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Triplex formation-based artificial transcription factor to recognize any upstream sequence of desired genes was developed to regulate expression of any target genes. The reporter beta-galactosidase activity in yeast was increased 1.5-2 times by the introduction of the artificial transcription factor. The novel factor may be a useful tool to regulate expression of any target genes and reveal unknown function of the target genes.

Accurate estimation of the glomerular filtration rate (GFR) is crucial for the detection of chronic kidney disease (CKD). In clinical practice, GFR is estimated from serum creatinine using the Modification of Diet in Renal Disease (MDRD) study equation or the Cockcroft-Gault (CG) equation instead of the time-consuming method of measured clearance for exogenous markers such as inulin. In the present study, the equations originally developed for a Caucasian population were tested in Japanese CKD patients, and modified with the Japanese coefficient determined by the data.The abbreviated MDRD study and CG equations were tested in 248 Japanese CKD patients and compared with measured inulin clearance (Cin) and estimated GFR (eGFR). The Japanese coefficient was determined by minimizing the sum of squared errors between eGFR and Cin. Serum creatinine values of the enzyme method in the present study were calibrated to values of the noncompensated Jaffé method by adding 0.207 mg/dl, because the original MDRD study equation was determined by the data for serum creatinine values measured by the noncompensated Jaffé method. The abbreviated MDRD study equation modified with the Japanese coefficient was validated in another set of 269 CKD patients.There was a significant discrepancy between measured Cin and eGFR by the 1.0xMDRD or CG equations. The MDRD study equation modified with the Japanese coefficient (0.881xMDRD) determined for Japanese CKD patients yielded lower mean difference and higher accuracy for GFR estimation. In particular, in Cin 30-59 ml/min per 1.73 m(2), the mean difference was significantly smaller with the 0.881xMDRD equation than that with the 1.0xMDRD study equation (1.9 vs 7.9 ml/min per 1.73 m(2); P0.01), and the accuracy was significantly higher, with 60% vs 39% of the points deviating within 15%, and 97% vs 87% of points within 50%, respectively (both P0.01). Validation with the different data set showed the correlation between eGFR and Cin was better with the 0.881xMDRD equation than with the 1.0xMDRD study equation. In Cin less than 60 ml/min per 1.73 m(2), the accuracy was significantly higher, with 85% vs 69% of the points deviating within 50% (P0.01), respectively. The mean difference was also significantly smaller (P0.01). However, GFR values calculated by the 0.881xMDRD equation were still underestimated in the range of Cin over 60 ml/min per 1.73 m(2).Although the Japanese coefficient improves the accuracy of GFR estimation of the original MDRD study equation, a new equation is needed for more accurate estimation of GFR in Japanese patients with CKD stages 3 and 4.

Definition and classification of chronic kidney disease: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Chronic kidney disease (CKD) is a worldwide public health problem, with adverse outcomes of kidney failure, cardiovascular disease (CVD), and premature death. A simple definition and classification of kidney disease is necessary for international development and implementation of clinical practice guidelines. Kidney Disease: Improving Global Outcomes (KDIGO) conducted a survey and sponsored a controversies conference to (1) provide a clear understanding to both the nephrology and nonnephrology communities of the evidence base for the definition and classification recommended by Kidney Disease Quality Outcome Initiative (K/DOQI), (2) develop global consensus for the adoption of a simple definition and classification system, and (3) identify a collaborative research agenda and plan that would improve the evidence base and facilitate implementation of the definition and classification of CKD.The K/DOQI definition and classification were accepted, with clarifications. CKD is defined as kidney damage or glomerular filtration rate (GFR) 30 mg/g in two of three spot urine specimens. GFR can be estimated from calibrated serum creatinine and estimating equations, such as the Modification of Diet in Renal Disease (MDRD) Study equation or the Cockcroft-Gault formula. Kidney disease severity is classified into five stages according to the level of GFR. Kidney disease treatment by dialysis and transplantation should be noted. Simple, uniform classifications of CKD by cause and by risks for kidney disease progression and CVD should be developed.

Suppression on both bone formation and absorption is a characteristic histology of adynamic (or aplastic) bone (ABD). This new entity of renal osteodystrophy started to appear in bone biopsy findings in 1983. Most significant etiology of adynamic bone is relatively lower serum PTH level. Any study has failed to demonstrate that ABD would increase the incidence of bone fracture in dialysis patients. However, ABD increases the risk of hypercalcemia because a decrease in calcium uptake by bone and might shorten the life span of dialysis patients.

