Posterior leukoencephalopathy syndrome during steroid therapy in a down syndrome patient with nephrotic syndrome [4]

[No abstract available

Rapid decrease of intact parathyroid hormone could be a predictor of better response to cinacalcet in hemodialysis patients

Purpose: Cinacalcet is effective for treating refractory secondary hyperparathyroidism (SHPT), but little is known about the response rates and clinical factors influencing the response. Materials and Methods: A prospective, single-arm, multi-center study was performed for 24 weeks. Cinacalcet was administered to patients with intact parathyroid hormone (iPTH) level greater than 300 pg/mL. Cinacalcet was started at a dose of 25 mg daily and titrated until 100 mg to achieve a serum iPTH level <300 pg/mL (primary end point). Early response to cinacalcet was defined as a decrease of iPTH more than 50% within one month. Results: Fifty-seven patients were examined. Based on the magnitude of iPTH decrease, patients were divided into responder (n=47, 82.5%) and non-responder (n=10, 17.5%) groups. Among the responders, 38 achieved the primary end point, whereas 9 patients showed a reduction in serum iPTH of 30% or more, but did not reach the primary end point. Compared to non-responders, responders were significantly older (p=0.026), female (p=0.041), and diabetics (p<0.001). Additionally, early response was observed more frequently in the responders (30/47, 63.8%), of whom the majority (27/30, 90.0%) achieved the primary end point. Multivariate analysis showed that lower baseline iPTH levels [odds ratio (OR) 0.96, 95% confidence interval (CI) 0.93-0.99], the presence of diabetes (OR 46.45, CI 1.92-1125.6) and early response (OR 21.54, CI 2.94-157.7) were significant clinical factors affecting achievement of iPTH target. Conclusion: Cinacalcet was effective in most hemodialysis patients with refractory SHPT. The presence of an early response was closely associated with the achievement of target levels of iPTH. © Yonsei University College of Medicine 2013

Changes in Intracellular Ca2+ Concentration of Rabbit Coronary Artery Smooth Muscle Cell during Ischemic Cardioplegic Period

To elucidate the possibility whether an elevation of intracellular Ca2+ concentration ([Ca2+]) in rabbit coronary artery myocytes during ischemic cardioplegic period may serve as one of the mechanisms of the 'no-reflow' phenomenon or not, the changes in [Ca2+]i were measured under ischemic cardioplegia conditions using a fluorescent Ca2+ indicator, fura 2/AM. When single cells were perfused with cardioplegic or ischemic cardioplegic solutions, [Ca2+]i was significantly increased and the degree of [Ca2+]i elevation was further augmented by the ischemic cardioplegic solution. Pretreatment of a sarcoplasmic reticulum emptying agent, 20 mM caffeine, had no effect on ischemic cardioplegia-induced [Ca2+]i changes, but application of a Ca2+ channel blocker, 5 × 10-7M nifedipine, or an antagonist of Na+/Ca2+ exchange, 5 mM Ni2+, significantly inhibited the [Ca2+]i elevation, respectively. The magnitude of ischemic cardioplegia-induced [Ca2+]i elevation was dependent on the Ca2+ concentration of perfusate in the range of 0 and 2.5 mM. When Ni2+ was added to the reperfusion solution, recovery of ischemic cardioplegia-induced [Ca2+]i elevation was very rapid compared with the controls. It is concluded that ischemic cardioplegia-induced [Ca2+]i elevation may serve as one of the mechanisms of the 'no-reflow' phenomenon in rabbit coronary artery smooth muscle, cells. We propose that Na+/Ca2+ exchange may serve as a key function in ischemic cardiopelgia-induced [Ca2+]i elevation

