Migration ; seconds ; Proximal ; Cysts

Nephrotoxicity is a major limiting factor in the use of aminoglycoside antibiotics, the mechanisms for which are still speculative. To clarify the mechanisms of renal tubular cell death induced by aminoglycosides, we examined the renal proximal tubule-like cell line, LLC-PK1, after inducing apoptosis through a chronic treatment with gentamicin (GM). Changes in the expression of the Fas were also investigated. On flow cytometric analysis, 5.7 +/- 3.3% of the control cells appeared in a region of decreased forward light scatter and increased side light scatter, where both indices represent the characteristics of apoptotic cell death. Compared to the control, treatment with 10 mM of GM for 15 days significantly increased the proportion of cells in the apoptotic region to 23.9 +/- 8.5%. This finding was supported by electrophoretic analysis of the DNA extracted from the GM-treated cells, where a series of bands corresponding to integer multiples of 180 to 200 base pairs was visualized. However, the 15-day GM treatment did not cause a significant elevation in the expression of the 45 kD Fas protein, the cell surface molecule that stimulates apoptosis, by Western blot analysis. In conclusion, long-term exposure to GM induces apoptosis of the renal tubular epithelial cells, and this process may contribute to some of the aminoglycoside nephrotoxicities. Further studies are needed on the mechanism(s) of apoptosis induced by GM.
Animal ; Antibiotics, Aminoglycoside/toxicity* ; Antigens, CD95/analysis ; Apoptosis/drug effects* ; Cell Line ; Gentamicins/toxicity* ; Kidney Tubules, Proximal/pathology ; Kidney Tubules, Proximal/drug effects* ; Swine

No abstract available.
Proximal Optimization Technique ; Coronary Vessels ; Percutaneous Coronary Intervention ; Drug-Eluting Stents

Perlman syndrome is a rare autosomal recessive congenital overgrowth syndrome caused by pathogenic variants of the DIS3L2 gene at 2q37 region. Clinically this syndrome is characterized by polyhydramnios, macrosomia, distinctive facial appearance, and renal dysplasia. Prognosis of the disease is poor, and survivors usually have mental delay and a high risk of developing Wilms tumor. At present, the pathogenesis of this disease is still poorly understood. This article intends to provide a review for this disease.
Female ; Fetal Macrosomia ; Humans ; Kidney Tubules, Proximal ; Pregnancy ; Syndrome ; Wilms Tumor

Perinatal asphyxia can cause ischemic injury to immature kidney of neonates. Proximal renal tubule is the most sensitive area, showing various manifestations ranging from mild reversible injury to irreversible tubular necrosis. Aminoglycosides can be nephrotoxic in therapeutic range in immature or damaged kidney. Thess are the very important factors to be taken into corsideration on fluid therapy and nephrotoxic drugs in neonates. The purpose of this study is to detect renal dysfunction resulting from asphyxia and gentamicin treatment. The results were as follows; 1) Urinary 2-microglobulin concentration was significantly higher in neonatal asphyxia group irrespective of meconium stain (p<0.05). The group with neonatal asphyxia only (Ia) showed a gradual decline in urinary 2-microglobulin concentration and no significant difference shown when compared with control group on 7 days old (p>0.05). The group with neonatal asphyxia and meconium stain (Ib) received gentamicin for 7 days. Their urinary 2-microglobulin concentration dropped on 4 the day and increased again on 7 th day (p<0.05). The group with meconium stain only(3) showed no significant difference in urinary 2-microglobulin concentration when compared with control group (p>0.05). 2) No differences were shown in serum creatinine, serum sodium level and urinary creatinine concentrations between each group (p>0.05). 3) No differences were shown in creatinine clearance between each group (p>0.05).Fractional excretion of urinary sodium (FENa) was significantly higher on lst day in group, I, but no differences were shown afterwards (p>0.05). 4) There is no relationship between urinary 2-microglobulin concentration and serum creatinine level, creatinine clearance of FENa. 5) No differences were shown in incidence of renal dysfunction between each group. In conclusion, acute tubular injury by perinatal asphyxia recovered soon after birth. But nephrotoxic gentamicin worsened the recovering tubular injury. In case of mild fetal hypoxia without neonatal asphyxia, proximal tubular injury was not significant.
Aminoglycosides ; Asphyxia* ; Creatinine ; Fetal Hypoxia ; Fluid Therapy ; Gentamicins* ; Humans ; Incidence ; Infant, Newborn* ; Kidney ; Kidney Tubules, Proximal ; Meconium ; Necrosis ; Parturition ; Sodium

OBJECTIVESTo study the long-term results of selective vagotomy plus antrectomy in treatment of duodenal ulcer.

