Hyponatremia is more frequently observed in elderly patients associated with exaggerated response of ADH release and attenuated response of renin-aldosterone system. Differentiation of SIADH and hyponatremia other than SIADH is essential in anticipating the therapeutic effect of water restriction to correct hyponatremia. Serum concentration of uric acid and urinary excretion of kallikrein are significant parameters in biochemical discrimination index to differentiate these two types of hyponatremia. In addition to sodium replacement, water restriction and mineral corticoid, newly developed nonpeptide ADH V₂ receptor antagonist, OPC-31260, seems to be a useful tool to correct hyponatremia.

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1, 5-Anhydro-D-glucitol, a 1-deoxy form of D-glucose, is one of the major polyols in human and rat blood plasma, and is regarded as a sensitive marker of glycemic control in diabetic patients. Although renal tubular reabsorption of 1, 5-anhydro-D-glucitol is thought to maintain the physiological plasma level of this polyol, the mechanism of its cellular uptake has not yet been established. In the present study, the transport characteristics of 1, 5-anhydro-D-glucitol in a kidney epithelial cell line, LLC-PK₁, were investigated. The uptake of 1, 5-anhydro-D-glucitol by the LLC-PK₁ cell monolayers was found to be a highly Na⁺-dependent process. The initial uptake rate of 1, 5-anhydro-D-glucitol was inhibited by the presence of D-glucose, D-mannose and methyl-α-D-glucoside, a nonmetabolizable D-glucose analogue. D-Mannose was taken up partially by LLC-PK₁ cells in a Na⁺-dependent manner. 1, 5-Anhydro-D-glucitol had an inhibitory effect on the uptake of both methyl-α-D-glucoside and D-mannose. Phlorizin inhibited the uptake of methyl-α-D-glucoside and 1, 5-anhydro-D-glucitol, but not of D-mannose. In contrast, phloretin inhibited the uptake of both 1, 5-anhydro-D-glucitol and D-mannose, but not the uptake of methyl-a-D-glucoside. The apparent Michaelis-Menten constant and maximum velocity values for 1, 5-anhydro-D-glucitol uptake were 29 mM and 240 pmol/mg protein/min, respectively. These findings suggest that the uptake of 1, 5-anhydro-D-glucitol across the apical mem-branes of LLC-PK₁ cells is mediated by the Na⁺/D-glucose cotransport system and probably by the Na⁺/D-mannose cotransport system.

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The present study was designed to identify the mechanism of increased oxidant stress in the rat model of anti-glomerular basement membrane nephritis. Sixty-three Sprague-Dawley rats were injected with nephrotoxic serum and evaluated 1 to 24 hours later. In these rats, CeCl3 deposition, an index of hydrogen peroxide production, was observed on the surfaces of glomerular endothelial cells and polymorphonuclear leukocytes, whereas no such depositions were observed in controls. Renal cortical level of lipid peroxidation products (phosphatidylcholine hydroperoxide) was significantly (p < 0.05) elevated at one hour after the injection and remained elevated at least for 24 hours. Protein levels of glomerular Mn-superoxide dismutase (SOD) decreased from 1.55 ± 0.38 μg/mg protein to 0.67 ± 0.18 μg/mg protein at one hour and normalized by 12 hours after the injection. The activity of the enzyme showed a similar trend. In contrast, Mn-SOD mRNA increased 3.4-fold at 3 hours after the injection. In situ hybridization showed increased Mn-SOD mRNA expression in glomeruli. Cu/Zn-SOD mRNA expression was transiently suppressed. These results indicated that both increase in local production of reactive oxygen species (ROS) and reduction in antioxidant enzyme activities are responsible for the enhanced oxidant stress in the heterologous phase of anti-glomerular basement membrane nephritis. The paradoxical increase in Mn-SOD mRNA expression indicates that the posttranscriptional down regulation of Mn-SOD (i.e., reduction in protein and activity) and the increased ROS may activate transcription of the gene.