황체막에서의 Ca++-ATPase의 특성

의학과/석사[영문] [한글] 세포내 Ca**++ 농도에 의해 황체기능이 조절된다고하며(Higuchi등, 1976: Gore 및 Behr man, 1984: Dorflinger등, 1984) 또 황체세포내 Ca**++ 농도의 조절은 황체세포막에 있는 Ca**++ -ATPase에 의해 이루어질 것이라고 하므로(Verma 및 Penniston, 1981) 이를 토대 로 황체에서 분리한 황체세포막의 light membrane과 heavy membrane(Bramley 및 Ryan, 19 78a, 1978b, 1980), 그리고 세포내 Ca**++ 저장소로 알려진 microsome분획 (Moore 및 Pas tan, 1978, 대부분이 endoplasmic reticulum)에서 Ca**++ -ATPase를 확인하고 그들의 물 리화학적 성질 및 반응속도론적인 (kinetic) 특성을 조사하였다. 황체에서 분리한 light membrane과 heavy membrane, microsome분획은 모두 Ca**++에 대 해 낮은 Ca**++농도에서 활성화되는(Km, 10∼30 nM) high affinity Ca**++-ATPase와 이보 다 높은 농도에서 활성화되는 (K1/2, 40 μM) low affinity Ca**++-ATPase 두 종류로 되 어 있으나 양자간에 서로 cooperativity는 없다. High 및 low affinity Ca**++-ATPase 활 성도는 어느 Ca**++농도에서나 light membrane에서 가장 높았고 microtome분회에서 가장 낮았다. High affinity Ca**++-ATPase의 경우 Hill's coefficient가 모든 membrane분획에 서 거의 1인 것으로 보아 Ca**++에 대한 결합부위(binding site)는 하나인 것으로 생각된 다.각 membrane 분획의 high affifinity Ca**++-ATPase는 ATP농도를 증가시킴에 따라 활 성도가 sigmoid하게 증가되며 Hill's coofficient가 거의 2인 것으로 보아 ATP에 대한 결 합부위는 둘이며 각 결합부위간에는 서로 positive cooperative effect가 있어 하나의 부 위에 ATP가 결합함으로써 다른 부위에 ATP의 결합을 용이하게 해주는 것으로 생각된다. 적정 pH는 light membrane의 Ca**++-ATPase는 pH 7∼8로 비교적 넓은 영역을 갖고 있으며 , heavy membrane과 microsome분획의 Ca**++-ATPase는 적정 pH가 8.5로 약간 알카리쪽으 로 이동되어 있는 것을 볼 수 있다. 황체막과 microsome분획에 있는 Ca**++-ATPase의 활 성도는 온도변화에 민감하여 생리적 온도보다(37℃) 낮은 온도에서 lipid phase의 전이가 일어나 Ca**++-ATPase의 활성을 변화시킨다. Ca**++-ATPase의 활성화에너지는 전이온도 이하에서는 각 membrane이 거의 같은데 반하여 이 온도 이상에서는 heavy membrane이 가 장 크고 microsome분획에서 가장 낮았다. 이상과 같은 결과는 황체의 기능을 조절하는 것으로 알려진 세포내 Ca**++ 농도는 낮은 Ca**++농도(0.1 μM이하)에서 활성화되는 황체막과 microsome분획의 high affinity Ca** ++-ATPase에 의해 조절되고 있다는 것을 암시해 준다. Characterization of physicochemical and kinetic properties of Ca**++ -ATPase system in luteal membranes Gyu Bog Choi Department of Medical Science The Graduate School, Yonsei University (Directed by Assistant Professsor Inkyo Kin, M.D.) It has been reported that the luteal function may be regulted by the intracellular calcium in luteal cells (Higuchi et al, 1976; Dorflinger et al, 1984; Gore and Behrman, 1984) which is adjusted partially by Ca**++ ATPase activities luteal cell membranes(Verma and Penniston, 