title: Higher rates of hemolysis are not associated with albuminuria in Jamaicans with sickle cell disease.
abstract: BACKGROUND
  Albuminuria is a marker of glomerular damage in Sickle Cell Disease (SCD). In this study, we sought to determine the possible predictors of albuminuria in the two more prevalent genotypes of SCD among the Jamaica Sickle Cell Cohort Study participants.
  
  
  METHODS
  An age-matched cohort of 122 patients with HbSS or HbSC genotypes had measurements of their morning urine albumin concentration, blood pressure, body mass index, haematology and certain biochemistry parameters done. Associations of albuminuria with possible predictors including hematological parameters, reticulocyte counts, aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) levels were examined using multiple regression models.
  
  
  RESULTS
  A total of 122 participants were recruited (mean age 28.6 years ±2.5 years; 85 HbSS, 37 HbSC). 25.9% with HbSS and 10.8% with HbSC disease had microalbuminuria (urine albumin/creatinine ratio  =  30-300 mg/g of creatinine) whereas 16.5% of HbSS and 2.7% of HbSC disease had macroalbuminuria (urine albumin/creatinine ratio>300 mg/g of creatinine). Mean arterial pressure, hemoglobin levels, serum creatinine, reticulocyte counts and white blood cell counts were statistically significant predictors of albuminuria in HbSS, whereas white blood cell counts and serum creatinine predicted albuminuria in HbSC disease. Both markers of chronic hemolysis, i.e. AST and LDH levels, showed no associations with albuminuria in either genotype.
  
  
  CONCLUSIONS
  Renal disease, as evidenced by excretion of increased amounts of albumin in urine due to a glomerulopathy, is a common end-organ complication in SCD. It is shown to be more severe in those with HbSS disease than in HbSC disease. Rising blood pressure, lower hemoglobin levels and higher white blood cell counts are hints to the clinician of impending renal disease, whereas higher rates of hemolysis do not appear to play a role in this complication of SCD.
authors.affiliation: Sickle Cell Unit, Tropical Medicine Research Institute, Mona Campus, University of the West Indies, Kingston, Jamaica. monika.parshadasnani@uwimona.edu.jm
authors.forename: Monika R
authors.initials: MR
authors.lastname: Asnani
authors.forename: Raphael A
authors.initials: RA
authors.lastname: Fraser
authors.forename: Marvin E
authors.initials: ME
authors.lastname: Reid
mesh_terms: D000328:Adult; D000419:Albuminuria / Q000097:blood / Q000150:complications*; D000755:Anemia, Sickle Cell / Q000097:blood / Q000150:complications*; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D005260:Female; D006461:Hemolysis; D006801:Humans; D007563:Jamaica; D008297:Male