NKF (National Kidney Foundation) launched the Dialysis Outcomes Quality Initiatives (DOQI) in 1995 and reported first guideline on dialysis therapy in Autumn of 1997. In 1999, DOQI was further developed into the Kidney Disease Outcomes Initiatives (K/DOQI), in which the target of clinical practice has included the entire phase of chronic kidney diseases (CKD). K/DOQI revised first guideline by DOQI in 2002 and also published the "Chronic Kidney Disease:Evaluation, Classification, and Stratification" in 2002 and "Proteinuria and Other Markers of Chronic Kidney Disease "in 2003, and then "Bone Metabolism and Disease in Chronic Kidney Disease" in the fall of 2003. These guidelines were prepared by working group and review team. For instance, the review team first searched 4,233 literatures and finally 467 relevant literatures was selected for citation as the basis of evidence. Based on the summary table of these literatures, working group prepared a draft guideline. Finally, the present guideline consists of 201 pages totally and reflects a dedicated effort by the team. K/DOQI has now started the effort to develop their guideline into truly a global one.

In Japan, three oral preparations (calcitriol, alfacalcidol and falecalcitriol) and two intravenous preparations (calcitriol and maxacalcitol) are now available for the vitamin D(3) therapy in renal osteodystrophy. In general, oral therapy is indicated for mild cases of secondary hyperparathyroidism (intact PTH300 pg/mL) to maintain adequate level of serum PTH except "calcitriol oral pulse therapy" for moderate to severe cases. Recently, intravenous therapy has been introduced to treat more severe cases by using the advantage of rapid clearance of these metabolites. In order to use these preparations safely, adequate level of both serum intact PTH (150-300 pg/mL) and Ca/P product (55) should be maintained to prevent from adynamic bone and vascular calcification.

Following four etiologies are considered as the possible reason for secondary hyperparathyroidism in the previous reports. First, a decreased serum concentration of 1,25(OH) 2 D 3 directly stimulates PTH secretion. Second, hypocalcemia directly stimulates PTH secretion which is independent of 1,25(OH) 2 D 3 action. Third, the presence of decreased calcemic response to PTH. Fourth, there is a strong possibility that hyperphosphatemia indirectly and/or directly may stimulate PTH secretion. The treatment of secondary hyperparathyroidism should be modified according to the stage of uremia. Excess suppression of PTH secretion could cause an adynamic bone disease. Early start of the treatment would be beneficial to prevent the bone from the development of PTH resistance.

BACKGROUND Soya foods, a staple in several Asian countries, have received increasing attention because of their nutritional properties and their high isoflavone content. We have shown recently abnormal pharmacokinetics of soya isoflavones following acute oral intake, in soya-naive end-stage renal disease (ESRD) patients. No information is available, however, about blood levels of soya isoflavones in ESRD patients with habitual soya intake. Additionally, no information is available about the conjugation profile of these compounds in ESRD patients. METHODS To assess the relationship between habitual soya intake on blood isoflavone levels in ESRD patients, we recorded dietary soya food intake and analysed circulating levels of soya isoflavones in randomly selected, clinically stable haemodialysis patients from the United States (n = 20), Thailand (n = 17) and Japan (n = 20). Dietary records and three weekly blood samples were collected from each participant. Combined isoflavones and individual genistein, daidzein, glycitein and O-desmethylangolensin (DMA) were analysed in serum by liquid chromatography/mass spectrometry. Lipid phase micronutrients, including tocopherols, carotenoids and retinol were also measured to compare ethnic differences in isoflavones with those of more common lipid soluble antioxidant micronutrients. RESULTS Soya intake was higher in Japanese than in Thai patients and it was negligible in the US patients. Blood levels of genistein were very elevated and significantly higher in the Japanese patients (1128 +/- 205 nM), as compared with the Thai and US patients (258 +/- 64 and 168 +/- 49 nM, respectively; P < 0.001). The other isoflavones followed the same trend. Daidzein was more concentrated than genistein in the dialysis patients. Robust correlation was present between weekly soya intake and blood isoflavone levels (r = 0.56, P < 0.001). Despite very high total isoflavone concentrations, the levels of unconjugated and sulphated isoflavones in the Japanese patients were comparable to those described in healthy subjects. Compared with the striking difference in isoflavones, more easily accessible dietary antioxidants, including tocopherols, carotenoids and retinol, differed only minimally or not at all in the three groups. CONCLUSIONS ESRD patients appear to accumulate isoflavones as a function of dietary soya intake, resulting in blood concentrations that are higher than those reported in subjects with preserved kidney function. Even in the presence of very elevated total isoflavone levels, the concentrations of the unconjugated and sulphated fractions are comparable to those of healthy subjects. A discrepancy is noted between accumulation of soya isoflavones and other more common lipid-soluble antioxidant micronutrients.