1981). However, the physicochemical and kinetic properties of Ca**++ -ATPase in luteal membranes were not fully characterized. This study was, therefore, undertaken to characterize the physicochemical and kinetic properties of Ca**++ -ATPase in luteal membranes and microsomal fractions, Known as an one of the major Ca**++ storage sites (Moore and Pastas, 1978), from the highly, luteinized ovary. Highly luteinized ovaries were obtained from PMSG-hCG injected immature female rats. Hight membrane and heavy membrane fractions and microsomal fractions were prepared by the differential and discontinuous sucrose density gradient centrifugation method described by Bramley and Ryan(1980). Light membrane and heavy membrane fractions and microsomal fractions from highly luteinized ovaries are composed of the two different kinds of Ca**++ -ATPase system. One is the highly affinity Ca**++ -ATPase which is activated in low Ca**++ concentration (km, 10-3OnM), the other is low affinity Ca**++ -ATPase activated in higher Ca**++ concentration (K1/2, 40μM). At certain Ca**++ concentrations, activities of high and low affinity Ca**++ -ATPase are the highest in light membrane fractions and are the Lowest in microsomal fractions. It appeares that high affinity Ca**++ -ATPase system have 2 binding sites for ATP (Hill's coefficient; around 2 in all membrane fractions measured) and the positive cooperativity of ATP bindings obviously existed in each membrane fractions. The optimum pH for high affinity Ca**++ -ATPase activation is around 8 in all membrane fractions measured. The lipid phase transition temperature measured by Arrhenius plots of high affinity Ca**++ -ATPase activity is around 25℃. The activation energies of high affinity Ca**++ -ATPase below transition temperature are similar in each membrane fractions, but at above transition temperature, it is the high test in heavy membrane fractions and the Lowest in microsomal fractions. According to the above results , it is Suggested that intracellular Ca**++ Level, which regulates the luteal function, may be adjusted by the high affinity Ca**++ -ATPase system activated in intracellular Ca**++ concentration range (below 0.1μM) .restrictio

