In order to test the accuracy of glycated hemoglobin (HbA1c) in predicting mean glycemia in HIV-infected patients, we recorded consecutive HbA1c measurements from 1238 non-HIV-infected and 112 HIV-infected patients, all devoid of any hemoglobinopathy, in a retrospective, transversal study. Mean fasting glycemia from the six previous weeks (measured-Gly) and HbA1c-estimated glycemia [HbA1c-Gly (1.85x%HbA1c-4.78) mM] were compared. Mean hemoglobin, red cell volume, serum creatinine, CD4 count, and HIV viral load from the same period were collected in HIV-infected patients. Although measured-Gly was not significantly different between non-HIV-infected (6.95+/-3.23 mM) and HIV-infected patients (6.62+/-2.42 mM), HbA1c underestimated the mean fasting glycemia by 12.3% in HIV-infected as compared to non-HIV-infected patients (p=0.0001). The difference "measured-Gly-HbA1c-Gly" was correlated with the red cell volume (p<0.0001) in HIV-infected patients. We then searched for the presence of subclinical hemolysis, a cause of both macrocytosis and reduced HbA1c levels, in HIV-infected patients. To this end, we prospectively measured serum haptoglobin in 249 consecutive samples from HIV-infected subjects without any known cause of hemolysis. A very low haptoglobin level, a marker of hemolysis, was frequent and negatively correlated with the red cell volume in these patients. Treatment with nucleoside analogues was significantly associated with macrocytosis and low haptoglobin. In conclusion, HbA1c could be inappropriately low in HIV-infected patients. Its underestimation of mean fasting glycemia could be due to an antiretroviral-induced subclinical hemolysis, but further studies are needed to explore this hypothesis. Self-monitoring of blood glucose and search for latent hemolysis should be promoted in diabetic HIV-infected patients.
Increased urinary total protein is a nonspecific and unreliable marker of renal function. Analysis of the pattern of proteinuria, however, can provide information regarding the pathophysiologic changes in the affected nephrons. In physiologic proteinuria, the range of daily urinary protein excretion is typically 40 -80 mg/24 h with an upper limit of 150 mg/24 h. Albumin represents the main component (30 -40%), whereas IgG, light chains, and IgA represent 5-10%, 5%, and 3%, respectively, of urinary proteins. The remainder consists mostly of Tamm-Horsfall protein.Patterns of pathologic proteinuria may be classified as glomerular, tubular, prerenal, mixed, or postrenal, with glomerular patterns the most frequent. Total urine protein excretion can exceed 2 g/day, with albumin representing the main component (ϳ70%) and other large-molecularweight proteins, such as transferrin and IgG, accounting for the remaining 30%. Tubular proteinuria is characterized by the dominant excretion of low-molecular-weight proteins such as ␣ 1 -microglobulin (A1M) or retinol-binding protein (RBP), which correlate better with the extent of tubulo-interstitial damage than does determination of total 24-h protein concentrations (1 ).Urinary total protein is frequently undetectable in predominantly tubular kidney disease, and common chemical methods also often fail to detect urinary total protein in predominantly tubular kidney disease, in which albumin usually represents Ͻ30% of the total protein content (2-8 ). However, some renal tubular disorders or interstitial nephritis (e.g., when caused by antibiotics and other tubulo-toxic substances) are easily treatable. Prerenal proteinuria (Bence Jones proteinuria), attributable to overproduction of light chains in monoclonal diseases, or lysozymuria in patients with leukemia and the resulting overload of tubulo-interstitial reabsorption in the kidney often lead to secondary kidney damage. Mixed proteinuria presents with glomerular and tubular protein fractions in urine, i.e., high-and low-molecular-weight proteins. Postrenal proteinuria closely resembles glomerular proteinuria but can be identified by the presence of ␣ 2 -macroglobulin.Early approaches to the evaluation of proteinuria were based on sodium dodecyl sulfate (SDS) electrophoresis (9, 10 ). This method, however, is time-consuming, is at best semiquantitative, and has a high analytical detection limit well above the reference interval for most protein bands (Ϸ20 mg/L), and interpretation is investigator dependent. Alternatively, urinary marker proteins can be measured quantitatively by immunoturbidimetry or nephelometry.At least two knowledge-based systems for the further evaluation of proteinuria are available, UPES (11 ) and MDI-LabLink (4 ). MDI-LabLink, developed by Regeniter et al. (4 ), screens for proteinuria with few marker proteins (albumin and A1M) but uses additional marker proteins (IgG, transferrin, RBP, and  2 -microglobulin) to enable comparison with the SDS-polyacrylamide gel electrophoresis (PAGE) classification s...
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