Kazumasa Shimamatsu

Germanium dioxide-induced nephropathy: a new type of renal disease.

Chronic renal failure developed in 5 patients who were taking germanium dioxide (GeO2)-containing compounds. Renal functional deterioration was slow but progressive and dialysis treatment was necessitated temporarily in 2 patients. After the discontinuation of GeO2, the impaired renal function tended to improve but remained abnormal for an observation period of 10-40 months. The lack of proteinuria and hematuria was characterized as the clinical manifestations. Renal biopsy specimens revealed the tubular epithelial cell degeneration containing hematoxylin-positive fine granules on light microscopy, and electron-dense inclusions in the swollen mitochondria on electron microscopy. These findings localized mainly in distal segment of the tubules. In the rats given GeO2 orally for 10 weeks, similar histological lesions were evident, as manifested by marked weight loss, anemia, azotemia, and negative proteinuria. In the rats given carboxyethylgermanium sesquioxide, these changes were not observed and Ge concentration of kidney was significantly lower than in the rats given GeO2. The present study indicates that chronic GeO2 intake causes progressive renal dysfunction characterized by the degeneration of distal tubules.

Idiopathic Membranous Glomerulonephritis Associated with Diabetes mellitus

The present study described 3 patients with idiopathic membranous glomerulonephritis associated with diabetes mellitus. Clinical characteristics of the 3 patients contrasted with diabetic glomeruloscl

1-Year Controlled Trial of 1α-Hydroxycholecalciferol in Patients on Maintenance Hemodialysis

A 1-year controlled trial was performed to confirm the effects of 1α-hydroxycholecalciferol (1α-OH-D3) in chronic hemodialysis patients. Initially, a daily dose of 2 µg of 1α-OH-D3

Massive Pulmonary Embolism Occurring with Corticosteroid and Diuretics Therapy in a Minimal-Change Nephrotic Patient

A 32-year-old female with a relapsing minimal-change nephrotic syndrome developed a massive pulmonary embolism during the treatment of prednisolone and diuretics. The use of diuretics in addition to a hypercoagulable state associated with nephrotic syndrome per se and corticosteroid was considered to be a direct causative factor for the event. The careful use of diuretics and a consideration of additional anticoagulant therapy are emphasized.

Does 1α(OH)D3 Treatment Affect Blood Pressure Levels in Maintenance Hemodialysis Patients

Forty-eight chronic hemodialysis patients were divided comparably into two groups (24 patients in each). Two micrograms of lα(OH)D3 was administered to one group for 3 months and its placebo to the other group. In the 1α(OH)D3-treated group, serum total calcium increased from 7.82 ± 0.11 (mean ± SEM) to 9.70 ± 0.27 mg/dl (p 10 mg/dl) at 3 months, no significant changes in blood pressure were found. Serum iPTH decreased from 2.83 ± 0.28 to 0.98 ± 0.23 ng/ml (p 3 treatment in maintenance hemodialysis patients does not accompany a rise in blood pressure, probably due to a concomitant suppression of PTH. The results also suggest that the hypocalcemic state found in hemodialysis patients is not associated with any significant change in blood pressure. The importance of PTH in blood pressure regulation was discussed.

