal or even decreased GFR (13). It is not clear how an increase in the GFR could, in the absence of solute diuresis, influence the concentration of urine during hydropenia.…”

Section: Cell Trait Subjects and (C) Sicklementioning

confidence: 99%

Hyposthenuria in Sickle Cell Anemia: A Reversible Renal Defect

Keitel¹,

Thompson²,

Itano³

1956

J. Clin. Invest.

142

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“…Large juxtamedullary glomeruli with dilatation of both the afferent and efferent arterioles have been described in the kidneys of children with sickle cell anemia (3,28). Furthermore, Etteldorf, Smith, Tuttle, and Diggs have shown that both the ratios of effective renal plasma flow/maximal transport of p-aminohippurate (TmPAH) and of effective renal blood flow/TmpAH as measurements of tubular purfusion by plasma are supranormal in children with sickle cell anemia, indicating increased vascularity or vasodilatation or both (7). Recent hemodynamic evidence from our laboratory, showing the extraction of PAH to be normal or decreased and the noncortical plasma flow to be normal or increased in young sickle cell patients, offers additional support to the concept of increased medullary blood flow (29).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, the hyposthenuria in these patients is present almost from birth and persists throughout the life of the individual (6). A correlation between progression of the concentrating defect and advancing age has been noted (6), as well as the slow decline in renal function after the third decade of life, when all clearance values tend to become significantly diminished (7). Continuing vascular damage in the kidney probably plays an important role in the early decline of renal function, as well as in the more advanced changes seen in those patients manifesting evidence of overt renal disease-[proteinuria (8), hematuria (9,10), or papillary necrosis (4)].…”

Section: Introductionmentioning

confidence: 99%

Nature of the Renal Concentrating Defect in Sickle Cell Disease*

Hatch¹,

Culbertson²,

Diggs³

1967

J. Clin. Invest.

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Summary. Free water reabsorption (TCeiO) measured during 10% mannitol diuresis and subsequently during 3% saline diuresis was compared in patients with sickle cell anemia and in normal subjects. During mannitol infusion, TCHSO progressively rose with increasing osmolar clearance (Cosm) and reached a maximal level in both groups studied. During hypertonic saline diuresis, TCH0o progressively rose in the normal subjects and exceeded the maximal levels attained during mannitol diuresis, with no evidence of a maximal TCH,0 level appearing. In contrast, none of the saline curves significantly exceeded the mannitol curves in the sickle cell patients but tended to parallel the mannitol curves at comparable rates of solute clearance.Since TCH,0 is an index of both solute (sodium) transport from the loop of Henle and solute accumulation in the hypertonic medullary interstitium, tubular sodium handling was examined in both sickle cell patients and control subjects alike. No difference in the tubular transport of sodium could be demonstrated either under conditions of sodium loading or under conditions in which the tubular sodium load was low (water diuresis).These data support the conclusion that the defect in urinary concentration in sickle cell patients is caused by a limitation in maintaining a high concentration of solute in the medullary interstitium, thus limiting the rate of TcH,0 from the collecting duct.

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Renal hemodynamic studies in adults with sickle cell anemia

Cited by 93 publications

References 2 publications

Glomerular Hyperfiltration in Adult Sickle Cell Anemia

Glomerular Hyperfiltration in Adult Sickle Cell Anemia

Hyposthenuria in Sickle Cell Anemia: A Reversible Renal Defect

Nature of the Renal Concentrating Defect in Sickle Cell Disease*

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