To what extent dietary salt intake is involved in the pathogenesis of progressive renal diseases has never been fully understood in humans. To this aim, we investigated the relationship between urinary sodium excretion (under a low salt & low protein diet) and urinary protein excretion/renal function in patients with three major renal diseases : chronic glomerulonephritis (GN), diabetic nephropathy (DN) and nephrosclerosis (NSS). The results were as follows; 1) A significant positive correlation was found between urinary sodium excretion (equivalent to the daily salt intake) and daily urinary protein excretion in patients with a GN and DN. However, no relationship w found between the two parameters in patients with NS.2) Reduction in salt intake led to a significant decrease in daily protein excretion, the effect of which was prominent in patients with GN and DN. 3) A significant positive correlation was found between urinary sodium excretion and estimated protein intake (EPI) in all three groups. 4) There was a significant positive correlation between EPI and urinary protein excretion in DN, but not in GN. 5) Reduction in salt and protein intake (calculated as an EPI) ameliorates the slope of reciprocal creatinine concentration(1/Cr) in patients with GN and DN. These results indicate that salt restriction is strongly associated with the preservation of renal function in patients with GN and DN, suggesting that this dietary strategy can be a useful measure for retarding the progressive nature of these diseases. Of note is that both salt and protein restriction was renoprotective only in patients with DN. Thus, patients with GN and DN must be followed-up on the basis of a salt restricted diet throughout their clinical course.

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Since the accumulation of intestinal putrefactive products, such as indole and phenol, is known to play a role in the exacerbation of chronic renal failure, reduction of these intestinal putrefactive products can be expected to retard the progression of renal failure. In the present study, an enteric capsule preparation containing Bijidobacterium longum (Bifidus HD®) was administered orally to 27 patients with chronic renal failure (CRF) for 6 months. Though no significant effect was found in the whole group, a significant retardation of the progression of renal failure was found in patients with an initial serum creatinine level ≥4.0 mg/dl or those with an initial seru inorganic phosphate level ≥4.0 mg/dl. There was no adverse effect observed in any case. Bifidus HD® is considered a useful tool for suppressing the progression of chronic renal failure (CRF) in the conservative period.

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In patients with systemic lupus erythematosus (SLE), interstitial cystitis (lupus cystitis) is an uncommon, but important manifestation. We report two Japanese patients with lupus cystitis. Case 1 was a 49-year-old woman diagnosed as having rheumatoid arthritis and membranous nephropathy. She was treated with prednisolone (5mg daily) . Case 2 was a 41-year-old woman also diagnosed as having rheumatoid arthritis previously and treated with a non-steroidal anti-inflammatory drug. Both cases presented abdominal pain, vomiting, dysuria and frequency of micturition. We diagnosed these cases as SLE on the basis of arthritis, renal disorder (proteinuria and hematuria), and positive antinuclear and anti-dsDNA antibodies. In addition, bilateral hydronephrosis was found in both cases. Thus, they were also diagnosed as probable lupus cystitis. The patients were treated with one cycle of methylprednisolone pulse therapy. Thereafter they were treated with 60mg/day of prednisolone and their symptoms resolved promptly. Furthermore, no abnormal finding was found by abdominal ultrasonography and/or the intravenous pyelogram after therapy. Renal biopsies were performed and both cases showed lupus glomerulopathy (case 1 : WHO class Vb, case II : WHO class IVb). Abdominal pain and/or dysuria, which is common in SLE patients, requires further examinations to evaluate the lupus cystitis.

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We experienced a coincidental case of two types of glomerulopathy associated with Graves' disease. A 64-year-old man, who had been treated with propylthiouracil (PTU) for Graves' disease for 15 years, was admitted to our hospital for macroscopic hematuria and rapidly progressive deterioration of renal function. Although his thyroid function had been within the normal range during treatment, the level of thyrotropin receptor antibody(TRAb) gradually increased from a year before admission. Serological tests revealed that he was positive for myeloperoxidase-antineutrophil cytoplasmic antibody (MPO-ANCA). The renal biopsy specimen showed necrotizing and crescentic glomerulonephritis (GN) superimposed on membranous nephropathy(MN). This is a rare case of MN complicated with ANCA associated crescentic GN in a Graves' disease patient. Association of these two renal alterations was not clearly defined. MN involved with Graves' disease also has been rarely reported. Some reports demonstrated deposition of thyroglobulin and other thyroid related antigens in the glomeruli. In the present case, long-term impair ment of Graves' disease and elevation of TRAb might have been responsible for the formation and deposition of thyroid-associated immune complex in the glomeruli. As for crescentic GN, PTU might have induced ANCA-associated GN independently of MN. This case is instructive for considering the relation between Graves' disease and renal injury

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