Evaluation of renal function in leprosy: a study of 59 consecutive patients.

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 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

Leptospiral antigens (L. interrogans serogroup ictero-haemorrhagiae) in the kidney of experimentally infected guinea pigs and their relation to the pathogenesis of the renal injury.

The search for leptospiral antigens (L. interrogans serogroup icterohaemorrhagiae) was carried out in 24 guinea pigs experimentally inoculated with 1 ml of culture containing 10(7)-10(8) leprospires and sequentially sacrificed from the first until the 6th day of infection. Semiquantitative analysis of histopathological variables comprising kidney interstitium, tubules and glomeruli was done in 1 micron sections of tissue embedded in glycolmetacrylate. Leptospiral antigen (LAg) and its glycolipoprotein (GLP) expression were detected through PAP in paraffin embedded tissue. The mild interstitial involvement of the kidney, manifested chiefly by oedema and focal interstitial nephritis seen at the 4th day, progressed to tubular damage at the 6th day, characterized by either swelling or cytoplasmic acidophilia of epithelial cells with loss of cell cohesion and sloughing of cells into the tubular lumina. Brush border alterations and mitochondrial changes were observed. Endothelial cell injury was noted in the interstitial vessels. LAg expression was parallel to the kidney changes: small deposits of elongated forms of LAg were detected at the 4th day either within the vascular lumen or free in the interstitium. A rise in the antigen expression was observed at the 5th day when it was seen either around tubules or in their walls. LAg was detected inside the tubular lumina at the 6th day of infection when granular LAg and GLP were abundant. This sequence reproduces the pathway of leptospires in the kidney and the crescent amounts of antigens detected toward the end of the experiment, with antigen concentration in cases of major tissue damage suggesting a direct action of the microorganisms and/or their products in the pathogesis of the lesions.

Renal lesions in leprosy amongst north Indian patients.

Sixty consecutive patients with leprosy were investigated for renal involvement. Clinically overt renal disease was present in 4 patients; 3 presented with a nephrotic state and one patient with progressive renal failure. Urinalysis showed daily protein loss ranging from 0.4 to 8.9 g in 8 patients and microscopic haematuria in 4 cases. Elevated levels of blood urea and creatinine were seen only in one patient with diffuse proliferative glomerulonephritis. Of the 36 patients in whom distal tubular functions were evaluated, concentration and/or acidification defects were detected in 9 patients (25%). Renal histology revealed no abnormality in any of these patients. Serum C3 levels were decreased in 5 patients with lepromatous leprosy and 3 patients with borderline leprosy. Histological evidence of renal involvement was detected in 9 patients (15%). Amyloid deposits were seen in 3 (5%) patients of whom 2 had lepromatous leprosy and one had tuberculoid leprosy with chronic trophic ulcers. Mesangial proliferative lesions were seen in 5 (8.3%) and diffuse proliferative lesions (with crescents in more than 70% of glomeruli) in one patient. All of them had lepromatous leprosy. Three of the 5 patients with mesangial proliferative glomerulonephritis had erythema nodosum leprosum at the time of biopsy. Immunofluorescence studies revealed granular deposits of IgA, IgM and C3 in one patient with mesangial proliferation and IgA/IgM with or without C3 in 3 more patients in whom renal histology was normal. Glomerulonephritis associated with leprosy appears to be immune mediated but confirmation requires identification of lepra antigen in the glomerular immune complex deposits.

Acute renal failure due to intravascular hemolysis in the North Indian patients.

Acute renal failure due to intravascular hemolysis is a common clinical problem in North Indian patients. It constituted 21.5 percent of 325 patients dialyzed for acute renal failure over an 11-year period at Chandigarh. Thirty patients had developed acute intravascular hemolysis in association with erythrocyte glucose-6 phosphate dehydrogenase (G-6PD) deficiency, 17 due to copper sulphate intoxication and 8 due to envenomation by snakes. Less frequent causes were insect stings, incompatible blood transfusion, intake of anti-leprosy drug--dapsone in non-G-6PD-deficient patients, and mercuric chloride toxicity in two patients each; naphthalene poisoning in one; and uncertain causes in six patients. Renal histology was available in 55 patients. Acute tubular necrosis was seen in 54 and bilateral diffuse cortical necrosis in one patient. Fifty patients (71.43 percent) survived and 20(28.6 percent) diet. G-6PD erythrocyte deficiency, which is present in 4.5 percent of the North Indian population, was the most frequent cause of acute renal failure in this group.