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Renal acidification in sickle-cell disease.
J Lab Clin Med. 1976 Sep; 88(3):389-401.JL

Abstract

Renal acidification was evaluated in patients with sickle-cell disease (HvSS) with both oral NH4CI and NaHC03 and the results were compared to those of subjects with sickle-cell trait (HbAS) and controls. The pH of arterial blood was normal in HbSS subjects but their PC02 and [HC03] were lower than those of controls. In response to NH4CI, six of 20 HbSS subjects had an abnormal minimal urine pH (greater than 5.3) and the entire HbSS group had a higher mean value than did either controls or HbAS subjects. Since none of the six HbSS subjects had evidence of proximal tubular abnormalities, it was concluded that they exhibited the syndrome of incomplete distal renal tubular acidosis. Only one of the six HbSS volunteers with an abnormal response to NH4CI and two of seven with a normal response increased their urinary PC02 normally after bicarbonate loading. PAH clearance was significantly higher and inulin clearance tended to be higher in HbSS subjects than in either controls or HbAS subjects. Maximal concentrating ability was decreased in both sickle-cell groups but more so in HbSS. No adverse effects occurred and no appearance or increase in per cent of sickled cells resulted from short-duration NH4CI acid-loading. No differences were found either in the clinical characterstics or in hematological, renal, and acid-base variables between the HbSS subjects with and without a normal response to acid-loading. The mechanism for the observed renal acidification abnormality remains unknown.

Authors

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

8574

Citation

Oster, J R., et al. "Renal Acidification in Sickle-cell Disease." The Journal of Laboratory and Clinical Medicine, vol. 88, no. 3, 1976, pp. 389-401.
Oster JR, Lespier LE, Lee SM, et al. Renal acidification in sickle-cell disease. J Lab Clin Med. 1976;88(3):389-401.
Oster, J. R., Lespier, L. E., Lee, S. M., Pellegrini, E. L., & Vaamonde, C. A. (1976). Renal acidification in sickle-cell disease. The Journal of Laboratory and Clinical Medicine, 88(3), 389-401.
Oster JR, et al. Renal Acidification in Sickle-cell Disease. J Lab Clin Med. 1976;88(3):389-401. PubMed PMID: 8574.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Renal acidification in sickle-cell disease. AU - Oster,J R, AU - Lespier,L E, AU - Lee,S M, AU - Pellegrini,E L, AU - Vaamonde,C A, PY - 1976/9/1/pubmed PY - 1976/9/1/medline PY - 1976/9/1/entrez SP - 389 EP - 401 JF - The Journal of laboratory and clinical medicine JO - J. Lab. Clin. Med. VL - 88 IS - 3 N2 - Renal acidification was evaluated in patients with sickle-cell disease (HvSS) with both oral NH4CI and NaHC03 and the results were compared to those of subjects with sickle-cell trait (HbAS) and controls. The pH of arterial blood was normal in HbSS subjects but their PC02 and [HC03] were lower than those of controls. In response to NH4CI, six of 20 HbSS subjects had an abnormal minimal urine pH (greater than 5.3) and the entire HbSS group had a higher mean value than did either controls or HbAS subjects. Since none of the six HbSS subjects had evidence of proximal tubular abnormalities, it was concluded that they exhibited the syndrome of incomplete distal renal tubular acidosis. Only one of the six HbSS volunteers with an abnormal response to NH4CI and two of seven with a normal response increased their urinary PC02 normally after bicarbonate loading. PAH clearance was significantly higher and inulin clearance tended to be higher in HbSS subjects than in either controls or HbAS subjects. Maximal concentrating ability was decreased in both sickle-cell groups but more so in HbSS. No adverse effects occurred and no appearance or increase in per cent of sickled cells resulted from short-duration NH4CI acid-loading. No differences were found either in the clinical characterstics or in hematological, renal, and acid-base variables between the HbSS subjects with and without a normal response to acid-loading. The mechanism for the observed renal acidification abnormality remains unknown. SN - 0022-2143 UR - https://www.unboundmedicine.com/medline/citation/8574/Renal_acidification_in_sickle_cell_disease_ L2 - http://www.diseaseinfosearch.org/result/6589 DB - PRIME DP - Unbound Medicine ER -