OBJECTIVES: lschemic acute renal failure(ARF) is characterized by an abrupt and sustained decline in GFR within minutes to days after renal ischemia and not immediately reversed on restoration of renal blood flow. The typical delay of a few days to a few weeks suggests reversible parenchymal damage awaiting cell regeneration for functional recovery. Many potentially cell damaging factors, such as ATP depletion, plasma membrane phospholipid degradatian and superoxide-induced membrane damage, play a central part in ischemic injury. More recently, much attention has been focused on the role of calcium, especially ischemic cell injury and the possible therapeutic role of calcium channel blockers emerged from studies conducted several years ago. In the past, it was thought that activation of renin-angiotensin system plays a role in the pathogenesis of ARF. Now the role of angiotensin in human renal ischemia also appears to be controversial. The following study was done in order to investigate the effect of a calcium channel blocker, nifedipine, on gene expression of renin during acute ischemic renal injury. METHODS: The Sprague-Dawley rats were divided into 4 groups, group I(n=3) as the control, group II (n=3) as the sham operation group, group III(n=15) as the ischemic renal injury group without nifedipine pretreatment, and group IV(n=15) as the ischemic renal injury model by right nephrectomy and left renal artery clamping for 40 minutes with systemic nifedipine pretreatment(10mg/kg), 1n ischemic renal injury model(group III and IV), rats were further divided into three subgroups according to reperfusion time of 1,24,72 hours. The non-ischemic right kidney removed at the time of initial procedure served as paired control. Total renal RNA was extracted by Chomczynskis method and electrophoresis was done in a 1% agarose gel containing 2,2M formaldehyde. Northern was performed at 42degrees C with isotope labeled renin probe for 18 hours, Autoradiographs were obtained and quantitated by a densitometer measured at 530nm. RESULTS: 1) The expression of renin gene was markedly decreased after renal ischemia and slowly recovered to one half of the control level after 72 hours of reperfusion. 2) Renin gene expression pattern of ischemic renal injury with prior nifedipine treatment was similar to the ischemic group without nifedipine pretreatment. CONCLUSION: These findings suggest that the renin gene expression was markedly decreased after renal ischemia and slowly recovered. Systemic nifedipine pretreatment does not have a significant effect on gene expression pattern of renin in ischemic renal injury.
Adenosine Triphosphate ; Angiotensins ; Animals ; Calcium Channel Blockers ; Calcium Channels* ; Calcium* ; Cell Membrane ; Constriction ; Electrophoresis ; Formaldehyde ; Gene Expression* ; Humans ; Ischemia ; Kidney ; Membranes ; Nephrectomy ; Nifedipine ; Rats ; Rats, Sprague-Dawley ; Regeneration ; Renal Artery ; Renal Circulation ; Renin* ; Renin-Angiotensin System ; Reperfusion ; RNA ; Sepharose

No abstract available.
Lupus Nephritis

PURPOSE: The purpose of this study was to determine the value of the intrarenal resistive index (RI),measured by Doppler sonography, in order to assess intrarenal vascular resistance in autosomal dominant polycystickidney disease (ADPKD) patients. MATERIALS AND METHODS: In 26 patients with ADPKD, RI was measured by Dopplersonography and correlated with the presence of hypertension, renal function (creatinine clearance) and anatomicalrenal severity index (RSI), thus indicating renal morphologic abnormalities during B-mode sonography . RESULTS:RI was significantly higher in 18 hypertensive ADPKD patients (0.64+/-0.65) (Mean+/-1SD; range: 0.52-0.74) than ineight normotensive patients (0.59+/-0.50) ( 0.48-0.64) (p<0.05). Statistically significant inverse correlation wasfound between RI values and creatinine clearance (r=-0.45, p<0.05), and statistically significant correlation wasfound between RI values and RSI, indicating the degree of renal parenchymal involvement. CONCLUSION: RIcorrelates with the development of hypertension, renal function and renal morphologic abnormality scoring by RSIduring B-mode Doppler sonography, and measured in this way may thus be used to assess renal vaseular resistance inADPRD patients.
Creatinine ; Humans ; Hypertension, Renal ; Polycystic Kidney, Autosomal Dominant* ; Vascular Resistance

