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Objectives: Perinephric fat invasion (PFI) of renal cell carcinoma (RCC) is known to be associated with adverse pathological features and poor prognosis. We analyzed these associations using a sub-group of the RCC registry of The Cancer Registration Committee of the Japanese Urological Association., Methods: The study cohort of 2998 non-metastatic cases was retrieved from RCC registry (3648 in total). We compared clinicopathological characteristics of cases with PFI (n = 256) and without PFI (n = 2742), and investigated the impact of PFI on cancer-specific survival using univariate and multivariate analyses., Results: Compared with non-PFI cases, PFI cases were older (P = 0.003), and more likely to be hypertensive (P = 0.034) and symptomatic at presentation (P < 0.001). PFI tumors were larger (P < 0.001), and more often have sarcomatoid component (P < 0.001) and tumor thrombus (P < 0.001). Cancer-specific survival was significantly shorter in cases with PFI than without (P < 0.001). The difference in survival tended to be greater in cases with large tumors but was significant in small tumor sub-groups. Cancer-specific survival was significantly shorter in cases with both PFI and renal vein involvement (RVI) in comparison to those with PFI or RVI alone (P = 0.011, P = 0.007, respectively). On multivariate analysis PFI with and without sinus fat invasion remained as an independent risk factor along with symptom at presentation, low body mass index, hypertension, multiple tumors, large tumor size (>7.0 cm), sarcomatoid component and RVI., Conclusions: PFI was associated with advanced age and aggressive pathological features. PFI is an independent prognostic factor in non-metastatic RCC., (© The Author(s) 2019. Published by Oxford University Press. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Dyslipidemia is a risk factor for the progression of chronic kidney disease (CKD). While conventional lipid lowering therapy provides a benefit to CKD management, the effect of statins on eGFR remains unclear., Methods: A prospective, multi-center, open-labeled, randomized trial. Total of 349 CKD patients with hyperlipidemia were randomized into 2 groups, and followed for 2 years. Group A included patients who were treated with atorvastatin. Group C were treated with conventional lipid lowering drugs other than statin. Primary endpoint was changes in eGFR. Secondary endpoints included changes in urinary albumin excretion, serum LDL-C, serum triglyceride, cardio-vascular events and all-cause mortality., Results: As the primary endpoint, eGFR decreased by 2.3 ml/min/1.73 m 2 in Group A and by 2.6 ml/min/1.73 m 2 in Group C, indicating that there was no difference in change of eGFR between the two groups. As secondary endpoints, atorvastatin succeeded to reduce serum LDL-C level significantly and rapidly, but conventional therapy did not. In fact, mean LDL-C level did not reach the target level of 100 mg/dl in Group C. Serum triglyceride was lowered only by atorvastatin, but not conventional drugs. The number of cardiovascular events and all-cause mortality did not differ between in two groups., Conclusion: The ASUCA (Assessment of Clinical Usefulness in CKD Patients with Atorvastatin) trial demonstrated that atorvastatin failed to exhibit reno-protections compared to conventional therapy in Japanese patients with dyslipidemia and CKD. It would be due in part to the ability of atorvastatin to more potently reduce serum LDL and triglycerides compared to conventional therapy.

In the present study, we tested the hypothesis that up-titrating the dose of an angiotensin receptor blocker (ARB) is superior to combined treatment with an ARB and a calcium channel blocker for the same degree of blood pressure (BP) reduction, with respect to urinary albumin excretion in diabetic patients treated with a standard dose of the ARB. Hypertensive patients with type 2 diabetes mellitus and albuminuria (≥30 mg g(-1) creatinine) were enroled in the study, and were either started on or switched to candesartan (8 mg per day) monotherapy. After a 12-week run-in period, baseline evaluations were performed and patients with BP ≥130/80 mm Hg were randomly assigned to receive either candesartan (12 mg per day) or candesartan (8 mg per day) plus amlodipine (2.5 mg per day) for a further 12 weeks. The primary end-point was a reduction in urinary albumin levels. Although there was no significant difference in the BP reduction between the two groups, the reduction in urinary albumin was greater in the up-titrated than the combination therapy group (-40±14% vs -9±38%, respectively; P<0.0001). Thus, up-titration of candesartan more effectively reduces urinary albumin excretion than combined candesartan plus amlodipine in hypertensive patients with diabetes for the same degree of BP reduction.