Calciphylaxis is a rapidly developing, fatal process of vascular calcium deposition with prominent cutaneous manifestation. We treated a long-term haemodialysis patient who developed an analogous disorder limited to the lungs. A 57-year-old man was admitted for initiation of peritoneal dialysis because limited cardiac reserve precluded further haemodialysis. He was treated successfully for pneumonia until hypoxia and progressive hypercalcaemia developed. 99mTc-methylene disphosphonate scintigraphy showed diffusely increased pulmonary uptake. Death supervened despite aggressive and successful treatment of hypercalcaemia. Autopsy studies included immunohistochemistry and morphometric studies of bone. Alveolar capillary walls showed diffuse calcium deposition. Both gross and microscopical findings differed from those of typical metastatic calcification in dialysis patients. Immunoreactivity for parathyroid hormone-related protein was present in the lesions. Bone histomorphometry indicated mild osteitis fibrosa. Pneumonia is believed to have caused local synthesis of parathyroid hormone-related protein that, along with high calcium × phosphorus product, contributed to calcium deposition. By analogy with the cutaneous process we termed the deposition ‘pulmonary calciphylaxis’.

To examine the effectiveness of 22-oxacalcitriol (OCT) injection on the improvement of severe osteitis fibrosa, we studied 10 hemodialyzed patients (age, 59 +/- 12 years). The initial OCT dose was 5 microg and was administered three times weekly at the end of each hemodialysis session. OCT doses (1, 3, 5, 10, 15, and 20 microg) were changed in subsequent weeks to maintain serum calcium levels at less than 11.5 mg/dL. Administration of OCT significantly suppressed serum intact parathyroid hormone (PTH) from an initial level of 1,193 +/- 584 to 775 +/- 552 pg/mL in the 24th week (n = 10). OCT increased PTH levels again to 857 +/- 635 pg/mL in the 48th week (n = 7). Among the 10 patients, 5 patients (high responders) showed more than a 50% suppression of serum intact PTH levels at the end of the study. The rest of the patients had hypercalcemia and did not receive increased OCT doses (low responders). At the start of the treatment, the only difference between high and low responders was serum calcium level. Serum calcium levels (adjusted for serum albumin level) increased from 9.7 +/- 0.7 mg/dL (n = 10) at the beginning to 10.5 +/- 0.6 mg/dL (n = 10) in the 24th week and to 11. 1 +/- 0.7 mg/dL (n = 7) in the 48th week. Six patients (1 to 6) agreed to undergo a second bone biopsy in the 24th week of OCT administration. In bone histomorphometric measurements, OCT significantly changed bone marrow fibrosis, mineralization (labeled mineralizing surface and bone formation rate), and osteoid formation (osteoid volume and thickness). In conclusion, intravenous OCT effectively suppressed PTH secretion and improved the bone histological characteristics of severe osteitis fibrosa, especially in patients with initial serum calcium levels less than 10 mg/dL. With concerns about OCT causing adynamic bone, additional bone histological data are needed to ensure the long-term safety of OCT.

Pregnancy-associated hypopituitarism (PAH) has been referred to as Sheehan’s syndrome and lymphocytic hypophysitis, both of which are occasionally disclosed several decades after delivery. We report the rare case of a 70-year-old woman diagnosed with PAH with empty sella 42 years after her second delivery; she had had an episode of hypovolemic shock during her second delivery. She had been referred to our hospital because of the emergence of non-sustained ventricular tachycardia and symptoms of appetite loss and general fatigue accompanied by hyponatremia, hypoglycemia, and hypothyroidism. Hypopituitalism and secondary adrenal insufficiency had been revealed after her hospitalization. She had suffered from Raynaud’s syndrome for the past several decades. Our testing revealed that the patient had autoantibodies for thyroid peroxidase, thyroglobulin, and centromere, indicating the diagnosis of chronic thyroiditis and limited scleroderma. Her series of symptoms had been treated successfully by hydrocortisone and thyroid hormone replacement therapy. To the best of our knowledge, latent PAH accompanied by limited scleroderma have not been described in the international literature to date though quite a few latent cases may exist. We assume that some autoimmune mechanism during the perinatal period may possibly be a common step in the pathogenesis of PAH, chronic thyroiditis and limited scleroderma.

