6-ketoprostaglandin-f1-alpha and Glomerulonephritis

The effects of dietary protein on glomerular and hormonal function were studied in twelve adults with a variety of glomerular diseases. They were randomly assigned, using a crossover design, to two 11-day periods, one on a high-protein diet (2 g.kg-1.day-1) and the other on a low-protein diet (0.55 g.kg-1.day-1). Improvement in glomerular permselectivity on the low-protein diet was manifested by a decreased 24-h urinary excretion of total protein, albumin, and IgG by 33, 40, and 25%, respectively (all P less than 0.02); a fall in the fractional clearance of albumin (10.1 +/- 6.3 X 10(-3) to 5.8 +/- 3.3 X 10(-3)), and IgG (6.9 +/- 5.1 X 10(-3) to 3.5 +/- 2.3 X 10(-3)) (both P less than 0.02); and a decreased fractional clearance of neutral dextrans of molecular radii 48-56 A (P less than 0.05), when measured on the final day of each dietary period. The high-protein diet was accompanied by a higher plasma renin activity (6.9 +/- 1.6 vs. 3.5 +/- 0.8 ng angiotensin I.ml-1.h-1) (P less than 0.02), and increased excretion of prostaglandin E and 6-ketoprostaglandin F1 alpha. We conclude that a low-protein diet rapidly improves the size-selective defect in glomerular permselectivity.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aldosterone; Blood Proteins; Dextrans; Diabetic Nephropathies; Dietary Proteins; Female; Glomerulonephritis; Hemodynamics; Hormones; Humans; Kidney; Kidney Failure, Chronic; Kidney Glomerulus; Male; Metabolic Clearance Rate; Middle Aged; Prostaglandins E; Proteinuria; Renin

We investigated whether the glomerular synthesis of prostacyclin modulates the renal blood flow and glomerular filtration rate in chronic glomerular disease. The urinary excretion of 6-keto-prostaglandin F1 alpha, a stable breakdown product of prostacyclin, was significantly (P less than 0.01) reduced in 20 women with chronic glomerular disease, as compared with 19 controls, whereas excretion of urinary prostaglandin E2 was unchanged. In 10 patients randomly assigned to one week of treatment with ibuprofen, excretion of urinary 6-keto-prostaglandin F1 alpha and prostaglandin E2 was reduced by 80 per cent, the level of serum creatinine was increased by 40 per cent, and creatinine and para-aminohippurate clearances were reduced by 28 and 35 per cent, respectively. The reduction of both clearances was inversely related (P less than 0.01) to the basal urinary excretion of 6-keto-prostaglandin F1 alpha but not of prostaglandin E2. No functional changes were detected in five healthy women, despite a similar suppression of renal prostacyclin synthesis by ibuprofen. In contrast, one week of treatment with sulindac did not affect renal prostacyclin synthesis or renal function in the other 10 patients, despite a marked inhibition of extrarenal cyclooxygenase activity. We conclude that in patients with mild impairment of renal function, the renal blood flow and glomerular filtration rate are critically dependent on prostacyclin production. In such patients sulindac may be a safe substitute for other nonsteroidal antiinflammatory drugs.

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Aged; Chronic Disease; Creatinine; Dinoprostone; Epoprostenol; Female; Glomerular Filtration Rate; Glomerulonephritis; Humans; Ibuprofen; Indenes; Kidney; Kidney Glomerulus; Middle Aged; p-Aminohippuric Acid; Prostaglandins E; Renal Circulation; Sulindac

