The histological grading and staging (G-S system) is proposed in addition to the common histological diagnosis of IgA nephropathy, aiming the more precise understanding and appropriate therapeutic approach to the disease process. The histological grade (G) is estimated by the occurrence of acute glomerular and tubulointerstitial lesions, and histological staging (S) is evaluated by the increase of extra-cellular matrices (sclerosis) of the glomeruli and interstitial fibrosis . The evaluation of the G and S is expressed semiquatitatively for more helpful use in the clinical side . The G-S system may be beneficial for the management and therapeutic selection of patients of IgA nephropathy .

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In many tissues, cell proliferation is counterbalanced by apoptosis. Hyperparathyroidism is one of the most important complications in long term dialysis patients and is characterized by remarkable cell proliferation of parathyroid cells. Therefore, alteration in the regulation and clearance of excess cells by apoptosis may occur in hyperparathyroidism. In the present study, we evaluated the expression of Ki-67 (proliferative cell associated protein) and Bcl-2 (apoptosis-preventing molecules), and the number of apoptotic cells in the nodular lesion of parathyroid glands with secondary hyperpara thyroidism (2°HPT), as compared with primary hyperparathyroidism(1°HPT) for clarification of the role of apoptosis in the development of 2° HPT. The number of Ki-67+ cells was remarkably increased in 2°HPT (12.02 ± 10.87, mean ± SD) compared to in 1° HPT (0.81 ± 0.53) (p<0.01). However, the number of apoptotic cells was significantly decreased in 2° HPT(0.10+0.06) compared to in 1° HPT(0.31±0.19)(p<0.05). To the contrary, Bcl-2+ cells were increased in 2°HPT(0.35+ 0.23) compared to in 1° HPT(0.10 ± 0.13) (plt;0.05). These results suggest that the mechanisms of parathyroid cell proliferation are different in each nodular lesion of 1° HPT and 2° HPT. Furthermore, the remarkable proliferation of parathyroid glands may have been due to the reduction of the apoptotic process via Bcl-2 expression in 2°HPT.

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Serum remnant-like particles-cholesterol (RLP-C), an atherosclerosis risk factor that strongly reflects disorders of chyromicron and VLDL metabolism and contains high levels of TG, was measured in patients on hemodialysis and CAPD. The purpose of this study was to determine the serum levels of RLP-C in 30 outpatients on hemodialysis (18 males, 12 females) and 84 patients on CAPD (53 males, 31 females). The serum RLP-C level was 8.1±13 mg/dl in CAPD patients and 2.7±0.2 mg/dl in hemodialysis patients (p<0.001). Patients who used dialysate containing over 150 g of glucose per day, showed higher levels of serum RLP-C than CAPD patients whose glucose consumption was under 150g(10.4±2.4 mg/dl vs. 5.5±0.6 mg/dl, p<0.01). There was no statistical relationship between age, sex, dialysis duration and serum RLP-C in CAPD and hemodialysis patients. Serum level of RLP-C was positively correlated with serum triglyceride, total cholesterol, apolipoprotein B and VLDL, and was negatively correlated with apoA-I/apoB in the dialysis patients. It appears that RLP-C, which is one of the risk factors of atherosclerosis, might reflect a disorder of triglyceride metabolism in patients on dialysis, especially on CAPD.

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It is well known that the myoglobinuric acute renal failure caused by drugs is an important clinical aspect of nephrology. On the other hand, neuroleptic malignant syndrome is an uncommon, but potentially fatal, idiosyncratic reaction to neuroleptics and is characterized by muscular rigidity, fever, autonomic dysfunction and altered consciousness. The most common serious complication of malignant syndrome is rhabdomyolysis. We investigated 10 cases with acute renal failure induced by haloperidol and other neuroleptics. At the time they developed acute renal failure, the patients were taking a wide variety of medications. However, seven of the patients who developed acute renal failure, had received haloperidol, phenothiazine and anticholinaergic drugs, and 2 cases with acute renal failure were taking lithium. Characteristic clinical manifestations of malignant syndrome were observed in 7 patients who had been administered haloperidol orally or intravenously. All of the patients with acute renal failure induced by haloperidol, lithium and other neuroleptics were treated succsessfully with blood purification therapy (HD or HDF). We concluded that acute renal failure associated with malignant syndrome evoked by haloperidol is an indication for blood purification therapy.

