糖尿病性腎症早期診断基準を改訂した。試験紙法で尿蛋白が陰性, あるいは+1程度の陽性を示す糖尿病症例を対象に, 午前中の随時尿でアルブミンを測定し, 尿中アルブミン値3回中2回以上が30～299mg/gCrであれば微量アルブミン尿と判定する。また, 腎肥大, 尿中IV型コラーゲン値上昇は糖尿病性腎病変の存在を示唆する。これらを参考に非糖尿病性腎疾患由来の微量アルブミン尿を鑑別し, 糖尿病性腎症を早期診断する。

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Inulin clearance (Cin) is widely believed to be the gold standard of the glomerular filtration rate (GFR). However, in Japan, Cin has not been officially recognized by the Ministry of Health, Labour and Welfare of Japan for clinical use. Creatinine clearance (Ccr) has been used to estimate the renal function of patients, but there have been many studies in which Ccr estimates were GFR falsely high because the metabolism and tubular excretion of creatinine widely varied according to the pathophysiological state of the patient. In the present study, we determined Cin and Ccr simultaneously in 116 adult patients with renal diseases and diabetic mellitus. The clearance study was performed by the modified Wesson's method. The inulin preparation was FFI-1010 (Fuji Yakuhin Co. Ltd.). Inulin in serum and urine was determined by the newly devised enzymatic assay (Toyobo Co. Ltd.), which is specific for inulin. The mean Cin was 35.0±14.4ml/min/1.73m². The mean Ccr (the enzyme assay) was 63.6±24.1ml/min/1.73m² and that of the kinetic Jaffe assay was 55.3±19.3ml/min/1.73m². Mean Ccr/Cin was 1.93±0.73, 1.69±0.62, respectively. This ratio was significantly different (p<0.05) in the degree of reduction of Cm, with values of 2.07±0.82 (Cin<40ml/min/1.73m²) and 1.64±0.32 (40<Cin<80ml/min/1.73m²), respectively. Only 8 patients were classified into the same degree of reduced renal function (the Guideline of Japanese Society of Nephrology).
The findings of this study suggest that the GFR determined by Ccr could misjudge the renal function of patient and delay the administration of proper treatment of the patient. Introduction of Cin into the clinical field is necessary to avoid this delay.

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Background: Kidney transplantation is the most ideal treatment in renal replacement therapy for patients with end-stage renal disease. However, the prevalence of transplantation is extremely low and most patients with ESRD should continue dialysis for their whole life. Recently, high transposition rate of renal transplantation from peritoneal dialysis (PD) was reported, however, it was unclear whether a difference in dialytic modality can influence the outcome. Therefore, we evaluated the influence of dialytic modality on the rate of kidney transplantation and outcome in our single center.
Methods: Forty-two kidney transplants were carried among 1, 573 dialysis patients from the years 1986 to 2004 in our center. Transposition rates from two modalities (HD and PD) and graft survival were compared. The incidence of acute rejection episode, complications after receiving transplantations, and coexisting diseases were also evaluated between the two modalities prior to transplantation.
Result: The number of patients who received HD was larger than PD (HD 77.1%, PD 22.9%, respectively). Forty-two patients undergoing dialytic therapy received a living-donor kidney transplantation. Overall graft survival was 92% at 5 years and 75% at 10 years. Among these cases, dialytic modality prior to transplantation was 57.1% in HD, and 42.9% in PD. The transfer rate from PD to transplantation was significantly (p=0.0036) higher (4.7%) than that of HD (1.9%). The reason for the high transfer rate of PD patients might be cooperation with their family and the provision of relevant information by nephrologists during PD. There were no differences between the two modalities prior to transplantation in the graft survival rate, incidence of acute rejection, and complications before and after transplantation.
Conclusion: Difference in pre-transplant dialysis modality did not affect the outcomes, however, the transfer rate from PD was significantly higher than from HD. Accordingly, PD is useful compared to HD as bridge therapy for kidney transplantation from the high feasibility of living donor kidney transplantation.