Although mildly reduced renal function is associated with increased risk for heart failure in patients with coronary artery disease (CAD), mechanisms underlying the association remain unclear. We tested the hypothesis that abnormal ventricular-arterial interaction may occur in mildly reduced renal function. We examined the relationships of the estimated glomerular filtration rate (eGFR) with various indices reflecting ventricular-arterial coupling [effective arterial elastance (the ratio of left ventricular (LV) end-systolic pressure to stroke volume, E (a)], LV end-systolic elastance (the ratio of LV end-systolic pressure to end-systolic volume, E (es)), and the total arterial compliance (the ratio of stroke volume to aortic pulse pressure)] and those of LV systolic and diastolic function [peak systolic and diastolic mitral annular velocities (S' and E') and the ratio of peak early diastolic mitral inflow to annular velocity (E/E')] in 320 consecutive patients who underwent cardiac catheterization for CAD and had normal (≥ 0.50) ejection fractions (EF). As eGFR decreased, E (a) and E (es) increased and total arterial compliance and E' decreased. eGFR did not correlate with E (a)/E (es), S', or E/E'. After adjusting for potential confounders, the findings were generally similar, but the correlation of eGFR with E' did not remain significant. In conclusion, reduced renal function may be associated with combined increases in ventricular-systolic stiffness and arterial load in known or suspected CAD patients with normal EF.

Objectives: Effective blood pressure (BP) control is difficult to achieve in diabetic patients. This study investigated factors that exacerbate resistance to antihypertensive medication in patients with diabetes., Methods: Hypertensive patients with type 2 diabetes (n = 108, 67 ± 9 years) were subjected to a step-wise upward titration of medication (step 1, routine dose of angiotensin receptor blocker; step 2, routine doses of angiotensin receptor blocker and calcium channel blocker; step 3, step 1 + double dose of calcium channel blocker; step 4, double doses of angiotensin receptor blocker and calcium channel blocker; step 5, step 4 + routine dose of diuretic; step 6, step 5 + routine dose of β-blocker; step 7, step 6 + routine dose of α-blocker; step 8, step 6 + double dose of α-blocker) implemented with a target home BP of below 130/80 mmHg. The step number at which target BP was achieved was considered the amount of antihypertensive medications needed for BP control., Results: All patients reached the target BP at step 4.0 ± 1.5. Multivariate regression analysis identified estimated glomerular filtration rate, but not measures of glycemic control, as an independent predictor of the number of drugs needed for BP control (P < 0.0001)., Conclusion: The number of antihypertensive medications needed for BP control in patients with diabetes mellitus is largely dependent on estimated glomerular filtration rate. Impaired kidney function could produce resistance to antihypertensive therapy in diabetic patients.

Background: There are plausible reasons to hypothesize that increased aortic stiffness and left ventricular (LV) dysfunction may occur in early renal insufficiency., Methods and Results: The correlation of glomerular filtration rate (GFR) with the augmentation index (AI) of ascending aortic pressure and indices of LV systolic and diastolic function (ejection fraction, LV pressure relaxation time constant, LV end-diastolic pressure and mitral inflow (E/A) and annular velocities (S' and E')) was examined in 359 consecutive patients undergoing cardiac catheterization for coronary artery disease (CAD). When patients were stratified according to GFR of 60, 75 and 90 ml x min(-1) x 1.73 m(-2), there was a progressive increase in AI and decreases in E/A and E' with decreasing GFR. There were no linear trends in other indices of systolic or diastolic function across GFR groups. After adjustment for potential confounders, reduced GFR was associated with increased AI, but not with decreased E/A or E'., Conclusions: Early renal impairment may be partly associated with increased aortic stiffness, but not with LV systolic or diastolic function in CAD patients.

We have postulated that the diminished renal capacity to excrete sodium causes nocturnal blood pressure (BP) elevation, which enhances pressure natriuresis in compensation for impaired daytime natriuresis. If such a mechanism holds, high BP during sleep at night may continue until excess sodium is sufficiently excreted into urine. This study examined whether the duration, defined as "dipping time," until nocturnal mean arterial pressure began to fall to <90% of daytime average became longer as renal function deteriorated. Ambulatory BP measurements and urinary sodium excretion rates were evaluated for daytime and nighttime to estimate their circadian rhythms in 65 subjects with chronic kidney disease. Dipping time showed an inverse relationship with creatinine clearance (C(cr); rho=-0.61; P<0.0001) and positive relationships with night/day ratios of mean arterial pressure (rho=0.84; P<0.0001) and natriuresis (rho=0.61; P<0.0001), both of which were also inversely correlated with C(cr) (mean arterial pressure: r=-0.58, P<0.0001; natriuresis: r=-0.69, P<0.0001). When divided into tertiles by C(cr) (mL/min), hazard ratios of nocturnal BP dip adjusted for age, gender, and body mass index were 0.37 (95% CI: 0.17 to 0.79; P=0.01) for the second tertile (C(cr): 50 to 90) and 0.20 (95% CI: 0.08 to 0.55; P=0.002) for the third tertile (C(cr): 5 to 41) compared with the first tertile (C(cr): 91 to 164). These findings demonstrate that patients with renal dysfunction require a longer duration until BP falls during the night. The prolonged duration until BP dip during sleep seems an essential component of the nondipper pattern of the circadian BP rhythm.

