Renal Acidification in Sickle Cell Trait

Oster, James R.; Lee, Stanley M.; Lespier, Laura; Pellegrini, E. L.; Vaamonde, Carlos A.

doi:10.1001/archinte.1976.03630010020004

Cited by 20 publications

(9 citation statements)

References 36 publications

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“…However, it is possible that the hyperkalemia was also partially due to a decreased tubular ability to excrete K. loads, as de scribed previously by DeFronzo et al [10], We did not evaluate the response to K loads in our patients in the light of reduced glomerular filtration rate and hyperkalemia. The ability to excrete acid has been shown to be defective in patients with sickle cell anemia [6,7], and it is also possible that our patient had some degree of inability to clear acid loads, which in turn could add to the already elevated serum K.…”

Section: Discussionmentioning

confidence: 97%

“…Hyporeninemic hypoaldosteronism has been described recently in a patient with sickle cell disease [12]. In most of the studies where renal rubular functions in sickle cell di sease were investigated, the renin-aldosterone axis was not evaluated [5][6][7][8]. Patients with sickle cell disease have been shown to have a high incidence of pyelonephritis and inter stitial parenchymal kidney disease [2,3]; although the exact nature of the kidney disease in our patient is not known, it is plausible to suggest an interstitial kidney disease which in turn might have affected the renin-secreting process.…”

Section: Discussionmentioning

confidence: 99%

“…The most common structural abnormality is diffuse interstitial disease associ ated with fibrosis [3][4][5]. Among the functional abnormali ties recently reported are renal tubular acidosis [6,7], ab normality in concentration of urine [8,9], and distal tubular dysfunction, resulting in inability to handle potassium loads [10].…”

Section: Introductionmentioning

confidence: 99%

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Hyporeninemic Hypoaldosteronism in Sickle Cell Disease

Yoshino

Amerian

Brautbar³

1982

Nephron

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A patient with sickle cell disease and persistent hyperkalemia in the face of mild stable renal failure is described. The adrenal response to ACTH stimulation was intact, nonstimulated renin and aldosterone levels were markedly low and did not increase in response to stimulation using acute volume reduction. The hyperkalemia responded to mineralocorticoids. It is suggested that patients with sickle cell disease might be at risk of hyperkalemia due to impaired ability to excrete potassium loads and impaired renin secreting aparatus.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

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Hyporeninemic Hypoaldosteronism in Sickle Cell Disease

Yoshino

Amerian

Brautbar³

1982

Nephron

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“…The prevalence of metabolic acidosis is unknown and is presumably low except in renal failure. Incomplete tubular acidosis was reported in several individuals (4)(5)(6)(7), suggesting that this feature may be potentially frequent without acidemia. However, the links between this incomplete tubular acidosis and SCAN (e.g., hyperfiltration, albuminuria, or chronic renal failure) are unknown.…”

Section: Introductionmentioning

confidence: 99%

Prevalence and Correlates of Metabolic Acidosis among Patients with Homozygous Sickle Cell Disease

Maurel¹,

Stojanovic

Avellino

et al. 2014

Clinical Journal of the American Society of Nephrology

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Background and objectives Very few studies report acid base disorders in homozygous patients with sickle cell anemia (SCA) and describe incomplete renal acidosis rather than true metabolic acidosis, the prevalence of which is unknown and presumably low. This study aimed to assess the prevalence of metabolic acidosis and to identify its risk factors and mechanisms.Design, setting, participants, & measurements This study retrospectively analyzed 411 homozygous patients with SCA with a GFR$60 ml/min per 1.73 m 2 , referred in a single center between 2007 and 2012. Acidosis and nonacidosis groups were compared for clinical and biologic data including SCA complications and hemolytic parameters. A subgroup of 65 patients with SCA, referred for a measured GFR evaluation in the setting of sickle cell-associated nephropathy, was further analyzed in order to better characterize metabolic acidosis.Results Metabolic acidosis was encountered in 42% of patients with SCA, with a higher prevalence in women (52% versus 27% in men; P,0.001). Several hemolytic biomarkers, such as lactate dehydrogenase, were different between the acidosis and nonacidosis groups (P=0.02 and P=0.03 in men and women, respectively), suggesting higher hemolytic activity in the former group. To note, fasting urine osmolality was low in the whole study population and was significantly lower in men with SCA in the acidosis group (392 versus 427 mOsm/kg; P=0.01). SCA subgroup analysis confirmed metabolic acidosis with a normal anion gap in 14 patients, characterized by a lower urinary pH (P,0.02) and no increase in urinary ammonium. Serum potassium, plasma renin, and aldosterone were similar between the two groups and thus could not explain impaired urinary ammonium excretion.Conclusions These results suggest that the prevalence of metabolic acidosis in patients with SCA is underestimated and related to impaired ammonium availability possibly due to an altered corticopapillary gradient. Future studies should evaluate whether chronic metabolic acidosis correction may be beneficial in this population, especially in bone remodeling.

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“…urinary bicarbonate ; urinary pH ; atmospheric carbon dioxide It seems to have been believed that the amounts of urinary bicarbonate of normal adults are negligible since the report of Picts et al (1949), and that the pH of urine of normal adults is around 5.5. Oster et al (1975) described that pH of urine obtained from six adults was less than 5.7. Stemmer et al (1986) reported that the contents of bicarbonate and pH of urine were not more than 2.7 mM and 6.3 in ten adult males.…”

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confidence: 99%