Changes in cytosolic Ca²˙ concentration of single rabbit coronary artery smooth muscle cell during ischemic cardioplegic period.

의학과/박사[한글] 허혈 손상이나 재관류 손상의 원인 규명 및 이를 최소화 할 수 있는 방법들이 거의 심근세포에 국한되어 시행되어져 왔으나, 심근세포의 직접적인 손상이외에 허혈성 심근정지시와 재관류 후 관상동맥에서도 혈관 기능의 손상, 혈관막을 통한 투과도의 변화 및 "low-reflow" 현상과 같은 여러가지 가역적인 기능 손상 뿐 만 아니라 "no-reflow" 현상과 같은 비가역적인 허혈-재관류 손상이 관찰되어겼다. 이러한 "no-reflow" 현상의 기전으로는 혈관 손상에 의해 유발되는 내피세포의 부종이 혈류를 차단하거나, 혈소판이나 혈전에 의한 혈류의 차단 또는 심근세포의 ischemic contracture가 관상동맥을 압박해 정상적인 혈류를 차단하여 일어나는 것으로 알려져 있으나 아직까지 그 기전은 명확하게 밝혀져 있지 않다. 또한 관상 혈류량 조절에 중요한 역할을 하고 있는 관상동맥 평활근 세포의 수축정도가 이같은 "no-reflow" 현상에 미치는 효과에 대해서도 아직 규명되지 못하였다. 따라서 본 실험에서는 가토 관상동맥으로부터 분리한 평활근 세포를 심근정지 용액으로 관류하면서 허혈 상태를 유발하였을 때, Fura-2를 사용하여 평활근 세포내 유리 Ca**2+ 농도의 변화양상을 측정함으로서 평활근 세포의 수축이 "no-reflow" 현상의 기전중의 하나로 작용할 수 있는지를 규명하고자 실험하여 다음과 같은 결과를 얻었다. 1. 심근정지시와 허혈성 심근정지시 평활근 세포내 유리 Ca**2+ 농도는 안정시에 비해 유의하게 증가되었는데, 허혈성 심근정지의 경우 세포내 유리 Ca**2+ 농도의 증가가 더욱 더 현저하였다. 2. 심근정지시 증가되었던 세포내 유리 Ca**2+ 농도는 caffeine을 반복 전 처치하여 sarco-plasmic reticulum (SR)내 저장된 Ca**2+ 을 고갈시킨 후 caffeine이 함유된 심근정지 용액으로 관류시 세포내 유리 Ca**2+ 농도의 증가가 대조군과 유사하였다. 그러나 Ca**2+ channel booker인 nifedipine이 함유된 심근정지 총액에 의해서는 심근정지시 세포내 유리 Ca**2+ 농도의 증가가 다소 감소되었으며, Na**+ -Ca**2+ exchange 차단제인 고농도 nickel이 함유된 심근정지 용액에 의해서는 완전히 억제되었다. 3. 평활근 세포에 caffeine을 반복 전 처치하여 SR내 저장된 Ca**2+ 을 고갈시킨 후 caffeine이 함유된 허혈성 심근정지 용액으로 관류시 세포내 유리 Ca**2+ 농도의 증가는 대조군과 유사하였다. 그러나 Ca**2+ channel bloker인 nifedipine이 함유된 허혈성 심근정지 용액에 의해서는 허혈성 심근정지시 세포내 유리 Ca**2+ 농도의 증가가 대조군에 비해 의의있게 감소되었으며, Na**+ -Ca**+ exchange 차단제인 고농도 nickel이 함유된 심근정지 용액에 의해서는 nifedipine 처치시 보다 더욱 더 억제되었으나 완전히 억제되지는 않았다. 4. Ca**2+ 농도가 다른 허혈성 심근정지 용액으로 평활근 세포를 관류시 세포내 유리 Ca**2+ 농도는 용액내 Ca**2+ 농도에 비례하여 증가되었으며, Ca**2 +이 제거된 허혈성 심근정지 용액의 경우 심근정지 기간에는 세포내 유리 Ca**2+ 농도가 증가되지 않았으나 재 관류시 다소 증가되었다. 5. 허혈성 심근정지 용액으로 평활근 세포를 관류시 증가되었던 세포내 유리 Ca**2+ 농도는 nifedipine이 함유된 정상 KH용액으로 관류액을 바꾸었을 때 대조군과 거의 유사하게 안정시 세포내 유리 Ca**2+ 농도로 회복되었으나, 5mM nickel이 합유된 정상 KH 용액 으로 평활근 세포를 관류시킨 경우 세포내 유리 Ca**2+ 농도는 대조군에 비해 매우 빨리 안정시 세포내 유리 C**2+ 농도로 회복되었다. 이상의 실험결과로 보아 허혈성 심근정지 또는 재판류시 관찰되는 평활근 세포내 유리 Ca**2+ 농도의 증가가 "no-reflow" 현상의 기전중의 하나로 작용할 것이라 추측된다. Changes in cytosolic Ca**2+ concentratlon of dingle rabbit coronary artery smooth muscle cell during ischemic cardioplegic Period Gyu-Bog Choi Department of Medical Science, The Graduate School Yonsei University (Directed by Professor Bok Soon Kang) No-reflow is a specific type of vascular damage occurring when removal of coronary occlusion does net lead to restoration of coronary flow. There are three major explanations for the no-re-flow phenomenon such as endothelial cell edema, microvascular Plugging by Platelets or thrombi and coronary occlusion by ischemic contracture of the myocardium. But detailed mechanisms of no-reflow phenomenon are not known. To elucidate the possibility whether elevation of cytosolic Ca**2+ concentration during ischemic cardioplegic period is mechanism of no-reflow phenomenon or not, chanties in cytosolic Ca**2+ concentration were measured under varying experimental condition. Free [Ca**2+] in the cytosole([Ca**2+]) of single rabbit coronary artery cells was measured with fluorescent Ca**2+ indicator, Fura-2. The results obtained were summarized as follows: Resting [Ca**2+], was 134.2 ±34 nM(n=43). When