Diastolic Blood Pressure and Progression of Chronic Renal Failure

Kazumasa Shimamatsu, MD, Shimamatsu Naika Iin (Clinic), Futsukaichi 709-1, Chikushino City 818 (Japan) Dear Sir, An increase in blood pressure has been considered as one of the factors which may contribute to the progression of chronic renal failure in patients with renal disease [1–5]. However, it has not been discussed in detail which blood pressure, i.e. the systolic or the diastolic (or mean), is more responsible for the progression of renal failure. Shimamatsu et al. [1] have previously reported that the diastolic blood pressure (but not the systolic) was significantly correlated with the progression (derived from plots of the reciprocal serum cretinine versus time) of renal failure in patients with chronic glomerulonephritis. As well, the progression rate of renal failure in patients with a diastolic blood pressure of less than 90 m Hg was significantly lower than that in patients with one of more than 90 mm Hg [1]. Bergstrom et al. [2] also reported that the retardation of progression of renal failure was associated with an improvement in diastolic blood pressure control from 93 to 90 mm Hg. On the other hand, Oldrizzi et al. [3] showed that the mean blood pressure did not affect the progression of renal failure. A recent paper by Brazy et al. [4] confirmed that a diastolic (but not systolic or mean) blood pressure of less than 90 mm Hg was associated with a slower rate of progression to end-stage renal disease. In this context, the study by Eliahou et al. [5] is of interest; they reported a favorable effect of the calcium channel blocker nisoldipine on the progression of renal failure. These authors stressed the beneficial effect of other factors rather than blood pressure control because no significant difference in the reduction of systolic blood pressure was observed between the nisoldipinetreated group and the group treated with placebo/standard antihypertensives. However, they also described a significant reduction in diastolic blood pressure from 90 to 85 mm Hg (p < 0.03) in the nisoldipine group while no significant change (from 93 to 91 mm Hg) occurred in the placebo group. Although the authors thought that this change in diastolic pressure was too small to be of clinical importance, I think that this significant difference in changes in diastolic pressure should not be ignored in clinical practice from the viewpoint of long-term control of blood pressure. These clinical studies suggest that the diastolic blood pressure may affect more significantly the progression of renal failure than the systolic or mean blood pressure, and also, from a practical point of view, the control of a diastolic blood pressure of less than 90 mm Hg may be important to preserve the renal function or to blunt the progression of chronic renal failure. References

Regulation of platelet count by erythropoiesis-stimulating agents – iron axis in hemodialysis patients

Higher doses of erythropoiesis-stimulating agents (ESAs) contribute to atherothrombotic cardiovascular disease in hemodialysis (HD) patients. Thrombocytosis is associated with increased mortality in ESA-treated HD patients. We investigated variables affecting platelet count and its variability (platelet count increment [Δplatelet count]) in HD patients. This retrospective longitudinal and observational study of HD outpatients was carried out over 3 years. The outcome was independent determinants of platelet count and Δplatelet count, which were associated with iron indices, ESA dose, and C-reactive protein. In univariate regression analysis, V-shaped relationship was observed between platelet count and transferrin saturation (TSAT), ferritin, serum iron, and hemoglobin (Hb) with the bottom of 0.21, 330 ng/mL, 49 µg/dL, and 10.3 g/dL, respectively. Mixed-effect multivariate regression analysis revealed that TSAT (inversely), Hb ≤10.3 g/dL (inversely), C-reactive protein, and ESA dose were independently associated with platelet count. Δplatelet count was independently and inversely correlated with ΔTSAT and directly correlated with Δferritin. TSAT was independently and inversely associated with ESA dose. ESA dose was directly correlated with iron dose and inversely correlated with TSAT, ferritin ≤330 ng/mL, and Hb ≤10.3 g/dL. ESA dose and TSAT were correlated in determining platelet count and Δplatelet count. Targets of iron indices that reflect iron supply sufficient to avoid platelet count increment and variability may be >21% of TSAT and 300 ng/mL of serum ferritin for appropriate ESA therapy in HD patients.

A case of chronic renal failure with ruptured aneurysm of the sinus of Valsalva treated by open heart surgery

Valsalva洞動脈瘤破裂は大動脈基部のValsalva洞が下外方に拡大突出し破綻する比較的稀な疾患である. 我々は本症を合併した慢性腎不全症例を経験した. 患者は44歳男, 昭和55年IgA腎症と診断され, 腎機能が低下傾向にあった. 昭和61年4月突然胸部圧迫感・労作時呼吸困難が出現, 連続性心雑音も認められ, 腎機能も急激に低下したため, 当科に入院した. クレアチニンクリアランスは6-8ml/minと比較的保たれていたが, 腎機能低下による心不全の増悪, ならびに心臓カテーテル検査・大動脈造影・開心術による腎不全の増悪の可能性を考慮し, 早期に血液透析に導入し, 根治術を施行し良好な結果を得た.