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The relative effect of renal transplantation on survival was examined in chronic dialysis patients in Okinawa, Japan. Of 3, 035 patients (1, 722 men and 1, 313 women) who were registered by the end of 1994 and followed up until April 1, 1995, 141 (91 men and 50 women) had undergone a renal transplantation during the follow-up period. The type of donor was a cadaver in 38 (26.9%) and a living relative in 103 (73.1%). At the end of the follow-up period, 12 (8.5%) of the patients with a renal transplant had died, 35 (24.8%) had returned to dialysis treatment, and 94 (66.7%) were alive with a functioning graft. In the patients who did not receive a transplant, 1, 134 (39.2%) had died and 1, 760 (60.8%) were alive and on dialysis. Cox proportional hazard analysis was performed with adjustment for sex, age at first dialysis, presence of diabetes mellitus, year of first dialysis, and predialysis co-morbid conditions. The hazard ratio (95% confidence interval) in the group with a transplant was 0.33 (0.18 to 0.59) when the hazard ratio of the group without a transplant was taken as 1.00. The patient survival rate was better in the former group. Our data provide fundamental evidence supporting the effectiveness of renal replacement as treatment. Whether the life-saving merit of renal transplantation is substantial enough to actively encourage donation remains to be clarified.

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We investigated whether the management condition of patients during dialysis therapy has an influence on the occurrence of complications after renal transplantation. Thirty-one patients who underwent renal transplantation were investigated: thirteen received kidneys from living related donors and 18 received cadaveric transplants. The relations between weight gain ratio, cardiothoracic ratio (CTR) and blood pressure during dialysis and the rate of episodes of acute rejection or infection after renal transplantation were analyzed. The rate of acute rejection tended to be higher among patients whose CTR was less than 45% than in those whose CTR was 45% or more. There was no relation found between the rate of infection after transplantation and weight gain ratio, CTR, or blood pressure during dialysis therapy. These results suggest the possibility that the management condition of patients during dialysis therapy influences the rate of acute rejection after these patients undergo renal transplantation.

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A 63-year-old man had anuria associated with a unilateral ureteral stone for 24 hours. Laboratory data indicated marked azotemia with the serum creatinine concentration of 7.2 mg/dL and urea nitrogen of 48 mg/dL. The radiological findings revealed contralateral hydronephrosis. Spontaneous discharge of the ureteral stone reversed the anuria and uremia. Both ureteral and vascular spasms were attributed to the anuria in this patient.

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We report here a 15-year-old girl with myeloperoxidase anti-neutrophil cytoplasmic antibodies (MPO-ANCA)-associated crescentic glomerulonephritis (CreGN) and subclinical autoimmune thyroiditis. She was found to have proteinuria and hematuria by a school mass-screening a year before the first visit to the hospital, where a routine examination revealed blood urea nitrogen (BUN) 36.8 mg/dl and serum creatinine concentration of 1.63 mg/dl, although she had no apparent disabilities. On admission, the additional laboratory findings showed proteinuria of 1.06 glday, hematuria of 3+, and a creatinine clearance of 30.1 ml/min. Hypocomplementemia was not observed. A renal biopsy revealed pauciimmune CreGN with 95% fibrocellular crescents, 84% sclerosis and/or hyalinosis and a massive cellular infiltration in the interstitium. She had MPO-ANCA of 865 EU/ml and an anti-thyroid microsome antibody titer of 1:1, 600 without the detection of anti-glomerular basement membrane antibodies. Laboratory tests and scintigraphies for the thyroid gland did not show any abnormalities. Under the diagnosis of MPO-ANCA-associated CreGN, cocktail therapy consisting of prednisolone, cyclophosphamide, dilazep hydrochloride and warfarin was started. Improvement of urinary abnormalities and suppression of further deterioration of renal function were observed. Serial renal biopsy 6 months after the initiation of therapy showed decrement of interstitial cell infiltration and no generation of other crescentic glomeruli. The patient's serum titer of anti-thyroid microsome antibody was not affected by the adsorption of MPO-reacted IgG, suggesting that MPO-ANCA was not crossreactive to thyroid microsome antigen.

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