Patients with infective endocarditis (IE) often have renal complications which may include infarcts, abscesses and glomerulonephritis (GN). Furthermore, it is generally accepted that there is an association between IE and anti-neutrophil cytoplasmic antibody (ANCA). Here, we report the case of a 24-year-old man who developed rapidly progressive GN in the course of IE due to infection with alpha-streptococcus. The initial clinical manifestation of the condition was severe sacroiliitis without fever. Sandwich ELISA showed that the patient was positive for PR3-ANCA at low titer, and the classical complement pathway was also activated. Renal biopsy demonstrated several lesions: focal embolic GN, GN with immune deposits and focal and segmental crescentic necrotizing GN. Treatment with antibiotics and steroids led to eradication of the infection, and resolution of the renal disease was accompanied by immediate disappearance of PR3-ANCA and hypocomplementemia. During a 4-year follow-up period, no recurrence was observed. There have only been 7 case reports of GN associated with IE and PR3-ANCA in which the renal pathology has been described, and the current report is the first to document renal pathology in a patient with isolated pulmonic valve IE and PR3-ANCA. Moreover, this report is the first to show a change in renal biopsy findings in response to treatment. A review of the 7 literature cases and that of our patient showed that none involved pauci-immune GN. Hence, further studies are needed to clarify the prevalence of pauci-immune GN in ANCA-positive IE patients.

We experienced two cases of renal infarction with atrial fibrillation who presented with acute abdominal pain. On initial urinalysis, both patients showed no hematuria, but the plasma lactate dehydrogenase level was markedly elevated with little or no rise in plasma transaminases. Their diagnosis was confirmed by contrast-enhanced CT of the abdomen on the second and third days of the crisis. We immediately initiated anticoagulant therapy, resulting in successful prevention of new embolism. Contrast-enhanced CT should be considered if abdominal symptoms develop in patients with atrial fibrillation. Renal infarction could be diagnosed in the early course, even in cases with incomplete occlusion of the renal arteries and normal renal function., (Copyright 2004 Lippincott Williams & Wilkins)

We investigated the prevalence of renal artery disease and outcome in a cohort of atherosclerotic patients with renal dysfunction. We studied 44 consecutive patients who were older than 50 years of age, who had renal dysfunction and in whom one or more of the following atherosclerotic diseases was confirmed: cerebral infarction, coronary artery disease or peripheral vascular disease. Renal artery stenosis was assessed by gadolinium-enhanced magnetic-resonance angiography. Patients who were treated medically were prospectively followed up in our outpatient clinic and the impact of renal artery stenosis on survival was evaluated. Renal artery stenosis was found in 22 (50%) of the 44 patients. Difference in kidney length and carotid artery stenosis were identified as independent predictors of renal artery stenosis. Among the patients who were treated medically (n=42), rates of mortality were 4.4, 12.7 and 18.1 per 100 patient-years in those without renal artery stenosis, those with unilateral renal artery stenosis and those with bilateral renal artery stenosis, respectively. The mortality and renal survival curves were significantly different among these three groups. These findings indicate that renal artery stenosis is common in patients with renal dysfunction and concomitant cardiovascular disease, especially in those with carotid artery stenosis, and that a substantial difference in the length of kidneys may be a predictor of renovascular disease. Patients with renal dysfunction resulting from renal artery stenosis are at risk of death from cardiovascular disease and end-stage renal failure.