sing1e cells were perfused with cardioplegic or ischemic cardioplegic solution, [Ca**2+], was significantly increased and the decree of [Ca**2+], elevation was further augmented by ischemic cardioplegic solution. Pretreatment of sarcoplasmic reticulum emptying agent(20 mM caffeine) had no effect on cardioplegia-induced [Ca**2+], change, but application of Ca**2+ channel blocker(5×17**-7 M nifedipine) or an antagonist of Na**+ /Ca**2+ exchange(5mM nickel) partially(nifedipine) or completely(nickel) inhibited the [Ca**2+], elevation. Pretreatment of caffeine had no effect on ischemic cardioplegia-induced [Ca**2+], chance, but application of nifedipine or nickel partially inhibited the [Ca**2+], elevation. Magnitude of ischemic cardioplegia-in-duces [Ca**2+], elevation was dependent on the Ca**2+ concentration of perfusate from 0 to 2.5mM. When nickel was added to reperfusion solution, recovery of ischemic cardioplegia-induced [Ca**2+],elevation was very rapid compared with control. From the above results, it may be speculated that ischemic cardioplegia-induced [Ca**2+], elevation may act as one of the mechanism of no-reflow Phenomenon in rabbit coronary artery. [영문] No-reflow is a specific type of vascular damage occurring when removal of coronary occlusion does net lead to restoration of coronary flow. There are three major explanations for the no-re-flow phenomenon such as endothelial cell edema, microvascular Plugging by Platelets or thrombi and coronary occlusion by ischemic contracture of the myocardium. But detailed mechanisms of no-reflow phenomenon are not known. To elucidate the possibility whether elevation of cytosolic Ca**2+ concentration during ischemic cardioplegic period is mechanism of no-reflow phenomenon or not, chanties in cytosolic Ca**2+ concentration were measured under varying experimental condition. Free [Ca**2+] in the cytosole([Ca**2+]) of single rabbit coronary artery cells was measured with fluorescent Ca**2+ indicator, Fura-2. The results obtained were summarized as follows: Resting [Ca**2+], was 134.2 ±34 nM(n=43). When sing1e cells were perfused with cardioplegic or ischemic cardioplegic solution, [Ca**2+], was significantly increased and the decree of [Ca**2+], elevation was further augmented by ischemic cardioplegic solution. Pretreatment of sarcoplasmic reticulum emptying agent(20 mM caffeine) had no effect on cardioplegia-induced [Ca**2+], change, but application of Ca**2+ channel blocker(5×17**-7 M nifedipine) or an antagonist of Na**+ /Ca**2+ exchange(5mM nickel) partially(nifedipine) or completely(nickel) inhibited the [Ca**2+], elevation. Pretreatment of caffeine had no effect on ischemic cardioplegia-induced [Ca**2+], chance, but application of nifedipine or nickel partially inhibited the [Ca**2+], elevation. Magnitude of ischemic cardioplegia-in-duces [Ca**2+], elevation was dependent on the Ca**2+ concentration of perfusate from 0 to 2.5mM. When nickel was added to reperfusion solution, recovery of ischemic cardioplegia-induced [Ca**2+],elevation was very rapid compared with control. From the above results, it may be speculated that ischemic cardioplegia-induced [Ca**2+], elevation may act as one of the mechanism of no-reflow Phenomenon in rabbit coronary artery.restrictio

