BACKGROUND: Renal abnormalities in leprosy have been largely described in medical literature, but there are few studies evaluating renal function in these patients. METHODS: This is a cross-sectional study in 59 consecutive paucibacillary (PB) and multibacillary (MB) leprosy patients. Glomerular filtration rate (GFR) was estimated by simplified-MDRD formula. Microalbuminuria was determined by 24 h urine collection. Urinary acidification capacity was measured after water deprivation and acid-loading with CaCl(2). Urinary concentration capacity was evaluated after desmopressin acetate administration, using the urinary to plasma osmolality (U/P(osm)) ratio. All parameters except microalbuminuria were measured in a control group of 18 healthy volunteers. RESULTS: Age and gender were similar between leprosy (MB or PB) and control groups. GFR <or= 80 ml/min/1.73 m(2) was observed in 50% of the leprosy patients. GFR and U/P(osm) in leprosy patients were significantly lower than in controls (P<0.001). Urinary acidification defect was found in 32% of PB and in 29% of MB patients and urinary concentrating ability was abnormal in 83% of PB and 85% of MB patients. Microalbuminuria was found in 4 patients (8.5%), leukocyturia was found in 13 (22%) and haematuria was present in 16 patients (27%). Plasma creatinine (P(cr)) >1.2 mg/dl was observed in 17.9% of MB patients and in none of the controls (P=0.020). A negative correlation was observed between GFR and time of treatment (r= -0.339; P=0.002). Age and time of treatment were independent risk factors for GFR <or= 80 ml/min/1.73 m(2) in multivariate analysis. CONCLUSIONS: Asymptomatic GFR changes and renal tubular dysfunction, including urine concentration defect and impaired acidifying mechanisms, can be caused by leprosy on specific treatment and without any reaction episodes.
BACKGROUND:Renal abnormalities in leprosy have been largely described in medical literature, but there are few studies evaluating renal function in these patients. METHODS: This is a cross-sectional study in 59 consecutive paucibacillary (PB) and multibacillary (MB) leprosypatients. Glomerular filtration rate (GFR) was estimated by simplified-MDRD formula. Microalbuminuria was determined by 24 h urine collection. Urinary acidification capacity was measured after water deprivation and acid-loading with CaCl(2). Urinary concentration capacity was evaluated after desmopressin acetate administration, using the urinary to plasma osmolality (U/P(osm)) ratio. All parameters except microalbuminuria were measured in a control group of 18 healthy volunteers. RESULTS: Age and gender were similar between leprosy (MB or PB) and control groups. GFR <or= 80 ml/min/1.73 m(2) was observed in 50% of the leprosypatients. GFR and U/P(osm) in leprosypatients were significantly lower than in controls (P<0.001). Urinary acidification defect was found in 32% of PB and in 29% of MB patients and urinary concentrating ability was abnormal in 83% of PB and 85% of MB patients. Microalbuminuria was found in 4 patients (8.5%), leukocyturia was found in 13 (22%) and haematuria was present in 16 patients (27%). Plasma creatinine (P(cr)) >1.2 mg/dl was observed in 17.9% of MB patients and in none of the controls (P=0.020). A negative correlation was observed between GFR and time of treatment (r= -0.339; P=0.002). Age and time of treatment were independent risk factors for GFR <or= 80 ml/min/1.73 m(2) in multivariate analysis. CONCLUSIONS: Asymptomatic GFR changes and renal tubular dysfunction, including urine concentration defect and impaired acidifying mechanisms, can be caused by leprosy on specific treatment and without any reaction episodes.
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