While cyclosporine A (CsA) is an effective therapy for nephrotic syndrome, it has nephrotoxic side effects. We compared the anti-proteinuric effects and nephrotoxicity in rats with passive Heymann nephritis (PHN) of CsA and mycophenolate mofetil (MMF).. PHN was induced in female Wistar rats. Two treatment groups consisting of 8 rats each received either 25 mg of CsA or 25 mg of MMF/kg body weight/day and were compared with untreated controls. Kidney function and proteinuria were monitored over 4 weeks. Western blots were used for densitometric analysis of renal cyclooxygenase-2 (COX-2) protein expression. Thromboxane B2 (TxB2) and 6-keto-PGF(1alpha) were determined by radioimmunoassays (RIAs) in renal tissue and urine.. Rats with PHN exhibited a marked proteinuria of 12.76 +/- 4.42 vs. 0.73 +/- 0.28 mg/24 h (p < 0.01) and showed increased glomerular concentrations of TxB2 and 6-keto-PGF(1alpha) (992.6 +/- 216.9 and 1,187.0 +/- 54.2 pg/mg protein, respectively) compared with healthy controls (595 +/- 196.17 and 729 +/- 297.84, respectively) and a strongly induced COX-2 protein expression. CsA and MMF treatment reduced PHN-related proteinuria to 2.10 +/- 1.47 and 1.47 +/- 7.2 mg/24 h, respectively. In rats with PHN, CsA induced a significant deterioration of renal function and enhanced urine excretion of thromboxane A2, paralleled by a significant, twofold increase in COX-2 protein expression and renal prostaglandins. By contrast, MMF treatment in rats with PHN was not nephrotoxic and had no effect on prostaglandin production. COX-2 protein expression under MMF was suppressed.. While the antiproteinuric efficacy of MMF and CsA in PHN was comparable, the absence of nephrotoxicity might favor MMF in the treatment of nephrotic syndrome. The CsA-induced increase in COX-2 expression and COX-2-dependent prostacyclin may indicate a mechanism that compensates nephrotoxicity in the diseased and CsA-exposed kidney.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Blotting, Western; Cyclooxygenase 2; Cyclosporine; Enzyme Inhibitors; Female; Glomerulonephritis; Mycophenolic Acid; Nephrotic Syndrome; Rats; Rats, Wistar; Thromboxane B2

To explore the effects of ligustrazine on proteinuria, urinary TxB2 (metabolism of thromboxane A2, TxA2) and 6-keto-PGF1alpha (metabolism of prostacyclines I2, PG I2), glomerular inducible nitric oxide(NO) synthase (iNOS) mRNA, urinary NO3-/NO2- (decomposing products of NO) and pathological changes in rats with passive Heymann nephritis (PHN).. A rat PHN model was induced by intravenous injection of rabbit anti-rat renal tubular antigen (Tub-Ag) antiserum, and ligustrazine was given intraperitoneally into PHN rats every 2 days for 1-5 weeks. Then, proteinuria, urinary TxB2 and 6-keto-PGF1alpha, glomerular iNOS mRNA, and urinary NO3-/NO2- were measured by sulfosalicylic acid, radioimmunoassay (RIA), Northern blot and nitric acid reductase methods, respectively. Moreover, the damage to the renal tissue of the rats was observed under light and electron microscopy and immunofluorescence (IF).. The urinary TxB2 in PHN rats was significantly higher than that in control rats, but the PHN rats treated with ligustrazine had significantly less proteinuria, urinary TxB2 and tissue lesions, and more urinary 6-keto-PGF(1alpha), glomerular iNOS mRNA and urinary NO2-/NO3- than the PHN rats without the administration of ligustrazine.. These data indicate that ligustrazine has inhibitory roles on the glomerular injury of PHN rats, which may associate with modulating the balance of TxA2-PGI2 and elevating synthesis of NO to a certain extent.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Epoprostenol; Female; Fluorescent Antibody Technique, Direct; Glomerular Basement Membrane; Glomerulonephritis; Immunoglobulin G; Kidney Glomerulus; Nitrates; Nitric Oxide; Nitric Oxide Synthase Type II; Nitrites; Proteinuria; Pyrazines; Rats; RNA, Messenger; Thromboxane A2

The antinephritic effect of DP-1904 [6-(1-imidazolylmethyl)-5,6,7,8-tetrahydronaphthalene-2-carboxylic acid hydrochloride], a thromboxane A2 synthase inhibitor, was evaluated using an experimental model of membranous nephropathy, viz. accelerated passive Heymann nephritis in which the glomerular injury is mediated by immune complexes. DP-1904 markedly inhibited the develop-ent of glomerular alteration as well as the elevation of proteinuria and plasma creatinine. When the treatment was started from the 22nd day, at which time proteinuria is fully developed, DP-1904 showed beneficial effects on proteinuria and glomerular histopathological changes. DP-1904 apparently decreased the deposition of both rabbit immunoglobulin G and rat immunoglobulin G on glomerular basement membrane in nephritic rats. A single administration of DP-1904 restored the decreased renal tissue blood flow, inhibited glomerular thromboxane B2 production and increased glomerular prostaglandin E2 and 6-keto prostaglandin F1 alpha production in nephritic rats. These results suggest that DP-1904 may be an effective agent for the treatment of idiopathic membranous nephropathy and that the beneficial effect of this drug may be due to the elimination of glomerular immune deposits and to an increase in renal tissue blood flow related to amelioration of the abnormal metabolism of arachidonic acid.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Antibodies; Azathioprine; Creatinine; Dinoprostone; Drug Interactions; Enzyme Inhibitors; Glomerulonephritis; Imidazoles; Immunoglobulin G; Immunosuppressive Agents; Kidney Glomerulus; Male; Methacrylates; Proteinuria; Rabbits; Rats; Rats, Sprague-Dawley; Renal Circulation; Tetrahydronaphthalenes; Thromboxane B2; Thromboxane-A Synthase