Objective: Studies of experimental animals show glomerular hypertension to be important in the progression of glomerular disease. We evaluated this connection clinically by examining the relationship between glomerular hemodynamics and histological changes in patients with immunoglobulin (Ig)A nephropathy., Methods: The subjects were 23 patients with IgA nephropathy. All patients underwent renal biopsies. Glomerular hemodynamics, in terms of glomerular capillary hydraulic pressure (PGC) and the whole-kidney ultrafiltration coefficient, were calculated from the renal clearance, plasma total protein concentration, and pressure-natriuresis relationship. The severity of glomerulosclerosis, tubulointerstitial damage and mesangial matrix expansion was evaluated semiquantitatively., Results: PGC ranged from 33-69 mm Hg, and the mean arterial pressure (MAP) from 79-112 mm Hg. Their correlation was not significant (r= 0.29, P= 0.18). PGC was significantly correlated with the glomerulosclerosis score, and also with the score for tubulointerstitial damage (r= 0.65, P < 0.001 and rs = 0.59, P = 0.007, respectively), but not with the score for mesangial matrix expansion (r= 0.08, P= 0.72). MAP was significantly correlated only with the score for tubulointerstitial damage (rs = 0.63, P = 0.004). In multiple linear regression analysis of the histological changes and hemodynamics, the glomerulosclerosis score and the score for tubulointerstitial damage were correlated with PGC, but not with MAP., Conclusion: These clinical results support the speculation that glomerular hypertension is involved in the glomerulosclerosis and tubulointerstitial damage that occurs in IgA nephropathy.

It has been postulated that glomerular capillary pressure is elevated in sodium-sensitive types of hypertension. In addition, the presence or absence of renal function reserve, in response to a chronic protein load, is thought to be useful in predicting the existence of glomerular hypertension. Intrarenal hemodynamic parameters in the sodium-sensitive type of essential hypertension were therefore calculated by analyzing the pressure-natriuresis curve, and the preservation of renal function reserve was evaluated. Fifteen patients with essential hypertension were maintained on a normal sodium diet for 1 week and a low-sodium diet for a second week in study 1. This protocol was repeated for low and high protein intake in 8 patients in study 2. Subjects in study 1 whose mean arterial pressure was reduced by more than 10% by sodium restriction were considered sodium sensitive (n = 7), with the remaining patients classified as non-sodium sensitive (n = 8). There were no significant differences in mean arterial pressure (125 +/- 2 mm Hg), glomerular filtration rate (80 +/- 3 ml/min), or renal plasma flow rate (355 +/- 24 ml/min) on the normal sodium diet between sodium-sensitive and non-sodium-sensitive patients. Glomerular capillary pressure (59 +/- 2 mm Hg vs 47 +/- 1 mm Hg, p < 0.0002) was estimated to be elevated in sodium-sensitive patients relative to that in non-sodium-sensitive patients, whereas the whole kidney ultrafiltration coefficient of glomerular capillary walls (0.068 +/- 0.009 (ml/sec)/mm Hg vs 0.221 +/- 0.042 (ml/sec)/mm Hg, p < 0.005) was decreased. Chronic protein loading increased both glomerular filtration and renal plasma flow rates in study 2. Although the sodium sensitivity of blood pressure showed no significant correlation with the increase in either glomerular filtration or renal plasma flow rate, it showed a weak negative correlation with the increase in filtration fraction (r = -0.69, p < 0.06), which is the ratio of the two rates. Taken together, these results suggest that glomerular capillary pressure is elevated and renal function reserve is impaired in patients with sodium-sensitive essential hypertension.

The renal mechanisms of hypertension were reviewed, and new way to classify hypertension based on renal mechanisms was proposed. Theoretically, the pressurenatriuresis relationship can be affected in two different ways; either a parallel shift along the blood pressure axis toward a higher blood pressure level or a depression in the slope. The parallel shift of the pressure-natriuresis relationship induces non-sodium sensitive hypertension, while the depressed slope induces sodium sensitive hypertension. Since the degree of the shift of the pressure-natriuresis relationship is determined by the preglomerular vascular resistance from heart to glomeruli, non-sodium sensitive hypertension should be based on the increased preglomerular vascular resistance. On the other hand, the slope of the pressure-natriuresis relationship is determined by glomerulo-tubular balance of sodium, which is mainly controlled by the difference between the whole kidney ultrafiltration coefficient and the rate of tubule sodium reabsorption. Therefore, sodium sensitivity of blood pressure is based on a decrease in the whole kidney ultrafiltration coefficient (due to a decrease in either filtration surface area per glomerulus, hydraulic permeability of glomerular filtration barrier or the number of glomeruli) and/or an increase in tubule sodium reabsorption. In sodium sensitive states, whether whole kidney ultrafiltration coefficient is reduced or tubule sodium reabsorption is enhanced, the glomerular capillary hydraulic pressure rises to compensate for the impairments in sodium excretory capability. If there is a linkage between sodium sensitivity of blood pressure and glomerular hypertension as proposed, renal failure may be expected to be more common in sodium sensitive types of hypertension than in non-sodium sensitive types.(ABSTRACT TRUNCATED AT 250 WORDS)