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We examined the relation of diurnal alteration of platelet-free Ca²⁺ to blood pressure and plasma vasoactive substances in 6 subjects with normal renal function (N group) (with both normal GFR and normal urine concentration, and with the renal biopsy finding of minor glomerular change) and 7 patients undergoing CAPD (CAPD group), then evaluated the pathophysiological difference in diurnal variations between both groups and the effect of native kidney function. Diurnal values of platelet basal-free Ca²⁺ concentration in N showed a positive correlation with the corresponding PRA levels. On the other hand, in CAPD they showed a positive correlation with the corresponding levels of plasma AVP. The larger increases in platelet-free Ca²⁺ concentration due to thrombin stimulation were observed in the daytime and the smaller increases in the nighttime in the N groups. The thrombin-induced changes showed a positive correlation with the diurnal levels of mean blood pressure in N (p<0.004). However, in contrast, in CAPD the increase in platelet-free Ca²⁺ due to thrombin tended to be larger in the nighttime and showed a negative correlation with the daily mean blood pressure levels (p<0.004). These findings suggest that there might be differences in the regula-tion of intracellular-free Ca²⁺ dynamics and the diurnal variation between subjects with normal renal function and patients undergoing CAPD. Those differences could affect the progression of vascular disturbance in CAPD patients.

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The aim of the present study was to examine the efficacy and safety of combination therapy with amoxicillin (AMPC), lansoprazole, and plaunotol for the eradication of H . pylori in dialysis patients. The subjects consisted of 15 dialysis patients (10 men and 5 women, mean age of 56±2.4 years) in whom H. pylori was found in the stomach. H. pylori status was evaluated by histology, culture and rapid urease test with biopsy specimens of the gastric mucosa . The patients were treated with AMPC 500 mg once a day for 3 weeks, lansoprazole 30 mg once a day for 8 weeks and plaunotol 80 mg three times a day for 24 weeks. In addition, the concentrations of serum gastrin and gastric juice ammonia were measured. Fourteen patients completed the treatment schedule, while one discontinued treatment because of nausea and diarrhea. Among the 14 patients, H. pylori was eradicated in 11 without any side effects (eradication rate 78.6%). Concentrations of gastric juice ammonia and serum gastrin were reduced significantly in patients who became H. pylori-negative. The present study indicates that combination therapy with AMPC, lansoprazole and plaunotol is safe and efficient for the eradication of H. pylori in dialysis patients. The results also suggested that elevated concentrations of gastric juice ammonia and serum gastrin in dialysis patients can be attributed, at least in part, to H. pylori infection.

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For the purpose of clarifying the changes occurring in thromboxane (TX) A₂ metabolism in the platelet of nephrosis patients, we investigated the changes in platelet sensitivity to TXA₂ and the changes in TXA₂ production in pediatric patients with nephrotic syndrome (N. S.) using STA₂ which is an analogue of TXA₂ and ONO 3708 which is a TXA₂ receptor antagonist. The subjects investigated in the present study consisted of 11 cases with initial onset of N. S. (onset group), 15 relapse patients (relapse group) and 15 children with N. S. without any recurrence in the past 6 months (remission group) as well as 25 normal children (control group). The results were as follows: (1) Platelet aggregation attributable to STA₂ stimulation was enhanced at the onset and relapse of N. S. (2) Sensitivity to TXA₂ was enhanced in the platelets of patients in the relapse group. (3) Though some demonstrated enhanced platelet sensitivity to TXA₂, while others in the onset group did not, enhanced sensitivity was observed in all the patients along with an improvement in hypoalbuminemia. (4) The amount of daily urinary excretion of TXB2 and 11-dehydro-TXB2 in the onset group and relapse group was increased in comparison with the status in the remission group and control group. The above results demonstrated enhanced platelet sensitivity to TXA₂ and increased biological production of TXA₂ in patients with N. S., suggesting that TXA₂ metabolism in the platelet is deeply involved in the pathophysiology of N. S.

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There is a strong association between epithelial crescent formation and the outcome of patients with Henoch-Schönlein purpura nephritis (HSPN), but little is known about the mechanisms of crescent formation in this disease. In this study, we examined whether or not glomerular endocapillary proliferation, fibrinoid necrosis and infiltrating inflammatory cells are involved in the process of crescent formation. Renal biopsy specimens were obtained from 19 patients (11 males and 8 females, 7.8±3.8 years old). The biopsies were performed within the initial 3 months after the onset of urinary abnormalities in all patients. Twelve patients had crescents (% glomeruli with crescents; 27.5±20.4%), and the other 7 did not. Renal tissues biopsied from 10 patients with asymptomatic hematuria served as controls for quantitative studies of glomerular leukocyte infiltration. Prominent endocapillary proliferation as well as fibrinoid necrosis were encountered in patients with crescents in contrast to patients without crescents. A positive correlation between crescents and endocapillary proliferation or fibrinoid necrosis was also observed. Significant increases in the number of glomerular CD68+ macrophages, CD45R0 + T cells and NP57+ neutrophils were observed in HSPN patients compared with the controls. When patients with or without crescents were compared, patients with crescents had a greater number of inflammatory cells. Although all kinds of inflammatory cells appeared in the endocapillary prolif erative lesion, only CD68 + macrophages and NP57 + neutrophils were present in the fibrinoid necrotizing lesion. In conclusion, the present study demonstrated that necrotizing lesions with capillary rupture may be essential in the process of crescent formation seen in HSPN. Although the mechanism by which capillary wall breaks occur is still unknown, this study indicates that infiltrating macrophages as well as neutrophils may be involved in capillary rupture leading to epithelial crescent formation.