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Blood ionized calcium (iCa) fraction is affected by the serum albumin (Alb) level, even though this effect might not be appropriately estimated by the formulae proposed previously. To clarify a reasonable regimen for predicting iCa from serum total Ca (tCa), we investigated the relationship of blood iCa, tCa, and serum Alb levels through 124 samples from 116 non-dialysis patients requiring iCa measurement at the Nephrology Section of Toride Kyodo General Hospital. The patients comprised 61 males and 55 females with the mean age of 66.9±1.4 years, including 9 cases of hypercalcemia, 110 of normocalcemia, and 5 of hypocalcemia based on their iCa levels. Their background diseases were 25 cases of chronic glomerulonephritis, 17 of nephrotic syndrome, 40 of diabetes mellitus, 4 of collagen diseases, and 30 of others. Their mean serum Cr was 2.44±0.21mg/dl, and 77 patients showed elevated Cr levels.
Four adjustment formulae: one derived from Payne's, two from the proposal of K/DOQI Clinical Practice Guidelines, and a theoretical one based on the previous in vitro experiments, were compared with the non-adjusted value (tCa itself) with respect to their suitability for estimating iCa. The correlation coefficient of tCa with iCa was higher than the values adjusted by the above four formulae. The difference of iCa from tCa divided by eight, which concisely predicted iCa based on the assumption that half the serum Ca is bound to protein, was less than 1/8th of the other adjusted Ca levels. Hence none of the adjusted Ca by the above formulae was superior to non-adjusted tCa from the point of estimating the iCa level. Moreover, the sensitivity for predicting hypocalcemia was the highest in tCa, even though its specificity was lower than the other adjusted values.
In conclusion, no adjustment formula is required to predict ionized Ca from tCa, and to screen hypo-or hypercalcemia.

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Herein we describe the case of a patient with focal segmental glomerulosclerosis (FSGS) following polycythemia vera (PV) on whom hemodialysis was started 7 years later. A 66-year-old woman who had been treated for PV with hydroxyurea and phlebotomy for three years was referred to our hospital because of nephrotic syndrome. Renal biopsy performed at her local hospital revealed FSGS. Although she had received prednisolone at an initial dose of 45mg/day, no significant improvement of proteinuria was achieved. The dose of prednisolone was tapered because the second renal biopsy revealed sclerosing glomerulopathy. We considered that FSGS was associated with PV because renal hemodynamic alterations in PV could result in FSGS as in any other secondary FSGS and there was no proteinuria at the initial detection of PV. On January 29, 1999, she developed massive proteinuria (9.6g/day) and the findings of the third renal biopsy worsened in comparison with that of the first renal biopsy. Thereafter, hydroxyurea or ranimustine was used in treating PV at an outpatient clinic. However severe thrombocytosis was difficult to control, and progressive renal dysfunction finally necessitated hemodialysis on January 18, 2005. In conclusion, physicians should be aware of the risk of progressive renal failure in patients with FSGS following PV, particularly in patients with persistent thrombocytosis.

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The present case was a 59-year-old woman who underwent a right nephrectomy at 30 years of age, and in whom renal dysfunction occurred at 51 years of age. In November 199X, when her creatinine level reached 7mg/dl, renal replacement therapy was recommended. She refused this therapy and began her own diet therapy, which consisted of taking only supplement beverage, but no food. Afterwards she became unable to do daily work, and entered our hospital in July of the next year.
On admission, her bleeding time was over 10 minutes, but coagulation function tests showed normal values. Platelet function tests showed that coagulation with the addition of ADP was mildly decreased and that coagulation with the addition of aggregation was severely decreased. These data and her bleeding tendency improved with hemodialysis. Therefore, a diagnosis of aggregation non-responsive uremic platelet dysfunction was made. On admission, we were not able to insert a catheter for hemodialysis because of her severe bleeding tendency. A platelet transfusion was made so that we could insert the catheter without severe bleeding. However, this hemostatic effect lapsed after about five to six hours. Six hours after insertion of the catheter, oozing from the orifice of the catheter was seen and a red blood transfusion was necessary. Three days after beginning hemodialysis, the bleeding tendency was no longer seen. Her platelet function and coagulation test results also improved.
We can make two conclusions regarding this case. The first is when the physician's medical strategy cannot be carried out due to uremic platelet dysfunction, a platelet transfusion can temporarily eliminate the bleeding tendency. The second is that the pathophysiology of uremic platelet dysfunction involves suppression of the primary step of platelet aggregation with collagen. Experience with the present case revealed the appropriate therapeutic strategy for the pathophysiology of uremic platelet dysfunction.

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