33 cases of acute glomerulonephritis treated with Ji Shen Mixture (JSM) were studied with 31 cases treated with Western medical therapy (WM) for comparison and 34 healthy subjects as controls. The levels of lipo-peroxide (LPO), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), theromboxane B2 (TXB2), 6-keto-PGF1 alpha and TXB2/6-keto-PGF1 alpha ratio were examined before and after treatment. Compared with healthy controls, the levels of LPO, TXB2, TXB2/6-keto-PGF1 alpha of patients increased and that of GSH-Px, 6-keto-PGF1 alpha decreased significantly, whereas SOD activity had no significant difference. After treatment, the level of LPO reduced and GSH-Px activities raised significantly, but the effect of JSM group was better than that of WM group. It indicated that JSM was more effective in clearing the free radicals. The TXB2, TXB2/6-keto-PGF1 alpha dropped and 6-keto-PGF1 alpha elevated significantly after treatment, the effects of JSM were markedly better than those of WM. Furthermore, JSM was more potent in raising the clearing rate of hematuria and proteinuria.

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Child; Child, Preschool; Drugs, Chinese Herbal; Female; Glomerulonephritis; Glutathione Peroxidase; Humans; Lipid Peroxides; Male; Superoxide Dismutase; Thromboxane B2

Several clinical studies have proposed that a T cell derived cytokine IL-4 is operative in glomerulonephritis; however, its biological activities on renal cells have not been investigated. To elucidate its possible role in glomerulonephritis, we have examined whether IL-4 has effect on cell growth and prostaglandins synthesis using cultured mesangial cells (MC). IL-4 dose-dependently suppressed DNA synthesis and cell proliferation. IL-4 (10 ng/ml) alone did not affect prostaglandin E2 (PGE2) synthesis by mesangial cells, though, it inhibited IL-1 alpha- and TNF alpha-stimulated PGE2 synthesis by 48% and 81%, respectively. Comparable inhibition was observed on the conversion of exogenous arachidonic acid to PGs by IL-1-stimulated cells, suggesting IL-4 down regulates PG endoperoxide synthase activity. These results demonstrated that IL-4 is antagonistic to inflammatory cytokines upon PG synthesis as well as anti-mitogenic with MC.

Topics: 6-Ketoprostaglandin F1 alpha; Arachidonic Acid; Cell Division; Cells, Cultured; Dinoprostone; Glomerular Mesangium; Glomerulonephritis; Humans; Interferon-gamma; Interleukin-1; Interleukin-4; Kinetics; Prostaglandin-Endoperoxide Synthases; Prostaglandins; Recombinant Proteins; Tumor Necrosis Factor-alpha

We investigated the relation between the changes of TXA2-PG1 alpha balance and glomerular injury, and the effects of Dazoxiben, Chuan Xiong on in situ immune complex glomerulonephritis (ISICGN) produecd by C-BSA in rats. After two weeks of immunization, the level of renal cortical TXB2 and urine protein was increased, while that of 6-keto-PGF1 alpha was decreased. Four weeks later, the changes as mentioned above were more significant, and platelet aggregation revealed an increase of maximal aggregation. Positive correlation was seen between urine protein and renal cortical TXA2, and negative correlation between urine protein and 6-keto-PGF1 alpha. Histological examination showed morphological changes. Two treated-groups showed significant reduction of urine protein and renal cortical TXB2, but increase of 6-keto-PGF1 alpha. Besides the changes like worm-eaten in electron-dense deposits, foot process fusion disappeared. The thickened GBM and mesangial proliferation were lessened, especially in Dazoxiben group. These results suggests that there is a TXA2-PG1 alpha imbalance in ISICGN, and TXA2 plays an important pathogenetic role in the onset and progression of glomerulonephritis. Dazoxiben and Chuan Xiong might improve TXA2-PG1 alpha imbalance and attenuate glomerular injury to some extent in ISICGN.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Antigen-Antibody Complex; Drugs, Chinese Herbal; Glomerulonephritis; Imidazoles; Kidney Cortex; Male; Rats; Rats, Sprague-Dawley; Serum Albumin, Bovine; Thromboxane B2; Thromboxane-A Synthase