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In order to investigate endothelial cell dysfunction in patients with impaired renal function, we measured circulating endothelin (ET-1) and thrombomodulin (Tm) concentrations used as markers for endothelial cell injury in patients with renal failure. 1) ET-1 and Tm were significantly higher in patients with renal failure and pre-dialysis patients than in normal subjects. Tm in CRF patients was significantly greater than that in ARF patients. In contrast, ET-1 was significantly greater in ARF than in CRF. 2) A positive correlation was found between serum creatinine concentration (Cr) and Tm in pre-dialysis patients. However, no correlation was found between Cr and ET-1. 3) A positive correlation was found between Tm and the duration of dialysis in HD patients, but not in CAPD patients. 4) With the improvement of renal function after regular HD treatment, a substantial reduction was found in ARF patients in both Tm and ET-1, but not in CRF patients. The present study suggests the presence of endothelial cell dysfunction in pattients with impaired renal function. The progression of endothelial cell damage may differ between patients on HD and those on CAPD.In addition, it is suggested that endothelial cell dysfunction reverses in ARF patients with improved renal function.

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It is well known that diet therapy is effective for inhibition of the advancement of chronic renal failure. Rhubarb, which can improve nitorogen metabolism, may allow delay in the introduction of the hemodialysis. After performing diet therapy with an energy intake of 35 Kcal/kg and a salt volume of less than 7g in 38 cases with chronic renal failure (CRF), 5 healthy volunteers (N) and 5 cases with liver cirrhosis (LC), 1.Og of rhubarb was adominisitered orally . The blood urea nitrogen (BUN) did not vary in N, decreased in cases with LC and CRF (rhubarb-administered group), but increased in cases with CRF (non-rhubarb-administered group). The serum creatinine (s-Cr) did not vary in N and cases with LC and CRF (rhubarb-administered group), but was elevated in cases with CRF (nonrhubarb-administered group). Serum methylguanidine did not vary in N and cases with LC, decreased in cases with CRF (rhubarb-administered group), and increased in cases with CRF (non-rhubarbadministered group). The chronological level of 1 / Cr in cases with CRF (rhubarb-administered group) was improved. In addition to the diet therapy, adminisitration of rhubarb inhibited increase of BUN and serum creatinine in cases with chronic renal failure and was effective for the reduction of uremic substances. Therefore, it was concluded that rhubarb can retard the introduction-period of hemodialysis and can also inhibit deterioration of the disease .

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We report a patient with rhabdomyolysis secondary to hyperosmolar nonketotic diabetic coma (HNKC), who progressed to acute renal failure. A 43-year-old male with diabetes mellitus for three years was admitted to our hospital because of loss of consciousness. The laboratory findings at admission were as follows: serum glucose 1792 mg/dl, serum Na 129 mEq/ 1, BUN 71 mg/ dl, serum creatinine 3.3 mg/dl, CPK 715 IU/l, plasma osmolality 370 mOsm/l, and negative urine ketone bodies. A diagnosis of HNKC was made. On the 2nd day, he had oliguria and the serum creatinine increased despite adequate treatment of HNKC by the administration of intravenous fluid and insulin. On the 4th day, CPK reached 47300 IU / 1, and serum myoglobin was also increased, indicating rhabdomyolysis. His renal function improved gradually and was almost normalized on the 20th day. Renal biopsy on the 23rd day showed myogloblin at the distal renal tubules, which appeared to be involved in the pathogenesis of renal failure by rhabdomyolysis. However, we found little abnormality association with diabetic nephropathy in the renal tissue. Since HNKC is known to induce acute renal failure rarely without diabetic nephropathy, these findings suggested that the acute renal failure was caused mainly by the rhabdomyolysis. Acute renal failure induced by rhabdomyolysis in patients with HNKC is rare, but fatal. The present study showed that the measurement of serum CPK and urine myoglobin was helpful for early diagnosis. Only 12 cases have been reported to have developed renal failure due to rhabdomyolysis among patients with HNKC. To our knowledge, we demonstrated for the first time, that myoglobin at the distal renal tubules after renal function was normalized.

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