Expression of epidermal growth factor in the developing rat kidney

Epidermal growth factor (EGF) is important in mammalian renal development. In our study, we investigated the detailed distribution and the time of the first appearance of EGF in developing rat kidney. Kidneys from embryonic 18 (E18)- and 20-day-old (E20) fetuses, postnatal 1 (P1)-, 3 (P3)-, 1 (P7)-, 14 (P14)-, and 21-day-old (P21) pups, and adults were processed for immunohistochemistry and electronmicroscopy. In adult rat kidney, EGF immunoreactivity was found in distal tubule including the thick ascending limb (TAL) and portion 1 of distal convoluted tubule (DCT1), whereas no EGF immunoreactivity was seen in portion 2 of distal convoluted tubule (DCT2) and connecting tubule. In developing kidney, EGF-positive cells first appeared at P3 and were localized in the middle portion of the differentiating TAL of the corticomedullary junction. By P7, the abundance of EGF expression had dramatically increased in the medullary TAL. Between P14 and P21, EGF immunoreactivity was found in the TAL and the DCT for the first time. However, EGF-positive and EGF-negative cells were in the TAL in developing rat kidney. EGF-positive cells did not differ from negative cells in the expression of sodium transport proteins or in the proliferation rate at P3 and P7. In the TAL, smooth-surfaced cells had strong EGF immunoreactivity, but no EGF immunoreactivity was seen in the rough-surfaced cells with well-developed microvilli. Our results suggest that the expression of EGF in developing kidney plays an important role in the regulation of growth and differentiation of the loop of Henle during kidney development and that this may act in the paracrine mode

Hypertensive hypokalemic disorders

Hypokalemia is a common clinical problem. The kidney is responsible for long term potassium homoeostasis, as well as the serum potassium concentration. The main nephron site where K secretion is regulated is the cortical collecting duct, mainly via the effects of aldosterone. Aldosterone interacts with the mineralocorticoid receptor to increase sodium reabsorption and potassium secretion; the removal of cationic sodium makes the lumen relatively electronegative, thereby promoting passive potassium secretion from the tubular cell into the lumen through apical potassium channels. As a result, any condition that decreases the activity of renal potassium channels results in hyperkalemia (for example, amiloride intake or aldosterone deficiency) whereas their increased activity results in hypokalemia (for example, primary aldosteronism or Liddle's syndrome). The cause of hypokalemia can usually be determined from the history. If there is no apparent cause, the initial step is to see if hypokalemia is in associated with systemic hypertension or not. In the former group hypokalaemia is associated with a high mineralocorticoid effect or hyperactive sodium channel as in Liddle's syndrome. In hypertensive hypokalemic patients, measurement of the renin, aldosterone, and cortisol concentrations would be of help in differential diagnosis

Serum globotriaosylceramide assay as a screening test for Fabry disease in patients with ESRD on maintenance dialysis in Korea

Background/Aims: Fabry disease is an X-linked recessive and progressive disease caused by α-galactosidase A (α-GaL A) deficiency. We sought to assess the prevalence of unrecognized Fabry disease in dialysis-dependent patients and the efficacy of serum globotriaosylceramide (GL3) screening. Methods: A total of 480 patients of 1,230 patients among 17 clinics were enrolled. Serum GL3 levels were measured by tandem mass spectrometry. Additionally, we studied the association between increased GL3 levels and cardiovascular disease, cerebrovascular disease, or left ventricular hypertrophy. Results: Twenty-nine patients had elevated serum GL3 levels. The α-GaL A activity was determined for the 26 patients with high GL3 levels. The mean α-GaL A activity was 64.6 nmol/hr/mg (reference range, 45 to 85), and no patient was identified with decreased α-GaL A activity. Among the group with high GL3 levels, 15 women had a α- GaL A genetics analysis. No point mutations were discovered among the women with high GL3 levels. No correlation was observed between serum GL3 levels and α-GaL A activity; the Pearson correlation coefficient was 0.01352 (p = 0.9478). No significant correlation was observed between increased GL3 levels and the frequency of cardiovascular disease or cerebrovascular disease. Conclusions: Fabry disease is very rare disease in patients with end-stage renal disease. Serum GL3 measurements as a screening method for Fabry disease showed a high false-positive rate. Thus, serum GL3 levels determined by tandem mass spectrometry may not be useful as a screening method for Fabry disease in patients with end stage renal disease

Relationship of peritoneal membrane transport characteristics to the nutritional status in CAPD patients