The authors investigated in 19 patients with chronic proliferative glomerulonephritis the effect of 100 mg acetylsalicylic acid (ACA) administered for 12 months and the effect of 50 mg ACA administered for the same period. They evaluated the effect of the two doses on the urinary excretion of PGI and TXA2 metabolites as well as the effect on proteinuria and glomerular filtraction (GF). The authors provided evidence that small and very small amounts of ACA did not affect the excretion of the PGI metabolite, while they reduced significantly the excretion of the TXA2 metabolite and of proteinuria, and significantly increased GF.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aspirin; Chronic Disease; Creatinine; Female; Glomerular Filtration Rate; Glomerulonephritis; Humans; Male; Middle Aged; Proteinuria; Thromboxanes

To determine the role of thromboxane A2 in the pathogenesis of experimentally induced immune complex glomerulonephritis, 12 concanavalin A-immunized Beagles were infused with 1 mg of concanavalin A via each renal artery and treated twice daily for 8 days with either 30 mg of CGS 12970/kg, PO, a specific thromboxane synthetase inhibitor, or placebo. The effect of treatment was assessed by measuring endogenous creatinine clearance and urine protein and eicosanoid excretion, and by evaluating changes in glomerular morphometric characteristics. On postinfusion day 8, urine protein, thromboxane B2, and 11-dehydro-thromboxane B2 excretion, glomerular epithelial crescent formation, and glomerular cell proliferation in the CGS 12970-treated dogs were significantly decreased when compared with values in the placebo-treated group. Differences were not observed in endogenous creatinine clearance, urine prostaglandin E2 and 6-keto-prostaglandin F1 alpha excretion, or glomerular polymorphonuclear leukocyte infiltration between groups in this study. These findings suggest thromboxane A2 has a role in the development of immune complex glomerulonephritis and that thromboxane synthetase inhibition may be beneficial in attenuating some of the functional and histological changes associated with immune complex glomerulonephritis.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Concanavalin A; Dinoprostone; Disease Models, Animal; Dogs; Glomerular Filtration Rate; Glomerulonephritis; Immune Complex Diseases; Kidney; Kidney Glomerulus; Male; Pyridines; Thromboxane A2; Thromboxane B2; Thromboxane-A Synthase

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Antioxidants; Benzoquinones; Drug Design; Drug Evaluation, Preclinical; Free Radicals; Glomerulonephritis; Humans; Leukotriene B4; Lipoxygenase Inhibitors; Molecular Structure; Oxygen; Puromycin Aminonucleoside; Rats; Structure-Activity Relationship; Thromboxane B2; Thromboxane-A Synthase

To determine if a selective thromboxane (TX)A2 synthetase inhibitor is clinically effective for the treatment of nephrotic syndrome, 11 patients with nephrotic syndrome were treated only with OKY-046, (E)-3-4-(1-imidazolylmethyl)phenyl-2-propenoic acid hydrochloride monohydrate, for at least 8 weeks. Urinary excretion of protein, TXB2, 2,3-dinor-TXB2, and beta-N-acetyl-D-glucosaminidase decreased with OKY-046. Creatinine clearance value, and urinary excretion of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), however, did not show any significant change, while serum albumin level increased. Two patients with minimal change nephrotic syndrome showed complete remission only with OKY-046. These results demonstrate that the selective TXA2 synthetase inhibitor is an effective drug for the treatment of chronic glomerulonephritis accompanied by nephrotic syndrome.