Split intrarenal hemodynamics in stenotic and contralateral kidneys of unilateral renovascular hypertension (RVH) were estimated by Gomez's formulae. Ten patients with RVH were studied. Split para-amino hippurate and inulin clearances were measured by ureteral catheterization as indexes for renal plasma flow and glomerular filtration rates, allowing the estimation of intrarenal hemodynamics such as preglomerular arteriolar resistance, postglomerular arteriolar resistance and glomerular hydrostatic pressure in each kidney. Renal plasma flow and glomerular filtration rates were lower in the stenotic kidney (83 +/- 12, 19 +/- 2 ml/min/m2) than in the contralateral kidney (170 +/- 19, 43 +/- 4). Preglomerular arteriolar resistance was elevated due to the stenotic lesion in the stenotic kidney (30,900 +/- 4,500 dyns.sec.cm-5) while the elevation in the contralateral kidney (11,300 +/- 1,000) was less. Postglomerular arteriolar resistance was high in both kidneys. Glomerular pressure was lowered in the stenotic kidney (54 +/- 1 mmHg), while elevated in the contralateral kidney (71 +/- 3). Although the stenotic kidney of RVH was protected from systemic hypertension (138 +/- 6 mmHg) by stenosis of the renal artery, the increase in preglomerular arteriolar resistance in the contralateral kidney was not sufficient, making glomerular pressure elevated. Thus, glomerular hypertension and hyperfiltration were demonstrated in the contralateral kidney of RVH.

Intrarenal hemodynamics were estimated clinically in essential hypertension. Two-week studies were performed in 30 patients with essential hypertension who were given a regular sodium diet in the first week and a sodium-restricted diet in the second week. Intrarenal hemodynamic parameters such as afferent arteriolar (preglomerular) resistance, efferent arteriolar resistance, and glomerular hydrostatic pressure were calculated from renal clearances and plasma total protein concentration measured on the last day of the regular sodium diet. Calculations were based on Gomez's equations with the assumption that the gross filtration coefficient of glomerular capillaries was normal. The increase in afferent arteriolar resistance (8,100 +/- 500 dyne.sec.cm-5) was significantly correlated with an elevation in mean arterial pressure (120 +/- 2 mm Hg), whereas glomerular pressure (56 +/- 1 mm Hg) and efferent arteriolar resistance (2,500 +/- 100 dyne.sec.cm-5) remained normal. The renal function curve (pressure-natriuresis relation) was drawn by plotting urinary sodium excretion on the y axis as a function of mean arterial pressure on the x axis, both of which were measured on the last 3 days of each week. The extrapolated x intercept (107 +/- 2 mm Hg) of the renal function curve was strongly correlated in a 1:1 fashion with the sum of the arterial pressure drop from the aorta to the renal glomeruli plus the opposing pressures against glomerular filtration at glomeruli (r = 0.7, p less than 0.001) on the regular sodium diet, suggesting that the difference between mean arterial pressure on the regular sodium diet and the extrapolated x intercept represented the effective filtration pressure across the glomerular capillaries on the regular sodium diet.(ABSTRACT TRUNCATED AT 250 WORDS)

The differences between sodium sensitive and sodium retaining hypertension were theoretically considered using a water tank model of body fluid volume-blood pressure regulation. If an outlet valve is attached to a tank with a base area corresponding to the reciprocal of total peripheral resistance (TPR) and water is poured into this tank at a rate corresponding to the amount of Na+ intake, then equilibrium should be achieved at a certain water level, volume and output from the outlet, which represent mean arterial pressure (MAP), cardiac output (CO) and urinary Na+ excretion. The height of the outlet from the tank bottom and the size cross-sectional area, of the outlet correspond to the x-intercept and slope of the renal function (pressure-natriuresis) curve, respectively. In both nonsodium sensitive hypertension, due to the shift of the curve toward a higher blood pressure level (elevated height of the outlet) without change in the slope (size of the outlet), and sodium sensitive hypertension, due to the depressed slope of the curve (reduced outlet size), not only MAP (water level) but also CO (water volume) are increased, resulting in sodium retaining hypertension, if TPR (reciprocal of base area) remained unchanged, while CO is relatively unchanged, resulting in nonsodium retaining hypertension, if TPR is elevated. Thus, the MAP and its sensitivity to sodium intake is determined by the renal function curve. Since body fluid volume is determined by both the renal function curve and TPR, however, changes in TPR during the development of hypertension is a major factor in determining whether or not the body fluid volume has to change only a small amount or a large amount. Therefore, the sodium sensitivity of blood pressure and sodium retention must be considered separately.