We studied 26 non-dialysed patients with chronic renal failure [creatinine clearance (CCr) 32.6 +/- 12.7 ml/min]. They were divided into three groups according to their CCr and serum intact parathyroid hormone (PTH) and were given 0.5 micrograms/day oral calcitriol (calcitriol group, n = 8), 3 g/day calcium carbonate (CaCO3 group, n = 10), or neither (control uraemic group, n = 8). Serum intact PTH decreased from 154 +/- 75 to 90 +/- 43 pg/ml in the calcitriol group (P < 0.01) and from 162 +/- 97 to 77 +/- 62 pg/ml in the CaCO3 group (P < 0.001). Calcium carbonate was also effective in suppressing serum tartrate-resistant acid phosphatase, alkaline phosphatase and intact osteocalcin levels, while calcitriol did not suppress serum osteocalcin. Secretion of interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) by phytohaemagglutinin A (PHA)-activated peripheral blood mononuclear cells (PBMC) was greater in uraemic patients than in age-matched healthy controls (n = 8). Calcitriol was effective in suppressing secretion of both cytokines, while calcium carbonate was capable of suppressing only TNF-alpha secretion. CCr decreased from 37.4 +/- 15.4 to 33.0 +/- 11.8 ml/min (P < 0.05) in the CaCO3 group, while it did not decrease in either the calcitriol group or the control uraemic group during a 6 month period. These results suggest that supplementation with calcitriol is necessary to maintain bone formation and normalize IL-1 beta and TNF-alpha secretion by activated PBMC in uraemic patients.

An ATP-dependent Ca2+ uptake system from rat renal cortical basolateral membranes was solubilized with Triton X-100 and reconstituted into liposomes with lecithin. In the presence of Mg2+, Ca2+ uptake in the reconstituted vesicles was time and ATP dependent and was inhibited by vanadate. Ca2+ uptake in basolateral membrane vesicles depleted of endogenous calmodulin was enhanced by exogenous calmodulin and depressed by R-24571. This sensitivity to calmodulin and R-24571 was lost upon reconstitution in the presence and absence of leupeptin. Vesicles containing Ca2+ uptake activity were separated by gradient centrifugation after Ca2+ was taken up and accumulated as calcium phosphate in the vesicles. This resulted in Ca2+ uptake activity that was enriched 25 times. However, Ca(2+)-dependent adenosinetriphosphatase (ATPase) activity was not enriched significantly. This Ca(2+)-ATPase had two kinetic forms for Ca2+: one was a high-affinity low-capacity form; the other had a low affinity and high capacity. The Ca(2+)-ATPase activity also had two kinetic forms for ATP. All kinetic forms were inhibited by Mg2+. Vanadate, calmodulin, and R-24571 had no effects on Ca(2+)-ATPase activity. A protein doublet of Ca(2+)-dependent hydroxylamine-sensitive phosphorylated intermediates was demonstrated at 125 and 136 kDa in the purified vesicles. This doublet was not altered by addition of leupeptin throughout the purification.

Parathyroid hormone (PTH) stimulates active Ca2+ reabsorption in the distal convoluted tubule of the rat and in the cortical connecting tubule, distal convoluted tubule, and granular portion of the cortical collecting tubule of the rabbit. The dominant mechanism of Ca2+ reabsorption in the proximal tubules is passive diffusion via the paracellular pathway and PTH does not stimulate this Ca2+ transport. The distal tubules are equipped with molecular mechanisms which favor active transcellular Ca2+ transport. 1,25(OH)2D3 dependent calcium binding protein (CaBPr) facilitates Ca2+ diffusion in the cytosolic space and increases the supply of the Ca2+ pump. PTH regulates the Ca2+ pump directly by increasing the affinity for cytosolic Ca2+ and by facilitating Ca2+ extrusion from the cell. Lack of CaBPr makes the proximal tubule less capable of transcellular Ca2+ reabsorption.

The authors report a case of rapidly progressive renal failure associated with Castleman's disease. Renal biopsy revealed crescentic glomerulonephritis associated with marked tubulointerstitial nephritis. This kind of renal lesion has never been reported in association with angiofollicular lymph node hyperplasia (Castleman's disease) or other immunoblastic disorders. The patient initially required hemodialysis therapy. However, steroid therapy was effective in treating the systemic manifestations of Castleman's disease and some renal function was recovered. The patient was finally withdrawn from hemodialysis therapy.