Background. The study was carried out to evaluate the role of individual peritoneal membrane transport characteristics in the nutritional status expressed as the composite nutritional index (CNI). Methods. Cross-sectional analyses of the overall nutritional status of 147 continuous ambulatory peritoneal dialysis (CAPD) patients were performed using the CNI. CNIs based on a scoring system of 10 nutritional indices including subjective global assessment, biochemical parameters and anthropometry were compared according to the results of a standard peritoneal equilibration test (PET). Results. Patients were classified as low (n = 16, 10.9%), low average (n = 59, 40.2%), high average (n = 54, 36.7%) and high (n = 18, 12.2%) transporters based on the D/P(Cr) after 4 h dwells. The mean 4 h D/P(Cr) was 0.65 ± 0.12 (0.34-0.95), and there was no significant correlation between D/P(Cr) and other demographic parameters such as age, duration of peritoneal dialysis and body surface area. D/P(Cr) was correlated with dialytic albumin loss (r = 0.47, P < 0.001), serum albumin (r = -0.46, P < 0.001), serum creatinine (r = -0.38, P < 0.001), serum IGF-1 (r = -0.37, P < 0.01) and LBM(Cr) (r = -0.26, P < 0.05). In high transporters, the serum albumin was significantly lower while dialysate protein and albumin losses were significantly greater compared with low transporters. Serum creatinine and IGF-1 concentrations as well as LBM(Cr) were also decreased in higher transporters. The mean CNI score was 8.1 ± 4.9, with a range of 0-24. CNI was positively correlated with age, duration of peritoneal dialysis, incidence of peritonitis, CRP and dialytic protein loss, whereas it was inversely correlated with ultrafiltration volume, haemoglobin and NPNA. The CNI score was significantly higher in high transporters compared with low transporters (11.7 ± 4.3 vs. 5.9 ± 1.6, P < 0.01). There was also a significant correlation between D/P(Cr) and CNI (r = 0.29, P < 0.05). Multiple regression analysis revealed that the incidence of peritonitis, duration of CAPD, CRP and D/P(Cr) were the independent factors affecting the CNI. Conclusion. Peritoneal membrane transport characteristics correlate with the overall nutritional status of peritoneal dialysis patients assessed by the scoring system of the CNI, although it is associated with a different impact on the individual nutritional indices. The results of this cross-sectional study also suggest that a high permeability state is a risk factor for malnutrition in CAPD patients. Prospective studies evaluating the changes in nutritional parameters among patients with different membrane transport rates are needed to understand better the relationship of peritoneal membrane characteristics to the nutritional status of CAPD patients

Effect of epidermal growth factor on the developing rat renal papilla

Background: Apoptosis plays an important role in the morphogenesis of the renal papilla. During kidney development, ATL is derived from the TAL in the inner medulla by apoptotic deletion of a fraction of TAL cells and the transformation of the remaining TAL cells. EGF is an important regulator of apoptosis in the kidney. Hypothesis: Exogenously administered EGF in postnatal rat affects renal papilla growth with cell proliferation and apoptosis in the loop of Henle. Methods: Rat pups received subcutaneous injections of EGF (0.3 μg/g body weight) or saline four times a day from after birth. Rats were sacrificed and the kidneys were preserved for immunohistochemistry on day 4 and day 7. The TAL was identified with antibody directed against Na-K-ATPase or BSC1, and type A intercalated cells were identified with antibody to anion exchanger 1 (AE1). Apoptosis was detected with TUNEL method, and cell proliferation with immunostaining for PCNA. Results - Primary and Secondary: EGF treatment resulted in the following: (1) reduced kidney weight; (2) shortened length of renal papilla; (3) delayed transformation of the cuboidal epithelium into the squamous epithelium of the ATL; (4) delayed elimination of type A intercalated cells in the medullary collecting duct; (5) decreased both apoptotic index and PCNA-positive cells in the TAL and the collecting duct of the renal medulla. Conclusion: These findings suggest that exogenous EGF delays the development of loop of Henle in the renal papilla by reducing both apoptosis and cell proliferation. Copyright © 2004 S. Karger AG, Basel