Plaque-forming activity and T-antigen-synthesizing activity in the crude preparation of simian virus 40 (SV40) decreased to 1/20-27 after treatment with 0.5% sodium deoxycholate (DOC) for 30 min at 37 degrees C. A full restoration of the activity occurred after incubation of DOC-treated virions with the extract of monkey CV-1 cells, host cells for productive infection with SV40. Analysis by sedimentation through 15% sucrose to CsCl cushion (rho = 1.327 g/cm3) revealed that virions in the [35S]methionine-labeled crude virus preparation sedimented to the interface between CsCl and sucrose, and that treatment with DOC resulted in the loss of infectivity and the appearance of virions sedimentable into CsCl cushion. The [35S]methionine-labeled purified virions (prepared after treatment with DOC and sedimentable into CsCl cushion) sedimented to the CsCl-sucrose interface after incubation with the cell extract, with restoration of infectivity. The infectivity-restoring activity of the cell extract was sensitive to ethyl ether, partially sensitive to heating at 75 degrees-97 degrees for 30 min, but resistant to treatment with DNase (50 micrograms/ml), RNase (40 micrograms/ml), or trypsin (0.05%) for 30 min at 37 degrees. These results suggest that lipid-related cellular components bind stably to virions of SV40 and facilitate an efficient infection.

The causative mechanisms of hypertension were investigated by studying the renal function (pressure-natriuresis) curve in patients with primary aldosteronism (n = 6) and renovascular hypertension (n = 6). Before and after radical operation (removal of adenoma in primary aldosteronism and percutaneous transluminal angioplasty in renovascular hypertension), dietary NaCl intake was altered from 10 to 13 g/day in Week 1 to 1 to 3 g/day in Week 2. Mean arterial pressure (MAP) and urinary sodium excretion were measured on the last 3 days of each week. By restricting sodium intake before operation, MAP was reduced from 122 +/- 7 to 113 +/- 7 mm Hg (p less than 0.025) in primary aldosteronism but not in renovascular hypertension (130 +/- 6 to 128 +/- 5 mm Hg). The renal function curve was drawn by plotting urinary sodium excretion on the ordinate and MAP on the abscissa before and after operation. The slope of the curve was analyzed between the plotted points, and each curve was extrapolated to zero sodium excretion as an estimate of the degree of shift of the curve along the MAP axis. Before, as compared with after operation, the extrapolated x-intercept of the curve was shifted rightward in both primary aldosteronism (111 +/- 7 vs 87 +/- 4 mm Hg; p less than 0.025) and renovascular hypertension (128 +/- 5 vs 95 +/- 2 mm Hg; p less than 0.025) and the slope was depressed in primary aldosteronism (16 +/- 1 vs 40 +/- 17 [mEq/day]/mm Hg; p less than 0.025) but not in renovascular hypertension (130 +/- 75 vs 40 +/- 13 [mEq/day]/mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Hashimoto Y, Kondo Y, Kimura G, Matsuzawa I, Sato S, Ishizaki M, Imura N, Akimoto M & Hara S (2004) Histopathology 44, 353–359 Cyclooxygenase-2 expression and relationship to tumour progression in human renal cell carcinoma Cyclooxygenase (COX), which catalyses the synthesis of prostaglandins from arachidonic acid, has two isoforms; COX-1 and COX-2. There is ample evidence to suggest an important role for COX-2 in cancer. The aim of this study was to evaluate the clinical significance of COX-2 expression and its localization in the development and progression of human renal cell carcinoma (RCC). The expression and localization of COX-2 were evaluated in human RCC tissues from 75 patients by immunohistochemistry. Immunoreactive COX-2 protein was observed in all cases of RCC, and the levels of COX-2 expression were correlated with tumour grade and pathological stage. Expression of COX-2 was higher in the granular cell subtype than in the clear cell subtype of RCC. Immunoelectron microscopy revealed that COX-2 was expressed in the nuclear membrane, rough endoplasmic reticulum, Golgi complex and mitochondrial membrane of RCC cells. COX-2 overexpression within these intracellular organelles in RCC may be associated with renal cell carcinogenesis and COX-2 may be a useful biomarker in RCC. [ABSTRACT FROM AUTHOR]