Deterioration of renal function produces various abnormalities, of trace element metabolism in the patients. The therapy of uremia such as an aluminum containing phosphate binder and hemodialysis also causes these abnormalities in the patients with chronic renal failure. These abnormalities could be an important causality of uremia.

Vanadium (V) has been reported to inhibit a number of enzyme activities such as those of Na(+)-K(+)-ATPase. The main excretory pathway of this element is via the kidney. These facts led us to study the V distribution in uremic patients. As a result, hemodialysis patients at our dialysis center exhibited extremely high levels of serum V (23.9 +/- 11.3 ng/ml, n = 43) as compared with healthy adults. Nondialysis patients did not show increased serum V concentrations. The V contents were significantly elevated in the skin and in the aortae of hemodialysis patients. It was found that the tap water from Kanagawa prefecture, Japan, had the highest V concentrations among the 21 cities in Japan and the US. In conclusion, oral ingestion of V-contaminated water has likely caused an accumulation of the metal in patients with end-stage renal failure.

107例の術後ないし出血性合併症をもつ血液透析患者を対象に, nafamostat mesilate (FUT-175; FUT) を抗凝固薬として使用した血液透析を平均7.5回 (約16日間) 施行し, その透析用局所抗凝固薬としての有用性を多施設共同研究にて検討した. FUTの有効投与量は34.2±1.2mg/hrと判定され, 本投与量投与時には, 対照としたヘパリンを用いた血液透析時 (減ヘパリン化法または局所ヘパリン化法) に比較して, 透析器内残血は減ヘパリン化法よりも有意に少なく, 局所ヘパリン化法とは差がなかった. また動・静脈側ドリップチェンバー内残血にヘパリン使用時との差は認められなかった. 血液透析中のセライト活性化凝固時間 (CCT) は体内循環血液で全く延長しないのに対し, 体外循環路内血液ではヘパリンと同等ないしそれ以上に延長し, 透析終了後15分でもCCTの延長は全く認められなかった. FUT使用中, 透析の開始により出血の増悪した透析は21/573 (3.7%) に止まり, 透析前から活動性出血がみられた145透析中134透析 (92.4%) で出血の増悪なしに血液透析が可能であった. またブラッドアクセス穿刺部抜針後の止血時間は70%の症例でヘパリン使用時に比して短縮した. FUT使用期間中透析・除水効率は高く保たれ, 全体としで異常な臨床検査値の変動は認められなかった. 副作用は嘔気, 嘔吐の消化器症状が4例, 頭痛, 全身掻痒感各1例の計6例にみられ, うち4例はFUTとの関連性は不明と判定された. 不明例を含め副作用発現率は症例数当り5.6%, 透析回数で1.2%であった. 局所抗凝固薬としてのFUTの薬効評価は有効率95.3%, 安全率97.2%, 有用率94.4%と判定された. 以上の成績より, FUTは血液透析用局所抗凝固薬として, 特に手術前後および出血性合併症を有する透析患者の血液透析に広く臨床効果が期待できる.

An abnormal level of serum lipids may be one of the major risk factors for the development of atherosclerosis in patients with chronic renal failure (CRF). In the present study, the effect of polyunsaturated fatty acid-rich and low carbohydrate diet on serum lipids and HDL-cholesterol was studied in 6 nonnephrotic and nondialyzed patients with CRF on an isocaloric basis. Serum triglycerides decreased significantly from 2.08 +/- 0.93 mmol/l (183 +/- 82 mg/dl) to 1.49 +/- 0.83 mmol/l (131 +/- 73 mg/dl) by consumption of polyunsaturated diet (p less than 0.01). The 'HDL-cholesterol ratio' increased significantly and LCAT decreased on a polyunsaturated diet. In conclusion, the consumption of a polyunsaturated fatty acid-rich diet tends to normalise increased serum triglycerides and lowered 'HDL-cholesterol ratio' in patients with CRF and may be effective for prevention of atherosclerotic vascular sequellae.

A 42-year-old woman presented with orthostatic hypertension. Increased plasma renin activity was noted and blood pressure rose gradually with standing. Selective renal arteriography indicated narrowing of the distal portion of the right renal artery and poststenotic dilatation and signs of arterial stenosis due to fibromuscular dysplasia. Greater arterial narrowing resulted from tortion due to nephroptosis brought about by excessive renin secretion. Thus, both renal arterial stenosis and nephroptosis were considered responsible for the present orthostatic hypertension. Percutaneous transluminal renal angioplasty was found very effective for normalizing standing blood pressure and renal blood flow.

