Proteinuria is an important predictor of renal outcome in a variety of renal diseases. Proteinuria exceeding 0.5 g/day is often considered to be a major indication of renal biopsy. In this study, we analyzed the clinical and histopathological data of 58 patients with mild proteinuria of less than or equal to 0.5 g/day. The histopathological diagnosis included 45 cases (77.6 %) of mesangial proliferative glomerulonephritis, 4 cases (6.9 %) of lupus nephritis, one case of membranoproliferative glomerulonephritis and only 6 cases (10.3 %) of minor glomerular abnormality. The percent sclerotic glomeruli exceeded 10 % in 17 cases (29.3 %) and reached 71.4 % in 2 cases. There were no significant differences in histopathological parameters (percent sclerotic glomeruli, tubulointerstitial change, arterio-arterio sclerotic change) between the groups with or without microhematuria. There was a positive correlation between age and percent sclerotic glomeruli. Percent sclerotic glomeruli in our cases were higher than in the healthy population reported by Kaplan et al. and the influence of glomerulonephropathy was obvious. During the follow-up period (mean 19.7 months), one patient progressed to chronic renal failure and 2 patients had increased urinary protein excretion, but the others did not. These results suggest the importance of clarifying the prognosis by renal biopsy even in cases with mild proteinuria.

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Cyclosporin A (CyA) is used frequently in the treatment of steroid-resistant or recurrent cases with nephrotic syndrome. Recently, a new microemulsion formulation of CyA (Neoral^(R)) has been developed and used preferably because of a more stable bioavailability than an oily formulation (Sandimmun^(R)). Nephrotic syndrome accompanies hyperlipidemia, and probucol is used in cases showing inadequate effects or some adverse reactions under therapy with HMG-CoA reductase inhibitors. We reported previously that combined use of probucol caused a decrease in blood concentrations of CyA to about half of those without probucol. In the present study, we evaluated the influence of probucol on the blood concentrations of CyA in patients with nephrotic syndrome following Neoral^(R).Coadministration of Neoral^(R) and probucol decreased the blood concentrations of CyA to approximately 75 % of the levels before combined use. The change of blood CyA concentrations appeared to be smaller compared to those in cases with Sandimmun^(R). Based on the present findings, we suggest that Neoral^(R) should be used preferentially instead of Sandimmun^(R) when the concomitant use of probucol is required, and that optimal dose adjustment of CyA is needed by frequent monitoring of CyA blood concentrations.

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In order to investigate the participation of monocytes/macrophages (Mo/MΦ) in the progression of various kidney diseases of children, Mo/Mm in urine and that infiltrating renal tissue were both measured as the number of CD68 positive Mo/MΦ(CD68⁺ Mo/MΦ), using anti-CD68 antibody. The number of CD68⁺ Mo/MΦinfiltrating in one glomerulus was significantly higher in Henoch-Schonlein purpura nephritis (HSPN) (p<O.01) in comparison with that in minimal change nephrotic syndrome (MCNS) (p<0.01), and a high tendency was found in IgA nephropathy(IgAN), proliferative glomerulonephritis(nonIgAN), focal segmental glomerulosclerosis (FSGS) and membranoproliferative glomerulonephritis (MPGN), respectively. The number of CD68⁺ Mo/MΦ infiltrating one mm² of tubulo-interstitium area was significantly higher in HSPN (p<0.05), FSGS (p<O.OI), Alport's syndrome (p<0.01), respectively, than that in MCNS. The number of CD68⁺ Mo/MΦ in one milliliter of urine correlated significantly with both that infiltrating the glomerulus and the tubulo-interstitium (both p<0.01). Moreover the number of urine CD68⁺ Mo/MΦ in a clinically active stage was significantly higher than that in an inactive stage in the AGN (p<0.05), IgAN (p<0.05), HSPN (p<0.05), non-IgAN (p<0.01) and MPGN groups (p<0.05), respectively. From these results, 1) It was suggested that the Mo/MΦ infiltrating renal tissue participated in the development of various kidney diseases. 2) It was predicted that CD68+ Mo/MΦ in urine reflected both the number of Mo/MΦ infiltrating the glomerulus and that in the tubulo-interstitium. 3) It was suggested that the number of CD68⁺ Mo/MΦ in urine indicated clinical activity in proliferative glomerulonephritis groups of children.

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A 52-year-old man was admitted to our hospital because of nephrotic syndrome. He had been monitored at our outpatient clinic for chronic hepatitis B, and had experienced histologically proven minimal change nephrotic syndrome at the ages of 40 and 51 years. Because of HBsAg positivity in his serum, steroid therapy was withheld in his earlier episodes and he recovered from nephrotic syndrome spontaneously. However, in the most recent episode the nephrotic syndrome was found difficult to control and the findings of renal biopsy showed FSGS, which is not expected in HBV-associated nephropathy. Finally, prednisolone was administered at the dose of 40 mg/day for four weeks, after which the dose was tapered. LDL apheresis was also administered three times because of the patient's incomplete response to prednisolone. His proteinuria was reduced from>10 g/day to<1 g/day, but the ALT levels and HBsAg titer increased. With stronger neominophagen C induction and very careful tapering of glucocorticoid, ALT levels and the HBsAg titer decreased. During the two-year period since the induction of glucocor ticoid therapy, urinary protein excretion has been maintained at less than 1 g/gcr, and ALT levels and HBsAg titer have not increased. We conclude that attention must be paid to dose modification of steroid therapy and strategies without immunosuppressive agents such as LDL apheresis should be considered in the case of treatment of nephrotic syndrome with HB virus.

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We report here a unique case of recurrent malignant hypertension after the removal of an adrenal tumor for primary aldosteronism. The patient had a history of hypertension for 15 years. In 1995, he developed drug-resistant hypertension with hyperreninemia, hyperaldosteronemia and hypokalemia. He was diagnosed as having primary aldosteronism with a right adrenal tumor. His blood pressure did not normalize and renal dysfunction continued after the adrenalectomy. Although antihypertensive treatment was continued for residual hypertension, he soon refused medication. In 1997, he developed recurrent malignant hypertension. It was considered that the different underlying mechanisms might be attributable to the two episodes of malignant hypertension in this patient.

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We report here two interesting cases of systemic lupus erythematosus (SLE) accompanied by antiphospholipid syndrome nephropathy (APSN). These cases satisfied the criteria for SLE established by the American College of Rheumatology 1997 and also satisfied the criteria for antiphospholipid syndrome (APS) established by the Sapporo International Workshop of APS 1998. Both cases had high blood pressure with elevated plasma renin activity, proteinuria and renal dysfunction. Their biopsied renal specimens showed the characteristic findings for APSN, such as mesangial proliferation, double contours, thickening of the capillary loops, and intimal hyperplasia, but there was no evidence for immune complexes in the glomeruli, which were examined by the indirect immunofluorescence methods and the electron microscopy method. These results indicated that their renal dysfunction was caused by APSN, but not by immune complex nephritis. In addition to treatment with prednisolone, they were administered anticoagulants (warfarin, or aspirin, or heparin) for APSN and an angiotensin II receptor blocker, candesartan, for the hypertension. Subsequently, their conditions recovered with the improvement of renal function and hypertension. Our experiences suggest that anticoagulant therapy in addition to corticosteroids offers advantages in the treatment of patients with SLE accompanied by APSN and renal dysfunction.

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