METHODSOne hundred and ninety-three patients with duodenal ulcer were subjected to selective vagotomy plus antrectomy from November 1977 to November 2001. These patients included 28 patients with refractory ulcer, 112 with recurrent bleeding, 41 with pylori obstruction, and 12 with duodenal and gastric ulcer.

RESULTSBAO, IMAO, PMAO and serum gastrin were decreased significantly after an 1 - 24-year follow-up after selective vagotomy plus antrectomy. The characteristics of inhibitory secretive were observed in parietal cells. Follow-up after operation for 1 - 10 years and 11 - 24 years showed that 95.60% and 96.61% of patients belonged to Visick grade I and II, and 4.40% and 3.39% of patients belonged to Visick grade III, respectively. No ulcer recurrence was seen during the 1 - 24 year follow-up after the operation.

CONCLUSIONSV + A is an effective method for duodenal ulcer, especially for complicated duodenal ulcer, with permanent reduction of gastric acid and no recurrence.

Adult ; Digestive System Surgical Procedures ; Duodenal Ulcer ; surgery ; Female ; Humans ; Male ; Pylorus ; Treatment Outcome ; Vagotomy, Proximal Gastric

An improved approach for determination of Na(+)-K(+)-ATPase activity in single proximal renal tubule of rat reported by Doucet and his colleagues has been suggested. The single proximal renal tubules were isolated by hand under stereomicroscope from collagenase II-treated renal cortical tissue in rats. The length of every single renal tubule segment obtained was measured. The single proximal renal tubules were treated with a hypoosmotic solution and with freeze-thaw successively, before incubation with [gamma-(32)P]-ATP. (32)Pi hydrolyzed from [gamma-(32)P]ATP by Na(+)-K(+)-ATPase in the single proximal renal tubules was assayed by liquid scintillation counting. The activity of Na(+)-K(+)-ATPase in the single proximal renal tubules was calculated by applying a modified formula. There was no significant difference in the measurement result of Na(+)-K(+)-ATPase activity between the method of Doucet et al. and the improved one, but the latter has advantage of less time, less reagents and being easy to operate.
Adenosine Triphosphate ; metabolism ; Animals ; Kidney Tubules, Proximal ; enzymology ; Male ; Microscopy ; Rats ; Rats, Wistar ; Sodium-Potassium-Exchanging ATPase ; metabolism ; Time Factors

HCO3(-) reabsorption in the renal tubules plays a critically important role in maintaining the global acid-base balance. Loss of HCO3(-) causes metabolic acidosis. Proximal renal tubule is the major site for HCO3(-) reabsorption, accounting for more than 80% of total HCO3(-) reabsorption along the nephron. Over the past more than half centuries, tremendous progresses have been made on understanding the molecular mechanisms underlying the HCO3(-) reabsorption in proximal tubules. The transepithelial movement of HCO3(-) involves the coordinated operation of machineries on both the apical and the basolateral membranes of the epithelial cells. On the apical domain, Na(+)-H(+) exchanger NHE3 and the vacuolar H(+)-ATPase are two major pathways mediating the apical uptake of HCO3(-)-related species. Taken together, NHE3 and H(+)-ATPase are responsible for about 80% of HCO3(-) reabsorption in the proximal tubule. The remaining 20% is likely mediated by pathways yet to be characterized. On the basolateral membrane, NBCe1 represents the only major known pathway mediating the extrusion of HCO3(-) coupled with Na(+) into the interstitial space. In the present article, we provide a historical view about the studies on the mechanisms of HCO3(-) reabsorption since 1940s. Moreover, we summarize the latest progresses emerging over the past decade in the physiological as well as pathological roles of acid-base transporters underlying the HCO3(-) reabsorption in proximal tubules.
Acidosis ; physiopathology ; Animals ; Bicarbonates ; metabolism ; Humans ; Kidney Tubules, Proximal ; physiopathology ; Sodium-Hydrogen Exchangers ; physiology ; Vacuolar Proton-Translocating ATPases ; physiology