Topics: 6-Ketoprostaglandin F1 alpha; Acrylates; Adolescent; Adult; Aged; Female; Glomerulonephritis; Humans; Male; Methacrylates; Middle Aged; Nephrosis, Lipoid; Nephrotic Syndrome; Proteinuria; Thromboxane B2; Thromboxane-A Synthase

Topics: 6-Ketoprostaglandin F1 alpha; Female; Glomerulonephritis; Humans; Hypertension; Kidney Diseases; Liver Cirrhosis; Male; Nephrotic Syndrome; Radioimmunoassay; Thromboxane B2; Uremia

Repeated subcutaneous (SC) injections of mercuric chloride (MC) in Brown Norway (BN) rats induce an autoimmune glomerulonephritis (GN) due to antiglomerular basement membrane (BM) antibody deposition in the glomeruli. The aim of this study was to investigate the effects on MC-induced autoimmune GN of OKY-046, a selective TXA-synthetase inhibitor herring oil (HO), which is rich in eicosapentaenoic acid (EPA) (5.6%) precursor of the three series of prostaglandins (PGs) and of (inactive) thromboxane (TXA3), and evening primrose oil (EPO), which is rich in linoleic acid (LA) (72%) and gamma-linolenic acid (GLNA) (9%), precursors of the one series of PGs, mainly PGE1, and of (inactive) TXA1. The administration of OKY-046 significantly inhibited proteinuria, partially prevented fibrin thrombi (FT) formation in the glomeruli, decreased urinary TXB, enhanced 6ketoPGF excretion and, increased survival rate of the animals from 60% (group receiving only MC) to 86%. However, OKY-046 did not prevent body weight (BW) loss or the development and deposition of IgG in the glomeruli. Increased intake of HO (80 days prior and throughout the experiment) and avoidance of arachidonic acid (AA) intake produced an effect comparable to that of OKY-046 in the rats. Furthermore, HO significantly inhibited the deposition of IgG in the glomeruli, increased the survival rate of the animals to 100% and further enhanced the increased urinary PGE excretion induced by MC. However, HO did not prevent BW loss in the animals. Increased intake of EPO and avoidance of AA intake produced an effect comparable to that of HO. Additionally, EPO completely prevented BW loss induced by MC in these animals. These findings suggest that the metabolites of AA, EPA and GLNA play an important role either in the development or in the modulation of this model of MC induced GN.

Topics: 6-Ketoprostaglandin F1 alpha; Acrylates; Animals; Autoimmune Diseases; Fatty Acids, Essential; Fatty Acids, Unsaturated; Fish Oils; gamma-Linolenic Acid; Glomerulonephritis; Hypolipidemic Agents; Immunoglobulin G; Linoleic Acids; Mercuric Chloride; Methacrylates; Oenothera biennis; Plant Oils; Prostaglandins E; Proteinuria; Rats; Thromboxane-A Synthase; Thromboxanes

Eicosanoid synthesis was studied in a model of in situ glomerulonephritis (gn) in the rat. Unilateral gn was induced by perfusion of left kidneys with 200 micrograms cationized human IgG followed by intravenous (i.v.) autologous anti-human IgG antiserum. Rats developed proteinuria in the first 24 hours and hypercellular gn with leukocyte infiltration in the left kidney. Synthesis of thromboxane B2 (TXB2), prostaglandin E2 (PGE2) and 6-ketoprostaglandin F 1 alpha(6-keto-PGF 1 alpha) was measured at 6, 12, 18 and 24 hours in isolated glomeruli by radioimmunoassay. In nephritic glomeruli there was a nine-fold rise in TXB2 at six hours (5.35 ng/mg glomerular protein) when compared to control (0.6 ng/mg). TXB2 was still elevated at 24 hours (2.7 +/- 1 ng/mg; control 0.7 +/- 0.2 ng/mg). There were no consistent changes in PGE2 or 6-keto-PGF 1 alpha. No changes were found in right kidneys of nephritic or control rats. Treatment of nephritic rats with a selective thromboxane synthetase inhibitor, dazmegrel (20 mg/kg 8 hourly intraperitoneally), suppressed glomerular TXB2 at 24 hours. TXB2 was also inhibited in right (non-nephritic) kidneys and serum. Dazmegrel did not inhibit proteinuria or glomerular hypercellularity. We conclude there is a major increase in glomerular TXB2 in this model which does not play an essential role in the development of proteinuria or cellular infiltration.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Dinoprostone; Glomerulonephritis; Imidazoles; Kidney Glomerulus; Prostaglandins E; Radioimmunoassay; Rats; Rats, Inbred Lew; Thromboxane B2; Thromboxane-A Synthase

