Short daily peritoneal dialysis and protein restriction.
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Biomedical subjects
Publications and source records attributed to G Capodicasa.
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Renal morphology was evaluated in 2 siblings with Wiskott-Aldrich syndrome (WAS) aged 12 and 4 years. They gave a typical history of recurrent episodes of respiratory infection and presented with microhematuria of glomerular origin and proteinuria. The study disclosed a membranoproliferative glomerulonephritis with IgA mesangial deposition in the elder child, while immunofluorescence was negative in the younger. The data indicate that (1) a specific nephropathy does not exist in WAS and (2) the IgA nephropathy is the result of recurrent infections and of related formation of IgA immune complexes scarcely removed by a deficient reticuloendothelial system. This view is consistent with presenting features in WAS (microhematuria, episodes of macrohematuria, proteinuria, Henoch-Schönlein syndrome) and with the fact that it takes years to develop as indicated by the negativity of immunofluorescence in the younger patient.
Cyclosporin A (CsA) in combination with 6-methylprednisolone was administered over a six-month period to 10 children with nephrotic syndrome (6 frequently relapsing and 4 steroid resistant) at a dose providing blood CsA concentrations of 200-400 ng/ml. In frequent relapsers 6-methylprednisolone was given initially at a dose of 60 mg/m2/day and subsequently at a dose of 35 mg/m2/48 h. In steroid resistant cases the steroid was given at an initial dose of 1 mg/kg tapering to 0.35 mg/kg by the end of the first month and to 0.22 mg/kg by the fourth month being also administered at the same dosage during the fifth and the sixth month. Among the frequent relapsers there were 30 relapsers in 116 months before CsA and 1 relapse during 70 months after CsA (in 5 patients urine was protein free and 1 relapsed after 7 months. Two of the steroid resistant cases healed. There was a modest incidence of CsA toxicity as evidenced by the usual clinical monitoring and by evaluation of creatinine clearance, plasma potassium and evolution of renal parenchymal cells as studied in the course of sequential fine needle aspiration biopsies.
This is a population based study on urinary excretion of sodium, potassium and creatinine in children from Southern Italy aged 3-16 years. Mean urinary creatinine excretion was 33 +/- 10 mg/kg. Mean sodium excretion was of 3.91 +/- 1.52 mM/kg. Urinary sodium, potassium and creatinine correlated with age, body weight, body mass index (BMI) and height and no difference was found in the comparison among sexes. The data point to an excessive sodium intake in these children and additionally claim for a reconsideration of urinary creatinine excretion in this age group.
A case of acute renal failure associated with cisplatin therapy for a stage IV neuroepitelioma of the chest wall is described. This case was associated with a normal magnesium concentration and with presence of fibrinogen in the Tubular Basement Membrane and of IgG in the interstitial infiltrates. Immunological activation was evidentiated by fine needle aspiration biopsy (FNAB) at the time of renal biopsy.
Cellular immune mechanisms have been shown to play a prominent role in glomerulonephritis. Cellular mediators of inflammation cause both acute and progressive glomerular and tubular injury. Understanding the mediation pathways offers the opportunity for therapeutic manipulation. In addition to polymorphonuclear leucocytes, monocytes/macrophages, B-cells and T-cells subsets are being enumerated in normal and diseased renal tissues. The correlation between immunological findings in peripheral blood and infiltrate composition in renal tissue, by using weekly Fine Needle Aspiration Biopsy (FNAB), for assessing the clinical status and monitoring the immunosuppressive therapy was the aim of this study. When determining the intensity of inflammation the numerical values of the Total Corrected Increment (T.C.I.) were defined as follows: less than 1.5 no inflammation; from 1.5 to 2.0 inflammation possible; greater than 2.0 inflammation. The ratio between OKT4 and OKT8 was used as the index: greater than 2.0 immunologic activation; greater than 2.0 no immunologic activation. When the T.C.I. was greater than 1.5 and the OKT4/OKT8 less than 2.0, or the T.C.I. less than 1.5 and the OKT4/OKT8 greater than 2.0 we used only a standard treatment. When both activation indexes were in the normal range we have not treated the patients. When the T.C.I. was greater than 1.5 and the OKT4/OKT8 was greater than 2.0 we treated the patients with standard treatment plus methylprednisolone pulses every time the activation indexes monitored by FNAB, showed an increase. A spontaneous improvement was obtained in untreated patients. The patients treated by standard therapy alone showed a different outcome. All patients treated with standard therapy plus methyl-prednisolone pulses showed a progressive clinical improvement.(ABSTRACT TRUNCATED AT 250 WORDS)
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