The present study was designed to investigate the effect of administration of adrenomedullin (ADM) into subfornical organ (SFO) on renal tubular Na(+),K(+)-ATPase activity in rats. Rats under anesthesia were injected with ADM 0.1 mL (20 ng/mL) via an implanted cannula into SFO (n=6). Plasma ADM and serum endogenous digitalis-like factor (EDLF) levels were assayed with radioimmunoassay, and urine samples were collected via a canoula intubated in bladder. Urinary sodium concentration was assayed with flame spectrophotometry. Single proximal renal tubule segments were obtained by hand under stereomicroscope and its Na(+),K(+)-ATPase activity was measured by liquid scintillation counting. In addition, single proximal renal tubule segments from normal rats (n=6) were incubated with serum from animals administered with ADM into SFO, and then the Na(+),K(+)-ATPase activity was determined. The results showed that both urinary volume and sodium excretion amounted to the peak value at 30 min after ADM administration, and sustained a significant high level at 60 min (P<0.01). At 30 min after ADM administration, there was a significant increase in serum EDLF and a decrease in Na(+),K(+)-ATPase activity of proximal tubule (P<0.01, respectively), but not in plasma ADM level. Na(+),K(+)-ATPase activity was decreased significantly in single proximal renal tubule segments from normal rats incubated with serum from rats administered with ADM into SFO (P<0.01). These results suggest that the diuretic and natriuretic responses following administration of ADM into SFO are associated with the inhibition of renal tubule Na(+),K(+)-ATPase activity. The inhibition of renal tubule Na(+),K(+)-ATPase activity is related to the increase in the serum level of EDLF.
Adrenomedullin ; pharmacology ; Animals ; Kidney Tubules, Proximal ; drug effects ; enzymology ; Rats ; Sodium-Potassium-Exchanging ATPase ; metabolism ; Subfornical Organ

The electrogenic sodium/bicarbonate cotransporter 1 (NBCe1) on the basolateral side of the renal proximal tubule plays a pivotal role in systemic acid-base homeostasis. Mutations in the gene encoding NBCe1 cause severe proximal renal tubular acidosis accompanied by other extrarenal symptoms. The proximal tubule reabsorbs most of the sodium filtered in the glomerulus, contributing to the regulation of plasma volume and blood pressure. NBCe1 and other sodium transporters in the proximal tubule are regulated by hormones, such as angiotensin II and insulin. Angiotensin II is probably the most important stimulator of sodium reabsorption. Proximal tubule AT(1A) receptor is crucial for the systemic pressor effect of angiotensin II. In rodents and rabbits, the effect on proximal tubule NBCe1 is biphasic; at low concentration, angiotensin II stimulates NBCe1 via PKC/cAMP/ERK, whereas at high concentration, it inhibits NBCe1 via NO/cGMP/cGKII. In contrast, in human proximal tubule, angiotensin II has a dose-dependent monophasic stimulatory effect via NO/cGMP/ERK. Insulin stimulates the proximal tubule sodium transport, which is IRS2-dependent. We found that in insulin resistance and overt diabetic nephropathy, stimulatory effect of insulin on proximal tubule transport was preserved. Our results suggest that the preserved stimulation of the proximal tubule enhances sodium reabsorption, contributing to the pathogenesis of hypertension with metabolic syndrome. We describe recent findings regarding the role of proximal tubule transport in the regulation of blood pressure, focusing on the effects of angiotensin II and insulin.
Acidosis, Renal Tubular ; Angiotensin II ; Blood Pressure* ; Diabetic Nephropathies ; Homeostasis ; Humans ; Hypertension ; Insulin ; Insulin Resistance ; Kidney Tubules, Proximal ; Plasma Volume ; Rabbits ; Rodentia ; Sodium ; Sodium-Bicarbonate Symporters