Renal tubular dysfunction in human visceral leishmaniasis (Kala-azar)

There are few studies about the functional tubular disturbances in human Kala-azar. The aim of this study was to investigate alterations in tubular reabsorption of urinary proteins, sodium, potassium, chloride, glucose, uric acid, inorganic phosphate and amino acids in patients with the chronic form of kala-azar.

This is a cross-sectional study of 55 patients with visceral leishmaniasis (Kala-azar). The laboratorial investigation was: creatinine clearance and daily urinary excretion of total proteins, albumin, IgG, beta2-microglobulin, sodium, potassium, chloride, calcium, inorganic phosphate, uric acid and glucose. Plasma and urinary protein electrophoresis were performed in agarose gel. Urinary light chains were determined by the nephelometric method and amino acids by chromatography. All data were compared to those of a control group.

Hypoalbuminemia, hypergammaglobulinemia as well as increased plasma levels of both IgG and beta2-microglobulins were found in all patients with Kala-azar. The mean urinary protein excretion was 277 +/- 66 mg/day. Increased albumin excretion was observed in 44% of patients accounting for 17% of the total urinary protein excretion. Proteinuria consisted predominantly of low molecular weight protein fractions that migrated with alpha1, alpha2, beta and especially gamma globulins. Urinary beta2-microglobulin excretion was elevated in all patients. Immune electrophoresis showed increased urinary excretion rates of kappa (27%) and lambda (42%) light chains. The Bence-Jones test was positive in 20% of patients. Immunofixation was negative for monoclonal peak. The principal alterations were hyponatremia 94.6%, hypokalemia 26%, hypochloremia 27.2%, hypocalcemia 32%, hypomagnesemia 41.8%, hypouricemia 14.3%, Increased urinary excretion fraction were: sodium 15%, potassium 26%, chloride 33.3%, calcium 32%, inorganic phosphate 27.2%, magnesium 100% with hypermagnesiuria, uric acid 44%. Glucosuria was found in one third of patients.

There was evidence of renal proximal tubular damage with alterations in the reabsorption of proteins and light chains with characteristics of a tubular proteinuria, Disturbances of tubular reabsorption of uric acid, calcium, phosphate, glucose and magnesium were also observed.