OBJECTIVE: To evaluate the effects of cyst ablation with absolute ethanol in autosomal-dominant polycystic kidney disease (ADPKD) patients with symptomatic cysts. MATERIALS AND METHODS: Using absolute ethanol, cyst ablation was performed in 11 patients with documented ADPKD who suffered cyst pain refractory to medical treatment. An ethanol solution was instilled into the largest symptomatic cysts through a catheter. We assessed the therapeutic efficacy of the procedure by tracking subjective pain relief during a 3 to 24-month follow-up period after ablation. RESULTS: At follow-up, we found that the duration of subjective pain relief was 12 to 24 months in seven patients, 4 to11 months in one, and less than 3 months in three. CONCLUSION: Selective ablation of a symptomatic cyst may be a valid option in managing chronic pain caused by one or a few large cysts in ADPKD patients.
Adult ; Aged ; Contrast Media/administration & dosage ; Ethanol/*therapeutic use ; Female ; Follow-Up Studies ; Human ; Male ; Middle Aged ; Pain, Intractable/etiology/physiopathology/*therapy ; Palliative Care/methods ; Polycystic Kidney, Autosomal Dominant/physiopathology/radiography/*therapy ; Sclerotherapy/*methods ; Solvents/therapeutic use ; Tomography, X-Ray Computed ; Treatment Outcome

PURPOSE: Recent studies have showed that epithelial-mesenchymal transition (EMT) is a key process of glomerular and tubulointerstitial pathology in many chronic kidney diseases. However, there are no data of EMT in humane autosomal dominant polycystic kidney disease (ADPKD). PATIENTS AND METHODS: ADPKD kidneys (N = 5) with end stage renal disease (ESRD) and control kidneys (N = 4) were analyzed immnunohistochemically. We evaluated alpha-SMA, E-cadherin, vimentin, TGF-beta1 and Smad 2/3 expression in ADPKD and compared them with those in control kidney. These immunohistochemical findings were quantitatively analyzed by computer-assisted image analyzer and positive tubules (%). RESULTS: There were severe interstitial fibrosis and proliferation of alpha-SMA+ myofibroblasts in ADPKD. Cystic tubular epithelial cells in ADPKD lost epithelial marker (E-cadherin) and expressed mesenchymal markers (alpha-SMA, vimentin). There were significant increases of alpha-SMA (34.3 +/- 11.7% vs 0.9 +/- 1.5%), vimentin (19.9 +/- 3.9% vs 3.3 +/- 1.4%), TGF-beta1 (5.42 +/- 2.83% vs 0%) and Smad 2/3 (3.4 +/- 1.7% vs 0.7 +/- 0.6%) in ADPKD kidneys compared with control kidneys evidenced by computer-assisted image analyzer. When we analyze the positive tubules (%), the results were the same as computer-assisted image analyzer. CONCLUSION: Our results showed that the end stage of ADPKD is associated with TGF-beta, Smad 2/3 and markers of EMT. It suggests that TGF-beta mediated EMT has a role in progression of ADPKD.
Aged ; Biological Markers/metabolism ; Cell Division ; Disease Progression ; Epithelial Cells/*pathology ; Female ; Fibrosis ; Humans ; Kidney Glomerulus/pathology ; Kidney Tubules/pathology ; Male ; Mesoderm/*pathology ; Middle Aged ; Polycystic Kidney, Autosomal Dominant/*metabolism/*pathology ; Transforming Growth Factor beta/*metabolism

One author's name is misspelled. Correct Seungho Rhu into Seungho Ryu.