The basolateral segment of the rat renal tubular plasma membrane possesses Ca2+-dependent ATPase activity which was independent of Mg2+. Two kinetic forms were found: one, was a high affinity (apparent Km for free Ca2+ of 172 nM) low capacity (Vmax of 144 nmol of Pi X min-1 mg-1 protein) type; the other, had low affinity (apparent Km of 25 microM) and high capacity (896 nmol of Pi X min-1 X mg-1 protein). Mg2+ inhibited both Ca2+-ATPases. The high affinity enzyme exhibited positive cooperativity with respect to ATP, with a n value of 1.6. Ca2+-ATPase activity was not affected by calmodulin and was not inhibited by vanadate. On the other hand, both high and low affinity Ca2+-ATPase activities were increased when 1,25-dihydroxycholecalciferol was given to vitamin D-deficient rats. Kinetically, the enhanced activities were due to an increase in the Vmax values; the apparent affinities for free Ca2+ were not changed. The physiological function of the vitamin D-sensitive, Mg+-independent, Ca2+-ATPase activities remains to be established.

The development of techniques for the isolation of highly purified baso-lateral membrane vesicles (BLMV) from the renal tubular epithelial cells enabled us to investigate the mechanism of calcium extrusion at this barrier of the cell. Two mechanisms of calcium transport known to exist in other tissues have been identified in the renal BLMV. These mechanisms are ATP-dependent Ca2+ transport and Na+/Ca2+ exchange. Yet, several aspects of these transporters are quite unique in the renal tubular cells.

Plasma concentrations of 6 essential trace elements were measured in undialyzed and hemodialyzed patients with chronic renal failure (CRF) and in healthy volunteers by tube-excited X-ray fluorescence analysis and atomic absorption analysis. The influences of hemodialysis on plasma concentrations of Al, Zn, Cu and Br were also studied. High plasma concentrations of Al and Cu and low concentrations of plasma Zn were found in nondialyzed patients with CRF. Plasma concentrations of Al and Cu increased and Zn and Br decreased in the hemodialyzed patients with CRF. An elevated concentration of plasma Al may be primarily caused by permeation from dialysate across the dialyzer membrane. The use of water produced by reverse osmosis will prevent the elevation of plasma Al concentration in patients with CRF.

Trace element concentrations in hair and fingernails and plasma of nondialyzed, hemodialyzed and hemofiltered patients with chronic renal failure and healthy volunteers were measured by atomic and flameless atomic absorption spectrophotometry and neutron activation analysis. Plasma aluminum concentrations in all three groups of patients were higher than in the controls. Aluminum levels in plasma and red blood cells were higher in hemofiltered patients than in dialyzed patients. The aluminum concentrations in the hair of both nondialyzed and dialyzed patients was higher than in the controls, while that in the hemofiltered patients it was not. These elevated aluminum concentrations appear to be mainly caused by the use of aluminum-contaminated dialysate. Calcium concentrations in the hair of nondialyzed and dialyzed patients were higher than in the controls. Plasma zinc concentrations in all the patients were lower than the controls, and the concentrations in hemofiltered patients were lower than in the dialyzed patients.

Serum lipids were studied in 98 nonnephrotic patients with chronic renal failure at pre-dialysis, dialysis and post-transplant stages. Hypertriglyceridemia was observed in pre-dialysis patients, altho

An ATP-driven Ca 2+ pump in the basolateral membrane of rat kidney cortex pumps Ca 2+ out of the cell at the expense of MgATP ( K m = 0.191 mM). This pump has a high affinity for free Ca 2+ (26 nM). Vanadate, lanthanum, N -ethylmaleimide and calmodulin inhibitor R24571 inhibited this pump activity. Dimethyl[2- 14 C]oxazolidine-2,4-dione ([ 14 C]DMO) was entrapped in the vesicles in association with the ATP-driven Ca 2+ influx. The ATP-driven Ca 2+ influx was stimulated by the intravesicular acid pH and an upper convex Lineweaver-Burk reciprocal plot suggested two possible kinetics; one is that this Ca 2+ pump is an allosteric enzyme with more than 1.72 H + binding sites and another is the presence of two Ca 2+ pumps with different affinities for H + . Valinomycin study indicated that the ATP-dependent Ca 2+ transport by the BLMV was electroneutral and voltage independent. These results strongly suggest that the ATP-driven Ca 2+ pump in the renal basolateral membrane catalyzes an electroneutral Ca 2+ /H + antipon.