Fludarabine in chronic lymphocytic leukemia with membranous nephropathy.

Chronic lymphocytic leukemia (CLL) is the most frequent form of leukemia in Western countries. Despite its relative frequency, the association of glomerular disease is extremely rare. We present a case of membranous nephropathy (MN) during CLL treated with fludarabine. A 74-year-old man was admitted to our hospital because of the onset of nephrotic syndrome (proteinuria was 7 g/24 h). Six years before, he had been diagnosed with CLL. Biochemical analysis showed the following results: creatinine was 1.7 mg/dL (creatinine clearance was 39 mL/min), urea was 64 mg/dL, hemoglobin was 8.6 g/dL, and white blood cells was 16,580/mm(3) (60% lymphocytes). The urine sediment revealed 7-8 red blood cells and many hyaline and granular casts. No monoclonal peak was demonstrated in either serum or urine electrophoresis. Bence-Jones proteinuria was negative. The patient underwent renal biopsy that showed MN with an extensive lymphocyte perivascular infiltration; immunohistochemistry on renal biopsy specimen showed that infiltrating lymphocytes were CD20+. Moreover, DNA from tissue fractions was analyzed by qualitative polymerase chain reaction-based detection of clonal gene rearrangements of the immunoglobulin heavy chain gene, confirming the monoclonality of the infiltrating lymphocytes. The patient was started on fludarabine as monotherapy, with complete remission of proteinuria and recovery of renal function (creatinine clearance was 75 mL/min) after 1 year of follow-up.

[Hypertensive nephrosclerosis: an exhaustive diagnosis?]. / Nefroangiosclerosi: entita' clinica definita?

Hypertensive nephrosclerosis is a much overused clinical diagnosis, largely unsubstantiated by biopsy data. It is in fact a clinical-pathological diagnosis implying a causal role of hypertension in the associated chronic kidney disease. However, such a simple, linear causality is often not obvious or easy to demonstrate. Further factors like age, Afro-American descent, genetic and immunological factors as well as dysmetabolic syndrome may contribute to the development and progression of arterionephrosclerosis independently of hypertension.