Although urinary tract infections are common in adults, pyelonephritis is rarely considered in the differential diagnosis of acute renal failure. Acute pyelonephritis without urinary tract obstruction, previous renal diseases or septic shock is a rare cause of acute renal failure. Despite appropriate antibiotic therapy, recovery of renal function could be slow and incomplete. We experienced a 45 year-old woman with diabetes who developed bilateral acute pyelonephritis followed by acute renal failure. The renal biopsy revealed diffuse edematous and focal fibrotic inters- titium with infiltration of lymphocytes compatible with interstitial nephritis. Although her renal function improved gradually with antimicrobial treatment, the process was incomplete and renal dysfunction persisted at about 10-month follow-up, suggesting permanent renal damage. Therefore, we report this case with brief review of related literature.
Acute Kidney Injury* ; Adult ; Biopsy ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Humans ; Lymphocytes ; Middle Aged ; Nephritis, Interstitial ; Pyelonephritis* ; Shock, Septic ; Urinary Tract ; Urinary Tract Infections

Central diabetes insipidus (CDI) is a clinical syndrome that result from a failure of the neurohypophyseal axis to produce or release a sufficient quantity of arginine vasopressin (AVP) to permit normal function of the urinary concentrating mechanism. Polyuria and polydipsia are the symptoms associated with CDI. The most common cause of CDI is idiopathic variety and head trauma, neurohypophyseal surgery, primary or metastatic brain tumors acount for most of the remaining cases. CDI in Langerhans cell histiocytosis (LCH) is thought to be to infiltration of the hypothalamus-neurohypophyseal system. We report a patient with CDI and LCH underwent water depriviation test, MR imaging of the pituitary-hypothalamic region, and VATS associated open lung biopsy.
Arginine Vasopressin ; Axis, Cervical Vertebra ; Biopsy ; Brain Neoplasms ; Craniocerebral Trauma ; Diabetes Insipidus* ; Diabetes Insipidus, Neurogenic ; Histiocytosis* ; Histiocytosis, Langerhans-Cell ; Humans ; Lung ; Magnetic Resonance Imaging ; Polydipsia ; Polyuria ; Thoracic Surgery, Video-Assisted

No abstract available.
Diagnosis* ; Polycystic Kidney, Autosomal Dominant*

PURPOSE: Klotho mutant mice showed abnormal calcium and vitamin D metabolism, hyperphosphatemia and vascular calcification. We observed the frequencies of klotho gene polymorphism and investigated their relation with some clinical parameters including serum osteoprotegerin (OPG) levels in maintenance hemodialysis (HD) patients. METHODS: Total 88 patients (mean age 58+/-13 years, male:female=47:41) on maintenance HD were enrolled. The genotypings for G-395A in promoter and C1818T in exon 4 of klotho gene were performed with real-time polymerase chain reaction. We measured blood pressure, body mass index (BMI), and serum calcium, phosphorus, parathyroid hormone (PTH), alkaline phosphatase, hs-CRP, lipid profiles and OPG. RESULTS: In G-395A in promoter, the distribution of genotypes was GG 66% (n=58), GA 23% (n=20) and AA 11% (n=10), respectively and the allele frequencies were 0.773 for G allele and 0.227 for A allele. In C1818T in exon 4, the distribution of genotypes was CC 63% (n=55), CT 30% (n=26), and TT 7% (n=7), and the frequencies were 0.773 for C allele and 0.227 for T allele. G-395A shows correlations with BMI and HDL-cholesterol (p<0.005). G-395A and C1818T in klotho gene show no statistical correlation with other clinical parameters of vascular calcification including OPG. CONCLUSION: Klotho G-395A and C1818T polymorphisms are not correlated with OPG in maintenance HD patients. Further research needs for the other klotho polymorphisms on chronic kidney disease and end-stage renal disease.
Alkaline Phosphatase ; Alleles ; Animals ; Blood Pressure ; Body Mass Index ; Calcium ; Exons ; Gene Frequency ; Genotype ; Glucuronidase ; Humans ; Hyperphosphatemia ; Mice ; Osteoprotegerin ; Parathyroid Hormone ; Phosphorus ; Real-Time Polymerase Chain Reaction ; Renal Dialysis ; Renal Insufficiency, Chronic ; Vascular Calcification ; Vitamin D