To determine factors mediating the aldosterone secretory response to orthostasis, we examined the effect of angiotensin-converting enzyme inhibition (CEI) on orthostasis in eight normal subjects and 10 normotensive patients with primary glomerulonephritis ingesting a normal sodium intake. On standing with CEI, the mean plasma aldosterone concentration (PAC) did not change [68.6 +/- 3.9 (+/- SE) and 63.4 +/- 6.9 pg/ml] in normal subjects, while PAC rose significantly from 72.3 +/- 7.5 to 129.5 +/- 13.2 pg/ml (P less than 0.001) in the glomerulonephritis patients without a concurrent rise in plasma angiotensin II, serum potassium, plasma ACTH, or mean blood pressure. There was a good correlation (r = -0.7064; P less than 0.03) between the changes in PAC and the changes in fractional sodium excretion in the patients. Pretreatment with indomethacin blunted the rise in PAC from 159.0 +/- 21.5 to 63.3 +/- 10.2 pg/ml upon standing with CEI, without a concurrent change in circulating 6-keto prostaglandin F1 alpha (from 57.7 +/- 9.5 to 56.0 +/- 11.1 pg/ml) in 4 patients. These results suggest that the aldosterone secretory response to orthostasis in patients with glomerulonephritis is dependent on factors blunted by pretreatment with indomethacin in addition to angiotensin II.

Topics: 6-Ketoprostaglandin F1 alpha; Adrenocorticotropic Hormone; Adult; Aldosterone; Angiotensin II; Glomerulonephritis; Humans; Indomethacin; Male; Posture; Potassium; Renin

To study the effects of uremia and hemodialysis on the production rates of antiaggregatory prostacyclin (PGI2) and proaggregatory thromboxane A2 (TxA2), we collected serial plasma samples from eight patients with chronic uremia before, during and after hemodialysis and assayed them for 6-keto-PGF1 alpha and TxB2, the stable metabolites of PGI2 and TxA2, respectively. In addition, the capacity of the platelets to produce TxB2 during spontaneous clotting was studied by measuring the TxB2 levels in serum incubated at +37 degrees C for 60 minutes. The PGI2 production of the uremia patients before hemodialysis was less (P less than 0.001) than that of healthy volunteers. It rose significantly following heparinization and remained elevated during hemodialysis. TxB2 generation by platelets during clotting was diminished in uremia. Plasma TxB2 levels were normal before, but increased during hemodialysis. Thus, profound changes in the PGI2/TxA2-system seem to be associated with uremia and hemodialysis.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Blood Platelets; Epoprostenol; Female; Glomerulonephritis; Heparin; Humans; Kidney Failure, Chronic; Male; Middle Aged; Prostaglandins; Pyelonephritis; Renal Dialysis; Thromboxane A2; Thromboxane B2; Thromboxanes; Uremia

Thirteen patients with active IgA glomerulonephritis (IgA GN), ten patients with a history of Henoch-Schönlein glomerulonephritis (HS GN) and nine healthy controls were studied during hydropenia (HP) and 3% volume expansion (VE) with isotonic saline. Clearance of inulin and para-aminohippurate, urinary excretion of Na, immunoreactive prostaglandin F2 alpha (PGF2 alpha) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were determined. The patients with a history of HS GN had normal blood pressure and renal function. As in the controls, the urinary excretion of PGF 2 alpha decreased and the excretion of 6-keto-PGF1 alpha increased during VE. In the patients with IgA GN the glomerular filtration rate (GFR) was normal, markedly reduced and supernormal. Five patients had hypertension and an increased NA excretion in relation to the GFR during VE. As a group, the patients with IgA GN increased their urinary excretion of 6-keto-PGF1 alpha during VE, while the excretion of PGF2 alpha did not change. In relation to the GFR, the urinary excretion of PGF2 alpha and 6-keto-PGF1 alpha was markedly increased in two patients with low GFR, which implies that these substances play a role in advanced renal disease. VE had little effect on PG excretion in these patients. In the hypertensive patients the urinary excretion of PGF2 alpha and 6-keto-PGF1 alpha was the same as in those with normal blood pressure. PGs are therefore not likely to mediate the increased natriuretic response to VE in hypertension.

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Child; Dinoprost; Female; Glomerular Filtration Rate; Glomerulonephritis; Humans; Immunoglobulin A; Male; Prostaglandins F; Water-Electrolyte Imbalance